A detailed functional anatomy of thalamus.

1. Dr Sudhakar Marella
DM Neurology

2. • 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

3. • 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.

4. • 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.

5. • 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)

6. • 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

9. • 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.

10. • 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

11. • 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

12. • 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.

14. • 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)

15. • 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.

16. • 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.

18. • 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.

20. • 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 mamillary
bodies 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.

22. • 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).

23. • 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

24. • 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.

25. 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

27. • 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.

28. • 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

29. • 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.

31. • 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

32. • 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.

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

34. • 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

36. • 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.

37. • 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).

38. • 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

40. • 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

41. 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:

42. 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.

43. • (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

44. 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 intralaminar
nuclei (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 intralaminar
nuclei.

45. • (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

47. 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.

48. 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

49. • 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

50. • 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).

51. • 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

52. • 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.

53. • 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)

54. • 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

55. • 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.

56. • 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.

57. • 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

58. • (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.

59. • 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

60. • 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

61. • 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).

62. • 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

63. • 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.

64. • 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

65. • 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.

66. • 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.

67. • 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.

68. • 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

70. • 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

71. • 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.

72. • 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

73. • 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.

74. • 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

76. • 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

78. • 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

80. • 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

82. • 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

83. • (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.

84. • 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.

85. • 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

86. • 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

87. • 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

88. • 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.

89. • 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.

90. • 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.

91. • 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

92. Anterior
VA
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

93. 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).

94. 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

95. 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

96. 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

97. • 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.