connection3 of the cerebral cortexbrainmaps.org/pdf/krieg3.pdfconnections of cerebral cortex 269...

CONNECTION3 O F THE CEREBRAL CORTEX

I . THE ALBIKO RAT . C . E X T R I N S I C C O N N E C T I O N S

WENDELL J . S . KRIEG Institute of Neurology. Northwestern Univers i t y Medical School.

Chicago. Il l inois

THIRTY-NINE FIGURES

CONTENTS Introduction . . . . . . . . . . . . . . . . .

Connections of the several cortical areas . . . . . . . . . . . . . . . . . . . . . .

Area 10 . . . . . . . . . . . . . . . . . Area 10a . . . . . . . . . . . . . . . . . Area 4 . . . . . . . . . . . . . . . . . . . Area 6 . . . . . . . . . . . . . . . . . . Areas 8, 8a . . . . . . . . . . . . . . . Area 11 . . . . . . . . . . . . . . . . .

Areas 2, 2a . . . . . . . . . . . . . . . Areas 3, 1 . . . . . . . . . . . . . . . . Area 7 . . . . . . . . . . . . . . . . . . . Area 40 . . . . . . . . . . . . . . . . . . Area 39 . . . . . . . . . . . . . . . . . .

Area 41 . . . . . . . . . . . . . . . . . Area 20 . . . . . . . . . . . . . . . Area 36 . . . . . . . . . . . . . . . . .

Area 17 . . . . . . . . . . . . . . . . . . Area 18 . . . . . . . . . . . . . . . . . . Area 18a . . . . . . . . . . . . . . .

Insular region . . . . . . . . . . . . . Areas 13, 14 . . . . . . . . . . . . .

Area 24 . . . . . . . . . . . . . . . . . Area 23 . . . . . . . . . . . . . . Area 29h . . . . . . . . . . . . . . . . Area 29c . . . . . . . . .

Retrohippocampal region . . . . Area 27 . . . . . . . . . . . . . .

Method of study . . . . . . . . . . . . . .

Frontal region . . . . . . . . . . . . . . .

Parietal region . . . . . . . . . . . . . .

Temporal region . . . . . . . . . . . .

Occipital region . . . . . . . . . . . . .

Cingular region . . . . . . . . . . .

267 269

270 271 271 273 274 275 2 76 276 277 277 282 283 283 284 285 285 285 286 286 286 287 288 289 289 290 290 291 291 292 294 294

Area 35 . . . . . . . . . . . . . . . . . . Area 28 . . . . . . . . . Cortical amygdaloid nucleus

Connections of the thalamic nuclei

Anterior group . . . . . . . . . . . . Habenula . . . . . . . . . . . . Stria medullnris . . . . . . . . . . . Suhmedius . . . . . . . . . . . . . . .

Ventrolateral region . . . . . . . . Nucleus ventralis . . . . . . . . . Lateral nuclei . . . . . . . . . . Medial geniculate . . . . . . . . . Lateral geniculate . . . . . . . Nucleus posterior thalami . .

Subthalamus . . . . . . . . . . . . . . . . Zona incerta . . . . . . . . . . . . . . Nucleus entopeduncularis . . . Nigra . . . . . . . . . . . . . . . . . .

Mid brain . . . . . . . . . . . . . . Superior colliculua . . . . . . . . Inferior colliculus . . . . . . . . . Tegmentum . . . . . . . . . . . . . Medial lemniscus . . . . . . . . . Posterior coniniissure . . . . . .

Red nucleus . . . . . . . . . . . . . . .

Thalamo-cortical relations . . . . General results . . . . . . . .

Summary . . . . . . . . . . . . . . . Literature cited . . . . . . . . . . . . . Figures . . . . . . . . . . . . . . . . . .

Medial region . . . . . . . . . . . . .

Pretectal region . . . . . . . . . . .

. . . . . Discussion . . . . . .

294 295 295 295 295 295 297 299 299 300 300 301 303 303 304 305 305 305 305 306 306 307 307 308 309 309 309 309 309 317 326 334 336

This work was aided by a generous grant f o r the study of the cortical connections from The John and Mary R . Markle Foundation .

267

THB JOURNAL O F COMI’ARATIVE N E l W O I . O O Y . V l l l . 86 . NII . 3 J U N E . 1947

268 WENDELL J. S. KRIEG

INTRODUCTION

This is a study of the coiinectioiis of the cerebral cortex of the albino rat, based on analysis and reconstruction of hlarchi series after specific lesions. The results of such a study must be analyzed and expressed in terms of specific cortical areas if they are to be comprehensible, or applicable to experimental work 011 other species. Since the cortical areas of the albino ra t had never been studied, it was first necessary to establish critically the identity, structure and location of the several areas, to furnish a firm basis for the tract studies to follow. This basic work was presented in a recent issue of this journal (Krieg, ’46a, ’46b).

This trio of papers aims to establish as exact a picture as possible of the cortical connections in a relatively simple brain, to serve as a point of departure and a basis of comparison with cortexes of greater complexity. I n selecting the rat for this purpose, the object was not to utilize the lowest accessible animal with any considerable iieocortex, or the opossum would have been the choice. Nor was it considered necessary to ad- here to the primate line a t all costs, or a lemur or marmoset would have been used. Rather, it was desired to select a species which has some elaboration of cortical development, is accessible, easily reared and handled, standardized, prefer- ably lissencephalic and small. The last consideration is especially important when brains a re to be mounted in serial sections and reconstructed in detail. The albino rat fulfills these conditions better than any other animal. It has been used extensively by experimental psychologists in studies of be- havior, but a systematic attempt has liever been made to discover just what a re the corinectioris of this animal’s cortex. Thus the albino rat, experimentally the most favored animal, has been anatomically neglected.

The writer’s long preoccupation with the rat brain has been coiitinued despite the wide gap that separates that animal from man and the greater persuasiveness of findings in the higher primates, because the results of a close study of a simple cortex would be fundamental to an understanding of

CONNECTIONS O F CEREBRAL CORTEX 269

tlie lruinan cortex - the ultimate goal. Fo r even if we knew every neuroii of the hunraii cortex, we still would not under- stand it. Firs t it would be necessary to discover the fundamental plan by a study of a simpler brain, and then on this to lay the secoiidary fabric. The further one studies the brain, the greater is one convinced of the essential uniformity of the plan. The cranial nerve and brain stem connections are similar throughout the vertebrates, and the thalamic nuclei and the cortical areas are remarkably uniform among the niammals.

METHOD O F STUDY

Jlarchi series exclusively were used for this phase of the general problem of cortical connections in the rat. The lesions were all made with a stereotaxic machine designed for small aiiinrals. A previous paper ( '46c) described the apparatus, illustrated the basis of stereotaxic coordinates, arid described the operation in detail, so those phases of the work need not be entered upon here.

A few remarks on the analysis of the sectioiis a re necessary, however. Sections were cut at 40 p in some cases and 80 p in others, and alternate sections mounted. I n addition, every fourth section was stained with acidified thionin. Without the use of a cell stain the identification of thalamic nuclei arid cortical areas would have been impossible. The courses of the trails of Marchi granules were then studied minutely in every section. After this, the degenerated connections were reconstructed in the following manner.

Successive sections were projected at a uniform magnification, and on a single sheet the outlines of the areas containing granules in a considerable sequence of sections were plotted, together with the principal landmarks. This resulted in a closely graded set of contour outlines which modulated in position and shape through the series. Additions and alterations of the outlines were then made where necessary after reexamination under the microscope. Then, by visualizing tlie appearance such structures would have in actual reconst ruc- tions, shading, lrighliglrts and shadows were worked up in


pencil. After this the pencil cartoons were transformed into stereographic drawings in ink. The finished set of drawings were then allowed to lie fallow for nearly a year while the cortical areas of the ra t were being studied. When it became possible to identify the cortical areas with certainty, the slides and drawings were reexamined in detail and the relations of the lesions and fiber degenerations to the cortical areas added to the reconstructions. At this time a detailed description of the findings in each case was written, and, in addition, the data on each connection were transferred to cards, and the cards were classified by area or nucleus involved. These cards were used as a basis for the descriptive portion of this paper, and reference was made to the reconstructions in its preparation. The legends to the illustrations were then written. As a final check the slides, reconstructions, and manuscript of this paper were subjected to the scrutiny of 4 graduate students who examined them critically as a major part of the subject matter of a course on the albino rat brain.

The method of graphic slice reconstruction has proven a most useful research tool. It furnishes a positive method of recording and illustrating findings on all of the sections, fairs any discrepancies from section to section, allows all of the data to be surveyed quickly, establishes a positive record not prone to subjective alterations of interpretation, and permits direct ccmparison between brains.

CONNECTIONS OF THE SEVERAL CORTICAL AREAS

I n the expository part of this paper, in order to avoid a multiplicity of headings, connections of any given area will be described according to the following plan arid in the indicated sequence:

Projectional Callosal Peduncular, pgraniidal Associational Thalamic (aff'rwnt and efferent) Irit raareal Subthalamic Interareal Collicular Efferent Tegmental ARerent

CONNECTIONS OF CEREBRAL CORTEX 271

Frontal region

Area 10. Area 10 occupies considerable space and is the seat of numerous lesions. These lesions are mostly small and on account of the thickness of the cortex here they are less likely to involve the underlying fibers. Only 1 small lesion, however, is distinctly apical (GI I I ) , but a t the caudal border there is an excellent series of small lesions ranging from medial to lateral. These are, in order: GH 11, FZ I, GN 11, GK I, F N IV. I n addition there is a very large lesion which cuts off all of the dorsal part of the frontal pole, but except for an involvement of the extreme of area 2, is nearly confined to area 10. Area 10 is also involved in 1 very extensive lesion (FR 11).

Immediately on leaving the cortex the projection fibers begin their caudal course, but they make a short lateral jog as they pass through the medulla. Fibers from the more lateral part of the lesion make a wider diversion within the medullary center. These fibers can be clearly seen in normal preparations. Even the medial fibers jog laterally and not medially as might be expected considering that they arise medial to the medial surface of the striatum. Since the medullary center forms an outer covering for the striatum the fibers then course through the striatum, always in the form of distinct and separate rounded fascicles surrounded by the substance of the caudate. The rat differs from many mammals, particularly the higher ones, in that the capsule is not sandwiched between caudate and putamen, but rather threads through the conjoined caudate-putamen. In spite of the fact that this arrangement is not truly capsular here, the portion within the caudate will be regarded as a part of the internal capsule in order to bring it into homology with the nomenclature of other animals. Even very small lesions (GH, GF) send fibers into several fascicles where they are apparently mixed with fibers from neighboring regions. These fascicles are rather individual through the length of the striatum but they blend and recombine to some extent, as is evident in a horizontal section through the basal part of the cerebrum. They keep their discrete arrangement in spite of this regrouping and there is little tendency to scatter. Their course, once in the caudate, is almost in the'sagittal plane. As the capsule becomes more compact at the caudal end of the caudate nucleus these fibers gather into its medial part, which is the first to become com- pacted. They are not the most medial or even the most dorsal of the fibers in this region, however, as might be expected, but rather are central at first (GI 11, GP I ) . As the cerebral peduncle becomes complete, fibers are seen to occupy the central part of the first or medial fifth. As the midbrain is reached, however, the fibers become rearranged by passing ventrally in the peduncle in the form of broad,

2’72 WENDELL J. S. KRIEG

palisade-like fascicles alternating with fascicles of other nature. As a result of this they attain .the ventral surface of the medial fifth, but it seems that nothing else is gained from this rearrangement (GI 11, G H 11, GK). Projection fibers may be followed past the nigra where they reach both deep and superficial surfaces of the peduncle, thence into the pons where they occupy the medial of the 2 pontile pyramids and are concentrated at its medial extreme. The fibers may be traced into the bulb but are scattered evenly through the bulbar pyramid. (There is no local topology within the bulbar pyramid.) Their further course has not been traced in this study.

Area 10 has a very strong callosal connection and seems to be rather definitely homeotopic, though the distal part of callosal degeneration is always faint and not easy to distinguish from such adventitious degeneration as there may be. At the medullary center fibers destined f o r the callosum diverge medially and backward from the laterally directed projection fibers. They are thus carried toward the anterior forceps of the callosum, gradually attaining the transverse plane, crossing, and bending forward again to the corresponding position on the opposite side. The callosal fascicles are quite distinct and limited in their position through their entire extent and have a location in the callosum which reflects their exact cortical origin. The fibers from the pole (GP) course back over the dorsomedial surface of the apex of the striatum and form the extreme fibers of the rostrum of the callosum. I n spite of the large size of the lesion of GP, a t the crossing the fibers are confined t o an extent of about 0.2 mm. The more rostral fibers are rostrally placed in the callosum and the more caudal fibers are situated caudal to them; the crossing fibers from GH 11, GK I, GN TI, F N IV being placed conGderably behind the rostral extreme of the callosum at level 59-59.4.?

It is interesting that at no point in the course of the projection fibers from area 10 can any divergent fascicles or components be seen. This is unusual for an area of this size. Ordinarily there is degeneration toward and within the thalamic nucleus which sends fibers to any particular area, but there is no thalamic degeneration in this case. It is well demonstrated that the medial nucleus sends fibers t o area 10 (GN I a and b, GU I1 f, F T I11 h, HH 11 c ) . This fact is established from thalamic lesions. The details will be discussed along with the medial nucleus. The theoretic significance of the absence of retrograde degeneration will be taken np in the discussion section of this paper. I n addition to the well established demonstration

“Levels” indicated in this work are traiisverse levels of the rat br:iin iii the stereotaxie macliiiie illustrated in Krieg ( ’46e)


of fibers from the medial nucleus 1 experiment (GX I1 b) demonstrates the presence of numerous fibers from the nucleus ventralis dorsalis to area 10.

Area 10 seems to receive numerous association fibers from area 2, since in extensive lesions of area 2 intracortical granules niay be traced throughout area 10 (FU I1 r ) .

Area 10a. This area was not distinguished in paper I, A, but is now recognized as a separate division of area 10 corresponding to its medial portion, paralleling area 24. The subdivision of the frontal area was recognized by ltose, area 10a forming the precent ralis agranularis and area 10 the precentralis granularis. The histological differentiation will not be entered into here, but the lesions involving this area will be summarized. Four lesions are specific to area 10a. None of them involves the underlying fibers and all are sniall ( F Z 11, GA 11, GF TI, HA I ) . GA involves less than half the thickness of the cortex but nevertheless produces the same degeneration as do the other lesions; H A I is the most medial and rostral; G F is the most caudal. In addition GH 11, a small lesion, straddles area 10 and area 10a; while GA I1 encroaches on area 10a.

The projection fibers are numerous and run a long distance. T1ii.y run diagonally laterally through the medial thick part of the medullary center but do not make as sharp a jog as the fibers from area 10. On reaching the dorsomedial edge of the caudate they pass through it in the form of discrete fascicles in an arrangement similar to that from fibers of area 10. They run almost precisely in the sagittal plane along the medial edge of the caudate, dropping ventrally. In the compact part of the internal capsule (FV JI, H A I a ) they lie in the medial quarter but are not the most medially placed. Instead they lie in the dorsomedial part of this quarter. I n the peduncle they reach its ventral aspect by fascicles which interdigitate with those of other nature, but Beep their medial position. They can be traced through the pontile pyramid where they occupy its medial extreme and into the bulbar pyramid where they become disseminated. Like the fibers from area 10, these projection fibers give off no visible connections to the thalamus, but in HA numerous fibers leave the tract a t the level of the rostral end of the mammillary body passing dorsally past the nigra and may be traced as far as the medial lemniscus, but are lost beyond this, so they probably terminate in the tegmentum of the midbrain. However, this lesion was the only one which encroached on area 24 and such fibers may actually come from area 24.

Area 10a sends numerous callosal fibers to the corresponding region of the opposite side. The callosal fibers diverge canclomedially


to become involved in the anterior forceps. The fascicles are very circumscribed and occupy precise positions within the rostral end of the callosum. They are distributed a t various levels depending on the position of the cortical area from which they arrived. Thus the fibers from HA, the most rostral lesion, begin at level 60.5, those of FZ are found at level 60, of GH a t 59.4, G F at 59, and GA a t 57.2, thus making a spread of over 3 mm within the callosum. All of the fascicles involved lie on the dorsal surface, indicating that there are no callosal fibers from area 24.

Area 10a receives fibers from the nucleus medialis in all of its parts, but not from the anterior nuclei. This is a rather difficult matter to ascertain since usually, when one of this group is involved the other is also. There is some evidence that the anterior nuclei contribute to area 10a (FS 11, FU I h ) , but in each of these cases the medial nucleus was slightly involved. At least, the greater portion of the anterior nuclei pass to the cingular region. The main part of the medialis shows connections to this region in F T 111 h, F U I h, G?: I c, and GS I1 lr. The posterior part of the medialis shows connections here in FO TI1 and IV m and GQ I b. The pars lateralis of the medialis sends fibers t o area 10a in HH 11. Apparently no other thalamic nucleus is suspected of sending fibers here, though i t is not impossible that parataenialis or reuniens contributes.

Area 4. The motor area is involved in 6 examples. Four of these (GH I, G F 11, HI1 11, GR I ) are electrode track lesions but on account of the narrowness of area 4 are adequate to damage a considerable proportion of it. G F I, an extension of an electrode track lesion, involves widespread damage in area 4 almost coextensive with its main part, but most of it is very superficial and is not accompanied by as much degeneration as would otherwise be expected. GI I is the most useful for study of the projection tract because it is massive, but it reaches the medulla and slightly undercuts area 3, consequently the degeneration in the callosum in this example must be discounted. In addition there is a minute shallow nick in area 4 in the opposite side of G F which only enters layer ii, nevertheless it is possible to trace a trail of granules into the fascicles of the caudate. This would indicate that some projection fibers have a supragranular origin.

The projection fibers may be seen in all of the examples, even from the small puncture wounds, and the impression is gained that area 4 has a heavy projection tract. In all of the cases the fibers are seen to diagonal through the medullary center, gaining a more lateral position. As soon, however, as they reach the caudate they turn directly ventrally and keep in the same sagittal plane throughout


the extent of the capsule. At first they are dorsal in the middle third of the extent of the caudate, but they migrate ventrally keeping a medial position and take up a position deep in the second fifth of the definitive capsule and peduncle. Their course is best seen in GI I. Within the peduncle they migrate to a ventral position, still in the second fifth, by means of coarse fascicles interdigitating with non- degenerated fibers. This position is maintained as the capsule flattens to clear the nigra, but beyond the nigra the more medial fibers either become lost or integrated with this group, so that they occupy the medial fourth of the lower end of the peduncle. I n the pons the tract is still strong and occupies the medial half of the pontile peduncle. It can be traced into the bulb. Oblique penetrating electrode tracks show that fibers take origin a t least halfway out in the cortex (GH I, GR I ) . There is no evidence that fibers are given off to any part of the thalamus or midbrain. The course of the tract in the bulb has not been followed. There are apparently no callosal connections.

There is no clear evidence that area 4 receives projections from any thalamic nucleus. Thalamic injuries which resq4t in scattered grannles through the dorsal part of the medullary center will also show granules underlying area 4, though this is usually the medial extreme of their extent. Thus, FH I1 k, G S I1 g after lesions to the ventral nucleus and FR I h aftpr an extensive injury in the region of the medial group of thalamic nuclei, indicate the possibility of fibers entering area 4. As was noted in paper I. B., p. 281, area 4 is poor in fibers and such radial fibers as there are do not extend into the supragranular layer. This perhaps is evidence of the meagre thalamic connections.

It was imagined that area 4 would show numerous association fibers from the parietal cortex, but such have not been forthcoming. Large parietal lesions adjacent to area 4 show no evidence of granules passing into the area in question

Area 6. This area is difficult to distinguish from its neighboring areas, consequently is difficult to locate in experimental series. I ts narrowness precludes its being the subject of a specific and inclusive lesion. The only example of a nearly specific lesion is GR 11. Though slightly impinging on area 2 and thus involving a faint trail of granules into the ventral thalamus this is a purely cortical involvement of the area. The fibers diagonal markedly through the medulla. The tract passes ventrally through the caudate nucleus in separate fascicles (GR I1 c) and takes its place near the deeper aspect of the

( F U I, F U 11).

a Ward et n7. ('46) have found only a restricted aniount of firing into area 6 under experimental strychnine stimulation.

276 WENDELL J. 6. KBIEQ

mid-part of the internal capsule. Fibers continue into the peduncle. lying in the niiddle of its dorsoniedial par t but cannot be followed below that level in this example because of adventitious degeneration. It seems rather clear that there is a callosal connection from area 6 (GR I1 d ) since the lesion does not approach the medulla. As with area 4, there is some evidence that thalamic lesions leave granules here, as for example FX I1 where cingular fibers from the anterior nucleus seem to extend to area 4, but i t is not possible to make definite conclnsions on the material a t hand.

Sreas 8, 80. Area 8 has not received a specific lesion in any case in this series. Its caudal part has been involved in a very estrnsive lesion of the lateral cortex, but this demonstrates little for this area except that it can have but a n insignificant contribution to the internal capsule since no granules are observable i n the underlying fiber bund1t.s which trace into 8. 8a is too small and linear to expert any specific lesions unless specially attempted. The rentrolateral aspects of the frontal lobe deserve further exploration.

On the other hand, i t is possible to make some very specific statements about the thalamic connections of this area. I n F O there are 2 nnusually specific circumscribed lesions of the nucleus parafascicularis of both sides. The projections from these nnclei can be clearly traced forward to the anterior thalamic radiation into the internal capsule and the medial par t of.the caudate to emerge from its extreme pole and its immediately contiguous ventrolateral aspect. These fibers, once in the niedullary center, tu rn sharply laterally and enter area 8 where the granules are quite numerous and may be traced fa r out into the cortes. They may go to area 8a too, but this is rather unlikely. At least they do not pass to area 10. In G F I, which injnres thr nucleus anterior ventralis and the medial part of the ventralis. the fibers from the parafascicnlaris arc probably severed also. A t any rate a similar tract can be traced forward, par t of which ends in area 8 almost as precisely as in the previous case. I n GIJ I1 f and in G F I e and F T I11 there are distinct fibers to 8a after thalainic lesions which hare in coininon the destruction of the nucleus snbrnedius (ovalis). Since this nucleus is not injured i n any other lesion and no other? send fibers here, it is reasonable to assiime the nuclens submedius is the chief nucleus of projection to this narrow strip of cortex.

Arm 11. Thongh this area is a sniall and hidden one and a specific lesion would be difficult to obtain, nevertheless an interesting obserration has been made with regard to its thalamic connections, for in G F I f there are abundant granules within the confines of area 11 cmanatinp from a thalamic lesion, involving particularl>-

CONNECTIOXS O F CEREBRAL CORTEX 277

the anterior ventralis, ventralis medialis parvocellularis, submedius, and blocking fibers from the medialis and parafascicularis. The anterior ventralis fibers are adequately taken care of by component g to the cingulum, leaving the other 2 nuclei directly involved as potentially sending fibers to area ll. The projection of the ventralis medialis parvocellularis seems to be demonstrated in OT I1 leaving, by subtraction, the nucleus submedius to supply area 11. This will be further discussed in connection with the thalamus.

Parie t a 1 region

Areas 2, 2a. These areas together form the largest unit of snb- division of the cortical areas and consequently have received numerous lesions, 12 in all. One of these (GU I ) is a sub-total and nearly specific lesion of area 2, although the underlying medulla is involved. FR I1 is a very extensive dorsal lesion which involves the upper half of area 2, while HD is a very extensive lesion implicating the lower half with area 2a. The other lesions are manageably small and localized. For purposes of description they may be divided into 3 classes : the rostromedial part includes GO, FO I, GQ I1 j the rostro- lateral part is involved in GM 11, GV I1 ; the caudomedial part in GW, F U 11, and GW I. There is no caudolateral quadrant since this is occupied by area 40. 2a, which cuts into the ventral part of 2, is the seat of a specific lesion in GVI.

I n view of the large number of lesions involving area 2, perhaps the most reasonable approach to their analysis is to describe the findings in GU where the entire area is destroyed and then to modify and extend this description from the other cases.

The projection system is quite massive, occupying a large part of the capsule and converging in the peduncle to the superficial half of its middle third. I n the lower part of the midbrain as the peduncle is flattened to clear the nigra this tract changes its shape to correspond. It passes into the pons and many of its fibers reach the pontile nuclei. At 2 places in the downward course there are components which diverge from the main tract : to the thalamus and to the tegmentum. The component to the thalamus (GU b) is quite massive. It begins to leave the tract near the anterior end of the thalamus, thus participating in the superior thalamic radiation. These fibers run in a diagonal direction to the nucleus ventralis occupying the coarse fascicles seen here. They quite completely fill this nucleus, except in this case its caudolateral part (the lesion did not involve the caudal part of area 2) . Both dorsal and ventral parts of ventralis contain granules but in the ventral part they are thickest. They do not extend beyond the ventralis or go to any other nuclei, but there is

278 WENDELL J. S. KRIEQ

every indication that the cells of the ventralis are connected with area 2. The tegmental radiation (GU c) diverges from the deep aspect of the tract a t level 53, the fibers running straight dorsally and caudally so that they keep in the lateral part of the tegmentum between the medial geniculate and the superior colliculus. They become lost here, indicating connection with the lateral nucleus of the tegmentum.

Of the projection fibers from the 3 lesions in the rostromedial quadrant GO is the most rostromedial. The small size of the lesion and its specificity furnishes a good basis for the study of the extent of scatter and the localization of this part of area 2 in the projection system. Only 4 or 5 of the coarse fascicles within the caudate contain granules, and in the internal capsule they are confined to the second fifth, but are scattered within this division. I n the peduncle they tend to scatter through the medial third, and in the pons they are widely disseminated through the pontile pyramid. GQ 11, a small specific lesion in the dorsal part of area 2 at the junction of the first and second thirds, sends off a distinct projection system, the fibers of which jog laterally as they pass through the medulla, the lateral ones more so than the medial ones. They gather in the lateral part of the caudate, form a circumscribed area in the middle of the superficial part of the capsule and peduncle and may be traced through the pons. The thalamic component of GQ branches off the capsular fibers a t the level of the anterior end of the ventral nucleus and a distinct group of fibers wends its way into the central part of the ventralis ventralis. They run caudally a considerable distance within it, gradually working their way toward the ventralis dorsalis. Some cell degeneration is seen outside the fascicles. The degenerated region is in the form of a long cylinder running practically the entire length of the ventralis. The tegmental radiation was not observed in this case. F O is a small shallow lesion which allows the degeneration to be traced only through the capsule. Nevertheless, it can be observed that the fibers jog distinctly laterally as they pass through the medulla and then take a downward course through the lateral part of the caudate. They are lost below this level. GV I11 is a t the rostroventral corner of area 2. The initial course of the fibers from this lesion is medially and caudally, so that a t first they lie in the horizontal plane. On being gathered into the compact part of the capsule they run directly caudally, lying in the superficial half of the second fifth of the capsule and peduncle (GV f ) . The thalamic fibers jog medially as they pass through the reticularis and enter the ventromedial part of the nucleus ventralis ventralis. They may be traced a considerable distance in this position (GV g) . GM is in


the middle of the rostra1 part of area 2. The lesion itself is small, but it involves the medullary center, which undercuts the region out- lined. The projection tract occupies approximately the middle of the caudate nucleus and in the internal capsule is in its superficial half, within the middle third. A t the upper end of the peduncle the bundle breaks into fascicles, alternating with fibers of other nature, but they maintain their superficial position. The thalamo-cortical connections take the oblique course through the reticularis already signalized, run through its entire longitudinal extent in the large fascicles of the medial third of the ventralis ventralis. Further caudally they extend into the medial third of the ventralis dorsalis also. Cells in this region are definitely fainter in thionin stains, .indicating retrograde degeneration. There is a distinct tegmental radiation, fibers coming off rostral of the nigra and passing far dorsally into the tegmentum. Two additional tegmental connections were observed in this case, to the nucleus entopeduncularis and to the nigra. The nucleus entopeduncularis lies within the region of the capsule which is occupied by projections from area 2. Distinct fine granules could be seen passing among the cells of this nucleus, particularly in its lateral part. Within the nigra there are 2 groups of fibers. The upper is composed of fine granules and the lower of coarse granules. Both converge on the lateral portion of the substantia reticulata of the nigra, so that it becomes heavy with granules, though the surrounding region or the opposite nucleus is not affected.

The lesion in GW 1 is a double one consisting of a small and a very small lesion separated by about a millimeter, both of which are in the posterior part of area 2. Through the caudate the fibers from each lesion are distinct. They jog laterally as they pass through the medulla and ea&h occupies a group of fascicles within the nucleus. At the compact part of the capsule they are indistinguishahle. From the combined bundle there are 2 distinct thalamic radiations. The upper one (b) leaves at the level 56.5 and goes into the ventralis ventralis in the dorsal part of its central region at 54.5. There is a definite cell loss to the area supplied. The lower thalamic radiation leaves at 54.7 and enters the middle of the ventral nucleus. Its course within the nucleus cannot be easily traced, but with respect to the upper group of degenerated fibers it is ventrolateral and caudal. The upper part belongs to the medial lesion which is closely adjacent to area 1, the lower group to the ventral part of the lesion adjacent to area 40. Thus, dorsal in the-cortex is represented dorsally in the thalamus, ventral in the cortex ventrally in the thalamus. The main projection tract can be followed into the pons as 1 bundle. The peduncular fibers are located in the superficial part of the fourth fifth, that is they are more lateral than the fibers previoudy considered.

280 WENDELL J. S. HRIEG

F R is a very extensive lesion which includes a large part of the frontal half of the dorsal cortex. As far as area 2 is concerned, however, it involves the rostrodorsal half. A large proportion of the capsule is filled with granules, approximately the medial two-thirds, and granules pass to a considerable number of the thalamic nuclei. As far as the ventralis is concerned, however, only its ventromedial third contains granules. This is in line with our previous observations on localization, and i t is possible now to make the statement that the rostra1 part of area 2 is represented medially in the ventralis, the caudal part is represented laterally. The relation of the thalamic fibers then is a simple and direct one and demonstrates that they run parallel in the thalamic radiation. A point for point relationship between ventral nucleus and area 2 is indicated by these experiments.

HD is another extensive lesion which involves most of the lateral part of the cortex. In area 2, however, i t injures approximately its ventral half. Considering the size of the lesions the degeneration in the peduncle is not as large proportionately as that in FR. I t is, however, more lateral and continues into the pons. The connection to the ventralis is interesting because it seems limited to the ventrolateral part of the ventralis ventralis. There is a distinct anterior component (g) which jogs far medially and enters the medial part of that nucleus, and a large lateral one (h) which goes to much more than the ventralis but as far as this nucleus is concerned enters on its lateral surface and is distributed to its ventrolateral part, though it passes deep in the nucleus. Its origin is in all probability from the region of area 2 because i t clearly comes from the dorsal part of the large lesion. FR I1 and HD I, though they are the most extensive lesions in the series, furnish valuable facts in the analysis when carefully reconstructed. They corroborate the evidence that the dorsal part of area 2 is represented dorsally in the nucleus ventralis ventralis, and the ventral part is represented ventrally.

It is questionable whether area 2a should be distinguished from area 2. The only lesion which involves 2a specifically is GD I. This sends a projection into the capsule and has a thalamic radiation, but its fibers are so close to those of lesion I1 that it is impossible in this case to separate the thalamic connections of the 2 lesions.

All of the lesions involving area 2 show definite callosal connections, as far as can be discerned, from the lesion to the homeotopicl region. I t is difficult in tracing callosal fibers to determine whether the area supplied is slightly larger than the area giving origin to the fibers, but any sort of aberrant fascicle would be easily discovered. There is a precise topology in the arrangement of the fibers within


the callosuni in that fibers from the rostral part of the area cross near the rostrum of the callosuni and take a distinct backarcl course to contribute to the anterior forceps. Observations are on hand to show that the fibers cross from plane 59 back to plane 56.5. These figures are approximate. The more dorsoniedial parts of the area send their fibers more dorsally in the callosum; the more ventral parts send them more ventrally, in fact they are among the most ventral fibers of the callosuni. I n GW, where there are 2 lesions close together on the same side, there are 2 separate callosal fascicles placed a t distances corresponding to the separation of the lesions (GW c, f ) . I n F O I, where the lesion is supragranular only, there is, nevertheless, a callosal .connection, giving some indication that callosal fibers may arise from layers ii and iii. Other observations have shown, though, that lesions restricted in depth must be interpreted very cautiously with regard to statements concerning level of origin of fibers.

There are 5 thalamic lesions which send fibers in considerable number to area 2 (GS 11, CX 11, GY 11, GZ I1 and HA 11). Three of these (GS, GX, GZ) involve parts of the ventral nucleus. GS involves the middle 2 quarters of the nucleus and projects to the dorsorostral end of area 2. GX involves the ventralis dorsalis and sends numerous fibers to the rostral end, but a sprinkling to all of area 2. GZ involves quite precisely the vrntromedial end of the nucleus and the rostroventral end of the cortical area. These observations do not add to the localization as seen from cortical lesions, but they do not con- trovert them. There is some indication that the ventralis dorsalis has a generalized distribution to area 2 rather than a localized one. Of the other 2 lesions one is to the posterior thalamic radiation sending fibers to a diagonal area along the dorsolateral aspect of the cortex and including some of area 2, while the other (HA) implicates the lateralis dorsalis and seems to spare the ventralis. Nevertheless, i t sends fibers to the caudomedial par t of area 2 . The significance of these last 2 cases cannot be appraised with the material at hand, but since the lateralis dorsalis contributes largely to the posterior radiation there is an indication that that nuclens also sends a few fibers to area 2, but that the ventralis in both its parts has a strong and topical projection to area 2.

Not many of the. cortical lesions are extensive enough to show cortical association fibers. F U 11, a large lesion, is the most informa- tive in this regard. I t shows numerous intracortical fibers passing backward to area 7 and forward to area 10 with a few laterally to area 40. I n addition there are numerous association fibers within area 2. This lesion involves the medullary center, consequently it is impossible to rule out the presence of backward running thalamic


fibers disturbed in the lesion, but those cited are from trails of granules whose course is entirely intracortical and have a different appearance from thalamic projection granules. In addition there is a contribution to the cingulum running its entire length, but it is quite possible that this is a thalamic connection to the cortex. HD interrupts dorsally running intracortical fibers which would almost have to come from the insular region (€ID a ) . In addition to this there is an interrupted intramedullary lamina which may come from the insula or from area 2 (HD b) which runs diagonally backward ending in areas 3 and 4. H E I, which is a specific lesion to area 40, sends association fibers dorsally into parietal area 2 along with 1 and 3 (HE I c). GV I11 j exhibits granules in area 2 dorsal to the lesion, indicating the presence of dorsally running intraareal association fibers. Considering the size and number of the lesions of area 2, however, it must be said that there is little evidence of inter- or intraareal association fibers. To study this problem specifically planned lesions would be necessary, or other methods must be resorted to since such fibers may be poorly myelinated and show up only by other methods.

Areas 3, 1. There are no impeccable lesions of areas 3 or 1. In each case they are involved as parts of a larger lesion. FU I involves area 3 at the surface but it undercuts area 4, whose fibers pass obliquely under area 3 anyway and are so numerous that they vitiate the results. G V I I involves area 3 but extends into area 4 and a considerable distance into areas 7 and 18. F R is a very extensive lesion including area 3. However, from the fibers from the anterior part of area 3 in GV I1 the projection fibers can be traced. They run diagonally lateralward and forward for a considerable distance in order to clear the hippocampal commissure. Having done so they bend slightly medially on assuming a descending course, and then keep pretty well in the sagittal plane. It is unfortunate that lesion I in area 2a sends its fibers so close to these fibers. They become fused, but the group passes down the brain stem. There is a very marked thalamic radiation, but it is possible to trace continuity between these granules and the granules from the lesion in the lateralis dorsalis, thus vitiating these results too. Hence in each case involving lesions of area 3 we are defeated in attempting to build up the picture. I n thalamic lesions it is not entirely clear which nucleus is most closely related to area 3. Lesions of the anterior part of the lateralis (FN, G X I I , G Z I I ) show projection fibers running around the anterior end of the hippocampal arch on the most inside curve. These (GZ I1 f ) run under area 3 and some may end there, but the actual observation is obstructed by the fact that in each case there is damage to area 3.


Lesions of the posterior part of the lateralis (HA 11) do not show granules further forward than area 7.

Area 7. There are 3 good lesions of area 7 ( F N I, GX 11, H A IT). The evidence presented by all of them is consistent enough t o allow a single description for the projection fibers. On leaving the cortex they pass about 2 nim laterally t o clear the arch of the hippocampus, then they bend ventrally and caudally, migrating medially in the posterior part of the internal capsule and in the peduncle they form scattered fibers within the fourth fifth. I n each case they disappear in the upper part of the peduncle and no radiations may be discovered passing into the tegmentum or elsewhere. No connections with thalamic nuclei have been observed after cortical lesions, but in GX I1 and H A 11 the field is confused by the presence of degenerating fibers from a thalamic lesion. There is a small callosal component at level 56.5 in HA. This component is small and in the other cases callosal fibers have not been observed. After a direct injury to the posterior thalainic radiation fibers have been seen passing to area 7, and other areas (GY 11). I n F O there are 2 nearly symmetrical lesions in the cortex which involve parts of 7, 29c and 18. I n F O I V area 7 is involved to a greater extent than in F O I11 and it has connections with the nucleus lateralis thalami, while F O 111 has not. The projection fibers from this lesion have a broad extent as they curve around the hippocampal arch. Those labeled c are from the forward end where area 7 is located. Those labeled d, not so numerous, are from the caudal end. I n an extensive lesion of area 2 ( F U 11) numerous association fibers are seen passing backward t o area 7 ( q ) . 4

Area 40. There are 2 specific lesions of area 40 (GW 111, HE I ) . GW shows a large amount of adventitious degeneration, but the latter is excellent €or the study of connections. I n neither case does the lesion involve the medullary center, except for a tiny extension, less than 0.1 mm diameter, under HE I. The following description is taken principally from the findings in HE I . The projection fibers are numerous and occupy the large fascicles in the caudodorsal part of the caudate. These pass medially and ventrally to join the posterior part of the compact capsule. I n the peduncle these fibers converge to its lateral third, occupying alternate vertical fascicles. There are a few thalamic fibers which run into the lateral extreme of the ventralis a t the middle of its longitudinal extent. At the level of the rostra1

‘ I n paper I.B, p. 285 the description of area 40 was wrongly repcated in the first paragraph on area 7. Hence the next to last paragraph on p. 2885 of that paper is t o be deleted.


end of the lateral geniculate there seems to be a dorsal outflowing to the zona incerta. At the caudal end of the thalamus there is another distinct dorsomedial outflow past the medial geniculate body and into the lateral tegmentum (not reconstructed). This outflow continues into the level of sections through the nigra passing into the tegmentum below the superior colliculus. Some fibers possibly contribute to the posterior commissure. Fibers within the peduncle may still be traced at the pontile level where they are distributed to the lateral half of the pontile pyramid. The same general findings characterize the lesion in GW, but another injury to the medial lemniscus has introduced granules in the ventral nucleus and the tegmentum obscuring any divergent fibers. In GX I1 b granules were seen in area 40 after a lesion to the nucleus ventralis dorsalis and apparently coming from its lateral part. I n GY I1 where the posterior thalamic radiation was severed area 40 is included in the widespread distribution of intracortical granules, but here they are not dense.

Area 40 seems to be rich in interareal association fibers. There are numerous connections dorsally within the cortex to the parietal areas 2, 1 and 3 (HE c) . Another group passes caudally and dorsally ending within area 17 and extending as far as area 18 in the retrosplenial region (e). The tiny medullary prolongation of the lesion injured a distinct fascicle (d) sending fibers a long distance caudomedially to area 29. This may come from the more ventral lying cortex (14, 13) or from the thalamus. The large injury to the parietal area in F U I1 demonstrates the existence of association fibers to area 40 ( r ) .

Area 39. The only lesion which involves this area specifically is F R I , but part of 18a is also included. There are numerous lesions of Ma, the connections of which can be rather well integrated. By comparing the degeneration from this lesion with other lesions involving 18a it is possible by subtraction to determine the probable connections of area 39. There are clearly projection fibers running forward parallel and just inferior to those of 18a. They turn into the capsule a t the posterior part of the arch of the hippocampus but they are separate from those of 18a, passing through fascicles in the dorsal part of the putamen. Keeping more ventral as they turn they become more lateral in the peduncle and soon branch off dorsally to enter the medial geniculate (FR I e) . No other lesions involving 18a sent fibers to the medial geniculate. Whether o r not the fibers continue in the peduncle cannot be determined in this example. Con- sidering its closeness to area 41, i t seems appropriate that, area 89 should have auditory connections.


Temporal region.

Area 42. Lesion G U I I I is a complete and exclusive involvement of the auditory area, 41. It does not injure the medulla. HH I is a shallow and incomplete lesion, but the description here will be based chiefly on GUII I . There are numerous projection fibers passing horizontally or obliquely through the caudal extreme of the putamen in large separate fascicles. They join the lateral extreme of the peduncle and continue in this position to the level of the medial geniculate body where they stream out dorsally as separate fibers. They do not enter the geniculate body, but clear it caudally, continuing caudodorsally for a long distance to enter the inferior colliculus, concentrating particularly in its outer fibrous covering. They end in the colliculus (m). Another bundle (n ) corresponds to the thalamic component, but it has a short course in combination with the projection fibers and it curves around the posterior extreme of the hippocampal arch to enter the posterior thalamic radiation, then runs directly caudally to the lateral geniculate and expands and breaks up to enter the medial geniculate from its medial and rostra1 aspect. There is an extensive but thin callosal component (p) which occupies most of the inferior part of the posterior half of the callosum. HH does not show the thalamic or callosal components, which suggests that these have an origin deep in the cortex. There is a distinct dorsocaudally running association lamina passing chiefly to 18a but continuing in reduced form under area 17. This lamina runs obliquely caudomedially so that points in area 41 project to points dorsocaudally of i t in area 18a. Area 41 also receives fibers from area 18 (or from 29c) as shown in HD I1 a. Projection of the medial geniculate body onto area 41 is clearly demonstrated in several cases (GY 11, HB I1 and HC 11) in which the geniculate or the beginning of the auditory radiation has been damaged by a specific lesion and the auditory projection has been shown to coincide with the extent of area 41. It was the establishment of this region as the true auditory cortex that served as the positive basis for renumbering of the cortical areas in this part of the brain, as compared with Brodmann and Rose. The details of the auditory radiation will be studied in connection with medial geniculate body.

Area 20. Area 20 is involved along with a part of 13 in GT 111. There is a distinct though weak projection system (GT 111 g ) which runs forward for a considerable distance in the medullary center and then crosses through the inferior edge of the putamen in its caudal part. These fibers are among the most caudal and inferior of the internal capsule. If area 20 is accepted as the forerunner of the temporal lobe, this is the homologue of the infralenticular capsnle.


The fibers enter the peduncle in the fourth fifth and, it is perhaps significant, not in the most lateral part. The tract is slight and cannot be followed far. There is a surprisingly large callosal component which runs backward and upward through the medulla curving broadly around the caudal end of the hippocampus to turn forward again in the retrosplenial region to form some of the most posterior fibers of the callosum (GT 111 h) . This represents the tapetum of the callosum which is destined to receive such a large development in man. HH I involves area 20, but the lesion is shallow and it shows no projection fibers, although there are numerous fibers from the adjacent area 41.

Area 36. GT I is a subtotal destruction of area 36, though it includes a little of area 35. GX I is a lesion about 0.5 mm in diameter which only goes through the supragranular layers. I n spite of the insignificance of the lesion and the undifferentiated cytology of this area a few fibers may be traced radially through the cortex to the medulla, then turning forward in the center, indicating that they are directed toward the capsule. In the larger lesion (GT I ) , however, there is a considerable forward running lamina of fibers in the medulla which turns medially in the posterior extreme of the putamen, occupying several of the large fascicles there and then turning caudally as extreme caudal fibers of the internal capsule and entering the lateral edge of the peduncle, to be directed downward and then to be lost a little below. This finding is of interest because area 36 is one of the least differentiated areas in its cytology, and yet it shows a well-marked projection tract into the peduncle, giving additional basis for the generality that nearly all of the cortical areas project into the peduncle. I n HB I1 d, where the auditory radiation and little else is damaged, while the great proportion of fibers end in area 41 some of them pass to area 36 (HB I1 g ) .

Occipital region

Area 17. The visual receptive area is large and is the seat of 5 small specific lesions in this series (FT I, FY 11, GY I, HB I, HF, not illustrated). It is involved with 18 in H C 1 and with 18a in HE 111, HD 111, F Y 111 and GS I.

I n each of the 5 examples of circumscribed lesions to area 17, as well as an additional case (HG I) where the medulla was damaged at the posterior extreme of area 17, there is a band of fibers running forward and ventrally for a long distance to curve around the stria terminalis and the hippocampal arch and enter the lateral fifth of the peduncle. These fibers form a discrete flat band in the medulla and the course in the various examples indicates that they are part


of an extensive radiation which centers a t the lateral side of the peduncle. This can hardly be the optic radiation since it enters the peduncle and not the thalamus. I n none of these small lesions can the fibers be traced any considerable distance. In F Y 111, where 18a is also involved, fibers in this position can be traced into the posterior thalamic radiation and toward the lateral geniculate body ( j ) . These are separate from a more dorsal group which runs also toward the lateral geniculate body, but has the position and appearance of true thalamic radiation fibers. There are definitely 2 components here, the j fibers probably coming from area 18a since none of the optic fibers previously observed went through the putamen. Thus the h fibers are probably from area 17.

There is no evidence that area 17 has a callosal connection as none of the pure lesions show it. F T touches the medulla a t one point, which vitiates the finding of callosal fibers. All of the specific lesions are small, however, and a larger one may bring out such connections.

There are association fibers to the visual cortex. In the large lesion H D I, a definite fascicle (d2) within the medulla ends in the medial part of 17. This may of course be from regions ventral. I n HE I c a tiny involvement of the medulla caused degeneration of a tract to area 17. This could come either from area 40 or below.

In this series there is no lesion of the lateral geniculate body to demonstrate the course of the optic radiation. It is possible, however, that the visual area should also receive fibers from other thalamic nuclei. In HA 11, where the lateralis posterior is destroyed, there are granules in the cortex of area 17 directly traceable to the lesion.

Area 18. Area 18 is involved in 8 lesions. Four of these ( F O IV, F U 111, G U I I , H D 11) are nearly or quite confined to this area. HC I impinges on area 17 slightly. GX I11 is combined with the caudal extreme of area 29, while F O I I I and FUIII include also parts of areas 3 and 7. All lesions show a thin laminar tract running forward and laterally f o r a great distance in the medulla under area 17 to reach the dorsocaudal part of the hippocampal arch ( F O I V c and d, F U I11 s, G U TI j, HC I e, HD I1 w). At that point they divide into 2 groups, at least in some examples. The ventral group entms the most lateral fifth of the peduncle on curving around the stria medullaris and fornix, and lies in the deep half of that segment. Within a very few sections, however, it streams dorsomedially almost bodily out of the peduncle (FU I11 t, HC I e) . The former example shows that they turn dorsomedially into the tegmentum so that they reach its dorsomedial quadrant. These fibers are gathered up and redistributed in the posterior part of the ventral nucleus. Some may enter lamina iv of the superior colliculus. The granules in-


volved in this degeneration are always more minute than most granules participating in the peduncle. The other division of the projection tract from area 18 makes a sharper t u r n which places it more dorsally on the hippocampal arch and is in the form of a thin and very flattened lamina. It keeps the most dorsal position possible and reaches the dorsal par t of the lateral geniculate body ( F U 111 u, HD I1 m, y ) . In both of these cases there is some undercutting of area 17 so that the fibers to the lateral geniculate could really belong to the visual receptive cortex.

There is also some evidence that area 18 connects with the lateral nucleus. I n F O IV e there are fibers to the lateralis nuclens from that portion of the lesion coming from 18, and reciprocally in H A I1 where the lateralis posterior is injured, the thalamic projection curving around the hippocampal arch sends cortical endings to area 18, but also to a wide region rostroventrally of it. I n GY 11, where the posterior thalamic radiation is interrupted, there is degeneration within area 18. No fibers can be followed in the peduncle, except for a very short space a t the teginental connection referred to as located there. The nature of most of the lesions does not permit a conclusion as to the presence of a callosal connection between opposite areas 18, since the medulla is usnally impinged on. IIC, which does not injure the medulla, shows a callosal connection passing through the middle of the dorsal, lightly-stained coinponent, and crossing a t the posterior extreme of the splenium.

F o r association fibers larger lesions of area 18 shorn a broad and unspecific association with the auditory and soniesthetic receptive regions (HD I1 u ) . There are fibers from area 17 ( F T I c) and from 18a (GS I d ) . I n addition there are intraareal association fibers passing backward within area 18 (HD 11, not drawn in) .

Area 18a. Area 18a is the seat of some 8 lesions. They cover all parts of the area ( F H IV, F R I, F T IT, GS I, G P 111, GZ I, HD 111, HE 111). Most of them are practically confined to 18a but F R I incliides most of area 39. while GS I and HE I11 include parts of area 1’7. Most of them do not involve the medulla, but a n exception to this is GZ I.

All of the lesions demonstrate the existence of a forward-running fibrous lamina within the medulla which drops ventrally as it passes toward the posterior arch of the hippocampus, around which it curves to enter the lateral fifth of the peduncle (except in HD, where the tract seems to dwindle away). In no case have fibers been traced into the peduncle below the midbrain, but radiations to the lateral part of the thalamus and to the midbrain may be discerned. The extent of the radiations ohserved varies considerably in the several examples, some (FH IV, F R I , GS I) showing numerous radiations, the others


exhibiting fewer. Projection fibers from the posterior part of the area keep close to the posterior arch of the hippocampus, those from the posterolateral part form the most caudal bundles which pass through the putamen (GZ I ) . They are immediately continuous with the fibers from area 39 as shown in F R I a . It is questionable whether any of the fibers from area 18a pass to any of the thalamic nuclei. I n GZ I a the main peduncular group passes to the medial geniculate, but the medulla is involved here, although this would include the optic area 17 rather than any areas of known auditory nature, and F R I e which includes area 39 sends fibers to the medial geniculate. Area 39 is quite possibly auditory in its connections. However, these are the only ones that have obvious medial geniculate connections. GZ I a shows fibers ending in the lateral geniculate, but here the medulla is damaged so that these fibers could come from area 17. All of the examples, however, show a heavy distribution of fibers to lamina iv of the superior colliculus ending within its outer layers (FH IV a, b, c, e ; F R I d ; GZ I a ; G S I b ; GS I1 4). These fibers constitute the termination of the tract which lies in the peduncle. There are 2 groups, the medial group which takes off a t the lower level runs directly dorsomedially and caudally in the form of fine fascicles which bend caudally under the superior colliculus to form layer iv. The other group, the lateral group, threads through and over the medial geniculate body, passes beyond it to enter layer ii of the superior colliculus. These are shown in FR d and c respectively. There is also a well marked connection with the lateral part of the tegmentum in F T I1 d and GS I11 m, n, while in FI-I IV d, f , there are fibers which pass either to the medial tegmentum or are commissural. It is noteworthy that all of these tegmental connections come from rostrally placed lesions. There are no well defined afferents to 18a. There is a possibility of a connection to the latcralis posterior and a destruction of the auditory radiation showed a few granules in the basal part of 18a.

Area 18a sends callosal fibers to the opposite side bnt these are not numerous ( F H IV, F R I f , H E I11 p ) . Theyewere not noted in F T 11, which, however, is a small lesion. The chief association fibers seem t o be with 18, these connections running under 17 (GS I b, CZ I b, HE 111 n ) . I n all of these cases the medulla is involved to some degree, so this does not preclude a more ventral origin of the fibers, say, from area 41. In HB I1 LI fibers from area 18 have been noted ending in 18a.

Insular region

areas 13, 14. IIR 111 is a destruction of the forward end of areas 13 and 14. H G is a pure lesion of the forward end of 13. HC is a


very small lesion in 13 giving no degeneration, while both these areas are extensively involved in the lower part of the large lateral lesion HD I. HC 111 was so small that it gave no perceptible degeneration. IIB I11 and HG are the most useful. I n GT the caudal part of area 13 is involved along with area 20, while in GS the caudal part of area 13 is undercut along with the more dorsally lying areas 35 and 36.

The projection fibers occupy the coarse horizontally placed fascicles in the lower part of the caudate. On reaching the capsule they bend to pass ventrally, medially and caudally, but unlike other fibers near them joining the caudate they are represented by much finer granules and they do not immediately turn to pass directly caudally. Instead, they keep near the outer surface of the peduncle at its upper part and filter between the caudally running fibers. When they reach the central part of the medial half they encounter the entopeduncular nucleus, the position of the granules corresponding exactly to the nuclear spaces. They cannot be traced below this level, and hence are regarded as ending on the cells of the entopeduncular nucleus. This is well marked in HB but in HG the actual endings cannot be averred because of the large amount of adventitious degeneration. There are callosal fibers as shown in H B n . I n the rostral part of H D I areas 13 and 14 are the chief ones involved and thus there exists a lamina of fibers in layer vi which terminate in areas 3, 1 and 2 (HD I a) . In the medulla itself there is a deeper lamina of fibers (IID I b) which end in area 3 and area 4. This observation should not be regarded as final. Lesions of the medulla just dorsal to the insula, as in HE I, show a trail of granules passing ventrally which indicates the presence of association or of callosal fibers to the insula.

Cingular region Area 24. I n spite of the large size of this area it has not been

involved to any extent. It is included with the medial part of 10a in HA I, but the fibers are so mixed with those from its neighboring area that it is not feasible to make any conclusions. Areas 32 and 25 were spared in all cases. These are small anteroventrally placed areas and will not be analyzed in this study. However, there are numerous examples of lesions of area 24. Medial thalamic damage involving the eingulum regularly shows granules within the cortex of area 24, and the arrangement of fibers is such that the most medial and rostral fibers of the cingulum are those which are in a position to end in area 24. These fibers stem froin the more medial and anterior parts of the cortex, chiefly the anterior nucleus, and it is generally considered that the radiation from the anterior nucleus terminates in part here. These are shown in GF I and FX IT. The relation


between the position of the fibers and the lesion indicates that it is the fibers from the anterior ventralis which terminate within this rostrally placed cingular region. However, lesions of the medial thalamus further back which do not involve the anterior nucleus also show degeneration of fibers in the same position. In I-IH I1 these were noted to come from the nucleus medialis pars lateralis. I n GU I1 f they seemingly arise in the nucleus ventralis medialis magnocellularis. It is possible, of course, that in injuring the anterior nuclei we are involving fibers of passage which actually originate in the nucleus medialis, and it is noteworthy that in GF I, previously referred to, the ventralis medialis parvocellularis and the submeclius are involved also. Hence, in this series in spite of the possibility of tracing the complete course of the fibers involved and in spite of the fact that others have well established that there is a direct relation between the nucleus anterior and the forward part of the cingular area, it is impossible to confirm this conclusion. I n G N I also there is an extensive involvement of the medialis, but the anterior medialis is destroyed also.

Area 23. Passage of a narrow electrode track through area 23 in GI I11 and G F I has injured a strip of cells within this area, but no projection fibers have been seen. It is not possible, however, to state that they do not exist, as the lesions are small. However, lesions of similar magnitude in area 29 have given well-marked degenerations of projection fibers. Thus one can only say that they are not as numerous as those from the posterior cingulum. Fibers pass to area 23 from lesions which give extensive degeneration within the cingulum. Thus FX I1 and GN I show granules here. However, there is some indication that they are not as numerous. I n examples where the cingulum is uniformly degenerated there are more granules seen in area 24 and in area 29 than in area 23.

Area 29b. There are several good examples of lesions within this region, which has a considerable longitudinal extent and thus has been involved in needle tracks when the object was to injure the thalamus. On account of the orientation of the elements of area 29b, vertical needle tracks are likely to involve one or the other layer in a continuous line. Thus, in GC I1 layer ii is involved to the exclusion of others. In GD I layer v is involved and in GQ I the basal apex of the region is injured. In the infragranular lesions, shown particularly well in GV I, there are well marked granules in the basal layer of the cortex indicating clearly that these fibers are passing radially t o the medullary center, on reaching which they bend forward and laterally, threading through the cingulum and the medulla for a considerable distance until they reach the middle of the anterior arch of the hippocampus. This places them in the dorsomedial corner

292 WENDELL J. S. RRIEG

of the head of the caudate. There they bend to run ventrally and caudally. They can be followed within the middle third of the deep par t of the capsule, but cannot be traced quite to the peduncle. Where they end is unclear. GQ I, which involves parts of both 29b and 29c, shows the presence of granules from the area under consideration and demonstrates that these are placed more rnedially than fibers from the corresponding plane in area 29c. Their position within the capsule is clearly indicated (GQ I a ) . Within the peduncle they are just rostromedial to area 4, but they cannot be traced further. The lesion invplving the supragranular cells presents a different picture. Here there are fibers passing radially to the base of the area, threading through the cingulum, but o n reaching its basal aspect r u n directly forward for about 2 mm and then bend laterally just above the callosum, where in this case they get lost among fibers of the contiguous involvement of area 4. Whether they project or are association fibers is not certain, but they do have a different course. There is no clear evidence of a callosal component or of any thalamic or peduncular connections.

Area 29c. Lesions GA I and GB T arc from needle tracks and show numerous fibers of projection. GI< I1 is A minute lesion a t the basal par t of 29c which demonstrates that even damage to a small group of cells confirms the findings of the larger lesions, GD I1 is a somewhat larger specific lesion and GQ I is a needle track which destroys small portions of both 29b and 29c. With the exception of GD I1 all of these lesions show the presence of radially directed fibers from the lower half of the thickness of the cortex which on reaching the cingulum pass almost horizontally through it, and through the medulla for a considerable distance to reach the middle of the hippocampal arch. Having cleared this obstacle they bend rentrally and caudally into the dorsal part of the internal capsule, as these levels are behind the candate, and they can be seen to take u p a position within the middle third of its deeper part. They have never been traced below thalamic levels. GD IT is nearly a t the caudal end of the area. It shows a somewhat different picture. The fibers run laterally and rostrally arid into the capsule. O n account of the great distance they run and the tendency of fibers to dwindle away the ftirther they are from their lesion, we may be merely not seeing the peduncular conn-ctinn. Bnt some fibers do make the turn around the dor.;o- caudal part of the hippocampal arch and pass into the d o r 4 part of the thalamus in the region of the lateralis posterior. Thus it is clear that there are descending fibers from both areas 29, but where they end has not been ascertained.

On the other hand, connections from several of the thalamic nuclei end within thcl areas 29. Parts b and c will be described in one ac-


count here. The cingulum runs the entire length of the brain under the cingular region and gives fibers to all parts of the cingular cortex. The medial part of the cingulum is thick and is made up of fibers coming forward from the thalamic nuclei through the rostral pole of the caudate and running the entire length of the cerebrum. Later- ally this tract gets gradually thinner while fibers are added to it in an orderly manner from successively more caudally entering contributions. I n fact, it is difficult t o say where the cingulum ends laterally. It may be regarded as a broad lamina of fibers which is more condensed toward its medial edge. Direct lesions anywhere within the cingulum, of which there are numerous examples, show the presence and orderly distribution of caudally running fibers terminating in specific long strips of the cortex which directly overlie those fibers. The orderly arrangement of the fibers and the specificity of the cortical strips into which they send granules has been repeatedly observed. The anterior nuclei contributing to the most rostral and medial parts of the cingulum send numerous fibers into areas 29b and c (FX 11, F T 111). The nucleus medialis pars lateralis, in a case tvhere the anterior nuclei were not involved, showed degenerated fibers under and granules within area 29c and, to a lesser degree, 29b (HH 11). This is also demonstrated in (33 I. I n this case many granules are seen within 29b but not in 29c. These granules continue all the way out to layer i, where in normal fiber preparations there is a considerable lamina of tangential fibers. In normal sections of 29b one can see numerous radiate fibers reaching the first layer, but in 29c they do not pass layer ii. I n fact the thalamic representation within 29 is even more extensive. I n HA 11, where the lateralis posterior is almost exclusively involved, the medial portion of the thalamic radiation here extends far caudoinedially to pass granules into area 29. I n GY 11, where the posterior thalamic radiation itself is severed, there is likewise a trail of granules coming from the lateral addition to the cingulum within the areas 29. This is the case also in FT I11 g, where an electrode track passing through area 7 severs fibers joining on the lateral part of the cingulum and ending in the caudal part of 29. These, of course, could be thalamic projection fibers. Hence there is reason to believe that the areas 29 in the rat receive strong representations from a variety of thalamic nuclei. I n F U I1 t, where area 2 and the underlying medulla is extensively damaged and in HE I d , where area 40 and its underlying medulla are involved, there is degeneration which can be traced into the lateral and caudal part of the cingulum. However, it is not impossible that these fibers actually originate in the thalamus, as in all lesions in which the medulla is involved such observations must be held questionable.


Retrohippocarnpal region

Area 27’. This area will be considered first here because it has proved to be a part of the cingular system, having similar afferent connections to the areas 29. There is only 1 case of direct damage to area 27 (HG). There is attendant damage to the adjacent region, but it is clear that there are not fibers running through the cingulum in the forward direction from this area. Whether there is any component t o the internal capsule or the callosum has not been determined. On the other hand, there is ample material on the afferent connections of area 27. There seems to be a great tendency for fibers from widely dispersed regions of the thalamus and cortex t o send fibers back to area 27. First, it is connected with the anterior nuclei. A restricted lesion to the anterior nuclei ( F X 11) demonstrates the passage of fibers forward through the anterior pole of the caudate, then turning backward over the polar end of the medullary center and running along the dorsomedial edge the entire length of the cerebrum in the cingulum and ending finally in area. 27. When the nucleus medialis pars lateralis is injured without involvement of the anterior nuclei there is likewise a clear connection to area 27, taking the course just described. The contribution of the anterior and medial nuclei is amply confirmed in other lesions where parts of both these structures are damaged (GN I, FR I, F T 111). It should be noted that in IIH II there is a possibility of damage to the anterior ventralis and it i s notable that in GQ I, where the medialis is damaged without the anterior, there is no cingular degeneration, though numerous granules can be followed through the frontal cortex. Damage to the rostroventral part of the thalamus, though it may involve the ventral nucleus, can also sever connections from the anterior or the medial nuclei, so that in lesions such as in FH caution must be used in interpretation. It is possible, however, that the ventralis also contributes to area 27. I n GT the ventralis medialis parvocellularis is destroyed almost completely and exclusively, and there are connections through the cingulum to area 27. It is possible here that the significant damage is to obliquely running medialis projection fibers. There are numerous examples of direct injury to the cingulum in all parts of its course, usually by needle track. In all these cases where the damage was large enough to permit tracing it, i t could be followed to area 27, the fibers keeping a very orderly arrangement.

A r m 35. There is one example of a specific damage to this small strip-like area (GX IV). The lesion is a critical one and shows a strong component to the corpus callosum which runs dorsomedially curving over the posterior extreme of the medullary center and then

CONNECTIOXS OF CEREBRAL CORTEX 295

on reaching the dorsomcdial angle of the medullary center runs forward to enter the pobterior extreme of the spleniuni of the callosuni. There is some evidence of forward running granules directed toward the hippocampal arch where they might reach the capsule. They are few however, and it is impossible to trace them more than a short distance forward.

Area 28. A n accidental damage to the occipital end of the cerebrum involved area 28. This lesion is also involved in part in the lower part of GU 111. I n both cases there is heavy degeneration in the posterior extreme of the medulla which curves around dorsomedially to reach the splenium of the callosum (GY IV, GU 111 f ) . I n GY ( h ) there is also a connection to the retrosplenial region which parallels through most of its extent the course of the callosal tract.

Cortical aniygdaloid nucleus. This structure, included with cortical areas because it comes to the surface and is adjoined by true cortex, was injured in HI1 I. Being a part of the amygdaloid it could not be expected to have the conventional connections of cortex. Instead there is a well marked tract to the basal amygdaloid nucleus ( d ) . These fibers run forward as a flat lamina along the edge of the hippocampus. Though the tract is very poorly myelinated it is well defined in this series, indicating the ability of the Narchi method to demonstrate even poorly myclinated tracts.

CONNECTIONS O F THE THALAMIC NUCLEI

Medial region Anterior group. The anterior nuclei have been injured by deeply

placed lesions in 6 cases (FR I, F T 111, F U I , FX 11, G F I, GN I ) . The only one which is inclusive and exclusive is FXII . The medial nucleus has been iiivolved in F T 111, FIT1 and G N I . In F R I , although other nuclei are involved, of the anterior group only the anterior medialis is injured. I n G F I the only division of the anterior nucleus involved is the ventralis, while the medialis is not concerned. Any extensive lesion of the anterior nucleus must include some of the projection fibers from the medial nucleus as these cut forward through the anterior ventralis.

In all cases involving the anterior group there is a great uniformity of thalamic projections. The condition in FX I1 can be considered as representing the standard. The granules indicating degeneration of the thalarno-cortical connections congregate ventrolaterally of the nucleus. After passing through the nucleus reticularis in the form of coarse fascicleh the fibers of the internal capsule are encountered. Running into the internal capsule at an angle, these fascicles insert themselves in cracks between fiber bundles of the capsule, but as they


run forward they gradually blend with the capsular fibers and continue in the fascicles in the medial third of the caudate as f a r ventrally as the anterior commissnre. The more dorsal of these fascicles are more nearly vertical in their course, and on continuing reach the medullary center which they penetrate. On attaining the outer aspect of the medulla they turn caudally and join the cingulum, always placing themselves lateral to any fibers which have accum- ulated a t a more rostral level. This continues through the entire length of the striatum, the most ventrally placed fibers coming through the apex of the striatum and forming the most roc;tral and medial of the fibers in the cingulum. It seems clear that there is little criss- crossing or mixture between the fibers, so that the lateral part of the anterior ventralis is represented in the lateral par t of the cingulum here, and the medial part of the anterior medialis gives rise to the most rostral and medial fibers. This constant feature is of some value in determining the areas and levels of distribution of the components of the anterior nucleus. Following the cingulum back, it lies under the cingulate cortex, and in general sends granules into the overlying cortex. I n this example few fibers run forward a t the pole or end in area 10. Area 24 receives a large share of them. I t is likely that areas 10a and 6 receive some fibers. .Succeeding area 24 caudally is area 23 and it seems clear in comparing the various lesions that this area receives fewer fibers than 24, but i t does receive some. As area 29 is reached, the granules are sparser in the lateral part of the cingulum and many pass out into the overlying cortex, 2%. The more medial part keeps its compact arrangement but sends a few fibers to 29b. This continues throughout the entire length of the retrosplenial cortex, 29c always getting the more fibers. The most medial fibers, however, continue furthest caudally and after turning laterally as the remains of the cingulum they are distinctly distributed to area 27 in all of its parts but do not go beyond. This observation of the distribution of the long fibers of the cingulum, which seem to come purely from the anterior nuclei, was made again and again, opportunity being given by the numerous minute puncture wounds or deeper lesions permitting fibers to be followed f a r back, keeping their exact relative places and ending partly in area 29 and distinctly in area 27. Since the most medial fibers run the greatest distance, that is to 29b, 29c and 27, we conclude that the anterior medial nucleus connects primarily with these areas. This is confirmed in F R I, where this is the only one of the anterior nuclei, and but few granules are seen in areas 24 and 23. On the other hand, where the anterior ventralis is most involved there are numerous endings in area 24, but the degeneration in the cingulum is only scanty in its


caudal half. As an example of an extensive lesion near the anterior end of the thalamus not involving the anterior nuclei is FHIII. I n this case most of the anterior thalamic radiation is filled with granules, however, and the fibers, in addition to passing to the parietal cortex, join the cingulum also, but do not contribute to its anterior or medial part. Hence, in spite of the fact that other thalamic nuclei may project to areas 29 and 27, the forward par t of the cingular area is exclusively the domain of the anterior nuclei.

GHI is one of those remarkably accurate lesions which only chance can produce; here, in spite of the tenuous form of the nucleus anterior dorsalis, the entire nucleus is destroyed except for a thin lamina of cells posterolaterally, and no other structure except the stria medullaris is damaged. The findings in such a lesion should take precedence over those of any other nuclear lesion. From this example it is possible to say that the nucleus anterior dorsalis does not have a strong thalamic radiation or any distinguishable cortical representation. There are a few fibers running almost directly laterally along the dorsal extreme of the middle thalamic radiation passing through the anterior ventralis and the dorsal hook of the reticularis here. These fibers tu rn dorsally toward the medullary center but become lost. A few of them arise fa r enough forward to be regarded as a part of the anterior thalamic radiation, but are the most dorsal fibers there. Strangely, however, no interanterodorsal commissure shows in this case. In G F I, where the commissure is interrupted, the fibers can be traced under the medialis to the opposite dorsal anterior nucleus.

The chief afferents of the anterior nucleus are from the mammillothalamic tract. This is severed just behind the anterior nuclei in G U I I . The fine granules can be traced in all parts of the anterior nucleus, but are of course densest in the anterior medialis. The question has been raised (Le Gros Clark, '32) whether the mammillothalamic tract conducts also toward the mammillary bodies. From the vantage point of this lesion we can say that the number of granules in the proximal par t of the tract is very reduced when compared to the distal part . TWO other lesions (FR I, G F I ) give a n opportunity to observe the retrograde degeneration in the tract. It is present there also, though very reduced in quantity. Extensive lesions ( F R I1 k ) of the parietal cortex show trails of granules passing into dorsal and ventral anterior nuclei. I t is possible here, of course, that we are dealing with retrogressively degenerated thalamo-cortical radiations, but this lesion does not involve any of the cortex to which the anterior ventralis is known to send fibers.

Habenula. I n GD I the lateral habenular nucleus was destroyed entirely and the medial nucleus partially without damage to sur-


rounding nuclei. I n F R I and G[J I1 the habenula is included in a larger lesion. The principal efferent connection of the habenula is the habenulo-peduncular tract. This structure was directly damaged in its course in F O I11 and IV and HE 11. All of these examples give information on the connections of the habenulo-peduncular tract. While it is commonly considered that this tract ends in the interpeduncular nucleus, these lesions have shown that fibers pass to other regions. The observations of HE are best on this, though the other examples gave corroborative evidence. Just before the tract enters the interpeduncular nucleus it divides into 2 components. The habenulo- peduncular tract contains only fine granules compactly arranged and directed toward the interpeduncular nucleus, but there is in addition an extensive system of more disseminated large granules which indicate that the fibers branch off the main tract and ramify in the surrounding region. The region supplied by the latter tract of fibers is a triangular interval between red nucleus, median plane, and interpeduncular nucleus as far down as the pons. Some fibers seem to be distributed to the opposite side. This region does not receive any unified designation in the work of Gillilan ( '43), but includes part of the ventral tegmental area of Tsai, though i t extends further dorsally than this. Nor does it conform to any one nucleus on cytological criteria. In this region adventitious granules begin to show and it is difficult to determine how far down the fibers pass, particularly as some probably cross the median plane. The situation in GU I1 is interesting, however, because the lesion barely misses (or slightly involves) the habenular nuclei and the mammillo-thalamic tract, though it damages the thalamus just lateral to them. Here the compact part of the tract is almost without granules but stands out clear in a sheath of coarse granules passing downward with it. These granules continue into the region dorsal to the interpeduncular nucleus just cited. It is thus possible that these fibers only accompany the habenulo-peduncular tract. Yet when one examines normal fiber preparations carefully he sees no clear evidence that fibers are diverging from the tract. In its upper part it is surrounded by fibers of the paraventricular system medially and fibers descending into the tegmentum laterally, chiefly from the striatum. In its lower part it is involved in a very dense accumulation of fibers, mostly of striatal origin, but i t keeps its compact arrangement to the interpeduncular nucleus which it enters laterally and breaks up within its interior. There are no lesions of the interpeduncular nucleus, but normal fiber preparations show a congregation of fibers medially on each sidr in the caudal part of the nucleus which pass dorsally and caudally as the dorsal tegmental tract of Gudden.

C O S N E C T I O N S OF CEREBRhL CORTEX 299

Stria medullark Partly due to the fact that the needle track for medial thalamic lesions had to pass through the stria medullaris and partly due to chance there is an unsurpassable series of lesions to the stria medullaris which give a remarkable uniformity of results and allow some novel conclusions to be made. Only one of these involved the entire cross section of the stria (FU I). Others damaged about half of the fibers (FY, GD I, GH I, GL, GM, GU 11). Four of them were tiny nicks to a part of the tract (GC 11, GJ, GQ I, HE 11) which in some eases were so small that they could hardly include over one-twentieth of a cubic millimeter, as in GJ. This fact is of interest in itself because it demonstrates the possibility of making more minute lesions than have been attempted before so far as this writer knows, and that such lesions may be useful in demonstrating connections. These lesions agree in demonstrating that the stria medullaris conducts in both directions and almost equally. They show that a large number of fibers cross the median plane in the habenular commissure and run forward the entire length of the opposite stria medullaris, so that except in the case of the smallest lesion, where the degeneration seemed to fade out on the opposite side, degeneration in the stria medullaris was approximately symmetrical. Fibers pass of course to the medial habenular nucleus and also, though in less degree, to the lateral habenular nucleus, but the interest of the findings was largely in showing the course of termination of the fibers. Even in normal preparations the stria medullaris can be easily followed around the anterior surface of the thalamus where it passes ventrally and enters the nuclear material medial to the base of the caudate. The extent of distribution of the granules in these cases, however, shows the exact ending. They may be seen to pass to the lateral hypothalamic nucleus in its lateral part. Some of the fibers bend and pass caudally for a short distance. Others, particularly observable in F U I, turn forward in this basal region ( F U I m) , migrating laterally as they do. Here they reach the lateral preoptic nucleus below the rostra1 end of the caudate. The stria medullaris does not send fibers to any other structure than the habenula in any part of its course.

Submedius. Though others of the medial and median thalamic nuclei were involved in lesions, it is not possible to make accurate conclusions as to their connections. Another series of lesions will have to be made t o analyze this region. However, the nucleus submedius, termed by Cajal nuclehs ovoidius and by the present writer in a previous work ('44) the nucleus gelatinosus, was involved in lesions in 3 cases ( F T 111, G F I, GU 11). These are all involvements of the caudal ventral part of the medial thalamus. In each the


Hvolved along with the sitbniedius and the position of the lesions is such as to interrupt fibers from the parafascicularis. As will be shown later, the parafascicularis projects to area 8 and in these cases numerous granules are seen in the lo117er half of 8, particularly rostrally. The thalamic projection in these 3 cases presents certain uniform characteristics not found in other lesions of the series. Only in these cases is the degeneration extended as fa r ventrolaterally i n the anterior thalamic projection. These fibers pass to the medial extreme of the compact part of the internal capsule immediately adjacent to the anterior comniissnre, home of them even r u n nncleriieath i t and lie at first nearly in the transverse plane. On reaching the base of the caudate nucleus they keep in its basal part and as it rounds off rostrally becomes caught in 'the fibers forming the ventrolateral capsule and follow the outline of the caudate here. Some of the fibers do not continue around the pole, however, but tu rn sharply ventrally to enter the basal cortical areas here: 8a and 11 ( G F I, e, f ) . The fibers to the basal part of 8a rostrally are particularly numeroils and indeed this nucleus may contribute to that area. However only lesions involving the submedius show fibers passing to 11 ( G F f ) . Area 11 is in the cleft between the olfactory bulb and the base of the frontal pole and so constitutes a primordium of the orbital area. We are thus able to conclude that the nucleus submedius or the nucleus ventralis medialis, or both, project to area 11.

Ventrolateral region

Nucleus ventralis. The correlation of the ventral nucleusl in both its ventral and dorsal portions, with area 2 is so close, both as regards degeneration after thalamic lesions and after cortical lesions, that the 2 aspects of the subject may be considered together. They have been completely analyzed as fa r as the material will permit in the section on area 2. This analysis will not be repeated here. There is a close correlation between regions of area 2 to which fibers pass after thalaniic lesions and regions of the nucleus ventralis with which granules connect after cortical lesions. It will be recalled that there is a close topological correlation of regions of the nucleus with regions of the cortex. There is a considerable tendency for degenerations involved after cortical damage to take the form of longitudinal columns which follow the course of the fascicles through the length of the ventralis, involving both ventral and dorsal divisions of the nncleus, but the region of the ventralis dorsalis involved is more caudal in position than that of the more ventral division.


Whether the nucleds ventralis projects to other areas of the cortex than area 2 is, however, another question. The possibility of supply to areas 1 and 3 is, of course, a crucial one, but there are not many specific lesions to the ventralis and the material does not permit a final answer. GFII, however, is a quite critical lesion iiivolving all except the medial third of the ventralis and fibers do pass to area 3. They also seem to pass in this case to areas 4 and 6. It is likely that brachium conjunctivum fibers end here and form connections with the motor areas as they do in higher mammals. Area 40 seems to get fibers when the ventralis dorsalis is injured (GX I1 b) and in EIE I a granules after injury to area 40 have been traced to the lateral extreme of the nucleus ventralis. This is the position which an orderly arrangement of the fibers would demand if there is to be any thalamic connection with area 40. I n 1 case (GX I1 b) a lesion of the ventralis dorsalis (GX I1 b) seems to send fibers to area 10. Certainly the great majority of the radiation from the ventral nuclei passes to area 2.

Lateral nuclei. The subdivision of the lateral nucleus of the rat is a problem. It extends almost the entire length of the thalamus, lying dorsally to and in a shallow notch between the entire anterior and medial groups medially and the ventral nucleus laterally. It is in all fields sparsely celled and not perceptibly divided into regions or zones. It takes on a more definite quadrilateral shape posteriorly where it lies lateral to the nucleus posterior, dorsal to the ventralis and medial to the lateral geniculate but there is no evidence that the cell type is changed. In this study it will be divided for convenience into anterior, middle and posterior portions. These three regions of this extensive nucleus do not seem to have identical connections. The material on hand showing lesions of the lateral nucleus is limited considering the extent of the nucleus. In F N and GX I1 there is damage to the anterior part, but it is clear that there are very few cortical projection fibers. I n view of the course of the fibers from the part of the ventralis which is damaged, many projection fibers that fall into the parallel pattern must pass to the areas dorsomedial to area 3, that is, areas 1 and 3. The middle part of the nucleus is injured in GZI I . Here there are definitely fewer fibers than from the damaged part of the ventralis (e) . Fibers from the lateralis ( f ) begin more dorsally and take a more dorsal course as they curve around the anterior part of the hippocampal arch. Directed sharply medially, they diagonal through the thickest part of the medullary lamina and the majority of the fibers reach the cingulum. Probably some end in area 3. They continue in the cingulum, rather scattered, throughout its entire length, ending finally in area 27, but probably passing also to area 29. Fibers


from the lateral nucleus are always distinct and separate from those from the ventral nucleus. There are 2 lesions to the lateralis posterior. Flt I is a superficial involvement of a considerable area and it shows obvious projection fibers. The interpretation, however, is rendered somewhat ambiguous by the fact that there is a lesion to areas 18a and 39 which projects fibers just under the nucleus. H A I I , however, is an impeccable lesion to the lateralis posterior. Here there is a considerable radiation. The fibers lie directly against the hippocampal arch, in this example in the middle and upper part of its posterior portion, spreading out in a fanwise manner. This spread of the projection of the lateralis is characteristic. On reaching the medulla they are redistributed to form a compact lamina containing numerous granules. This lamina lies under the middle extent of the dorsolateral part of the cortex and the areas which it underlies are probably indicative of those which it supplies. There are numerous fibers t o the caudomedial corner of area 2, but these might come from an involvement of the ventral nucleus. The lamina continues broad as i t passes caudally under 18a, 17, 18 and 29c. Fibers pass conspicuously to 29c all along its course. There are definite granules within 18, particularly caudally, and in 17, though these are not so numerous and cannot be traced beyond layer vi. Area 29b receives no fibers. The more medial granules lie within the cingulum as did those from the middle part of the nucleus. I n this same lesion there are damaged caudally-running fibers t o the inferior colliculus (k) , but these are, no doubt, fibers of passage from the cortex.

Granules traceable to the lateral nucleus after cortical lesions are suggestive of these findings. It takes a rather large cortical damage to produce a trail of granules into the lateralis. I n F R I I , a very extensive lesion to the dorsorostral cortex, fibers may be traced into the lateralis anterior as well as to most of the other thalamic nuclei. I n F T I1 there is, however, a small lesion to area 18a which allows a few granules to be traced into the lateralis anterior. As far as the posterior part of the nucleus is concerned, in the large lesion HD I there are numerous fibers passing through the lateralis and probably some of them end there. There is, however, in GD I1 a small lesion to area 29c which allows a tiny but definite trail of granules to be followed into the lateralis posterior.

Thus it seems possible to conclude that the nucleus lateralis projects to the cortex medial to the main sensory area and caudal to it involving areas 3, 7, 18, possibly 17 and 18a, 29c and 27, these forming a continuous strip along the dorsomedial part of the cortex just beyond the cingulate areas. I n GW I1 h, in which the lateral lemniscus was damaged in the midbrain, a few fine granules could be traced into the lateral nucleus.


Medial geniculate. There are 4 examples of circumscribed lesions of the medial geniculate or of its radiations (GY 11, HR 11, HC 11, HD I ) . Of these only HC I1 involves the cells of the medial geniculate. The others are in the thalamic part of the course of the radiation as it passes medial to the lateral geniculate body. The details of the degenerated radiation agree in all important particulars in each of these cases. HC 11. involving the medial geniculate in a minute lesion near its outer surface, is the most critical. It shows the auditory radiation (b) passing forward medial t o the lateral geniculate body. The auditory radiation is especially condensed in size just rostra1 to its nucleus of origin. This is characteristic of the auditory radiation in man also. It expands rostrally as i t curves around the posterior part of the hippocampal arch and on curving around the stria medullaris breaks up into coarse fascicles laterally and dorsally directed through the putamen. The details of this distribution are better shown in H B I I e . Some of the fibers run dorsally a t the putamen to reach the medulla and most of the others thread through its largest portion as far ventrally as its lower extremity. The lower fibers do not run directly to the putamen but make a ventral genu as they pass from the capsule to the putamen. The lowest fibers make an extreme digression, even passing parallel to the optic tract f o r a distance, and then bending sharply laterally to form the lowest fibers of the auditory radiation. I n the medulla they form an extensive lamina, passing dorsally and caudally under area 41. By far the greater portion of these end in area 41. There are a few fibers passing further dorsally to 18a and the candalmost of these pass to area 36. The details of the cortical terminations are echoed in H B g.

Where the cortical area 41 is destroyed (GU 111 n ) the same pathway is shown passing to the medial geniculate, indicating that we are perhaps dealing with a retrograde degeneration of fibers. In OZ I a after injury of area 18a granules can be traced to the medial geniculate body. Thus it seems possible to conclude as the result of all these experiments that the medial geniculate body projects through the auditory radiation which curves around the posterior arch of the hippocampus and scatters widely in the putamen to be ultimately distributed preponderately to area 41 but also to areas 18a and 36. H C I1 a shows that the superficial fibers on the medial geniculate pass to lamina ii of the superior colliculus. They are of optic nature and descending.

Lateral geniculate. There is little information forthcoming on the efferent connections of the lateral geniculate body. No lesions were planned to include it and it is situated in too isolated a position to be involved accidentally. However, the existence of the optic


radiation is one of the best established facts in the whole subject of cortical connections. HC I1 came close to the lateral geniculate and produced some interesting results, particularly the degeneration of a tract (HC I1 d ) running down the optic tract toward the chiasma from the lower part of the lateral geniedate body, as a thin flat lamina between the peduncle and the optic tract. Fibers are distributed in both sides of the chiasma. Presumably it passes into the optic nerves as it is not found in the opposite optic tract or supraoptic commissures. The fibers passing over the surface .of the lateral geniculate come from the optic tract (HC TI a ) and enter the outer fibrous lamina of the superior colliculus and are distributed t o its cellular cortex (HC I1 a, OX TI d ) . It is assumed that the geniculo- cakarine tract passes only to area 17.

Cortical lesions to area 17 have not produced degeneration toward the lateral geniculate body. However, these are all small in this series. Those in HG I b and GZ I a may come from area 17 or 18. Two lesions of area 18 ( F U I11 LI, HD 11 w, y) show the presence of a forward running tract curving around the posterior hippocampal arch and ending in the lateral geniculate body.

Nucleus posterior. thalami. Gurdjian recognized the compact rounded nucleus medial to the caudal end of the nucleus lateralis posterior a t the transverse level of the posterior commissure as nucleus posterior thalami. It is questionable whether this is a pretectal nucleus or a genuine thalamic nucleus. HD I IC involves this nucleus and some of the nucleus lateralis posterior. From this caudal thalamic nucleus there are but few cortically directed fibers through the posterior thalamic radiation. Those which exist keep a dorsal and caudal position in the posterior thalamic radiation and curve sharply backward once they have rounded the dorsolateral part of the hippocampal arch and then are directed toward the caudo- niedial angle of the cerebrum. There are many fibers passing through this region, however, and these have been extensively damaged. They are of 3 categories. The most numerous are those to layer iv of the superior colliculus which thus shows extensive degeneration throughout the entire length of the colliculus. Some of the fibers destined for layer ii are are also damaged by the passage of the electrode track, in this case quite broad (HD IT 9). Rostrally directed fibers from the lower part of the lesion end distinctly in the zona incerta ( H D 11 9). There is also shown a strong descending tract to the lateral deep nucleus of the tegmentum in its ventral region and seeming t o continue in the diffuse tegmental nuclei dorsomedial to the nigra as far as the pons ( H D 11 r) . The con- servative appraisal of this group is that they are descending pallidal fibers, since such are numerous in this region.


SUBTHALAMUS

Zona incerta. The zona incerta was not directly damaged in any of the lesions. There is no clear-cut evidence that any of the cortical areas send fibers to this region, nor do any of the thalamic nuclei medial o r rostral to it. Lesions at its lateral angle, however, uniformly show a tract running parallel to its long axis in a ventromedial direction (GY I1 f , IIB I1 k, HC I1 c) . These lesions are all to the region rostral and medial to the medial geniculate body. Where the fibers come from cannot be said but they are apparently not cortical. A lesion to the caudal part of the thalamus involving the nuclei posterior and lateralis posterior indicates forward running fibers from or through the lesion to the caudal aspect of the zona incerta, where they end. These are likely to be fibers of passage stemming from the tegmentnm. Direct lesions of the incerta and of the pallidus would be necessary to clarify its connections, but it does clear the air sonie- what to be able to say that the zona incerta stands out of the thalamic and cortical realms.

Nucleus entopedzcnczclaris. I n GAl TI, where the rostral end of area 2 was destroyed, there is a heavy peppering of fine granules within the spaces occupied by the nucleus entopeduncnlaris. The portion of the peduncle surrounding it is also degenerated but the granules are larger. The insular region also sends fibers into this nucleus by way of a niedially directed fasciculus under the peduncle (HB 111, HG).

Nigra.. Lesions involving area 2 are apt to show fibers passing to the nigra (FR I1 q, GN 11, GIJ). It is important here to distinguish between the fibers leaving the peduncle and passing into the tegmentum and those which actually end in the nigra. Both types are found in the same preparations. The fibers to the tegmentnm arch over the top of and through the nigra, slanting laterally, and may be followed into the central lateral part of the tegmentuni ( F R IT 9) . However, in G M , as stated in the protocol, " These fibers leave in two groups, an upper and a lower. The upper is in the form of finer fascicles and the lower in the form of coarse fascicles whose granules cannot be traced beyond the nigra, but on the other hand the lateral portion of the reticular part of that nucleus is heavily peppered with fine grannles. There is a strong tendency fo r the fibers to turn laterally. The entire lateral portion of the reticulata is affected. The opposite side has very few granules."

There is a tendmcy in many of the series studied for the interstitial tissues of the caudate and of the nigra to show very fine black granules usually in floccular formation, which cannot be connected with any degenerating fiber tract. This is perhaps due to the large


amount of iron stated to be in these nuclei acting as a reducing substance on the osmium tetroxide. This phenomenon has been liberally discounted in the interpretations of the sections and rigid tests must be applied before concluding that any cortical area connects with the nigra. I t mould seem, however, that area 2 does.

MIDBRAIN

Superior colliculus. The superior colliculus is abundantly pro- vided with fibers from the cortex, especially from areas 2 , 18 and Ma, as we shall see. These fibers enter the colliculus either through the superficial fibrous lamina (lamina i i ) or through the deep lamina (lamina iv) . The connections of lamina ii will be considered first. Lesions of area Ma, particularly rostrally, send fibers to lamina ii of the superior colliculus. These are well shown in FR I c where, after rounding the hippocampal arch, fibers destined to this layer keep a n extreme dorsomedial position as they begin to run caudally on the outside of the lateral geniedate body. il similar appearance was observed in GZ I a. When the injury is directly over the lateral geniculate (HB 11) or over the medial geniculate (GY IT, HC I1 a) these fibers are also shown diagonalling caudally lateral to the pretectal region and then distributing themselves throughout lamina ii. They- are ultimately distributed to the superficial cellular lamina forming the cortex of the superior colliculus. There is another component to lamina 2 which is brought out by damage to the nucleus lateralis posterior ( H A IT k ) . This indicates the presence of fibers from more anterior regions. There is a third contribution to lamina ii well shown in 4 cases of damage to the pretectal region ( F N I I , FR I, F Z g, k). This layer of fibers can be seen abundantly in normal preparations on the surface just rostral to the superior colliculus proper. I n 1 case (GW 11) the superior colliculus itself was damaged a t its rostral end, exhibiting the expected degeneration in lamina ii.

Lamina iv comes to light in numerous cases of cortical damage. I n F U I1 e, after damage to the dorsal part of area 2 and to area 1, fibers leave the projection tract a t the midthalamic level, then diagonal dorsomedially through the posterior extreme of the thalamus and then run directly caudally to enter lamina iv. This is an isolated example, however, for even in the nearly total destruction of area 2 in GlJ I there are no fibers to the superior colliculus. This holds, too, for the very extensive lesion F R 11 which includes the entire front half of the dorsal cortex. I n both these examples thew were numerous tegmental fibers, so i t is not a question of impregnation. Area 18a has been amply shown to send a large component to lamina iv. I n

C O N N E C T I O N S O F CEREBRAL CORTEX 307

FH IV, an anterior lesion, these fibers radiate from the projection tract in 2 groups. Some are in the form of fine granules entering the posterior thalamic radiation (a, b, c) and continuing with it medial to the lateral geniculate body and then bending dorsomedially through the lateral nucleus to converge and form a part of layer iv. Other fibers diverge dorsally from the main tract as soon as it has reached the capsule and run dorsally in an almost transverse plane through the lateral geniculate body, ultimately joining with the preceding group in lamina iv. The fibers of F R I d are similar in their course to the former of the 2 groups just mentioned. GS I b shows granules in the position of the fibers of the latter group. GZ I a demonstrates both components, some fibers leaving from the peduncle itself and other fibers attaching themselves to the lateral geniculate as soon as they can reach it. I n GS I11 the 2 components are represented by groups q and r respectively and amply shown in the reconstruction. Damage to any part of this fiber system will light up degeneration, of course. Whether the injury is to the thalamic part of the posterior radiation (GY I1 e, HB I1 j ) , or whether near the posterior commissure (GB), or in the caudal end of the lateralis posterior (HD I IC f ) there is abundant degeneration in lamina iv. This tract is heavy and degeneration can be followed in gradually decreasing degrees to the caudal end of the superior colliculus.

Irzferior colliculus. Fibers may be traced into the inferior colliculns when the auditory cortex is extensively damaged (GU I11 m, HD I n ) . That they really come from area 41 is shown by GU I11 n, where the damage is almost exclusively to the auditory receptive cortex. These fibers form the principal par t of the downward projection through the putamen into the lateral extreme of the peduncle. They continue in the peduncle to the level of the medial geniculate where they stream out dorsally as separate fibers passing caudomedially of the medial geniculate, running dorsally to the inferior colliculus and scattered throughout it, but are particularly numerous in its outer fibrous covering. In H D I n the damage is extensive, but those fibers passing to the inferior colliculns are similar in their course to those just described. H H I is a partial injury of the auditory cortex which sends fibers down to the lateral extreme of the peduncle and dorsally into the tegmentum, but here they are not numerous enough to be traced to their termination, although when last seen they are directed toward the inferior colliculus.

Tegmerztum. Cortical fibers ending ultimately in the tegmentum were seen in numerous cases after cortical lesions to various areas. I n F U I I d , e , a connection with area 2 was shown with the dorso-


medial tegmtntum, fibers leaving a t the nigra level passing dorsomedially, then tnrning downward. The exteniive anterodorsal lesion (FR I1 p, q ) shows many descending tegniental fibers but it does not permit localization as to exact area. Lesions involving area 18 regularly show numerous tegmental connections which, when they can be traced far, pass into the clorsomedial tegrrientuni (FII I V d, F O IV j, F U 111 t, HC I e ) . This tegnieiital radiation uniformly leaves the lateral par t of the peduncle traveling dorsomedially i n the form of discrete fascicles nearly in tlie transverse plaiie and then turning caudally under lamina i r of the superior colliculus in the dorsoniedial part of the tegnientum. In an extensive lesion of 18a (GS I1 m, n ) a tegmental radiation was also observed, the fibers passing directly dorsally and caudally in the rostra1 part of the tegmentum and ending in the lateral part of the tegmentuni. The principal connection of area 18a is with lamina iv of the superior colliculus, but these fibers are separate. They were not specifically observed in the other lesions involving 18a. They may be present and not separated from collicular fibers in the analysis. Coniiectiori from area 40 is shown in HE I a. The othtr lesion of area 4C (GW 111) has so much degeneration in the tegnientuni due to a leni- niscal lesion that such a connection would be difficult t o coiifirm here. I-ID I m, from an extensive lesion in the lateral part of the cortex, shows tegmental fibers to the lateral deep nucleus. Extensive caudal lesions of the thalamus, however, do not show descending thalaniic connections. This was denionstrated in GI1 I1 h, where the entire medial half of the thalamus was destroyed in the caudal region, and in GZ 11, where the ventral nucleus was damaged. In- juries to the caudolateral extreme of the thalamus, as the ventralis posterior, show many tegmental connectioiis because tlie descending striatal fibers pass through here.

Medial leninisczis. A lesion planned to demonstrate the extent of distribution of the medial leniniscus (GW 11) shows the distribution of that tract throughout the entire extent of the nucleus ventralis. particularly in its ventral part, though in this case the medial and lateral ends were not damaged. The granules avoid the bundles of cortico-thalamic fibers. There is a sharp boundary laterally a t the reticularis. Degeneration exteiidr into the ventralis dorsalis throughout and a few fine graniiles are found in the lateralis arid in the medialis ( h ) . There was no retrograde degeneration in the medial lemniscus beyond a millimeter and the cells of the nuclei gracilis and curieatus showed no perceptible degeneration in the affected side. This lesion, where it involved the tegmentum, also showed numerous other connections (g-s) indicating the value minute lesions of the rat


tegmentum would have in elucidating the connections of this poorly uderstood region. Some of the revelations of this single lesion are: lateral tegmental contributions to the medial longitudinal fasciculus (m) , the distribution of the posterior commissnre (n ) , the presence of the ventral tegniental commissure ( lr) and of an extensive ascending tract from the ventral tegmentum (11).

GB I shows a small lesion to the anterior edge of the posterior commissure. There is degeneration to both sides, all in a downward direction, the fibers passing to the medial part of the tegmentum. A few drop ventralward into the region of the habenulo-peduncular tract, but the majority continue caudally well into the midbrain, lying among the tegmental fibers between the medial longitudinal fascieulus and the red nucleus. GW T I n confirms this observation. I n HD I1 t, where the damage is to the nucleus posterior, there are a few crossing fibers, but these may come from the striatuin.

Pretectal regioa. The region of the pretectal nucleus is damaged in F B I, GB I and GK 111. These lesions agree in showing descending connections to layer ii of the superior colliculus only. There were no observed ascending connections, indicating that the pretectal nucleus does not belong to the thalamus.

Red nucleus. This structure vas directly dainBged in GW I1 allowing the rubro-spinal tract (k) to be followed the length of the brain stem. I n Fft I1 r there is indication that the region of the red nucleus receives fibers from the anteroilorsal cortex, but otherwise there is no clear eSidence that the cerebral cortex sends radiations to the rubral complex.

Posterior conzmissure.

DISCUSSION

Thalamo-cortical relat iom A survey of the history of our knowledge of the relations

between thalanius and cortex may be sharply divided into 2 periods, the first from 1872 to 1913 in which the principal facts were worked out chiefly with lower mammals, and the second period from 1932 to the present day during which much of the previous work on lower mammals was repeated, the methods were applied to higher animals, and the findings generally made more precise.

As long ago as 1872 Gudd'en demonstrated that the extirpa- tion of isolated par ts of the cerebral cortex of the rabbit brought about atrophy of isolated iiuclei within the thalamus.

310 WENDELL J. S. I iRIEG

The operations were performed on newborn animals and they were sacrificed a considerable time later.

This finding interested von Monakow (1882) who in a series of 15 o r more cases extirpated isolated parts of the cerebral cortex of the newborn rabbit and identified the thalamic nuclei which failed to differentiate as a result of the operation. He established in a general way the site of distribution of the following nuclei : lateral geniculate, medial geniculate, lateral, ventral, anterior and medial. It may truly be said that until Lashley established local representation within the individual nuclei in 1941 the subject was not materially advanced.

In 1902 lllunzer and Wiener showed that extensive removals of the cortex caused extensive degeneration in the thalamus. They did not, however, produce by any means a complete decortication. I n 1913 Nissl found that after complete de- corticatioii the only thalamic nuclei remaining were the habenular, ventral parts of the external geniculate and the posterior or pre-bigeminal.

The experimental work of Sachs ( '09) was ahead cf its time and is still as modern in approach as the most recent in- vestigations. Working in Horsley 's laboratory' he was one of the first to apply the stereotaxic machine. He made cortical and thalamic lesions and studied the resulting Marchi degeneration. It must be remembered that a t that time proof of the very existence of thalamo-cortical fibers was a contribution and that the importance of a regard in experimental work for the finer subdivision of thalamus and cortex was not current. He was mistaken about the anterior nuclei, stating that they connected with the caudate ; but he did show degeneration passing to the ventral nucleus after precentral and postcentral damage, and to the pulvinar and medial geniculate after temporal lesions. He also established a rough topology of the body on the somesthetic cortex.

The year 1932 marked the beginning of the new era of studies of thalamo-cortical relatibns, for in that year appeared the results of Marchi experimentation on rats by LeGros Clark and on monkeys by Poljak. Poljak's monograph estab-


lished the origin, course and distribution of the somesthetic, visual and auditory radiations to the cortex of the monkey and he illustrated his findings beautifully.

LeGros Clark ('32) reported a t length on a series of 8 cortical and 7 thalamic lesions, together with 2 in the brain stem. He achieved his lesions of the cortex by damage to a region of the order of l m m of the surface; and of the thalamus by thrusting a needle deeply into the brain, fre- quently going far beyond the median plane, I n spite of the small number of cortical lesions he was able to indicate the general region of the termination of the following nuclei : anterior ventralis, medialis, ventralis and lateral geniculate, though of course he could not show the extent of cortical fields of these nuclei. Marchi preparations were used for all series. The degeneration toward the thalamus after cortical lesions was apparently regarded as cortico-thalamic instead of retrograde degeneration of axons of thalamic cells killed by the lesion. After the thalamic lesions the anterior nuclei were regarded as independent of the cortex. The ventral nucleus projects to the anterolateral cortex, the nucleus lateralis to the mid-dorsal cortex and the medial nucleus connects with the frontal pole. The submedius, the pretectalis, the nuclei of the midline, have no cortical connections.

Since Clark's paper of 1932 there have been no compre- hensive reports of attempts to trace thalamic or cortical connections in lower mammals by means of the Marchi method primarily. Making practical use of the now well-known fac t that localized cortical damage is followed by localized thalamic cellular degeneration, Waller ('34) made a study of thalamic degeneration following localized cortical destruction in 36 rats. Lashley ('41) made a similar study on the rat after several hundred localized cortical lesions. Bodian ( '42) by the method of retrograde cellular degeneration, traced the thalamo-cortical projections of the opossum. Thew 3 studies were similar in scope and were devoted entirely to the establishment of topical correlation between points in the thalamus and points in the cortex using retrograde degen-


eration as observed in cell-stained series. Except for the 8 lesions of Clark referred to, in which only connections with the thalamus were described, no systematic attempt has been made to trace the fibers from the cortex in lower animals.

Nearly all of the lesions of Waller encroach extensively on the medulla arid it is clear that he did iiot make allowance for the fibers of passage in the medulla to more outlying portions which were damaged as a result. This is especially vitiating in the posterior half of the cerebrum, where the capsular fibers often run long distances in the medulla in a caudalward direction, and in the dorsal par t of the cerebrum, where most of the fibers have to run medially for a long distance. This is another example of the folly of studying cell bodies while ignoring fibers, whether in anatomic or physiologic endeavors. Nevertheless he was able to obtain a closely fitting map of thalamic projections on the cortex which cover nearly every part of the neocortex. The cor- respondence of his findings in the r a t with those of von Mona- kow in 1882 in the rabbit is remarkable. It is this writer’s opinion that in any investigation localization within the thalamus should be based on an identification of cortical areas involved in the lesions to be of localizing value. At that time there was no study of the cortical areas of the albino ra t and Waller was forced to fall back on the charts given for Mus decumanus by Fortuyn and of Spermophilus by Brodmann. Whatever may be the value of the 2 studies for the form under investigation, they a re not a t all applicable in their topography to the albino rat , so that the discussion of the correlation of Waller’s findings with the cortical areas involved can have but little value. Nevertheless, a definite contribution was made by Waller in showing the general regions of the cortex in the rat to which most of the thalamic nuclei projected. He did not indicate a cortical projection of the medial, posterior, pretectal or midline nuclei.

LeGros Clark and Boggon (’33) included lesions in the retrocingular cortex of the rat in their study of the connections of the anterior nuclei and found degeneration in the

CONNECTIOITS OF CEREBRAL CORTEX 313

anterior ventralis but not in the aiiterior dorsalis. The extension of their lesions onto the dorsal region was followed by degenerations in the lateral nucleus.

Gerebtzofl' ( ' 37 ) from a series of 7 frontal and 6 parietal lesions, all of which damaged the medullary center, purported to establish the region of cortical projection of 10 thalamic nuclei and to demonstrate the truth of a group of principles of tlialamo-cortical systematization and of a set of rules of morphologic reflection of the thalamus in the cortex. His historical review is useful, however.

In 1938 appeared Walker's book on the primate thalamus, which is included here because of i ts importance in clarifying the subject of thalamic projection generally.

Stoffels ('3%) made a special study of the retrograde degeneration observed in the anterior nuclei of the rabbit after damage to the medial cortex. He also ('39b) discussed the organization of the thalamic projection to the cerebral cortex.

Lashley 's report ( '41) 011 the thalamo-cortical connections of the ra t brain by retrograde cellular degeneration after localized cortical damage, is based on 154 diverse lesions and 200 "additional cases for crucial evidence. " Having available a large and varied assortment of lesions, Lashley was able to make a map of the total extent of all of the lesions which did not damage a particular nucleus and a supplementing map of the parts common to those lesions which do injure the nucleus being studied. Moreover, he was able in most cases to make topical correlations of thalamic and cortical regions. He found that in the case of most of tlie principal nuclei there was a very sharp boundary to the cellular degeneration in the thalamus. Fo r most of the nuclei the representation of the cortex was found to be a t right angles to1 the axis of the thalamic radiations, indicating a direct course of the fibers and that the bi-climensionality of the cortex was projected on the thalamus in a 2-dimensional manner, so that any point in the cortex would be represented as a narrow prism in the thalamus corresponding to a unit of the thalamic radiation. This observation was confirmed in the present work, particularly in the case of tlie ventral nucleus.


In summarizing Lashley’s thalamic cortical fields it may be said that they are for the most part quite similar to those of Waller except that there are 3 extensive areas to which Lash- ley finds no specific thalamic projection. They are as follows :

1. A strip medial to the projection of the lateral geniculate body corresponding to our area 18.

2. A triangular area lateral to the projection of the lateral geniculate and caudal to the projection of the medial geniculate corresponding to our areas 18a and 36.

3. The entire frontal pole, with the exception of a ventrolateral area for the submedius, plus the anterior half of the dorsomedial cortex. This corresponds to our 10,10a, 6 and 4. It was recognized by Lashley, however, that this receives the projection of the medial nucleus. It was found in the present work that, though any damage to the medial nucleus would give a distinct projection to the frontal cortex, subtotal damage to the frontal cortex would not show granules in the anterior thalamic radiation nor retrograde degeneration of the cells of the medial nucleus. This is an example of where the use of retrograde cellular degeneration as a research method may give deceptive results and tends to confirm the belief that most of the fiber degeneration directed toward the thalamus after cortical injury represents decay of the fibers whose cell Bodies have been deprived of any outlet of their impulses. Presumably the cells of the medial nucleus have other connections. The fact that there was no localization of degeneration within the medial geniculate nucleus after localized injury to the auditory area has apparently disturbed Lashley considerably and caused misgivings as to the “relevance of the spatial differentiation of thalamus and cortex and such questions of functional organization.’’ Since his work, however, it has been established (Woolsey and Walzl, ’42) that there is tonal localization within the auditory cortex. This lends even more significance to the relevance of spatial differentiation than if there were point for point localization within the medial geniculate body since this might be regarded

CONNECTIOXS O F CEREBRAL CORTEX 315

as merely due to a natural orderly arrangement of fibers instead of a seemiiig necessity for unscrambling of the cochlear scale. Like Waller, Lashley made an attempt to correlate regions of thalamic projection with areal units of cortical structure, but the correlation was foredoomed because he did not use the areas as found in the albino rat, but instead con- structed a chart for the rat similar to that of Rose for the mouse. Jus t why investigators of cortical localization will attempt to translate the cortical maps of other writers on other species of animals to the form on which they are working instead of localizing their own lesions in terms of the cortical areas of that form is not clear to the present writer. As stated by Lashley “Lorente de N6 has pointed out serious defects in cyto- and myelinoarchitectonic studies unconfirmed by other methods,” but it seems to be piling confusion on error to modify these unconfirmed architectonic charts on the basis of intuitional judgment.

The study by Bodian ( ’42) of retrograde thalamic cellular degeneration after localized cortical injury of the opossum presents essentially similar findings to those of Waller and Lashley in the rat. While the opossum is a lower animal than the ra t and belongs to a different order, the plan of the thalamic nuclei and cortical areas is much like that of the ra t except for simplification and differences in proportion. Bodian had the advantage over the previous workers in the fact that Gray (’24) had previously worked out cortical areas in the same species so that it was possible to niake more meaningful correlations of thalamic nuclei with cortical areas. Most of’ the findings se,em well established but the material was not adequate to enable that writer to make conclusive statements about the connections of the anterior nuclei and the projections of the lateral nuclei are not entirely clear-cut. The failure to observe degeneration in the nuclei parafascicularis, parataenialis and paracentralis was perhaps due to the non- involvement of the orbital frontal region in any of the lesions analyzed. I t is interesting that in the opossum a polar frontal lesion is followed by a marked degeneration in the medial


nucleus, but this observation is not forthcoming in the rat. The incomplete degeneration of the medial geniculate nucleus was observed and regarded as due to intrathalamic connections. As with the work previously discussed, involvement of the medullary center has been a vitiating factor.

Essentially, the results of the various workers on thalanio- cortical projections are in agreement in spite of theoretical objections to the method of analysis. There is no point with which the findings of the present study are on serious variance with those just discussed. The work of Lashley with its large number of cases gives a much finer grained picture of intra- nuclear localization than does the present study. The paucity of lesions in the cingular region does not permit a study of retrograde degeneration in the anterior nucleus in our series. However, several facts are added in thalamo-cortical projection, particularly that of the cortical area for the parafascicularis, the submedius and ventralis medialis. Rose and Woolsey ('43), by complete and partial decortications of the rabbit and a study of the retrograde cellular degeneration in the thalamic nuclei showed that all of the nuclei of the dorsal thalamus proper degenerate after teleiicephalic ablation and it is hence considered that all dorsal thalamic iiuclei project to the cortex. According to Rose's subdivision of the thalamus there are 3 parts : epithalamus containing the paraventricular complex, the habenular nuclei and the pretectal group ; the dorsal thalamus, constituting the greater bulk of the thalamus ; and the ventral thalamus composed of the reticular nucleus, ventrolateral geniculate body and suprahypothalamic group. The first and last of these subdivisions do not degenerate under the conditions of the experiment so are considered as independent of the cerebral cortex (a part of the reticular complex is connected with the cortex).

It is to be borne in mind, however, that the correlation of points on the cortex with points in the thalamus is only a small part of the present work. The main object has been to discover the total connections of the cortex whether thalamic, projectional, callosal, tegmental, associational or otherwise,


and there has simply been no spsteniatic work on this subject in the lower mammals so it is impossible to extend the comparison of findings into these fields. Several attempts have been made to trace nonthalamic cortical connections in higher animals but these are so incomplete and the topographic differences a re so great that an attempt at comparison would not he instructive.

General results

This work has convinced the writer of the value and relia- bility of the llfarchi method, especially in the Swank-Daven- port procedure, as a tool for analysis of neural connections. I n the cerebrum and thalamus the backgrounds a re so clear and free from adventitious degeneration that sections of 80 p thickness may be studied to advantage. In general the statement that only the distal portion of a severed neuron degen- erates may be depended on. However, it is well known that under certain conditions injury to an axon results in prompt death of the cell. The best example of this is in the thalamus, where the sequence of events is so reliable that it is used as a research tool. If the cell dies, certainly i ts axon must die, and also the myelin sheath. Hence, after cortical lesions, any granules traceable to the thalamus are not necessarily cortico- thalamic in direction. If their position corresponds to known thalamo-cortical connections, as found after thalamic lesions, they must be conservatively regarded as arising from thalamic cells. This vitiates any Marchi evidence on supposed cortico- thalamic fibers in this or any other work. Such evidence can only be admitted if the connections a re to nuclei which a re kiiown not to send fibers to the region under question. The only certain way of determining whether reverberatory cortico-thalamic connections exist is actually to demonstrate the passage of axons of cortical origin into the thalamus.

Of the nuclei known to conduct to the cortex the medial is a n exception, since its cells do not degenerate retrogressively after localized frontal cortex damage, nor is there a trail of Marchi granules. Perhaps the axons from the other nuclei


are strictly projectional, and when deprived of aZZ exit for their impulses must eventually die, while tliose of the medial nucleus send collaterals to other nuclei or areas, and having an outlet, continue to live. Such collaterals have not been demonstrated, but the problem is an important one. At present we can only say that, if the above principle is correct, the cells which project to the cortex do not possess collaterals. This does not negate the existence of other thalamic cells which send fibers to other thalaniic nuclei.

Aside from this uncertainty, the results of this study have been gratifying to the writer and aid in giving a fixed point of departure in future work. I n addition to the specific connections of the individual cortical areas, certain generalities may be gleaned.

The belief of most workers on the thalamus that every nucleus (possibly excepting anterior dorsalis) of the true dorsal thalamus in the sense of J. Rose ('42) projects to the cerebral cortex is supported by the present work inasmuch as every thalamic lesion gave rise to degeneration to the cerebral cortex. Some of the smaller nuclei have not been involved and damage to some has not been separated from more inclusive lesions. On the other hand, some nuclei whose areas of cortical association were not previously known have been demonstrated, viz., parafascicularis, submedius, ventralis medialis. As a corollary to this, no connections of any dorsal thalamic nuclei have been shown to pass to any other structure than cerebral cortex. I n an anatomical stud:- of all of the more medial nuclei of the thalamus made several years ago (Krieg, '44) a singular dearth of internuclear connections was noted. This is in agreement with the complete- ness of cell loss observed after decortication, and the unity of cell type in Nissl and Golgi prepai.ations. (The medial nucleus proper is a possible exception.) As fa r as de< oenera- tion experiments have shown, the connections of the dorsal thalamus are esclusivcly to the cortex. The existence of iiiter- nuclear connections is not excluded but it shifts the emphasis


in degeneration experiments to a study of cortical connections and functions.

The afferents of the non-sensory thalamic nuclei are still poorly understood, and this investigation was not designed to show them. However, there is some evidence that such nuclei as the medialis and lateralis receive lemniscal collaterals.

An important goal in future work on the thalamus will be to determine what sort of afferent impulses are conveyed by each of the many thalamic nuclei to its cortical area and what is the significance of each in the economy of the organism. This will not be easy, but there is some comfort in the belief that the problem can be largely shifted from deeply lying thalamus to the more accessible cortex. However, it will be necessary to know much more concerning the thalaniic afferents.

The extensiveness of the descending projection connections of the cortex is regarded as one of the most significant findings. In the recent literature on the cortical connections of higher forms surprise has repeatedly been expressed as one area or another, except area 4, has been shown to have brain stem connections. In this work practically every cortical area has a descending connection at least as far as the peduncle, even discounting all possible cortico-thalamic connections. This fact does not lead one to suspect that a significant correlation between numbers of Betz cells in area 4 and number of fibers in the bulbar pyramid would be demonstrable.

It is also apparent that the cerebral cortex potentially connects with every part of the neuraxis, but in these experiments no myelinated fibers have been seen to end in striatum or hypothalamus. Radiations have been seen ending in subthalamic complex, colliculi, tegmentum, pons and bulb. Thus nearly all parts of the neuraxis may receive a cortical influence. This is in line with recent physiological investigation.

It is not denied that the hypothalamus may receive fibers from the basal frontal areas, as there were no lesions here. The study of normal preparations and physiological investi- gations support this.

320 WEEDELL J. S. KBIEG

The failure to show cortical connections to the striatum may come as a surprise to those who have found activity of the striatum paralleling cortical excitation. It is quite possible that all the cortical fibers to the striatum are unmyelinated collaterals. Even in a Cajal preparation there is no clear evidence of fibers diverging from the internal capsule.

Most of the areas showed a well-marked callosal connection. Some areas have abundant callosal fibers, some scant. This is not particularly correlated with any known aspect of function. The frontal areas make a massive contribution to the anterior forceps. Of the sensory receptive areas the somesthetic and auditory a re well represented, but there seems to be none for the visual. At least some of the retrohippocampal areas sliow a strong commissural connection, but the cingular region apparently has none. Some of the most outlying areas have definite callosal connections.

There is every indication that fibers of the callosnm are entirely parallel, a t least until the median plane is crossed. Localized damage in the cortex produced degeneration in only a limited region of the callosum and in definite positions for each cortical station. Thus the cortex may be imagined as projected onto a median sagittal section of the callosum as though viewed from the dorsolateral aspect, except that the areas are represented in much flattened form, and in different proportions.

As fa r as could be observed, all callosal coilneetiom are homeotopic. Callosal degeneration is never very heavy and the granules are small. There is a tendency for the intensity to decrease after the median line is crossed. Where the component is heavy, as in that from areas 10 and 2, granules in the opposite cortex correspond well in extent to that of the lesion on the opposite side. At any rate, no aberrant callosal fascicles were observed. Though some lesions were shallow there was no difficulty in deinonstrating an expected callosal component. This casts some doubt on whether the callosal fibers arise from the deepest layers as some believe.


The status of tlie associational system is of particular interest. It is the most poorly understood of the main groups of cortical connections. The nature and extent of interareal pathways is a matter of conjecture and theory but is of importance in an understanding of areal relations and functions. There seems to be a general belief that parts of the cortex in the primitive condition are interrelated by a diffuse feltwork of connecting neurons, mostly short, running in all directions arid equipotential. I n the evolution of the cerebrum as functions become impressed on regions, the more useful of these would become more pronounced and the others drop out, until in the highest forms there are definite long association pathways together with numerous “arcuate” fibers. It seems that a conditioiz more nearly the reverse of this holds true. Instead, in the lower brain there seem to be few association fibers of any sort. Here any unit of the cortex receives thalamic fibers, puts its stamp upon them and projects them to a definite place in the neuraxis. In fact, associational areas are greatly reduced in size in the rat, still more so in the opossum (Gray, ’24). One has only to look a t a section of the rat brain to realize how small a thickness of the medullary center could possibly be associational, once the obvious callosal and projection fibers are subtracted. The cingulum proper is a thalamic projection tract, not an associafion pathway.

It is apparent though that such association fibers as exist are intracortical. As shown in paper I, B (Krieg, ’46b) tlie inf ragranular laminae of many areas are packed with tangential fibers regarded as associational. The present work has confirmed this belief, f o r usually when laminae of granules pass to other areas they lie in layers v and vi. I f tliey run a long distance they tend to blend in with the medullary center. This leads to the generality that when associatioii fibers are first developed they tend to pass directly through the cortex to their termination. With an increase of such fibers they mass and become crowded deep to the cortex. This accounts


for the dearth of myelinated fibers of tangential nature in the deeper parts of the cortex of higher animals.

The most widespread association system in the rat brain is a lamina which accumulates from a wide region of the cortex and converges toward its caudomedial pole, i.e., t o areas 29 and 27. Many fibers in this lamina are tbalamic and many drop out a t various places along the route, Neverthe- less, there is a striking tendency for cortical prisms to become associated with prisms more caudoniedially located. This lamina forms the outer layer of the medullary center and blends laterally with the cingulum.

Another abundant association lamina, this one iiitracortical, gathers in area 2 and the other parietal areas and passes chiefly into area 10, but apparently not directly to the motor areas. Other fibers pass caudally. The primary sensory areas are to some extent centers of origin of intracortical association fibers, and these pass to contiguous nonsensory cortex. The undifferentiated areas receive few association fibers, and send fewer.

One of the major questions of general nature which this work should help to answer is that of degree of specificity of thalamic nuclei and of cortical areas. A study of thalamic cell degeneration after cortical lesions is not the most impeccable approach to this subject for even though a small cortical lesion niight result in specific thalamic cell loss, the possibility is not excluded that any cell unit of the thalamus supplies a relatively wide region of the cortex. For most locations this requires minute thalamic lesions, smaller than is practicable in the rat. The situation in the lateral nucleus is different, for. lesions here show that a number of areas are supplied. TT7hether or not there is orderly representation of these areas within the nucleus is uncertain. Perhaps the lateral nucleus transmits a general excitation to certain of tlie cortical areas, which by increasing or decreasing their excitation raises or lowers feeling tone or sharpens or dulls perception. At least no other thalaniic nucleus seems capable of this general influence.


Everything that has been observed about the cortical areas admits their being regarded as specific in their connections, and thus presumably specific in functions. The fact that a description of results subdivided by cell areas is possible without repetition is indicative of the essential soundness of this view. Specificity of thalamic connections alone would be sufficient to establish functional differentiation ; but the efferent connections reacclaim this specificity. Some areas, however, do not seem to have the same connections throughout their entire extent. Apparently only the rostra1 part of 18a has tegmental connections. Perhaps in such cases, we are dealing with 2 areas of which the anatomical differentiation has not been made. It would be unjustifiable to assume that in every case differences of connection are reflected in dif- ference in structure which we can detect in an architectonic study. The association fibers may not show specificity of connections as clearly as do projection tracts for they are not so distinctly arranged in fascicles passing to distinct nuclei. They are, however, arranged in laminae of parallel fibers which give every indication of being disposed in an orderly manner and thus furnishing the basis for the strictest specificity.

The orderliness of arrangement of fibers becomes inereas- ingly apparent wherever a new part of the nervous system is subjected to a closer study. As connections develop they tend strongly to follow direct courses and to keep parallel. All of the sense organs except smell and taste have an orderly internal arrangement either topically on the body, or with reference to the outside world, or with reference to the scale range within their modality. This pattern tends to be projected onto the secondary centers by the operation of the laws of growth of neurons, That this is extended into the thalamus has been adequately demonstrated for vision and somesthesis. Once the thalamus is reached the repetition of this pattern is practically assured, as the thalamic radiations have an undifferentiated matrix to grow in and are not strongly subject to space demands or primary distortion.

324 WENDELL J. S. I iRIEG

Descending projection fibers tend, likewise, to grow down along the outside of others, and to gather in the peduncle in an orderly manner. The Rlarchi studies illustrate this eloquently. Projection fibers in every case are locally segre- gated within capsule and peduncle. Within the poiitile pyramid they tend to scatter considerably however, and a t the junction of pontile and bulbar pyramids they become re- grouped so that fibers from any lesion a re almost evenly distributed.

The geneial subject of local segregation and extent of scatter within tracts is one on which the present study should furnish infoi-mation. Those cases in which there were 2 adjacent lesions separated by a short space allow observations on this subject. Such findings may be gleaned from the reconstructions. 111 general, bundles remain very separate through the capsule, but fibers from closely adjacent regions begin to blend as the peduncle is reached. Another aspect of this problem is the extent of scatter from any minute prism of the cortex. Some of tlie smallest lesions and most of the needle tracks allow one to see that, for example, in the frontal area even a minute lesion shows granules in several large fascicles though none of these is completely degenerated. I n the cing-ulate region the granules disperse considerably and in all these cases become lost in the capsule. Such con- siderations might be made the subject of a special study, but anyone interested can gain a tolerable impression from an inspection of tlie reconstructions. These do not always sliow such fibers as are isolated or outlying, however.

A few remarks might he made on the bearing of tlie study of the extent of involvement of the lesions themselves on the viability of cortical neurons under various insults. These ohservations a re made possible 1 1 , ~ tlie possibility of cor- rela tine on one section Marchi granules in tlie immediate vicinity of the lesion with recognizable cell damale. Most lesions were characterized by a complete destruction of tissue with removal of debris, but there is a zone of variable width in which only nerve cells are destroyed. This is usually only

CORNECTIONS O F CEREBRAL CORTEX 323

several cells wide. The neighboring area for a short space usually contained numerous Marclii granules not arranged like degenerating neurons. I n such areas the cells were to all appearances living and functional. Such accumulations were regarded as intercellular debris from the destroyed tissue. However, i f , for example, the supragranular layers were destroyed, the cells of the infragranular layers showed an entirely normal picture. Even if the cortex were extensively undercut, the outer layers would seem to have a normal appearance, though in area 2 there was a loss of the pyramidal cells of layer v-a. Such observations were repeatedly made and indicate that studies of retrograde degeneration are not applicable to the cortex as they are to the thalamus. To ex- plain them one can have recourse to the axiom that where there are collaterals not severed in the lesion, the cell remains alive. Cortical cells have numerous collaterals.

Finally, it should be stated that this work has left many unsolved problems concerning the cortical connections. By no means all points on the cortex were reached by critical lesions. No lesions of the cingular region were sufficient to determine the actual endings of the efferent fibers, and the connections of the caudal edge of the cerebrum are still largely unknown. The projections of some of the smaller thalamic nuclei are not known, in spite of the relatively large amount of work on the thalamus. A continuation of the methods used in this study should give answers to these problems.

There are problems remaining on the rat cortex which re- quire other approaches. It is to be remembered that nothing has been contributed in this series of papers on the intrinsic mechanisms of the cortex. The ground has been laid in establishing cortical areas and extrinsic connections, but what are now required are painstaking reconstructions of the neurons and endings in all parts of the cortex from Golyi material now largely prepared, supplemented by other methods. It is perhaps better to do this work on one form, and this should be the species which has been most thoroughly studied otherwise.


The more distant future presents possibilities of psychophysiological testing of animals after planned lesions, and the possibility of electrical determination of the conditions of activity of the circuits and neurons. The application of the latter, however, awaits refinements in electrophysiologic equipment which, like microchemistry, requires a new tech- nolo,gy.

The obvious extension of the study of cortical connections is to higher forms, and ultimately to man, a s fa r as conditions permit, and it is on these subjects that the writer’s efforts are now being applied.

SUMMARY

I n an attempt to determine the connections of the cerebral cortex of the albino rat 100 small lesions were placed with a stereotaxic machine in various parts of the cortex and thalamus, the degenerated axons visualized by the Marchi method, and their courses demonstrated by graphic slice reconstructions. Findings were synthesized and expressed in terms of cortical areas and thalamic nuclei.

Cortical areas Fro+zfaZ region. Area 10 sends numerous fibers through

the entire length of the hrain; they run almost in the sagittal plane and give off no radiations in their course. It has a strong callosal connection through the anterior forceps. The well- recognized projection of the medial nucleus to this area is not corroborated by cortical lesions, there being no retrograde degeneration of the thalamic radiations. Area 10 receives numerous association fibers from area 2.

Area 10a, newly separated from the medial portion of area 10, sends fibers the entire length of the brain through the pyramids without sending off any radiation on the way. It has numerous callosal fibers throuph the anterior forceps and rostrum of the callosum.

Area 4 sends numerous fibers into the bulb through the medial par t of the internal capsule and the second fifth of the

COBNECTIOGS O F CEREBRAL CORTEX 327

peduncle. No radiations may be observed throughout their course. Area 4 apparently does not receive projections from any of the thalamic nuclei nor does it receive any noticeable component of association fibers from other areas of the cortex.

Area 6 projects fibers which pass a t least into the peduncle, taking up a position lateral to those of area 4. There seems to be a considerable callosal connection.

Areas 8 and 8a seem to send no fibers into the capsular system. Area 8 receives the projection of the nucleus parafascicularis. 8a receives the projection of the nucleus submedius or of the ventralis medialis, or both.

Area 11 perhaps receives thalamic fibers from the submedius.

Purietol region. Areas 2 and 2a. This large region has numerous and distinct connections. There is a massive projection extending the entire length of the brain which, in the cerebral peduncle, occupies the superficial half of its middle third. A massive thalamic radiation connects with all parts of the ventral nucleus in its ventral and dorsal portions 0:-

cupying the coarse fascicles. Cortical lesions are accompanied by degeneration of the nucleus or the part of it which passes to the region damaged. There are also numerous fibers to the nucleus entopeduncularis and to the nigra. The dorsal part of area 2 is represented dorsally in the thalamus and the ventral part ventrally. The rostra1 part of the area is represented medially in the ventralis and the caudal part is represented laterally. In the peduncle more caudal parts of the area are represented more laterally. At the level of the nigra there is a distinct dorsally running teamental radiation traceable to the dorsolateral quadrant of the midbrain tegmentum. A well-marked callosal connection to the corresponding region of the opposite side exists. These fibers pass through a considerable extent of the ventral part of the callosum and are strictly localized within the area 2 region, the representation being like a much flattened version of area 2. Area 2 sends association fibers to areas 7 , 10 and 40

328 WEKDELL J. S. KRIEG

as well a s numerous fibers to other parts of area 2. These fibers lie in layer vi of the cortex or immediately under it.

Area 3 sends a projection tract down the brain stem and has a considerable thalamic radiation connected with the forward part of the lateralis or tlie ventralis dorsalis or both. It receives fibers from tlie rostra1 par t of the lateralis.

S r e a 7 . The projection tract from area 7 bends laterally and forward and then caudally within tlie fourth fifth of the peduncle, but disappears. From cortical lesions there is some evidence that area 7 is connected with the lateralis.

Area 40. There is a considerable projection tract through the lateral par t of the peduncle and poiitile pyramid. The thalamic connection is with the lateral extreme of the ventralis and there is a more caudally placed radiation to the zona incerta and a dorsally running radiation to the lateral tea- nientum. An interchange of association fibers exists between this area and areas 2, 1 arid 3. Other fibers pass backward to aseas 17 and 18.

Area 39 sends fibers through the dorsal par t of the putamen into the lateral par t of the peduncle to enter the medial g enicula te.

T c i n p o ~ n l region. Area 41. The auditory area sends a considerable projection tract through the lateral extreme of the peduncle whose fibers stream dorsally in the midbrain to elid in the inferior colliculus. The thalamic radiation, in this case caudal to thc main tract, curves sharply to enter the medial geniculate. These is a broad but thin callosal connection. Area 41 sends fikers to lb'a and to 17 and receives fibers from 18.

Area 20 sends a few fibers forward a coiisiderable distance to enter the internal capsule and has a large callosal connect ion.

Area 36 contrihutes to the most extreme caudal fibers of the internal capsule, but their termination is unknown.

Occipitnl ,ogiow. Area 17. The visual receptive area has a projection into the peduncle in addition to the visual radiation. The tesminatioii of these fibers cannot be traced, how-


ever. There is no evidence that area 17 has a callosal connection. There are some association fibers from the more rostra1 areas.

Area 18 sends a thin laminar tract forward which reaches the lateral extreme of the peduncle and divides into two. The ventral part soon leaves and turns into the dorsomedial tegmentum. The dorsal part keeps an outside position and ends in the dorsal part of the lateral geniculate body. Area 18 probably has a callosal component through the posterior extreme of the splenium and the area also probably connects with the lateral nucleus in its posterior portion. Area 18 has reciprocal connections with a widespread region of the cortex, particulady the auditory and somesthetic, but also from 17 and 18a. In addition there are intraareal association fibers passing backward.

Area 18a. Area 18a sends a forward running lamina curving around the posterior arch of the hippocampus to join the peduncle and immediately diverge dorsally. Many fibers pass to the superior colliculus in laminae ii and iv. Other fibers pass to the tegmentum. Area 18a sends a few callosal fibers to the opposite side and interchanges association fibers with area 18.

Iv~sular regior?. Areas 13, 14. Projection fibers run directly medially through lower part of caudate and outside of peduncle to end in entopeduncular nucleus. Callosal connections exist. Intracortical association fibers run dorsally to areas 3, 1 and 2 and the insula receives fibers from more dorsal region.

Cingulnr rcgion. Area 24 receives fibers from the medial portion of the thalamus, probably from the the anterior vent r alis.

Area 23 receives fibers through the cingulum from the medial part of the thalamus, but its afferent and efferent connections are less numerous than in the other cingular areas.

Areas 29b and c send numerous projection fibers laterally and forward into the internal capsule, but they cannot be followed into the peduncle. The areas 29 receive afferents

330 WENDELL J. S. IiRIEG

from a wide variety of sources. A large number of the fibers from tlie medial tlialamus carried back by the cinguluiii terminate here, but contributions a re received widely from the anterior arid intermediate thalamic radiations coming from the entire extent of the lateral nucleus. These fibers are laterally placed and connect with more caudal points in the areas.

Retrohipyocai,apal region. Area 27. Area 27 has extensive afferent connections from tlie thalamic nuclei. The anterior nuclei discharge into i t through the cingulum and the nucleus medialis pars lateralis as well as the ventralis in both of its main and its medial parts all contribute to it, adding on to the cingulum laterally.

Area 35 sends callosal fibers through the splenium and has some forward running fibers, probably projectional.

Area 28 sends some fibers to the splenium. Cortical amygdaloicl nucleus connects with the basal amyg-

daloid.

Coniicctioiis of the thalamic izuclei

Anterior group. The anterior nuclei form the greater par t of the cingulum. The fibers passing forward bend dorsally to reach the cingulurn all the way from the anterior end of the thalamus to the t ip of the caudate. They are distributed to the entire cingular and retrohippocampal regions. The anterior ventralis contrihutes mostly to the anterior part of the cingulum and the anterior medialis to the posterior part. The anterior dorsalis could not be shown to send a cortical radiation, but if it does it should be located fa r caudally in the limbic region. There is a true interanterodorsnl com- niissure. The mainmillo-thalamic tract supplies all parts of the anterior nucleus. I f it conducts toward the mammillarp bodies also, i t is only to an insignificant extent.

HabenuZa. The projection of tlie habenula to tlie interpeduncular nucleus is amply demonstrated, but ail additional connection is iidicated to the ventromedial tegmental region.


Stria medullaris . The stria medullaris contains crossing fibers through the habenular commissure which begin in the nucleus preopticus lateralis and hypotlialamicus lateralis and end in the same nuclei of the opposite side.

The nucleus subniedius and the nucleus ventralis medialis canriot be distinguished for sure in this series as regards their area of cortical projection. After lesions to these nuclei fibers run forward to the most ventral part of the anterior thalamic radiation to area 11, the primordium of the orbital areas.

Pe~~tro la tcr t r l group. Ventralis. The nucleus ventralis in both its parts projects to area 2. The topology is summarized under area 2. The lateral part of the nucleus connects with area 40 and it is likely that ventral nucleus fibers pass to areas 1 and 3. The anterior part rnay connect with the motor areas. Dorsal and ventral divisions seem to have similar coii- riections and the topolo,gy of the dorsal division repeats that of the ventral.

Xucleus lateralis. Sends off an extensive lamina forming the most dorsal fibers of the intermediate radiation. These end in the various areas of the caudomedial half of the cortex, possibly excepting 29b.

Xedial geniculate. Projection of the iiiedial geniculate body corresponds to the auditory radiation, passing through the putamen some of the fibers taking a quite aherrant course. They end in area 41 and to some extent in 18a.

Lateral geniculate. There is evidence for an antidromic tract along the optic tract, but no information is available on the nature of the optic radiation.

Nucleus posterior. This structure seems to send a few fibers in the dorsal caudal part of the posterior thalamic radiation toward the caudomedial angle of the cerebrum. There are numerous fibers of passage in the nucleus and near it, to the superior colliculus and from the striatum.

Sub t ha1 amus Z o m incerta. A tract in the region rostromedial to the

medial geriiculate body ends in the zona incerta. Other con-


nections come through the dorsocaudal region of the thalamus. The origin of these is not known.

Nucleus entopedumulnris. Area 2 and area 13 send fibers to this nucleus through the cerebral peduncle.

Nigra. Area 2 sends fibers to the nigra and there are many fibers which pass through this to the teamenturn from this and other areas.

Midbrain STuperior collic2~lzcs. The superior colliculus receives abun-

dant fibers from 18, 18a and possibly from 2. These converge in the 2 fibrous laminae of the superior colliculus (laminae ii, iv) which run its entire length and terminate in the more superficial layers throughout its estent. Fibers of lamina ii converge from 3 main sources: (1) from 18a over the surface of the geniculate bodies; (2) a group which passes through the nucleus lateralis posterior and (3) another which occupies the pretectal region. The abundant fibers of lamina iv come chiefly from 18a but possibly from 2 also. They are in 2 groups, one of which radiates dorsally from the peduncle, running medially to the lateral geniculate, and the other which never reaches the peduncle but runs through the lateral genicula t e.

Inferior coZ2icz~2us. Fibers to the inferior colliculus begin in area 41 running through, the putamen with the auditory radiation but reach the lateral extreme of the peduncle which they soon leave streaming dorsally to become exhausted in the inferior colliculus.

Tegmeiztum. There are numerous descending connections to the tegmentum chiefly from area 2 where they stream dorsally through the nigra, particularly from area 18 where they run from the lateral part of the peduncle directly dorsally to the dorsomedial tegmentum: a few from 18a and some from area 40. There are few or no descending tegmental fibers originating in the thalamus, though of course there are many from the striatum which pass through the caudolateral part of the thalamus.

CONNECTIONS OF CEREBRAL COR,TEX 333

Medial Zesianiscus. The medial lemniscus ends abundantly in both parts of the ventral nucleus and passes also to the medial and the lateral nuclei.

Ge Neralities The Marchi method is of great value in the study of the

connections of the cerebral cortex, but it cannot be expected to show the direction of conduction of fibers connecting thalamus and cortex after cortical lesions. Thalamic neurons probably degenerate after cortical lesions because they possess no collaterals; the medialis then would be an exception.

Every nucleus, except possibly the anterior dorsalis, and certain others insufficiently examined, send fibers to the cortex. The cortical areas of some thalamic nuclei have been identified for the first time. In our preparations none of the dorsal thalamic nuclei send axons anywhere else than to the cortex. Internuclear myelinated thalamic connections are very scant in the rat.

Nearly every cortical area sends nonthalamic projection fibers to the cerebral peduncle o r further. These connections pass to nearly every main division of the brain, though in this study none have been seen to pass to the striatal complex or to the hypothalamus.

Most areas have a homeotopic callosal connection. These are systematically arranged in the callosum. No heterotopic callosal connections have been observed, though the possibility has not been excluded.

There is no evidence of an undifferentiated feltwork of interareal association fibers. Most association fibers of the rat are intracortical throughout their course. There is a strong tendency for points in the cortex to send fibers to points caudomedially placed, so that the retrohippocampal region receives from widespread thalamic and cortical regions. As- sociation fibers of all sorts are relatively few in the rat.

There is a high degree of point for point correlation both in the thalamo-cortical connections (except for the lateral and

334 WENDELL J. 8. KRIEG

medial nuclei), and in interareal association fibers. The descending corinectioris a re specific for the several areas. These occupy limited regions within the internal capsule alld peduncle, but such a s continue to tlie bulbar pyramid become mingled.

Destruction of the outer layers of the cortex, or undermining of the cortex does not result in substarltial cell loss of the rernainiiiq layers. This is regarded as predicated by the iiumerous collaterals of cortical cells. Retrograde degeneration is not regarded as a fruitful inethod of investigation of the cerebral cortex.

Future problems are the clarification of the connections of cortical regions riot thoroughly studied in this series, the aiialpsis of intrinsic rnecliaiiisins in each of the cortical areas, the use of psychophysiological testing after planned lesions, the applicatioii of electi.ophysiologica1 methods of detection, and an extension to higher forms.

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the rat. Pliilos. Trans. Roy. Soc. Lond., B, B?: 1-28. C L ~ R K , W. E. LE GROS, A S D R. H. BOGGON 1933 On the coiniections of the

anterior nucleus of tlie tlialnmus. J. Annt., 67: 215-226. GERERTZOFF, M. A. 1937 Svst6in:itiwtioii des conuexions thalnnio ($01 ticnles des

aires frontales, centrales et pari6talPs. La Cclllule, 46: 7-54. GILLILAN, L. A . The nuclear pattern of the nontrctal portions of tlie mid-

brain and isthmus in rodents. J. Comp. Ncur., 78: 413-251. GRAY, P. L4., JR. The cortical lamination pattern in the opossum. Didelphys

virginiana. J. Conip. Neur., 37: 221-261. GCIRDJIAN, E. S. 1927 The dicncep1i:ilon of the albino rat. J . Comp. Neur., 43:

1-114. D'HOLLANDER, F. 1913 Reclierches anntomiqucs sur les couches optiques. La

topographie d e ~ nopaux tlialainiqucs. La NBvraxe, 25: 471-519. KRIEG, WENDELL J. R. The medial region of the th:ilamus of the albino

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Topography of the cortical areas. J . Comp. Neur., 8 4 : 221-275. __-__ 1946b Conneetions of the cerebral cortex. I. The albino rat. B.

Structure of the cortical areas. J. Comp. Neur., 84: 277-324. 1 9 4 6 ~ Accurate placement of minute lesions in the brain of the

alhiiio rat. Quxr. Bull. Northwestern Univ. Med. School, 20 : 199-208.

1943

1924

1944


LASHLEY, I<. S. 1941 Thalamo-cortical connections of the rat’s brain. J. Comp. Neur., 75: 67-121.

MONAKOW, C. VON 1882 Ueber einige dureh Exstirpation circuniscripter Hirn- rindenregionen bedingte Entwickeli~ngshemmungen des Kaninchen- gehirns. Arch. f . Psych., 19: 141 and 535.

MUNZER, E., AND H. WIENER Das Zwisehenhirn und Mittelhirn des Kanin- chens. Monatschr. f. Psych. und Neur., 12: 241.

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POLIAX, S. 1932 The Main Afferent Systems of Primates. Univ. of Calif. Pub. in Anatomy, 2: xiv + 370 pp., Univ. of Calif. Press, Berkeley, Calif.

ROSE, J. E. 1942 The ontogenetic derelopment of the rabbit diencephalon. J. Comp. Neur., 77: 61-129.

ROSE, J. E., A N D C. N. WOOLSEY A study of thalanio-cortical relations in the rabbit. Bull. Johns Hopkins Hosp., 73: 65-128.

ROSE, hf. 1939 Cytoarchitektonischer Atlas der Grosshirnrinde der Maus. J. f . Psychol. u. Neur., 40: 1-51.

1931 Cytoarchitektonischer Atlas der Grorshirnrinde des Knnin- cheiia. J. f . Psychol. u. New., 4 3 : 353-440. 1909 On the structure and functional relations of the optic thalamus.

Brain, 32: 95486 . La projection des nogaux anterieiirs du thalamus sur I’ecorce

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1902

52: 867-953.

1943

SACHS, E.

RTOFFELS, J. 1939a

1939b

1938

1934

WARD, ARTHUR A., J. K. PEDEN AND 0. SITGAR

453-461. WOOLSEY, C‘. N., A N D E. M. WALZL 1942


EXPLANATION O F FIGURES

Nearly all of the illustrations are slice reconstructions of transverse sections prepared by the Marchi method. Except for outlines arid landmarks they show only the lesion and the degenerated neural connections. The brain is regarded as divided into several slices which are imagined as transparent. The lesions are depicted as hollow shells with blackened walls; the tracts a re viwalized as solid cords, strands or trunks, the direction and depth of the contour shading indicating their course. Their direction of conduction and course is shown by little conical ' ' bullets. ' '

The various brains are not divided in the same transverse plane. Whatever section plane and thickness was expedient was used. The approximate positions of the slices are indicated by the numbers a t the lower right hand side. These refer to the transverse planes established for the stereotaxic machine, and illustrated at millimetric intervals in a prerious paper (Rrieg, '46c). The plane of section does not exactly correspond to the plane of the stereotaxic machine, however.

There a re from 1 to 4 lesions in each brain, and each is designated by a Roman numeral (I, 11, etc.). Each group of fibers receives a lower case letter designatioii (a, b, c, etc.), enahling it to be followed in all of the slices of any one brain. The extent of the cortical areas concerned is indicated hy radial dotted lines or by faintly drawn sloping walls, and designnted with arabic numerals preceded by a double cross (#l, #2) . In some cases the extent of distrihution of granules is indicated by a transparent envelope.

It is inevitable in such reconstructions tha t representations must be highly con- ventionalized, tracts represented as solid or divided into firm cords and rigid boundaries set up, bu t every attempt was made to conform to the actual situation as f a r as limitations would permit.

All transrerse reconstructions were built up by actual projection of sections a t a magnification of 20 X but in reproduction were reduced by 37% to 50%, de. pending on size of original drawing.

LEGENDS FOR FIGURES

Figitre 1. F H .

thalamic par t of lesion 111. On left of first drawing is a dorsal reconstruction of course of fibers from

11. Lesion shallow, fused with I V , no degeneration. 111. Lesion t o anterior end of thalamus including radiation and touchini inter-

nal capsule; h, descending capsular connections from direct damage ; j , tegmental radiation from h to layer i v of superior colliculus; k, thalamic radiation to cxten- sive region of dorsal cortex (Th-Go).

TV. Rostra1 par t of #18a damaged: a , h, c, to la,ver iv of superior cnlliculus; d, t o lateral tegmentum; e, throrigh lateral geniwlate to lamina iv of superior rollicu- 111s (S.C.iv) ; f , t o medial tegmentrm; g , projection tract, becoming dissipated in lateral par t of pediinclr.


Figure 1 A

Figure 1 B


Figlire 2. F N . 1. Damage to middle of # i : a, i ts projeetion tract. 11. Cortical part. Extensive damage to caudal part of #B and #7 and rostra1

part of #18: l), pro,jection, extmsive; c, thalamic radiation toward lateral nucleus; d , eingiilar fibers damaged 1)y lesion.

Figure 2 A

CONNECTION 6 OF CEREBRAL CORTEX 339

11. Hipp. Damage to hippocampus touching nucleus lateralis posterior : e, to

111. Needle track ending in hippocampus: f, projection fibers severed in corona

IV. Small lesion (not shown) to caudolateral part of #lo: h, projection fibers

lamina ii of superior colliculus, no fibers are contributed t o thalamic radiation.

radiata; g, direct damage to cingulum.

into peduncle blending with b.

Figure 2 C


Figuve 3. FO. I. Small shallow injury to medial end of #Z through layer iii: a, projection tract

disappearing within caudate ; b, callosal fibers. 111, IV. Cortical part; nearly symmetrical damage t o middle dorsal cortex ex-

cept I11 is smaller. Lesion I V includes more of #7 and #18: c, projection tract from region of #7

continuing through bulbnr pyramid; d, projection tract from #29c; e, cortico-

Figure i B


Figure 3 C

Figtire 3 D

thalamic degeneration from #4 to lateral nucleus; f , descending cortical fibers over thalamus to superior colliculus ; g, extensive callosal connection from both cortical lesions: 11, needle track damage to forn i r longus; cingulum also damaged above callosum ; j , pedunculnr radiations from d to dorsomedial tegmentum.

111, IV. Thalamic pa r t ; pure lesions of parafascieularis bilaterally: k, parn- fascicular projection fibers from thalnmns forward through caudate leaving a t anterior pole of caudate t o terminate in #S, a few, m, pass into #10a.


Figure 4. FR. I. Cortical pa i t (I Co.). Small lesion a t junction of #39 and #18a; a, projection

fibers forward, above and through dorsal extreme of putamen curving downward t o lateral pa i t of peduncle; b, radiation to thalamus; c, radiation from a through lateral geniculate to layer ii of superior colliculus; d, radiation from a through caudal part of ventral nucleus to layer iv of superior collieulus; e, direct radiation t o medial geniculate ; f , sparse callosal fibers ; g, caudomedially directed association tract over medullary center to #17.

I. Thalamic par t (I Th.). Extensive lesion t o left habenula (Hab.), para- ventricularis (Pv.) , most of medialis (Med.), parataenialis (Pt.) , anterior medialis (A.M.), and lateralis: h, projection into intermediate and anterior thalamic radiations, the most caudal fibers a re in intermediate thalamic radiation and end in #3, the more anterior ones join the eingulum, the most rostral being most medially placed in cingulnni, connections t o #Z9c and #27 through length of eingulum ; S.D., interanterodorsal commissure.

11. Very extensive lesion involving entire rostral half of dorsal cortex: j, extensive projection system involving most of fibers of caudate and occupying medial half of peduncle extending through bnlbar pyramid ; k, thalamic radiation from j to ventralis anterior (Vent. Ant.) , anterior lateralis (A.L.), anterior dorsalis (A.D.) and lateralis anterior ( L A . ) , dorsolateral two-thirds of ventralis free of granules; m, caudal cwriponc~nt of thalamic radiation sweeping through nucleus ventralis to caudal part of nucleus ventralis dorsalis; n, from j to zona incerta a s fascicles through \ entralis dorsalis into dorsomedial tegmentum, some possibly C I ossing in postei ior cornmisswe; p, midbrain radiation similar to n hut stopping a t anterior plane of superior ca l l icu l~~s ; q, radiation from j through nigra into central tegmentnm, some fibers ending in nigra (see text: n ig ra ) ; r, radiation from j to ventromedial tegmentum, possibly to red nucleus (manv granules in pontile tegmentum of affected side) ; s, lateral contribution t o cingulum rxtending remainder of its length ; t, extensive ca1lo~:il degeneration.

Figure 4 -4


Figure 4 B

Figure 4 C


P’igure 4 D

Figure 4 E

C O N N E C T I O N S OF CERPBRAL CORTEX 345

Figure 5. F T . The first drawing is a dorsal reconstruction of the degenerated fibers ending in

cortex. I. Small cortical lesion in anterior part of #17: a, projection fibers into lateral

part of capsule, dwindling away, some passing to region of lateral geniculate; b, rallosnl fibers; c, cortical association caudally and medially to #IS.

JI. Small cortical lesion in anterior par t of #18a: d, projection tract in lateral extreme of peduncle dwindling away therein, *, a separate lateral fascicle diverges here to lateral tegmentum medial to medial geniculate ; e, sparse thalamic connection probably to lateralis dorsalis (L.D.).

111. Damage to medial part of medialis (Med.), anterior medialis (A.M.) and, posteriorly, rhonlboideus (Rh.) and submedius (Sub.) ; f , severed projection fibers in medullary center; g, severed fibers of lateral extension of cingulum; h, thalamo- cortical fibers through medial third of caudate entering cingulum and extending its entire length to end in #lo, #10a, #24, and #29b (j).

Figure 5 A

346 WENDELL J. S. ICRIEG

Figure 5 B

Figure 5 C

CONNECTIONS O F CEEEBRAL CORTEX 347

Figure 6 . FU. I. Cortical part (I Co.). Destroys most of #3, extends t o #4 and #l: j, exten-

sive projection system through medial part of caudate and deep part of middle third of peduncle becoming medially placed a t midbrain level and continuing into bulbnr pyramid; k, thalamic radiation toward nucleus lateralis ; w, interrupted component to lateral extension of cingulum joining h laterally.

Figure 6 A

Figure 6 B


Figure 6 0

Figure B D

I. Thalamic part (I Th.). Small lesion involving all of anterior nuclei, rostral part of nuclei medialis, parataenialis and rostral end of reticularis, including much of anterior thalamic radiation and severing stria medullaris ; g, cortically directed fibers in anterior thalamic radiation and rostral par t of intermediate radiation running dorsally throughout entire anterior medial pa r t of caudate, contributing to cingulum, the more posterior fibers being more lateral; h, continuation of g into cingulum throughout its length ending throughout medial cortex; m, two-way degeneration in stria medullaris to lateral hypothalamic nuelpus and anterior olfartory nucleus ; M.Th.deg., degeneration in mammillothalamic tract.


11. Extensive cortical and medullary lesion to middle part of #2 and most of #l; n, extensive capsular component becoming middle third of peduncle, continued in bulbar pyramid, + ; a, radiations to nucleus ventralis dorsalis passing through central par t of nucleus ventralis ventralis (b ) and sending fibers there, and running most of length of lateral par t of ventralis; c, a more caudal radiation under dorsal thalamus becoming dorsomedially directed behind thalamus, ending in laper iv of superior colliculus; d, a radiation at midbrain level into dorsal tegmentum; e, more lateral fibers of similar nature; p, severed fibers to lateral wing of cinguliim ending in #29c and #27; q, strictly intracortical association fibers to #7 and caudal par t of #2; r, rostra1 and ventral intracortical association fibers to #40, anterior part of #2 and #lo.

111. Cortical lesion to middle of #IS undermining adjacent #17; 8, projectional (and interrupted callosal) fibers running forward to join lateral extreme of peduncle ; t , tegmental radiation from s, passing under thalamus to dorsomedial tegmentum; u, projection fibers from s to lateral genieulate probably optic in nature; v, interrupted callosal fihers from medullary par t of lesion 111.

Pigare 7. PI. I. Small cortical lesion just behind middle of medial part of #lo, projection fibers

run as f a r as peduncle, callosal fibers (ex.) through anterior forceps. 11. (Crosshatching.) Destroys all 3 parts of anterior nucleus (A.D., A.V., A.M),

projection fihers forward through medial par t of caudate turning dorsally to form cingulum and extending most of its length, t o #lOa (interrupted fibers from nucleus medialis), #24, #6, few to #33 and #29b, many to #2Rc and #27; passage of needle track (not shown) through medullary center below #4 interrupts fihers of lateral wing of cingulum ending in anterior par t of #29c (see sectional diagrams a t left. Th designates cingular fibers from thalamus; c, indicates fibers interrupted 11j needle).

Figure 7 A


Ptgure 8. PI'. I. Cortical lesion t o middle of #4 extending into #3: a, numerous projection

fibers along medial aspect of caudate into deep par t of middle third of peduncle continued a t least through pons (I Co) ; b, tlialamic radiation from a to nucleus ventralis; c, radiation from a to zona incerta; d, interrupted cingular fibers from ventral spur of lesion; e, callosal connection.

11. Small cortiral lesion a t anterior junction of #17 and #IS or #7 : f , projection tract to lateral part of peduncle; there are thalamic radiations to nucleus lateralis (To Lat.) . 111. Destruction of posterior par t of #Ma, encroaching on # 1 7 : g, projection

tract t o dorsal par t of putamen; h, in extreme caudal par t of posterior thalamic radiation keeping superficial position on thalamus, ending in lateral geniculate ; j , continuation of g i n ventral part of posterior th:rlarnic radiation to or past lateral geniculate.

Figure 8 A

CONNECTIONS O F CEREBRAL CORTEX

Figure 8 B

Figure 8 C

353 WENDELL J. S. K R I E G

Figure 9. FZ. I. Superficial damage to preoptic region lighting up filwrs running in medial

part of layer i i superior colliculus. 11. Cortical in,jury to rostra1 part of #10n showing projection tract tllrough

caudate into medial par t of internnl capsule and pedmiclc; there is n callosal component to rosti um of callosum.


Figure 10. G A . I. Narrow needle track through #29c: a, projection tract from cells of #29c

into medial part of internal capsule, lower par t of lesion in hippocampas permitting fornix fibers (d ) to be followed to mammillary body; there are no fibers given off to hypothalamus along course of fornix.

11. Cortical lesion to caudal medial end of #10a: b, !ong projection fibers along medial edge of caudate and second quarter of deep half of pediincle.

Anterior eommissiire is drawn in a R a landmark only.

.Figure 10 A

Figure 10B


Figlcre 11. G B . I. (',ortical portion. Necdle track in forward par t of #29c and cingulum: a,

projection fibers from cells of #29c into dorsomedial part of internal capsule, becoming lost ; b, interrupted cingular fibers running remainder of length of cerehrunl ending in #29b and #87. I. Thalamic portion, small part of pretectal nucleus and posterior conlmissure :

c, d, commissural fibers into medial part of tegmentilm from :interior extreme of commissure; e, interrupted fibers of medial par t of lamina i v of superior colliculus.

Anterior extreme of #59c touching #4 : numerous fibers into internal capsule. I I .

Figure 11 A

Figure 11 B


Figure 11 C Figure 12. GC.

I. Small lesion a t junction of #IS, #4, #3 and # 7 : a, extensively distributed projection tract through peduncle and to bulbar pyramid ; b, callosal fibers.

11. Needle track through #29b, layer ii: b, from layer ii cells into cingulum running forward 2 mm then lateralward, becoming lost; d, e, bilateral degeneration in stria medullaris from direct damage, ending in lateral part of lateral hypothalamic nucleus.

Figure 12 A

356 WEKDELL J. S. KRIEO

Fiyur r 13. G D . I. Cortical part. Needle track damage t o layer v of #29b: a, projection tract

into middle third of deep half of capsule, becoming lost ; b, caudally degenerating fibers interrupted in cingulurri.

I. Thalaniic par t ; nearly complete destruction of habenular nuclei impinging slightly on caudal par t of nucleus niedialis : c, habenulopeduncular tract degenera tion (see text: liabeiiulopeduncular t rac t ) ; d, fibers in anterior thalamic radiation from caudal par t of medial nucleus running forward under anterior nuclei through medial par t of ventral nucleus and medial part of caudate to polar part of #lO, some passing to #S and #11: e, f , bilateral degeneration t o stria medullaris frotn direct damage.

11. To posterior part of #29c: g, fibers running f a r laterally and rostrally tir coming deeper in medullary center, possibly reaching thalamus ; h, rostrolaterally directed radiation around hippocampal arch to 1ater:ilis posterior; j , callosal fibers directly damaged.

(Anterior conmiissure not degener:itcd.)

Figure 1:: A


Figure 13 B

Figure 13 C


Figure 14. GF. I. Cortical part . Extensive damage to medial part of #4 : a, projection fibers

through capsule and a t least through pons. 1. Thalamic par t ; only portion of anterior nucleus damaged is anterior ventralis

(A.V.) and this completely, extends to involve ventralis medialis parvocellularis (V.Pa.), mammil1oth:ilamic tract (M.Th.) and submedius (Sub.) : b, thalamo- cortical fibers through medial par t of ventral nucleus fanning out in medial part of caudate, some running laterally (c) others dorsally (a) the remainder remaining medial and piercing rostral end of caudate; e, to #S; f , t o #11; g, the most rostral e n d medial cingular fibers, ending in #24; h, more lateral cingular fibers possibly to #23, also degenerated is interanterodorsal commissure and some granules caudally toward medial nucleus ; j, interrupted cingular fibers from needle track.

11. Small lcsion t o medial part of #10a: k, projection fibers through most medial part of pontilr pyrnnlid ; ni, callosal fibers through dorsal part of anterior forceps.

(Anterior commissure not degenprated.)

Figlire 14 A


Figure 14 B

Figure 14 C

360 W E N D E L L J. 6. KKIEG

Ftgrrre 15. G H . 1. Puncture of main par t of #4 extending through medullary center and de-

stroying lateral half of stria medullaris (S.M.) : a, b, projection fibers a t least through pons ; c, d, two-way degeneration in stria medulkris across habenular commissure (hx.) extending to lateral hypotlislamic nuclei on both sides; e, laterally directed fibers of lamina zonalis thalami tu iinknown destination.

11. Damage to caudomedial part of # lo : g, projection tract through capsule and peduncle a t least tlirough pontile pyramid : 11, callosal conlponel~t t o anterior forceps.

Figure 15 A


Figure 1 5 B

Figure 15 C


Figure 16. GI. I. Extensive damage t o main par t of #4 and #S undermining medial end of #2

somewhat: a, projection fibers running entire length of brain (cortico-spinal tract) ; b, callosal component t o anterior forceps.

Figure 1 6 A

Figure 1 6 B

COXNECTIONS O F CEREBRAL CORTEX

i u I

Figure 16 C

363

Figure 18 D

11. Small cortical lesion a t apex of # lo ; c , projection tract running entire leiigtli

Cross-sectional diagrams illustrate position of degenerated f ascicles witiiiri of brain; d, callosal component.

peduncle and pontile pyramid a t levels designated.

3134 WENDELL J. S. XRIEG

Figure 17. G J . Lesion is a vertical needle track through middle of #29 parallel to i ts surface

slightly nicking stria medullaris: a, projection tract through middle of deep par t of capsule becoming lost a t beginning of peduncle where fibers are scattered in second fourth of deep portion; b, a few degenerated fibers in stria medullaris t o lateral hypothalamic nucleus.

Figure 17 A -

Figure 18 .4


Figure 18. GE.

pontile pyramid ; b, callosal connection. I. Small lesion in caudal and lateral part of #lo : a , projection tract through

11. Needle track involving fibers froni #89c: c, projection fibers into capsule. 111. Superficial injury to fibers over pretectal region: (1, interrupted fibers to

layer ii of superior colliculus.

Figure 18 B

Figure I8 C

WENDELL J. S. ICRIEG

Figure 19. G M . Lesion, a perforation tangential to anterior end of #S extending slightly into

caudate: a, interrupted forward-running fibers to #Z ; h, interrupted projection from anterior end of #2 giving distinct connectioos to entopeduncular nucleus and nigra not diagrammed here; c, to medial third of rentrolateral nucleus; d, eallossl connection t o anterior forceps : e, bilateral degeneration in stria medullaris from another lesion not analyzed here (position indicnted by *).

Figure 19 A

E’igure BO. G N . The fir& drawing is a dorsal view of a reconstruction of the degeneration from

lesion I. I. Destruction of entire medialis of one side together with pnrataenialis and

anterior medialis and some of rhomboidalis : a, thalamic radiation constricted between reticulsris and anterior nuclei and joining cingulum a t all levels, some passing to frontal pole; b, degeneration in cingulum entering cortex along course of same; d, anterolateral offshoot to #8.

11. Small lesion to caudal part of # l o : e, projection tract running directly caudally through pontile pyramid ; f , callosnl connection.

367

.e 2 0 A

Figure 2 0 B


Figure 21. GP. Direct damage t o middle of #10 with undermining of lateral part of #lo and

rostra1 end of #2, radiating lines and dots indicate aTeas undermined: a, projection fibers running through nicdial part of peduncle ; b, tegmental radiation ; c, thalamic radiation t o a strip within medial part of ventralis the granules being located in both ventral (vent.) and dorsal (Vent.P.dors.) portions of nucleus ; d, callosal connection through anterior forceps.

Figure 21 B


Figure 88. GQ. I. Cortical part; needle track through #29b and c: a, projection fibers through

medial part of internal capsule disappearing before midbrain. I. Thalamic part; in caudal half of medial nucleus (Med.) : b, cortical projec-

tion through medial extreme of nucleus ventralis, caudate and cortex of frontaI pole. IT. Cartical lesion in middle of anterior half of #2: c, projection fibers through

pons; d, thalamic radiation a t anterior end of ventralis running longitudinally through ventralis ventralis in its middle part continuing in ventralis dorsalis ; e, callosal connection.

Figure 2 2 A

Figure 2 2 B

370 WENDELL J. S. ICRIEO

Fl<Jlirt' 23. GR. I. Needle track producing: a, cnpxiilar degcneration and b, cingular degen-

eration. 11. To lateral part of #ti and #4: c, projection tract as far as peduncle with

1~OHsihle connections t o ~ e n t r a l i s ( * ) ; d , callosal connections.

Figure 23 A


Figure 24. GS. 1. To anterior half of #18a extending t o #17, involving nledullary center con-

siderably: a, projection fibers running a t first forward through putamen and di- viding -into 2 groups as they round hippocampal arch, the main portion runs into peduncle where it disappeais, while the dorsal portion (b ) skirts lateral gellieulate and enters lamina iv of superior colliculus; c, interrupted callosal fibers; d, association tract to caudal end of #IS; e, interrupted ventrally running fibers of external capsule.

11. Cortical part. Small perfoiation on boundary between #4 and #3: f , its projection tract distinrt from adjacent corticothalamic fibers and traceable into peduncle. XI. Thalamic par t ; destruction of middle third of ventralis ventralia (V.V.) and

dorsalis (V.D.) : g, thalamocortical fibers dorsalward through intermediate radiation and dorsal part of internal capsule sending granules (h) into cortex at dorsorostral extreme of #2, t o #4 and #S and a few to #3 and #lU; these thalamocortical fibers continue through cinguliini indicating tha t ventral nuclei distribute to cingular cortex; j, retrogressively degenerated fibers to medialis. 111. An irregular lesion primarily t o #18a in i t s rostral par t bu t considerably

undermining #36 and #35; k, principal projection tract from #18a around posterior a r rh of hippocampus terminating as tegmental radiation : m, n, to dorsolateral par t of tegmentum forming capsule around medial and caudal aspects of medial geniculate possibly ending in inferior colliculus (p) ; (1, retrothalamic fibers from

Figure 24 A


Figure 2 4 B

projection tract as it enters peduncle, running in medial part of layer iv of superior colliculus; r, from k curring caudal to lateral genieulnte entering lateral part of lamina iv of superior colliculus ; s, intracortienl association fibers from #35 to #36 : t, interrupted dorsomedially running fibers similar to those of lesion I, d which pass to #IS; u, ventrally running fibers of external capsule; v, contribution of #35 and #36 to interual capsule through inferior part of putamen, separate frorri k and skirting niedially along ien t ra l part of capsulopeduneular junction.


Figure 15. GT. I. Subtotal destruction of #36, extending into #35 ; f , projection tract through

ventrocaudal extreme of putamen into lateral extreme of capsule, becoming lost. 11. Cortical part; a needle track interrupting projectional and eingular fibers. 11. Thalamic part ; a peculiar lesion with long rostrocaudal extent involving

nearlv exclusively rentralis medinlis p;irvoc.cllulnri.s and medial end of reticillstis

GT 61-28

Figure 25 A

Figure 2 5 B

374 WENDELL J. S. KRIEQ

(V.Pa. & Ret.) : a, thalamic radiation, most of which is in anterior radiation but a few fibers are in intermediate radiation, these passing t o cingulum ; b, numerous granules in anterior extreme of #2 from grazing of ventralis ventralis by lesion, and some diffuse granules within #lo; c, cingular fibers derived from a, running length of cerebrum showing numerous endings in #23, some in #29 and #27, and a few in #3.

111. Destroys most of #20 and caudal extreme of #13; g, projection tract to ventral par t of caudal region of putamen into lateral third of peduncle; callosal fibers curving around caudal end of hippocampus becoming some of most posterior fibers of splenium.

Figure 26. GU. I. Extensive lesion destroying upper par t and undermining lower par t of #2 so

tha t #2 is nearly completely and exclusively destroyed; little damage to caudate: a, massive projection fibers through capsule and peduncle, many ending in pontile nuclei bn t continuing into bulb ; b, extentive thalamic connection through large fascicles in ventralis extending through both parts of ventralis except in lateral th i rd ; r, conspicuous radiation from a to dorsolateral tegmentum, there are fibers ending in nigra (unlabeled); d, numerous association fibers t o #3 only, within layer vi.

11. Cortical par t ; circumscribed injury to rostra1 extreme of #IS; 3, projection of #IS into internal capsule; k, interrupted fibers of cingulum running t o its caudal end. 11. Thalamic par t ; damage chiefly t o ventralis medialis magnoeellularis (V.Ma.)

and submedius (Sub.) extending t o caudal extreme of medial par t of medialis and lateral habenular nucleus bu t avoiding ventralis (V.V.) ; f , projection tract in anterior radiation fibers presumably from medialis, ending throughout #lo, from magnoeellularis ending in #24 but not passing caudally through cingiilum ; also granules in #8a from submedius; degeneration of mammillothalamic tract (M.-Th.) in medial and ventral anterior (A.M.,A.V.) nuclei shown, also forward connection to rhomboidalis ( to rhomb.) ; g, ventrally directed, and h, caudally directed sparse fibers to tegmentum.

IIIa. Total and exclusive destruction of #41 witliout subcortical damage ; m, projection fibers through caudal extreme of putamen around hippocampal arrh into lateral extreme of peduncle, diverging dorsally in tegmentum, terminating in inferior rollieulns ; 11, thalamic radiation taking lateral position, entering medial geniculate rostrally and medially and distributed there ; p, extensive but thin callosal component in inferior par t of posterior half of callosum; q, intracortical association fibers t o #18a and t o a slight extent to #17 directed raudomedially, ventrally directed fibers, possibly medullary.

I I Ib . A t junction of #13, #35, #28 and #51b; s, extensive callosal contribution curving aroimd posterior extreme of hippocampus to form caudal extreme of medullary center and splenium.


Figure 2 6 A

Figure 2 6 B


Figure 26 C

Figure 2 6 D


Figure 37 . G V . I. I n dorsal par t of #2a; a, projection fibers into capsule and peduncle joining

with b; c, callosal fibers; e, corticothalamic degeneration confused with thalamo- cortical fibers from 11.

11. Cortical part. Destroys most of #3 and extends caudally to medial par t of #7 and into #18; c, projection fibers joining a in peduncle.

II. Thalamic par t ; involves lateralis dorsalis ; e, numerous projection fibers to parietal region, mixed with thalamic connections of I.

111. Injures rostroventral extreme of #Z and touches # S ; f , projection fibers to peduncle, and g , radiation to ventroniedial part of centralis ventralis and dorsalis; j , intraareal association laniina ; h , callosal connrction.

G V 6 0 - 5 8 7 Figure 2 7 A

Figure 27 B


Figure 28. GW. Ia. Tiny lesion to dorsal end of middle zone of #2: a, its projection tract; h,

its thalamic radiation to dorsal par t of ventral tlucleus; c, its callosal connection. Ib. Small injury behind middle of #Z; d, its projection joining a and continu-

ing at least to the pons; e, i ts thalamic projection to raudal middle par t of ventral nucleus; f , callosal fibers distinct from and caudal to c.

11. The only tegmerital lesion in the series, directed toward medial lemniscus but extending irregularly to peduncle : g, termination of medial lemniscus fibers interrupted by lesion throughout entire ventralis (except medial and lateral extremes), occupying interstcies between coarse cortical fibers, some fibers extending dorsally to nucleus lateralis (Lat.) ; 11, component of medial lemniscua to nucleus medialis; j, some ventral fibers possibly to nigra; k, rubrospirial tract degenerated, although red nucleus is only grazed laterally; m, fibers from region just lateral to red nucleus running downward with medial longitudinal fasciculus ; n, tegmental fibers which pass through posterior commissure to opposite side; p, a ventral tegmental commissure (tectospinal?) ; q, descending lateral tegmental fibers interrupted by electrode track ; r, medial descending tegmental fibers interrupted by principal lesion; s, interrupted fibers to medial edge of tegmentum, descending; t, cortical projection fibers from cortical par t of electrode track (not shown) ; v, interrupted peduncular fibers through pons and bulb which decussate and give off a Pick’s bundle ascending medial to spinal V tract. 111. Pure #40 lesion: w, projection fibers from #40 into lateral extreme of

peduncle, becoming lost.

7 3 n

3

Figure 28 A


Figure 28 B

Figure 28 C

GW 52-51 Figure 2 8 D


GW 5 1 . 4 9 Figure 28 E

Figure 29. G X . I. Tiny shallow lesion of #36 allowing a few fibers to be traced forward a short

distance on medullary center. 11. Cortical part; lesion principally in #7 extending to #3: c , projection tract

into peduncle. 11. Thalamic part; a pure and nearly complete destruction of lateralis dorsalis

and ventralis dorsalis : b, thalamic projection through coarse fascicles of ventralis ventralis into dorsolateral quadrant of caudate entering medullary center on lateral dorsal apical portion, ending in caudal par t of #10 freely, t o rostra1 end of #2 and #40, sparsely to #1 and #3, but continuing in fair numbers throughout extreme end of #2, all these presumably from ventralis dorsalis, but some fibers run directly laterally through intermediate thalamic radiation and lenticular, turn dorsally, and run to dorsomedial cortex: d, caudally running interrupted fibers to layer iv of superior eollieulus ; e, cingular continuation of lateralis radiation, actually cortical fibers of lateral nncleus.

111. Damage to caudomedial angle of cortex, injuring caudal extreme ofl#18 and #29: f , g , thalamic or associational fibers caudolaterally.

IV. Rather precise destruction of #35: a , callosal fibers forming caudal extreme of medullary center and of spleniuni.


Figure 20 A

n

Figure 29 B

382 WENDELL J. s. KRIEG

Figure 30. G P . I. Tiny damage to middle of #17 with projection tract running forward and into

lateral extreme of peduncle. 11. Lesion within posterior thalamic radiation, where condensed between lateral

geniculate and ventral nucleus : a, posterior thalamic radiation involving extensive areas running obliquely caudalward and dorsally terminating in #41, #40, #2,

Figure 30 A

Figure 3 0 B


#3, #7, #18 and #29c; b, lowest fibers of auditory radiation; c, d, envelope of cortical endings of damaged par t of radiation; e, interrupted fibers to lamina iv of superior colliculus; f , fibers to incerta region; g, callosal fibers from a lesion of #28, not analyzed here.

IIT. Lesion to middle par t of #18a sending fibers i n t o peduncle.

Figure 31. GZ. I. Damage to middle of #18a, but in medullary center, undermining it forward;

a, projection fibers through dorsal part of putamen into lateral extreme of peduncle, then turning dorsally to end in medial geniculate; as hippocampal arch is cleared the radiation passes outside of and through lateral geniculate, converging to lamina iv of superior colliculus; b, intracortical association lamina to #18; c, interrupted deep fibers of medullary center to #27b; d, interrupted callosal fibers. 11. Partial injury of nucleus lateralis expanding to destroy medial end of

ventralis in both i ts parts; e, thalamic radiation from ventralis diagonalling through internal capsule and striaturn to rostroventral quadrant of #2 but not beyond; f, scattered fibers from nucleus lateralis curving sharply in intermediate radiation to'enter cingulum and dorsomedial cortex.

TTI. Insignificant.

Figure 31 A

384 WENDELL J. S. KRIEO

Figure 31B

Figure 31 C

Figure Sd. H A . Destruction of frorital half of #lOa, touching #34: a , projection t rnr t entering

pole of caudate, continuing ventromedinlly in caudate and in medial extreme of capsule and peduncle, going a t least to bulbar pyramid arid not coririecting with pontile nuclei; dorsal radiatiou exists past nigra to region of medial lemniscus; b, stroug callosal connection.

I.


Figure 32 A

..m

I.? 51 5

11. Cortical par t ; shallow damage in #7 sending projection tract, c, among most anteromedial fibers of hippocampal arch into second fifth of peduncle, be coming lost.

11. Thalamic par t ; almost confined to lateralis postrrior but extending slightly more caudally: d, extensive radiation extending fanwise around anterior part of hippocampal arch (e) becoming redistributed in medullary center ( f ) supplying fibers to overlying regions (h , j ) and extending caudomedially in conjunction with eingulum ( g ) to retrosplenial areas; k, interrupted fibers to lamina ii of superior colliculus; 1, same for lamina ir. 111. Infinitesimal lesion of superior collicnlus causing degeneration of several

tectotegrnental fibers.

386 WENDELL J. S. IIRIEG

Figure 33. € I D . I. Minute destruction of caudomedial estreme of #1T: a, projection lamina

traceable to hippocampal arch ; ti, interruption of a few cingular fibers t o #37. 11. Cortical part; needle track damage interrupting ( c ) forward running pro-

jection tract and (d ) caudomedially ruiining fibers t o #IS. 11. Thalarnic part; localized damage to fibers gathering medial to medial genicrr-

late : e, destruction of auditory radiation showing divergent and aberrant fibers to lower part of putamen; f , expansion of auditory fibers in medullary center; g , extensile termination in #41 estending to #36 and #I&; h, massive bundle t o medial geniculate, probably retrogressively degenerated auditory radiation; j, interrupted fibers t o lamina iv of superior collicnlus; k, to zona incerta.

111. Almost coextentive with rostra1 half of #13; m, projection tract through center of peduncle at leafit as f a r a s midbrain; n, callosal fibers.

H B Figure 33 A


Figure 3 3 B

Y

H B r2 5-79 5

Figure 33 C


Figure 34. H C . I. At junction of #17 and #18 near their middle: e, projection lamina ronverg

ing to fascicles into lateral part of peduncle aud diverging dorsally into lateral tegmentum.

11. Minute lesion on outer surface of medial genirulate: a, interrupted fibers to lamina ii of superior rolliculus; b, part of auditory radiation endinq in #41: c, a tiny rostrallp directed fascicle ; d, lamina paralleling optic tract traceable through chiasma.

111. Minute lesion to #I3 giving no degeneration.

H C 575 -5-4 Figure 3 4 A

Figure 34 B


Figure 35. HD. I. Massive lesion involving most of lateral aspect of cercbrum: a , extensive

lamina of intracortical association fibers to #3, #1 and #Z throughout ; b l , extensive lamina of fibers within medullary center ending chiefly in #4, possibly thalamic; b2, interrupted association fibers in medial par t of #17; c, extensive callosal connection; p, broad lamina of association fibers probably from #41 ending throughout #Ma; d, diffuse degeneration in basal telencephalic nucleus; e, envelope of actual degeneration within cortex; f , projection fibers mostly from #Z and indicating insignificant contribution from #8, #13 and #14 ; g, radiation to medial par t of ventralis ; h, extensive involvement of posterior thalaniic radiation partly to entire middle section of ventralis but in caudal part continuing as k fibers to lamina iv of superior colliculus ; j , radiation fibers on lateral geniculate ; 1, to medial geniculate and beyond; m, tegmental radiation to lateral deep nucleus of tegmentum; n, isolated fascicle to lateral aspect of inferior colliculus. I1 A, I1 B. Damage to #18a and medullary center, complex, not analyzed here

I1 C. To caudal part of nuclei lateralis posterior and posterior thalami: q, forward to zona incerta ; r, to iiacleus mesenceplialicus profundus pars lateralis continuing through tegmental nuclei; s, interruption of fibers to lamina iv of superior colliculus, also to lamina ii ( t ) .

(u, ", Y).

F.gure 35A

390 WENDELL J. 6. KRIEG

Figure 35 B

Figure 3 5 C


Figure 36. HE. I. Circumscribed destruction of #40: a, projection tract in caudodorsal part of

caudate and lateral third of peduncle and lateral half of pontile pyramid with radiation into lateral extreme of ventralis, also :t tegmeiital radiation laterally; c, association fibers to #3, #1, # 2 ; d, e, froin minute extension t o medulla, fibers to cnudomedinl cortex.

Figure 36 A

Figure 36 B


11. Cortical part. Penetration to #4 bhowing ( f ) projection fibers and (g ) interrupted cingular fibers to #29b.

11. Thalamic part ; needle track through stria niedullaris causing degeneration (h), expanding in posterior hypothalamic nucleus, causing degeneration i n peri- ventricular fibers, j ; k, degeneration in habenulopeduncular tract.

111. To caudal part of #18a and #17: m, forward running projection fibers; n, caudal association fibers; p, calloval fibers.

Figure 37. H G . I. Lesion chiefly to #27 with damage to medullary center: b, interrupted pro-

jection tract from caudal end of #17 t o lateral geniculate; c, callosal fibers directly damaged.

C

Figure : i i A

Figure $8. LIB. I. Irregular lesion damaging #41 and #20 superficially and cortical amygdaloid

nucleus deeply: a, projection fibers from #41 t o tegmentum medial to medial geniculate ; b. poorly myeljnated but conspicuous lamina from cortical amygdaloid to basal amygdaloid.

11. Damage to nucleus medialis pars lateralis: c, anterior thalamic radiation through medial par t of caudate turning dorsally into cingulum along considerable extent; d, termination of these cingular fibers to #10 and #24; e, to #3; f , to #29c; g, continuation througli cingulnm t o #29b and #27a; h, capsu1:ir fibers from cortical part of lesion.


58-55

Figure 38 A

Figure 38 B

394 WENDELL J. S. ICRIEG

Fzgrire 39. Locations of all cortical lesions. The network of tliin lines indicates boundaries

of cortical areas as identified by the diagram in Krieg, '46n, p. 227. Lines of dots indicate electrode tracks seen in profile.

Figure 39 A

Figure 39 B

connection3 of the cerebral cortexbrainmaps.org/pdf/krieg3.pdfconnections of cerebral cortex 269...

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