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• 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 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.
• 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 precentral
  gyrus.
• 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
• 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
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.
• (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
• 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
• 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
Functional Connections
                                        Lesion: contralateral loss of pain/temp, discrim touch

                                                                                           Globus Pallidus
                                                                                           Substantia Nigra
                Mammillary Body
                                                                                                        Premotor Cortex
                                                                                                        Prefrontal Cortex

               Cingulate Gyrus                                            VA                                         GP
                                                           Anterior                                                  SN
                                                                                                                     Cerebellum (Dentate)
                                                                                 VL                              Primary Motor Cortex (4)
                          Cingulate                                                                              Supplementary Motor Cortex (5_
                                                                       LD
                                                                                                                  Spinothalamic and DC/ML
                                                                                                                    Sensory Cortex (3,1,2)
                                                              DM
  Superior Parietal Cortex
                                                                        LP        VPL VPM                             Solitary Nucleus
  (5,7)
                  Amygdala                                                                                            Sensory Cortex
                  Hypothalamus
                  Olfactory Cortex                                                               Lesion: contralateral loss of pain/temp, discrim
              Prefrontal Cortex                                                                  touch in head; ipsilateral loss of taste

                                                                           Pulvinar      LGN                             Right Optic Tract
          Lesion: memory loss (Wernicke-Korsakoff)
                                                                                      MGN                          Primary visual Cortex (17)
                                                                                                                   (lingual gyrus, cuneus)
                                                                                                    Lesion: Left Homonymous Hemianopsia
                  Lesion: Sensory Aphasia
                                                                                        Primary Auditory
                                      LGN, Superior Colliculus                          Cortex (41,42)
                                                                                                        Brachium of Inferior
                                      Association areas of temporal, occipital, parietal lobes          Colliculus
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.
THALAMUS OVERVIEW
THALAMUS OVERVIEW

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THALAMUS OVERVIEW

  • 1.
  • 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
  • 7.
  • 8.
  • 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.
  • 13.
  • 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.
  • 17.
  • 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.
  • 19.
  • 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.
  • 21.
  • 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
  • 26.
  • 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.
  • 30.
  • 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
  • 35.
  • 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
  • 39.
  • 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
  • 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
  • 46.
  • 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
  • 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
  • 69.
  • 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
  • 75.
  • 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
  • 77.
  • 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
  • 79.
  • 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
  • 81.
  • 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. Functional Connections Lesion: contralateral loss of pain/temp, discrim touch Globus Pallidus Substantia Nigra Mammillary Body Premotor Cortex Prefrontal Cortex Cingulate Gyrus VA GP Anterior SN Cerebellum (Dentate) VL Primary Motor Cortex (4) Cingulate Supplementary Motor Cortex (5_ LD Spinothalamic and DC/ML Sensory Cortex (3,1,2) DM Superior Parietal Cortex LP VPL VPM Solitary Nucleus (5,7) Amygdala Sensory Cortex Hypothalamus Olfactory Cortex Lesion: contralateral loss of pain/temp, discrim Prefrontal Cortex touch in head; ipsilateral loss of taste Pulvinar LGN Right Optic Tract Lesion: memory loss (Wernicke-Korsakoff) MGN Primary visual Cortex (17) (lingual gyrus, cuneus) Lesion: Left Homonymous Hemianopsia Lesion: Sensory Aphasia Primary Auditory LGN, Superior Colliculus Cortex (41,42) Brachium of Inferior Association areas of temporal, occipital, parietal lobes Colliculus
  • 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.