shrinking retrograde amnesia1 - bmjd. frankbensonandnormangeschwind in he would deny that it was a...

J. Neurol. Neurosurg. Psychiat., 1967, 30, 539

Shrinking retrograde amnesia1D. FRANK BENSON AND NORMAN GESCHWIND

From the Departments ofNeurology, University Hospital and BostonVeterans Administration Hospital, and the Aphasia Research Center,Boston University School ofMedicine, Boston, Massachusetts, U.S.A.

Memory disturbance has long been recognized as akey feature of post-traumatic encephalopathy butone feature of this abnormality, the shrinking ofretrograde amnesia, has received scant attention.First described by Russell (1935), and in greaterdetail by Russell and Nathan (1946), this phenom-enon has been neglected by both clinicians andanimal experimenters. Recently Deutsch, Hamburg,and Dahl (1966) have demonstrated a similarphenomenon in animal studies. We feel that re-cognition of shrinking retrograde amnesia is ofdistinct importance in the clinical appraisal ofpost-traumatic memory disturbance and in additionhas several significant implications for any theory ofmemory function. We present here a case of post-traumatic memory loss which clearly demonstratesshrinking of retrograde amnesia and discuss both theclinical and theoretical considerations of thisphenomenon. Another clinical feature commonlyseen in acute traumatic encephalopathy, denial ofillness, was also present in this case and will bediscussed.

CASE REPORT

J.R., a 33-year-old right-handed man, was admitted to theUniversity Hospital, Boston, Massachusetts, on 26 Nov-ember 1965 with a large subcutaneous haematoma in theright temporal-parietal region and deep lacerations acrossthe forehead. He was stuporous but not totallyunconscious and there was a mild right hemiparesis. Nohistory was available concerning the cause of injury.

Later additional history was made available. Thepatient was married and had a family living in Washing-ton, D.C., but two years earlier he had separated fromhis wife and moved to Boston. He had worked as a busdriver in Washington. Since his arrival in Boston thepatient had held two jobs, first as a messenger for a drugstore and later as a labourer in a mattress factory. He hadfinished work on the evening of 25 November and was tohave taken a bus trip to Washington. He had not takenthe bus and it was assumed, although never definitely

"This study was supported in part by grant no. NB.06209 from theNational Institute of Neurological Diseases and Blindness to BostonUniversity School of Medicine.

proven, that he had gone on a binge. The patient'sdrinking history was noteworthy; he was not a regulardrinker, but on rare occasions he would go on bingeslasting several days. He had never needed treatment foralcoholism or its complications. In fact his health hadbeen excellent, his only medical complaints for manyyears having been minor disturbances of the feet andvision.During the first hospital week the state of conscious-

ness varied from stupor to semicoma, the righthemiparesis persisted and it was felt that he was aphasic.Radiographs of the skull showed no fracture, lumbarpuncture had normal pressure, no cells, and protein of68 mg. per 100 ml. An electroencephalogram wasabnormal and was considered compatible with asubdural haematoma. A brain scan and a left carotidarteriogram were performed and both were considered tobe normal. After one week the patient began to improve,the state of consciousness lightened, the paresis recededand then disappeared but a consistent language disturb-ance remained. Originally described as pure jargon, thespeech later was described as fluent with paraphasia. Inaddition there was an abnormal behaviour patternwith jocularity, facetiousness, unreliability, and top-ographical disorientation in the hospital.He was seen in consultation by members of the Boston

University Aphasia Research Unit on 26 December 1965,exactly one month after admission. By that time he wastotally free of disturbance of primary motor or sensoryfunctions and there was no evidence of visual fieldabnormality. He was bright, alert and apparently attent-ive to the examination but notably distractable. Digitspan was recorded at 6 forward. When questions wereasked he would respond, not with answers, but withadditional questions as to why the examiners were seekingsuch information. He was totally disoriented for time,giving dates at least three or four years before the time ofthe examination. When asked to give the date the patientwould often evade the question suggesting that theexaminers actually knew the date and that he did notneed to provide this information. He consistently statedthat he was in Washington, D.C., despite being toldregularly that he was in Boston. If asked about employ-ment he would reply that he was working as a bus driverin Washington. He was totally unable to remember thenames of the physicians and nurses attending him. Hecould not retain three unrelated words for three minutes.When questioned as to the type of building that he was

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D. Frank Benson and Norman Geschwind

in he would deny that it was a hospital giving a varietyof responses some of which were paraphasic. Thus onereply was 'some kind of malingua place-you use it a lotin South America'. If the examiner insisted that thebuilding was a hospital the patient would not argue. If hewas immediately asked why he was in the hospital hewould either claim that he was visiting or would presenta seemingly irrelevant disorder as the cause of hospital-ization. On several occasions he stated that he was inhospital because of eye problems; at other times hementioned difficulties with his feet or legs. He adamantlydenied any difficulties in the use of language or memorywhen specifically questioned concerning these.

His speech was fluent and well articulated but empty ofmeaning and both literal and verbal paraphasias werepresent. Comprehension of spoken language was con-sidered normal for ordinary conversation. Repetition andserial speech were normal. He could name simple objectsonconfrontationbuthaddifficultyif askedto namepartsofobjects. Thus the crystal on his watch became 'clystal',the watch stem was called a 'spicket', and the lead of apencil became 'rubber'. He was able to give the names ofonly three out of 10 colours. He had great difficulty inpresenting word lists; thus he could list the names of onlytwo makes of automobiles in 60 seconds and named only'ocelot' and 'bear' when asked for a list of animal names.Reading (aloud and for comprehension) was adequate.Orthography was good but the content of his writingwas circumlocutory and empty. Right-left orientationand finger localization were intact. He had great difficultyin construction tests, particularly when asked to copydrawings. He was able to calculate.The patient was transferred to the Boston Veterans

Administration Hospital on 27 December 1965 where itwas immediately apparent that memory disturbance wasthe most severe disability. He wandered off the ward,could not find his own bed, would lie downon any bed that was handy, and was frequently seenlooking for objects in other patients' bedside stands. Atone time he was found wandering in the hospital parkinglot, at another time he was watching television threefloors below his own ward. Because of this tendency towander he was transferred to a locked ward on29 December 1965. During his stay on the locked ward,the jocular, facetious, evasive behaviour, the inability toremember the name of the physicians, the nurses or thehospital, and complete disorientation for time persisted.During this period there was improvement in languageso that his speech became more definite and the previouslynoted paraphasia disappeared. He consistently stated thathe was in Washington, D.C., that his last job was that ofa bus driver, and he denied illness or memory defect.An electroencephalogram done during this period was

mildly abnormal with suggestion of a slow wave focus inthe left posterior temporal region. A brain scan on20 January 1966 was normal. A pneumoencephalogramon 17 January 1966 showed the size of the lateralventricles at the upper limits of normal, the fourthventricle slightly enlarged but the third ventricle ofnormal size. The left temporal horn was slightly largerthan the right but it was not felt that the pneumo-encephalogram showed evidence of either mass lesion or

hydrocephalus. Spinal fluid taken at that time showednormal pressure, total protein of 48 mg. per 100 ml., andno cells were present.The patient's status remained essentially the same

except for the improvement in the use of language untilabout the first of March 1966. During a period of one ortwo days the ward nurses noted a marked change in hisbehaviour, for the first time caring about the way hedressed and handled his food, asking them for theirnames and then correctly using their names later.Re-evaluation was performed on 2 March 1966, at whichtime he was able to recall three unrelated words afterthree minutes, to remember the name of the doctor, toremember the name of the hospital after it had been givento him, to recite the names of the ward nurses, and to tellthe number and location of the ward. He still manifesteda retrograde amnesia since he could not remembermoving away from Washington, D.C., but was willingto accept that he was now a patient in a Boston hospital.He no longer denied head injury but stated that he hadonly recently been told of this injury. He was transferredback to the Neurology Service and had no difficulty nowin locating his bed, in getting about the ward and theentire hospital. His behaviour pattern also changed as hebecame less evasive but remained jocular and facetious.Language evaluation at this time was normal except forminimal evidence of word finding difficulty. He was ableto give the names of eight animals in a period of 60seconds, only slightly below normal levels.During the remaining period in hospital, the retrograde

amnesia consistently improved. Thus when he firstreturned to the Neurology Service he was unable toremember living in the Boston area. Three or four dayslater he spontaneously recalled separating from his wifeand moving to Boston. Several days later he rememberedthe job that he held when he arrived in Boston and thename of his employer. He was unable to remember anyother job in Boston. Within a few days, however, herecalled the second and last job but was still vague as tohow long he had worked there. Before discharge theretrograde amnesia had cleared to the point that heremembered quitting work on the day before the injury,approximately 24 hours before admission to the Univer-sity Hospital. It is likely that the patient began drinkingat that time but this was not confirmed by the patientnor any other history available to us.On the day before discharge an amytal interview was

performed. The patient was given approximately 400 mg.of sodium amytal intravenously, sufficient to produceboth drowsiness and nystagmus. He was questioned aboutorientation and retested for aphasia. There was a recur-rence of the tendency to locate the hospital in Washington,D.C., and to deny that he had suffered a head injury. Heagain stated that he had been brought to the hospital byhis mother because of eye problems. The aphasic deficitsnoted when he first came to this hospital did not reappearunder the influence of amytal. The interview wasinitiated by two examiners who later were joined by athird person. The day following the interview the patientclaimed no memory of the interview and did notremember the third person joining the group despite thefact that he had conversed freely with this examiner

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during the interview. At the time of discharge the patientstill had total amnesia for a period starting about24 hours before admission to hospital at the UniversityHospital until he suddenly found himself in the lockedward at the Veterans Administration Hospital. He wasquite aware of details from that point on. Followingdischarge the patient returned to Washington, D.C.,where he was seen on three occasions in a VeteransAdministration clinic. There was no evidence of aphasiaor memory deficit so he was discharged from the clinic.

COMMENT

This case demonstrates several clinical featureswhich deserve discussion. The most dramatic obser-vation was the rather rapid reappearance of theability to learn new material followed by a slower butprogressive shortening in the duration of theretrograde amnesia. This course in the recoveryfrom traumatic memory loss (shrinking retrogradeamnesia) has been described previously (Russell andNathan, 1946) but is not widely recognized in theliterature of memory defects. This phenomenon hasimportant implications for both the clinical andexperimental evaluation of memory loss.Changes in memory following head trauma are

most often described as consisting of two types of'amnesia', post-traumatic (anterograde) and retro-grade. The first of these, post-traumatic amnesia, isdefined as 'the interval during which current eventshave not been stored' (Russell and Smith, 1961). Tothe clinician post-traumatic amnesia is most vividlydemonstrated when a patient, evaluated long afterrecovery from head injury, describes total amnesianot only for the period of unconsciousness but formany additional days or weeks, a period duringwhich the patient had apparently regained normalmental function. Older authors described 'recoveryof senses' (Jackson, 1932) or of 'vigilance' (Head,1926) indicating that this was the termination ofimpaired consciousness but it must be emphasizedthat a patient may be entirely alert and the 'impair-ment of consciousness' in post-traumatic amnesiamay be confined to an inability to store currentevents.The second major division of post-traumatic

memory loss is a retrograde amnesia, an inability torecall events preceding the injury. After full recoverythe retrograde amnesia is usually quite short, oftenencompassing only a few seconds before the injuryand only rarely exceeding a few minutes. In ourpatient the permanent retrograde amnesia could notbe ascertained since we did not know the exact timeof injury, but it could not have exceeded 24 hours.Our estimation of the retrograde amnesia is furthercomplicated because our patient may well have beenintoxicated for many hours preceding the trauma.

In patients who suffer a permanent post-traumaticloss of the ability to acquire new memory, however,a much different retrograde amnesia is noted, usuallycovering several years before the injury. In this lattercharacteristic the post-traumatic retrograde amnesiais similar to that seen in other disorders withpermanent memory loss such as the metabolicKorsakoff's syndrome in which one usually findsa retrograde memory loss of several years before theonset of recognized memory disturbance. Aninteresting dichotomy is thus present in retrogradeamnesia, one type with an amnesic duration ofseconds or minutes, and the other with retrogradeamnesia lasting at least several years. The patientwith shrinking retrograde amnesia thus representsa transitional form between those with long andthose with short retrograde amnesia. The observationthat permanent retrograde amnesia is usually eithervery long or very short and that a permanentretrograde amnesia of, let us say a month's duration,is extremely unusual, is of great interest in the theoryof memory function and will be discussed in detail.As post-traumatic amnesia and retrograde amnesia

are terms usually used in describing traumaticmemory loss another set of terms is indicated fortheoretical discussion. The three categories ofimmediate recall, recent memory, and remotememory have been recognized for many years andhave been proved to indicate separate and distinctfunctions.Immediate recall (also called immediate memory

and short-term memory) has been studied intensively(Brown, 1964). It is described as the ability to retainmaterial for 10 to 30 seconds and is differentiatedfrom the retention of material for several minutes orlonger. This type of 'memory' does not entail apermanent coding of the material.

Recent memory can be defined as the ability toretain new material for several minutes or longer.Stated another way, recent memory is the ability to'learn' new material. It is generally accepted thatpathological changes in the limbic system (hippo-campal region and mamillary bodies are the mostfrequently cited) are present in cases with loss ofrecent memory (Barbizet, 1963). It has also beensuggested that these structures must be intact for theconsolidation of newly learned material.Remote memory may be considered to be the

ability to recall material learned before the onset ofthe patient's illness. Included in this previouslylearned information are basic capabilities such asuse of language and numbers, feeding and dressingskills, and significant past history (i.e., birth andmarriage dates, career milestones etc.) plus purelylearned material (i.e., names of presidents, importanthistorical dates, etc.).

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A period of post-traumatic amnesia clearly cor-responds to a period in which there is loss of recentmemory function. Such a loss may be limited intime or may be permanent. A corresponding totalloss of remote memory function does not occur.Even in the most severely involved patient with aKorsakoff's syndrome much of remote memory isretained. In general the loss for the years immediatelypreceding the illness is most severe. Remote memorytherefore is not involved in as global a fashion asrecent memory. It would appear that older, probablyoverlearned material (e.g., language, the activities ofeating, dressing, etc.) is more resistant than morerecently acquired material. The inability to recallmaterial acquired in the period preceding the onsetof the illness is usually ascribed to the fact that thememory of this material is not 'consolidated' andtherefore is more readily wiped out by, for example,a head injury. This explanation carries with it theimplication that the process of 'consolidation' maytake several years.

It appears to us that the thesis of the abolition ofpoorly consolidated memory traces as the explana-tion for retrograde amnesia does not explain thefindings of shrinking retrograde amnesia. It isobvious that many of the remote memories which thepatient is incapable of recalling in the periodimmediately following his head injury are notabolished, since the patient does recall them at a laterdate. The disturbanceis therefore a failureof retrievalrather than a loss of established memories. Bycontrast the post-traumatic amnesia seems mostlikely to represent not a failure of retrieval but afailure to establish new memory traces. The perma-nent post-traumatic retrograde amnesia of seconds,to minutes' duration does, however, probablyrepresent the true abolition of memories not yetconsolidated.According to this view remote memory would fall

into three groups. There is a period of seconds tominutes in which a memory is fragile and may bepermanently abolished. There is a longer period inwhich the memory is consolidated but in whichretrieval may be impaired. Finally many memories,especially old and overlearned ones, may beretrieved despite influences which abolish the mostrecently acquired memories and affect the retrievalof many later memories.

It seems possible, furthermore, that the retrievalprocess depends on the same system that is necessaryfor the laying down of new memories. This wouldexplain the fact that the shrinking of retrogradeamnesia runs generally parallel to the recovery ofrecent memory function. It would also account forthe fact that a patient with a permanent recentmemory deficit has a permanent long retrograde

amnesia. Furthermore, the fact that in metabolicKorsakoff's syndromes a permanently long retro-grade amnesia is associated with a permanent recentmemory loss militates against the assumption thathead injury has some unique effect on memory. Itwould therefore seem probable that those limbicstructures which are necessary for the laying downof new memories are also necessary for the retrievalof the more recent or less over-learned oldermemories.The permanent long retrograde amnesia of either

the metabolic or post-traumatic Korsakoff's syn-drome is then a retrieval deficit. It is thus conceivable-that by some means it might be possible to makethese memories capable of retrieval although this.would not help the patient materially since he wouldstill be suffering from inability to lay down newmemories. The consideration must be entertained,however, that in other disturbances of the higherfunctions, e.g., some aphasic syndromes, retrievaldeficits are present, reversal of which, by as yetunknown means, might markedly improve the:patient's functional capacities.

Retrograde amnesia and the dramatic phenom--enon of shrinkage of retrograde amnesia have-important implications for animal experimentationdealing with memory. Until recently the spontaneous.return of memory after a lapse of time following.artificially induced amnesia had never been recordedin animals (Deutsch, 1962). A series of experiments-reported by Deutsch et al. (1966) suggested a'memory loss' which disappeared with time, a finding.which agrees with the clinical observations recordedin the present case. This shrinkage of retrogradeamnesia was not recognized in many of the earlieranimal experiments and theories ofmemory functionbased on such incomplete experiments must be,viewed with some doubt. Particular question mustbe raised concerning those studies which purportedto find that the process of 'consolidation' wasprolonged. It seems likely that most of these studiesactually demonstrated difficulties in retrieval.The late recovery of memory function is of

significance clinically. The behaviour problems assoc-iated with memory loss demand protective care ofthe type most often provided by psychiatric insti-tutions. Admission is usually by commitment andrecovery of memory function is unexpected, leadingto prolonged incarceration. Thus the potentiality ofexcellent recovery of memory function, even manymonths after brain injury, deserves emphasis.

This case demonstrated another dramatic phe-nomenon, denial of illness,which hasbeenrecognizedand discussed for many years. It has been suggestedby some that a parietal lesion was necessary for suchdenial (Schilder, 1934; Nielsen, 1938), by others that

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denial was a manifestation of clouding of conscious-ness (Spillane, 1942; Sandifer, 1946), or that denialof major neurological defect suggested impairedrecognition of body scheme (Gerstmann, 1942;Critchley, 1953). Weinstein and Kahn (1955) suggestthat denial is actually motivated and represents apsychological defence mechanism occurring in apatient with widespread dysfunction of the nervoussystem who is unwilling to accept the presence of amajor deficit.The present patient had clear denial of illness

when first seen and the denial persisted, essentiallywithout change until the post-traumatic amnesiacleared. During this time the patient adamantlyrefused to admit head injury, language disorder, ormemory loss, and if pushed by interrogation wouldstate that he was in the hospital because of visualdifficulty or foot trouble. There was consistentdisorientation for time, most often evasive, but iffirmly pushed the patient would give a date severalyears before the time of his injury. He consistentlyinsisted that he was in Washington, D.C., his formerhome.Taken out of context these findings could be

considered motivated with the patient activelydenying his obvious defects. It seems preferable,however, to describe this as confabulation, anattempt by the patient to fill a void in his knowledgeof present occurrences with past knowledge. Thisfits a current theoretical view (see, for example,Barbizet, 1963) which suggests that confabulationis an attempt on the part of a patient, unable to learnnew information, to provide requested informationfrom the only source available to him, his pastmemory. Our patient continued to deny his neuro-logical defects and remained disoriented until herather rapidly regained normal recent memoryfunction at which time all denial symptoms dis-appeared. In our opinion the denial and memoryloss were probably results of the same process. Thusit is not entirely correct to state that our patientdenied his illness but would be more accurate to saythat he was unable to remember the present difficultyand attempted to fill this void by providing older,previously overlearned information.A defect in word finding was clearly demonstrated

in this patient and was such a prominent feature inthe early part of the hospital course that at least onecompetent examiner considered the major difficultyto be anomic aphasia. Weinstein and Kahn notedword finding defects in many of their patients whodenied illness. In their opinion, the naming defectappeared to be more pronounced for hospitaloriented items (i.e., thermometer, stethoscope,urinal, etc.) than for other objects. They suggestedthat this was not a true naming defect and that the6

'paraphasia' demonstrated in these patients wastruly a non-aphasic misnaming of stress-producingitems. In the present case this theory cannot besubstantiated. It is true that our patient had difficultyin naming hospital oriented items but he had just asmuch difficulty naming other items. While it wouldbetempting to link his memory disturbance with hisanomia it is difficult to do so since our experience aswell as that of others confirms the existence ofsevere memory loss in adults without anomic dis-orders. It is most likely that our patient's anomicdisturbances were secondary to cerebral contusion.

Finally it is worth discussing the results demon-strated by the amytal interview. This technique wasused by Russell and Nathan and was also usedextensively by Weinstein and Kahn. In the presentcase we were interested mainly in the possibility ofreappearance of aphasic symptoms so we did notattempt to demonstrate regrograde amnesia nor didwe realize during the interview that we had actuallyproduced a period of recent memory loss. However,in an interview with the patient the following day itwas quite apparent that he had no memory whatso-ever of occurrences during the interview and in factdid not realize that a third person had joined theinterview team, a person whomheknew verywell, andwho had talked to him during the interview. Quitepossibly better observation on our part would havedemonstrated a distinct reappearance of retrogradeamnesia but even our limited observations suggestedits recurrence. One of the most significant parts ofthe interview was the reappearance of the denial ofillness. The patient strongly and adamantly deniedthat he was in the hospital because of any head orbrain injury and again told the story of being broughtto the hospital by his mother because of eyeproblems. Before the amytal interview the patientwas no longer telling this story and following theamytal interview he was quite aware of the reasonfor hospitalization. Thus with amytal we were ableto produce many of the findings that were seen duringthe acute state of the disorder and suggest thatone of the effects of amytal is to impair the functionof those regions involved in new learning and in theretrieval of more recent (less overlearned) pastmemories.

SUMMARY

A case of post-traumatic encephalopathy with athree month period of post-traumatic amnesia hasbeen presented. Particular attention was given to thestriking shrinking of retrograde amnesia whichoccurred after recovery of recent memory functionhad taken place and to the denial of illness seen inthe course of the illness.

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Two types of permanent retrograde amnesia aredemonstrated by this case and other cases of memoryloss, a long retrograde amnesia of several years'duration and a much shorter retrograde amnesia,usually of less than one day's duration. Retrogradeamnesia of intermediate length appears to occuronly during the period of shrinking of the retrogradeamnesia. Long-term retrograde amnesia is associatedwith a continued defect in recent memory whereasshort-term retrograde amnesia is present only inindividuals with intact ability to learn new inform-ation. The fact that memories that are unavailableduring long-term retrograde amnesia can returnwithout a process of r-leaming shows that thesememories are not lost, but that the ability to retrievethis material is lost during long-term retrogradeamnesia. Thus it is suggested that the same anatom-ical substrate necessary for laying down newmemories is probably necessary for retrieval ofless overlearned or more recently acquired pastmemories. This has significant implications foranimal experimentation dealing with memory,particularly those concerned with the time course ofmemory 'consolidation'.

Denial of illness was notable in this case up to thepoint that recent memory function returned at whichtime the denial abruptly ceased. This suggests thatthe denial was actually a confabulation caused byinability to learn new information, specifically thedetails of the present illness. After recovery ofmemory function we wcr- able to reproduce thedenial of illness, the recent memory defect andlengthening of the retrograde amnesia by use of

intravenous amytal, again suggesting the linkage ofthese disturbances.

The authors wish to acknowledge the valuable assistanceof Donald Urrea, M.D., in the clinical evaluation ofthis case.

REFERENCES

Barbizet, J. (1963). Defect of memorizing ofhippocampal-mammillaryorigin: a review. J. Neurol. Neurosurg. Psychiat., 26, 127-135.

Brown, J. (1964). Short-term memory. Brit. med. Bull., 20, 8-11.Critchley, M. (1953). The Parietal Lobes. Arnold, London.Deutsch, J. A. (1962). Higher nervous function: The physiological

bases of memory. Ann. Rev. Physiol., 24, 259-286.-, Hamburg, M.D., and Dahl, H. (1966). Anticholinesterase-

induced amnesia and its temporal aspects. Science, 151, 221-223.Gerstmann, J. (1942). Problem of imperception of disease and of

impaired body territories with organic lesions: relation to bodyscheme and its disorders. Arch. Neurol. Psychiat., 48, 890-913.

Head, H. (1926). Aphasia, and Kindred Disorders of Speech. Univer-sity Press, Cambridge.

Jackson, J. H. (1931-32). Selected Writings ofJohn HughlingsJackson,edited by J. Taylor. Hodder & Stoughton, London.

Nielsen, J. M. (1938). Gerstmann syndrome: finger agnosia, agraphia,confusion of right and left and acalculia: comparison of thissyndrome with disturbances of body scheme resulting fromlesions of the right side of the brain. Arch Neurol. Psychiat., 39,536-560.

Russell, W. R. (1935). Amnesia following head injuries. Lancet, 2,762-763.

, and Nathan, P. W. (1946). Traumatic amnesia. Brain, 69, 280-300.

, and Smith, A. (1961). Post-traumatic amnesia in closed headinjury. Arch. Neurol. (Chic.), 5, 4-17.

Sandifer, P. H. (1946). Anosognosia and disorders of body scheme.Brain, 69, 122-137.

Schilder, P. (1934). Localization of the body image (postural modelof the body). Res. Publ. Ass. nerv. Dis. 13,, 466-484.

Spillane, J. D. (1942). Disturbances of the body scheme: anosognosiaand finger agnosia. Lancet, 1, 42-44.

Weinstein, E., and Kahn, R. (1955). Denial of Illness. Thomas,Springfield, Illinois.

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