Dr Sudhakar Marella

DM Neurology

• The term thalamus derives from a Greek word that

means “inner chamber” or “meeting place”

• Use of the terms optic thalamus and chamber of vision

relates to the tracing, in the second century A.D., of optic

nerve fibers to the thalamus by Galen.

• The prefix optic was dropped when it was discovered that

sensory modalities other than vision are also processed

in the thalamus

• The thalamus is the largest component of the

diencephalon

• Rostrocaudal dimension of about 30 mm, height of about

20 mm, width of about 20 mm, and an estimated 10

million neurons in each hemisphere.

• The term diencephalon includes the following structures:

epithalamus, thalamus (including the metathalamus),

hypothalamus, and subthalamus.

• Thalamus lies medially in the cerebrum. Dorsal aspect

form the floor of the IV ventricle, bounded medially by III

venticle, laterally by internal capsule and basal ganglia;

ventrally it is continuous with subthalamus.

• The thalamus serves primarily as a relay station that

modulates and coordinates the function of various

systems

• Locus for integration, modulation, and

intercommunication between various systems

• Has important motor, sensory, arousal, memory,

behavioral, limbic, and cognitive functions

• The largest source of afferent fibers to thalmus is

cerebral cortex and cortex is the primary destination for

thalamic projections

• Many systems and fibers converge on the thalamus.

• Characteristically, thalamic connections are reciprocal,

that is, the target of the axonal projection of any given

thalamic nucleus sends back fibers to that nucleus.

• Nevertheless, thalamocortical projections are often larger

than their corticothalamic counterparts (e.g., the

geniculocalcarine projection)

• It is subdivided into the following major nuclear groups on

the basis of their rostrocaudal and mediolateral location

within the thalamus:

-Anterior

-Medial

-Lateral

-Intralaminar and reticular

-Midline

-Posterior

• The thalamus is traversed by a band of myelinated fibers,

the internal medullary lamina, which runs along the

rostrocaudal extent of the thalamus.

• The internal medullary lamina separates the medial from

the lateral group of nuclei.

• Rostrally and caudally, the internal medullary lamina

splits to enclose the anterior and intralaminar nuclear

groups, respectively.

• The internal medullary lamina contains intrathalamic

fibers connecting the different nuclei of the thalamus with

each other.

• Another medullated band, the external medullary lamina,

forms the lateral boundary of the thalamus medial to the

internal capsule.

• Between the external medullary lamina and the internal

capsule is the reticular nucleus of the thalamus.

• The external medullary lamina contains nerve fibers

leaving or entering the thalamus on their way to or from

the adjacent capsule

• The anterior tubercle of the thalamus (dorsal surface of

the most rostral part of the thalamus) is formed by the

anterior nuclear group.

• consists of two nuclei: principal anterior and anterodorsal.

• The anterior group of thalamic nuclei has reciprocal

connections with the hypothalamus (mamillary bodies)

and the cerebral cortex (cingulate gyrus).

• The anterior group also receives significant input from the

hippocampal formation of the cerebral cortex (subiculum

and presubiculum) via the fornix

• The anterior nuclear group of the thalamus is part of the

limbic system, which is concerned with emotional

behavior and memory mechanisms.

• Discrete damage to the mamillothalamic tract has been

associated with deficits in a specific type of memory,

episodic long-term memory, with relative sparing of short-

term memory and intellectual capacities.

• Of the medial nuclear group, the dorsomedial nucleus is

the most highly developed in humans.

• In histologic sections stained for cells, three divisions of

the dorsomedial nucleus are recognized: a dorsomedial

magnocellular division located rostrally, a dorsolateral

parvicellular division located caudally, and a paralaminar

division adjacent to the internal medullary lamina.

• The dorsomedial nucleus develops in parallel with and is

reciprocally connected with the prefrontal cortex (areas 9,

10, 11, and 12), via the anterior thalamic peduncle, and

the frontal eye fields (area 8)

• It also receives inputs from the temporal neocortex (via

the inferior thalamic peduncle), amygdaloid nucleus and

substantia nigra pars reticulata, and adjacent thalamic

nuclei, particularly the lateral and intralaminar groups.

• The dorsomedial nucleus belongs to a neural system

concerned with affective behavior, decision making and

judgment, memory, and the integration of somatic and

visceral activity.

• Bilateral lesions of the dorsomedial nucleus result in a

syndrome of lost physical self-activation, manifested by

apathy, indifference, and poor motivation.

• The reciprocal connections between the prefrontal cortex

and the dorsomedial nucleus can be interrupted

surgically to relieve severe anxiety states and other

psychiatric disorders.

• This operation, known as prefrontal lobotomy (ablation

of prefrontal cortex) or prefrontal leukotomy (severance

of the prefrontal-dorsomedial nucleus pathway), is rarely

practiced nowadays, having been replaced largely by

medical treatment that achieves the same result without

undesirable side effects.

• The lateral nuclear group of the thalamus is subdivided

into two groups, dorsal and ventral.

1. Dorsal Subgroup• This subgroup includes, from rostral to caudal, the lateral

dorsal, lateral posterior, and pulvinar nuclei.

• The lateral dorsal nucleus, although anatomically part of

the dorsal tier of the lateral group of thalamic nuclei, is

functionally part of the anterior group of thalamic nuclei,

with which it collectively forms the limbic thalamus.

• Similar to the anterior group of thalamic nuclei, the lateral dorsal nucleus receives inputs from the hippocampus (via the fornix) and an uncertain input from the mamillarybodies and projects to the cingulate gyrus

• The borderline between the lateral posterior nucleus and the pulvinar nucleus is vague, and the term pulvinar–lateral posterior complex has been used to refer to this nuclear complex

• The pulvinar–lateral posterior complex has reciprocal connections caudally with the lateral geniculate body and rostrally with the association areas of the parietal, temporal, and occipital cortices . It also receives inputs from the pretectal area and superior colliculus.

• The pulvinar is thus a relay station between subcortical

visual centers and their respective association cortices in

the temporal, parietal, and occipital lobes.

• The pulvinar has a role in selective visual attention.

• There is evidence that the pulvinar nucleus plays a role in

speech mechanisms.

• Stimulation of the pulvinar nucleus of the dominant

hemisphere

has produced anomia (nominal aphasia).

• The pulvinar nucleus also has been shown to play a role

in pain mechanisms.

• Lesions in the pulvinar nucleus have been effective in the

treatment of intractable pain.

• Experimental studies have demonstrated connections

between the pulvinar nucleus and several cortical and

subcortical areas concerned with pain mechanisms

• The pulvinar–lateral posterior complex and the

dorsomedial nucleus are known collectively as

multimodal association tha-lamic nuclei.

• They all have the following in common:

-They do not receive a direct input from the long

ascending tracts.

-Their input is mainly from other thalamic nuclei.

-They project mainly to the association areas of the

cortex.

Ventral Subgroup• This subgroup includes the ventral anterior, ventral lateral, and

ventral posterior nuclei.

• The neural connectivity and functions of this subgroup are

much better understood than those of the dorsal subgroup. In

contrast to the dorsal subgroup, which belongs to the

multimodal association thalamic nuclei, the ventral subgroup

belongs to the modality-specific thalamic nuclei.

• These nuclei share the following characteristics:

-They receive a direct input from the long ascending

tracts.

-They have reciprocal relationships with specific cortical

areas.

-They degenerate on ablation of the specific cortical area

to which they project

• This is the most rostrally placed of the ventral subgroup.

It receives fibers from several sources.

• Globus pallidus A major input to the ventral anterior

nucleus is from the internal segment of globus pallidus.

-Fibers from the globus pallidus form the ansa and

lenticular fasciculi and reach the nucleus via the

thalamic fasciculus.

-Pallidal fibers terminate in the lateral portion of the

ventral anterior nucleus.

• Substantia nigra pars reticulata Nigral afferents

terminate in the medial portion of the nucleus in contrast

to the pallidal afferents, which terminate in its lateral

portion.

• Intralaminar thalamic nuclei.

• Premotor and prefrontal cortices (areas 6 and 8)

• The inputs from globus pallidus and substantia nigra are

GABAergic inhibitory.

• The inputs from the cerebral cortex are excitatory

• The major output of the ventral anterior nucleus goes to

the premotor cortices and to wide areas of the prefrontal

cortex, including the frontal eye fields.

• It also has reciprocal connections with the intralaminar

nuclei.

• Thus the ventral anterior nucleus is a major relay station

in the motor pathways from the basal ganglia to the

cerebral cortex. As such, it is involved in the regulation of

movement.

• The medial (magnocellular) part of the ventral anterior

nucleus is concerned with control of voluntary eye, head,

and neck movements.

• The lateral (parvicellular) part of the nucleus is concerned

with control of body and limb movements.

• Lesions in this nucleus and adjacent areas of the

thalamus have been placed surgically (thalamotomy) to

relieve disorders of movement, especially parkinsonism

• This nucleus is located caudal to the ventral anterior nucleus

and, similar to the latter, plays a major role in motor

integration.

• The ventral anterior and ventral lateral nuclei together

comprise the motor thalamus.

• The afferent fibers to the ventral lateral nucleus come from

the following sources :

• Deep cerebellar nuclei The dentatothalamic system

constitutes the major input to the ventral lateral nucleus. this

fiber system originates in the deep cerebellar nuclei (mainly

dentate), leaves the cerebellum via the superior cerebellar

peduncle, and decussates in the mesencephalon. Some fibers

synapse in the red nucleus, while others bypass it to reach the

thalamus.

• Globus pallidus (internal segment) Although the pallidothalamic fiber system projects primarily on ventral anterior neurons, some fibers reach the anterior (oral) portion of the ventral lateral nucleus.

• Primary motor cortex There is a reciprocal relationship between the primary motor cortex (area 4) and the ventral lateral nucleus

• The efferent fibers of the ventral lateral nucleus go primarily to the primary motor cortex in the precentralgyrus.

• Other cortical targets include nonprimary somatosensory areas in the parietal cortex (areas 5 and 7) and the premotor and supplementary motor cortices

• The parietal cortical targets play a role in decoding

sensory stimuli that provide spatial information for

targeted movements.

• Thus the ventral lateral nucleus, like the ventral anterior

nucleus, is a major relay station in the motor system

linking the cerebellum, the basal ganglia, and the

cerebral cortex.

• Deep cerebellar nuclei have been shown to project

exclusively to ventral lateral thalamic nuclei, whereas the

projection from the globus pallidus targets mainly the

ventral anterior nucleus.

• As in the case of the ventral anterior nucleus, lesions in

the ventral lateral nucleus have been produced surgically

to relieve disorders of movement manifested by tremor

• This nucleus is located in the caudal part of the thalamus.

• It receives the long ascending tracts conveying sensory

modalities (including taste) from the contralateral half of

the body and face.

• These tracts include the medial lemniscus, trigeminal

lemniscus (secondary trigeminal tracts), and

spinothalamic tract.

• Vestibular information is relayed to the cortex via the

ventral posterior as well as the intralaminar and posterior

group of thalamic nuclei.

• The ventral posterior nucleus is made up of two parts: the

ventral posterior medial (VPM) nucleus, which receives

the trigeminal lemniscus and taste fibers, and the ventral

posterior lateral (VPL) nucleus, which receives the medial

lemniscus and spinothalamic tracts.

• Both nuclei also receive input from the primary

somatosensory cortex

• The output from both nuclei is to the primary

somatosensory cortex (SI) in the postcentral gyrus (areas

1, 2, and 3).

• A group of cells located ventrally between the ventral

posterior lateral and ventral posterior medial nuclei

comprises the ventral posterior inferior (VPI) nucleus.

Cells in this nucleus provide the major thalamic projection

to somatosensory area II (SII).

• The ventral posterior lateral and ventral posterior medial

nuclei are collectively referred to as the ventrobasal

complex

• The intralaminar nuclei, as their name suggests, are

enclosed within the internal medullary lamina in the

caudal thalamus.

• The reticular nuclei occupy a position between the

external medullary lamina and the internal capsule

1. Intralaminar Nuclei• The intralaminar nuclei include several nuclei, divided

into caudal and rostral groups.

• The caudal group includes the centromedian and

parafascicular nuclei.

• The rostral group includes the paracentral, centrolateral,

and centromedial nuclei.

• The intralaminar nuclei have the following afferent and

efferent connections:

1. Afferent connections

• Fibers projecting on the intralaminar nuclei come from

the following sources.

• (1) Reticular formation of the brain stem : This constitutes

the major input to the intralaminar nuclei.

• (2) Cerebellum : The dentatorubrothalamic system

projects on the ventral lateral nucleus of the thalamus.

Collaterals of this system project on the intralaminar

nuclei.

• (3) Spinothalamic and trigeminal lemniscus : Afferent

fibers from the ascending pain pathways project largely

on the ventral posterior nucleus but also on the

intralaminar nuclei.

• (4) Globus pallidus : Pallidothalamic fibers project mainly on

the VAN. Collaterals of this projection reach the intralaminar

nuclei.

• (5) Cerebral cortex : Cortical fibers arise primarily from the

motor and premotor areas. Fibers originating in the motor

cortex (area 4) terminate on neurons in the centromedian,

paracentral, and centrolateral nuclei. Those originating from

the premotor cortex (area 6) terminate on the parafascicular

and centrolateral nuclei. In contrast to other thalamic nuclei,

the connections between the intralaminar nuclei and cerebral

cortex are not reciprocal.

• (6) Other Afferent Connections : Retrograde transport studies

of horseradish peroxidase have identified afferent connections

to the intralaminar nuclei from the vestibular nuclei,

periaqueductal gray matter, superior colliculus, pretectum, and

the locus ceruleus.

2. Efferent Connections

• The intralaminar nuclei project to the following structures.

• (1) Other thalamic nuclei : • The intralaminar nuclei influence cortical activity through other

thalamic nuclei.

• There are no direct cortical connections for the intralaminar nuclei.

• One exception is direct projection from one of the intralaminarnuclei (centrolateral) to the primary visual cortex (area 17).

• The significance of this finding is twofold. First, it shows that intralaminar nuclei, contrary to previous concepts, do project directly to cortical areas. Second, it explains the reported response of area 17 neurons to nonvisual stimuli (e.g., pinprick or sound); such responses would be mediated through the intralaminarnuclei.

• (2) The striatum (caudate and putamen) : The striatal

projection is topographically organized such that the

centromedian nucleus projects to the putamen and the

parafascicular nucleus to the caudate nucleus

2. Midline Nuclei• Consist of numerous cell groups, poorly developed in

humans, located in the medial border of the thalamus

along the banks of the third ventricle.

• They include the paraventral, central, and reunien nuclei.

• Their input includes projections from the hypothalamus,

brain stem nuclei, amygdala, and parahippocampal

gyrus.

• Their output is to the limbic cortex and ventral striatum.

They have a role in emotion, memory, and autonomic

function.

• The intralaminar and midline nuclei comprise the

nonspecific thalamic nuclear group.

3. Reticular Nuclei• The reticular nucleus is a continuation of the reticular

formation of the brain stem into the diencephalon.

• It receives inputs from the cerebral cortex and other

thalamic nuclei.

• The former are collaterals of corticothalamic projections,

and the latter are collaterals of thalamocortical

projections.

• The reticular nucleus projects to other thalamic nuclei.

• The inhibitory neurotransmitter in this projection is GABA.

• The reticular nucleus is unique among thalamic nuclei in

that its axons do not leave the thalamus.

• Based on its connections, the reticular nucleus plays a

role in integrating and gating activities of thalamic nuclei

• Thus the intralaminar nuclei and reticular nucleus

collectively receive fibers from several sources, motor

and sensory, and project diffusely to the cerebral cortex

(through other thalamic nuclei).

• Their multisource inputs and diffuse cortical projections

enable them to play a role in the cortical arousal

response.

• The intralaminar nuclei, by virtue of their basal ganglia

connections, are also involved in motor control

mechanisms, and by virtue of the input from ascending

pain-mediating pathways, they are also involved in the

awareness of painful sensory experience

• The awareness of sensory experience in the intralaminar

nuclei is poorly localized and has an emotional quality, in

contrast to cortical awareness, which is well localized

• The term metathalamus refers to two thalamic nuclei, the

medial geniculate and lateral geniculate.

1. Medial Geniculate Nucleus• This is a relay thalamic nucleus in the auditory system.

• It receives fibers from the lateral lemniscus directly or,

more frequently, after a synapse in the inferior colliculus.

• These auditory fibers reach the medial geniculate body

via the brachium of the inferior colliculus (inferior

quadrigeminal brachium).

• The medial geniculate nucleus also receives feedback fibers

from the primary auditory cortex in the temporal lobe.

• efferent outflow from the MG nucleus forms the auditory

radiation of the internal capsule (sublenticular part) to the

primary auditory cortex in temporal lobe (areas 41 and 42)

• Small hemorrhagic infarctions in the medial geniculate nucleus

are associated with auditory illusions such as hyperacusis and

palinacusis and complete extinction of the contralateral ear

input.

• It may have roles in spectral analysis of sound, sound pattern

recognition, auditory memory, and localization of sound in

space, in addition to matching auditory information with other

modalities

• This is a relay thalamic nucleus in the visual system.

• It receives fibers from the optic tract conveying impulses

from both retinae.

• The lateral geniculate nucleus is laminated, and the

inflow from each retina projects on different laminae

(ipsilateral retina to laminae II, III, and V; contralateral

retina to laminae I, IV, and VI).

• Feedback fibers also reach the nucleus from the primary

visual cortex (area 17) in the occipital lobes.

• The efferent outflow from the lateral geniculate nucleus

forms the optic radiation of the internal capsule

(retrolenticular part) to the primary visual cortex in the

occipital lobe.

• Some of the efferent outflow projects to the pulvinar

nucleus and to the secondary visual cortex (areas 18 and

19)

• This group embraces the caudal pole of the ventral

posterior group of thalamic nuclei medial to the pulvinar

nucleus and extends caudally to merge with the medial

geniculate body and the gray matter medial to it.

• It receives inputs from all somatic ascending tracts

(medial lemniscus and spinothalamic), as well as from

the auditory pathways and possibly the visual pathways.

• Neurons in this part of the thalamus are multimodal and

respond to a variety of stimuli.

• The outflow from the posterior group projects to the

association cortices in the parietal, temporal, and

occipital lobes

• The posterior nuclear group is thus a convergence center

for varied sensory modalities.

• It lacks the modal and spatial specificity of the classic

ascending sensory systems but allows for interaction

among the divergent sensory systems that project on it.

• Unlike the specific sensory thalamic nuclei, the posterior

group does not receive reciprocal feedback connections

from the cerebral cortex.

• There are several nomenclature systems for thalamic

nuclei based on shared features of fiber connectivity and

function.

• Two such nomenclature systems are used commonly.

• The first nomenclature system groups thalamic nuclei

into three general categories:

(1) modality-specific,

(2) multimodal associative, and

(3) nonspecific and reticular.

• The modality-specific group of nuclei shares the

following features in common:

• (1) they receive direct inputs from long ascending tracts

concerned with somatosensory, visual, and auditory

information (ventral posterior lateral and medial, lateral

geniculate, medial geniculate) or else process

information derived from the basal ganglia (ventral

anterior, ventral lateral), the cerebellum (ventral lateral),

or the limbic system (anterior, lateral dorsal);

• (2) they have reciprocal connections with well-defined

cortical areas (primary somatosensory, auditory, and

visual areas, premotor and primary motor areas,

cingulate gyrus); and

• (3) they undergo degeneration on ablation of the specific

cortical area to which they project.

• The multimodal associative group, in contrast,

receives no direct inputs from long ascending tracts and

projects to association cortical areas in the frontal,

parietal, and temporal lobes.

• These nuclei include the dorsomedial nucleus and the pulvinar–

lateral posterior nuclear complex.

• The nonspecific and reticular group of nuclei are

characterized by diffuse and widespread indirect cortical

projections and by inputs from the brain stem reticular

formation. These nuclei include the intralaminar, midline,

and reticular nuclei

• Low-frequency stimulation of the modality-specific

thalamic nuclei results in a characteristic cortical

response known as the augmenting response. This

response consists of a primary excitatory postsynaptic

potential (EPSP) followed by augmentation of the

amplitude and latency of the primary EPSP recorded

from the specific cortical area to which the modality-

specific nucleus projects

• Stimulation of the nonspecific nuclear group, on the other

hand, gives rise to the characteristic recruiting

response in the cortex. This is a bilateral generalized

cortical response (in contrast to the localized augmenting

response) characterized by a predominantly surface-

negative EPSP that increases in amplitude and, with

continued stimulation, will wax and wane

• The other nomenclature system groups thalamic nuclei into the following categories: (1) motor, (2) sensory, (3) limbic, (4) associative, and (5) nonspecific and reticular.

• The motor group receives motor inputs from the basal ganglia (ventral anterior, ventral lateral) or the cerebellum (ventral lateral) and projects to the premotor and primary motor cortices.

• The sensory group receives inputs from ascending somatosensory (ventral posterior lateral and medial), auditory (medial

geniculate), and visual (lateral geniculate) systems.

• The limbic group is related to limbic structures (mamillary bodies, hippocampus, cingulate gyrus).

• The following neurotransmitters have been identified in

the thalamus:

(1) GABA is the inhibitory neurotransmitter in terminals

from the globus pallidus, in local circuit neurons, and in

projection neurons of the reticular nucleus and lateral

geniculate nucleus; and

(2) glutamate and aspartate are the excitatory

neurotransmitters in corticothalamic and cerebellar

terminals and in thalamocortical projection neurons.

• Several neuropeptides have been identified in terminals

of long ascending tracts. They include substance P,

somatostatin, neuropeptide Y, enkephalin, and

cholecystokinin

• Blood supply of the thalamus is derived from four parent

vessels: basilar root of the posterior cerebral, posterior

cerebral, posterior communicating, and internal carotid.

• The basilar root of the posterior cerebral artery, via

paramedian branches, supplies the medial thalamic

territory.

• The posterior cerebral artery, via its geniculothalamic

branch, supplies the posterolateral thalamic territory.

• The posterior communicating artery, via the tuberotha-

lamic branch, supplies the anterolateral thalamic territory.

• The internal carotid artery, via its anterior choroidal

branch, supplies the lateral thalamic territory.

• A multiplicity of neurologic signs and symptoms has been

reported in disorders of the thalamus.

These reflect

• (1) the anatomic and functional heterogeneity of the

thalamus,

• (2) simultaneous involvement of several nuclei even by

discrete vascular lesions due to the fact that arterial

vascular territories in the thalamus cross nuclear

boundaries, and

• (3) simultaneous involvement of neighboring areas such

as the midbrain in paramedian thalamic vascular lesions,

the internal capsule in lateral thalamic vascular lesions,

and the subthalamus in posterior thalamic vascular

lesions.

• The conglomerate of signs and symptoms associated with

thalamic lesions includes the following: sensory disturbances,

thalamic pain, hemiparesis, dyskinesias, disturbances of

consciousness, memory disturbances, affective disturbances,

and disorders of language.

• Correlation of signs and symptoms with affected thalamic

territory is best with vascular lesions (infarcts) of the thalamus.

• Most thalamic infarcts are reported in the posterolateral and

the medial thalamic territories supplied by the

geniculothalamic and paramedian arteries, respectively.

• Only a few cases are reported in the anterolateral and

posterior territories supplied by the tuberothalamic and

posterior choroidal arteries, respectively.

• Infarcts in this thalamic territory are due to occlusion of

the geniculothalamic (thalamogeniculate, posterolateral)

artery, a branch of the posterior cerebral artery.

• Thalamic structures involved by the infarct are the

primary sensory thalamic nuclei, which include the

ventral posterior lateral, ventral posterior medial, medial

geniculate, pulvinar, and centromedian nuclei

• The clinical hallmark of posterolateral thalamic territory

infarcts is a pansensory loss contralateral to the lesion,

paresthesia, and thalamic pain.

• In addition, one or more of the following may occur:

transient hemiparesis, homonymous hemianopsia,

hemiataxia, tremor, choreiform movements, and spatial

neglect, all contralateral to the lesion in the thalamus.

• An athetoid posture of the contralateral hand (thalamic

hand) may appear 2 or more weeks following lesions in

this territory.

• The hand is flexed and pronated at the wrist and

metacarpo-phalangeal joints and extended at the

interphalangeal joints. The fingers may be abducted. The

thumb is either abducted or pushed against the palm.

• The conglomerate of signs and symptoms associated with posterolateral thalamic territory infarcts comprises the thalamic syndrome of Dejerine and Roussy.

• In this syndrome, severe, persistent, paroxysmal, and often intolerable pain (thalamic pain) resistant to analgesic medications occurs at the time of injury or following a period of transient hemiparesis, hemiataxia, choreiform movements, and hemisensory loss

• Cutaneous stimuli trigger paroxysmal exacerbations of the pain that outlast the stimulus. Because the perception of “epicritic” pain (from a pinprick) is reduced on the painful areas, this symptom is known as anesthesia dolorosa, or painful anesthesia

• Infarcts in the anterolateral territory of the thalamus are usually secondary to occlusion of the tuberothalamic branch of the posterior communicating artery.

• Thalamic nuclei involved in the infarct include the ventral anterior, ventral lateral, dorsomedial, and anterior.

• The clinical manifestations include contralateral hemiparesis, visual field defects, facial paresis with emotional stimulation, and rarely, hemisensory loss

• Severe, usually transient neuropsychological impairments predominate in lesions in this thalamic territory.

• Abulia, lack of spontaneity and initiative, and reduced quantity of speech are the predominant findings.

• Other impairments consist of defects in intellect, language, and memory in left-sided lesions and visuospatial deficits in right-sided lesions

• Infarcts in the medial territory of the thalamus are

associated with occlusion of the paramedian branches of

the basilar root of the posterior cerebral artery.

• These branches include the posteromedial, deep

interpedun-cular profunda, posterior internal optic, and

thalamo-perforating.

• The thalamic nuclei involved include the intralaminar

(centromedian, parafascicular) and dorsomedial, either

unilaterally or bilaterally.

• The paramedian territory of the midbrain is often involved

by the lesion.

• The hallmark of the clinical picture is drowsiness.

• In addition, there are abnormalities in recent memory,

attention, intellect, vertical gaze, and occasionally, mild

hemiparesis or hemiataxia.

• No sensory deficits are as a rule associated with lesions

in this territory.

• Utilization behavior (instrumentally correct but highly

exaggerated response to environmental cues and

objects) that is characteristic of frontal lobe damage has

been reported in medial thalamic territory infarcts

• Two syndromes have also been reported in medial

thalamic territory infarcts: akinetic mutism and the Kleine-

Levin syndrome.

• In akinetic mutism (persistent vegetative state),

patients appear awake and maintain a sleep-wake cycle

but are unable to communicate in any way.

• In addition to thalamic infarcts, akinetic mutism has been

reported to occur with lesions in the basal ganglia,

anterior cingulate gyrus, and pons.

• The Kleine-Levin syndrome (hypersomnia-bulimia

syndrome) is characterized by recurrent periods (lasting

1 to 2 weeks every 3 to 6 months) in adolescent males of

excessive somnolence, hyperphagia (compulsive eating),

hypersexual behavior (sexual disinhibition), and impaired

recent memory, and eventually ending with recovery.

• A confusional state, hallucinosis, irritability, or a

schizophreniform state may occur around the time of the

attacks

• Infarcts in the lateral territory of the thalamus are associated with occlusion of the anterior choroidal branch of the internal carotid artery.

• Structures involved in the lesion include the posterior limb of the internal capsule, lateral thalamic nuclei (lateral geniculate, ventral posterior lateral, pulvinar, reticular), and medial temporal lobe.

• The clinical hallmarks of the infarct are contralateral hemiparesis and dysarthria.

• Lesions in the lateral thalamic territory may manifest with only pure motor hemiparesis.

• Other clinical manifestations include hemisensory loss of pain and touch, occasional visual field defects, and neuropsychological defects.

• The latter consist of memory defects in left-sided lesions and visuospatial defects in right-sided lesions

• Infarcts in the posterior thalamic territory are associated

with occlusion of the posterior choroidal branch of the

posterior cerebral artery.

• Thalamic nuclei involved include the lateral geniculate,

pulvinar, and dorsolateral nuclei.

• Clinical manifestations include contralateral homonymous

quadrantanopsia and hemihypesthesia, as well as

neuropsychological deficits, including memory defects

and transcortical aphasia.

• Inconsistent signs include contralateral hemiparesis and

choreoathetosis

• Four types of pain syndromes have been described in

association with thalamic lesions .

• The four types are differentiated from each other on the

basis of the presence or absence in each of central

(thalamic) pain, proprioceptive sensations (vibration,

touch, joint), exteroceptive sensations (pain and

temperature), and abnormalities in somatosensory

evoked potentials

• Discrete lesions of the thalamus can cause severe and

lasting memory deficits

• There are three distinct behavioral and anatomic types of

memory impairment associated with diencephalic lesions:

• (1) Severe encoding defects are associated with lesions

in the mamillary bodies, mamillothalamic tracts, midline

thalamic nuclei, and the dorsomedial nucleus.

Performance of such patients never approximates normal

memory.

• (2) A milder form of memory deficit characterized by

severe distractibility occurs in lesions of the intralaminar

and medial thalamic nuclei

• (3) Disturbances in verbal memory (retrieval, registration,

and retention) occur in lesions of the left thalamus that

include the ventrolateral and intralaminar nuclei and the

mamillothalamic tract.

• Memory disturbances, which may be transient or

permanent, are most common with bilateral thalamic

lesions but do occur with unilateral lesions of either side.

• The essential role of the thalamus as the sole

mechanism for cortical arousal has been challenged.

• It is now acknowledged that cortical activation is

mediated by two mechanisms:

• (1) an indirect mechanism, via the thalamus, comprised

of the ascending reticular activating system (ARAS), and

• (2) a direct mechanism (nonthalamic), via cholinergic,

serotonergic, noradrenergic, and histaminergic arousal

systems that originate in the brain stem, basal forebrain,

or hypothalamus and do not pass through the thalamus.

• This syndrome consists of sensory disturbances confined

to one hand and to the ipsilateral mouth region.

• It is associated with focal lesions in the ventral posterior

thalamic nucleus.

• A similar syndrome has been reported with lesions in the

somatosensory cortex, border of the posterior limb of the

internal capsule and corona radiata, midbrain, and pons.

• The involvement of the hand and mouth areas suggests

that the sensory representation of these two areas is

contiguous not only in the primary somatosensory cortex

but also elsewhere in the neuraxis

• The alien hand syndrome is defined as unwilled,

uncontrollable movements of an upper limb together with

failure to recognize ownership of a limb in the absence of

visual cues.

• The syndrome was first described by Goldstein in 1908.

• Most cases are associated with lesions in the corpus

callosum and mesial frontal area, alone or in

combination.

• The condition has also been reported in infarcts involving

the posterolateral and anterolateral thalamic territories

(supplied by the geniculothalamic and tuberothalamic

arteries, respectively). The lesion usually involves the

ventral posterior, ventral lateral, and dorsomedial nuclei

• Infarctions in the left anterolateral thalamic territory

supplied by the tuberothalamic artery have been reported

to produce acalculia.

• The lesion usually involves the ventral lateral and

dorsomedial thalamic nuclei

• Dominant hemisphere thalamic lesions may cause a

transient deficit in language.

• Three types have been described: (1) medial, (2)

anterolateral, and (3) lateral.

• In the medial type, involving the dorsomedial and

centromedian nuclei (medial thalamic territory), the

language deficit is characterized by anomia and

attentionally induced language impairment. Lesions in

this area are associated with memory and attention

deficits.

• In the anterolateral type, the lesion involves ventral

anterior and anterior ventral nuclei (anterolateral thalamic

territory). This type is associated with an aphasic

syndrome resembling transcortical aphasia.

• In the third type, the lesion involves the lateral thalamic

territory. The language deficit in this type is characterized

by mild anomia.

• Because the thalamus is small, several of the nuclei and

even several of the functional regions are usually

affected simultaneously, even by discrete lesions such as

infarcts.

• Because arteriolar vascular territories cross the nuclear

boundaries, as a rule ischemic disease affects several

nuclei, often partially.

• In addition, many lesions are not restricted to the

thalamus, but involve neighboring areas of the brain as

well.

• Except for sensory deficits, unilateral thalamic lesions result in transient deficits. By contrast, bilateral lesions or unilateral lesions, such as hemorrhages or tumors, which press against the contralateral thalamus or impinge on the midbrain, may render the patient comatose or akinetic and mute.

• Timing has a particular impact on the clinical expression of thalamic lesions. As the effects of an acute lesion recede, neglect may disappear, inability to walk may yield to mild ataxia, and hemisensory loss diminishes. Other findings, however, particularly the so-called positive symptoms (tremor, pain), usually become more pronounced within a few weeks after the injury

AnteriorVA

VL

VPLVPM

LD

LP

Pulvinar LGN

MGN

DM

Functional Connections

Mammillary Body

Cingulate Gyrus

Amygdala

Hypothalamus

Olfactory Cortex

Prefrontal Cortex

Globus Pallidus

Substantia Nigra

Premotor Cortex

Prefrontal Cortex

GP

SN

Cerebellum (Dentate)

Primary Motor Cortex (4)

Supplementary Motor Cortex (5_Cingulate

Superior Parietal Cortex

(5,7)

Spinothalamic and DC/ML

Sensory Cortex (3,1,2)

Solitary Nucleus

Sensory Cortex

Right Optic Tract

Primary visual Cortex (17)

(lingual gyrus, cuneus)

Brachium of Inferior

Colliculus

Primary Auditory

Cortex (41,42)LGN, Superior Colliculus

Association areas of temporal, occipital, parietal lobes

Lesion: memory loss (Wernicke-Korsakoff)

Lesion: Sensory Aphasia

Lesion: contralateral loss of pain/temp, discrim touch

Lesion: contralateral loss of pain/temp, discrim

touch in head; ipsilateral loss of taste

Lesion: Left Homonymous Hemianopsia

Anterior Thalamic Region:

• Discrete lesions may be silent or cause language

disturbances when they affect the dominant hemisphere.

• They may also cause inattention, which results more

often when the right hemisphere is involved.

• Bilateral lesions may cause akinesia, amnesia, and

attentional disturbances.

• Lesions extending to the subthalamic area may cause

athetosis, chorea, or postural abnormalities (thalamic

hand).

Medial Thalamic Region:

• Lesions in this location may pass unnoticed when they

are small and unilateral.

• Large or bilateral lesions cause impairment of recent

memory, apathy or agitation, attention derangements,

and somnolence or coma.

• Lesions that extend to the midbrain-diencephalic junction

may cause contralateral tremor and vertical gaze palsy,

affecting particularly downward gaze

Ventrolateral Thalamic Region:

• Sensory loss, paroxysmal pains, and hemiataxia in the

contralateral side of the body are the most striking

sequelae of lesions in the posterior portion of this region.

• More anterior lesions cause postural abnormalities, such

as disequilibrium and restriction of axial supportive

movements or delayed tremor.

• Hemineglect and language disturbances may appear

transiently

Posterior Region

• Basal lesions in this region may cause hemianesthesia,

pain, and visual field defects.

• Dorsal lesions give rise to attentional disorders of the

ipsilateral hemisphere, resulting in transient aphasia

when the dominant hemisphere is involved.

• Some patients may have myoclonic dystonia

• Discrete lesions in various regions of the thalamus, and, more recently, deep brain stimulation (DBS) through implanted electrodes, are increasingly used for the treatment of parkinsonian and essential, dystonia, pain, epilepsy, and the manifestations of Gilles de la Tourette's syndrome.

• Treatment of the tremor is the most extensively used and best understood DBS thalamic procedure.

• Essential tremor can be treated by DBS with electrodes in the ventrolateral nucleus. The ventrolateral nucleus includes the nuclei Ventralis Intermedius (Vim) and ventralis oralis posterior (Vop). The ideal location of the stimulating electrodes seems to lie in the Vop nucleus immediately anterior to the cerebellar receiving area, Vim.