The document discusses the neuroanatomy and neurolocalization of the basal ganglia and thalamus. It describes the basal ganglia as a collection of gray matter nuclei involved in motor control. It notes their role in initiating and modulating movement. It then describes the specific nuclei of the basal ganglia - the caudate, putamen, globus pallidus, subthalamic nucleus, and substantia nigra. It also discusses the direct and indirect pathways between these nuclei and their role in movement. Finally, it briefly discusses some movement disorders associated with lesions in different basal ganglia structures.

1. Neuroanatomy and neurolocalization of
basal ganglia and thalamus
Presenter: Dr Dagnaw.M NR2
Moderator: Dr Biniyam A (neurologist)
Jan 16, 2021
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2. Objective
• To know the macro and micro anatomy of the BG and
thalamus.
• To know the vascular supply
• To be able to neurolocalize with the clinical
correlates.
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3. BASAL GANGLIA
• The basal ganglia are a collection of gray matter nuclei located
deep within the white matter of the cerebral hemispheres.
• Principal component of the extrapyramidal motor system.
• Extrapyramidal system serves to modulate the activity of the
pyramidal system and does not project to the spinal cord.
• Primarily involved in control and regulation of activities of
motor and premotor cortical areas.
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4. PHYSIOLOGY
• These basal ganglia are involved in the control of complex
patterns of motor activity.
• There are two aspects to this involvement.
 The first concerns the initiation of the movement.
 The second concerns the quality/modulate the performance of
the motor task.
• In addition, some of the structures that make up the basal
ganglia are thought to influence cognitive aspects of motor
control.
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5. • It is not directly concerned with the production of voluntary
movement but is closely integrated with other levels of the
motor system to modulate and regulate the motor activity that
is carried out by way of the pyramidal system.
• The main components of the basal ganglia are the caudate
nucleus, putamen, globus pallidus, subthalamic nucleus,
and substantia nigra.
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6. • The caudate and putamen are histologically and
embryologically closely related and can be thought of as a
single large nucleus called the neostriatum or simply
striatum.
• The striatum receives virtually all inputs to the basal ganglia.
• The caudate and putamen are separated by penetrating fibers
of the internal capsule
• but remain joined by cellular bridges
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7. Lateral view showing basal ganglia, amygdala, and lateral
ventricle of the left hemisphere
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8. • Just medial to the putamen lies the globus pallidus meaning
“pale globe,” so named because of the many myelinated fibers
traversing this region.
• The globus pallidus has an internal segment and an external
segment .
• The putamen and globus pallidus together are called the
lenticular or lentiform (meaning “lentil- or lens-shaped”)
nucleus.
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9. Substantia Nigra
• The SN is a gray mass that lies in the cerebral peduncle between the crus
cerebri and the tegmentum of the midbrain.
• The SN is composed of two parts: the deep pars or zona compacta (SNc),
which contains the large, melanin-containing, dopaminergic neurons and
the more superficial zona reticulata (SNr), which contains large, multipolar,
nonpigmented, GABAergic neurons.
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10. Major Nuclei
• Striatum
– Caudate nucleus
– Putamen
• Globus Pallidus
– Globus pallidus external (GPe)
– Globus pallidus internal (GPi)
• Substantia Nigra
– Pars compacta (SNc)
– Pars reticulata (SNr)
• Subthalamic nucleus (STN)
Neostriatu
mm
Paleostri
atum
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16. Blood supply of basal ganglia
• Corpus striatum is supplied by lenticulostriatal branch of
MCA.
• Recurrent artery of heubner (branch of ACA) supply anterior
portion of Lentiform nuclei and head of caudate nuclei.
• Anterior choroidal artery supplies medial Globus pallidus.
• In hypertension, the lenticulostriate arteries are prone to
narrowing, which can lead to lacunar infarction as well as to
rupture, causing intracerebral hemorrhage.
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20. Inputs to the Basal Ganglia
• The main input to the basal ganglia comes from massive
projections from the entire cerebral cortex to the striatum.
• The putamen is the most important input nucleus of the
striatum for motor control pathways.
• Most cortical inputs to the striatum are excitatory and use
glutamate as the neurotransmitter.
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21. • Another important input to the striatum is the substantia nigra
pars compacta.
• This dopaminergic nigrostriatal pathway is excitatory to some
cells and inhibitory to others in the striatum.
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22. Major inputs
• Cereberal Cortex – Corticostriatal Fibers
• Thalamus -Thalamostriatal Fibers
• SN - Nigrostriatal Fibers
• RAPHE NUCLEI- Raphe Nuclei Striatal Fibers
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24. Outputs from the Basal Ganglia
• Basal ganglia outputs arise from the internal segment of the
globus pallidus and from the substantia nigra pars
reticulata.
• For motor control, the substantia nigra pars reticulata appears
to convey information for the head and neck, while the internal
segment of the globus pallidus conveys information for the
rest of the body.
• These output pathways are inhibitory and use the
neurotransmitter gamma-aminobutyric acid (GABA).
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25. • The main output pathways are to the ventral lateral (VL) and
ventral anterior (VA) nuclei of the thalamus via the thalamic
fasciculus.
• The substantia nigra pars reticulata also projects to the
superior colliculus, to influence tectospinal pathways.
• Which influences both the lateral motor systems (e.g., the
lateral corticospinal tract) and the medial motor systems (e.g.,
the reticulospinal and tectospinal tracts) .
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27. Intrinsic Basal Ganglia Connections
• There are two predominant pathways from input to output
nuclei through the basal ganglia.
• The direct pathway travels from the striatum directly to the
internal segment of the globus pallidus or the substantia nigra
pars reticulata.
• The indirect pathway takes a detour from the striatum, first to
the external segment of the globus pallidus and then to the
subthalamic nucleus, before finally reaching the internal
segment of the globus pallidus.
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28. • The direct pathway serves to facilitate cortical excitation and
carry out voluntary movement.
• The indirect pathway serves to inhibit cortical excitation and
prevent unwanted movement.
• The input and output nuclei are connected by the direct and
indirect loops.
• Disease of the direct pathway produces hypokinesia and
disease of the indirect pathway produces hyperkinesias.
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32. Lesions of the Basal Ganglia
• Pathologic processes affecting the BG are often diffuse.
• When discret,they usually also affect neighboring structures
like internal capsule and hypothalamus.
• Therefore except for hemiballismus, often associated with
damage to the contralateral STN,correlation b/n BG lesions
and clinical motor dysfunction tend to be obscure.
• Behavioral and mov’t disorder are common.
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33. • Lesions of the caudate rarely caused motor disorder /eg.
Chorea , dystonia/ but were more likely to cause behavioral
problem especially Abulia/ or disinhibition.
• Lesions of the putamen and globus pallidus rarely caused
abulia and disinhibition, but commonly dystonia, particularly,
when putamen involved. These emphasize the motor roles of
these structures.
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34. Movement disorders
• Hypokinetic movement disorders, such as (parkinsonism), are
thought to result from an increase of the normal inhibitory
effects of the BG output neurons.
• Hyperkinetic movement disorders—such as (chorea,
hemiballismus, and dystonia )—presumably result from a
reduction in the normal inhibition.
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35. 35
• Tardive dyskinesia:
- most common pattern– repetitive, rhythmical mov’ts occuring in
the oral-lingual-buccal area
 result from treatment with neuroleptic drugs
• Ballismus: an involuntary hyperkinesia often confined to one half
of the body (hemiballismus);
 characterized by sudden, paroxysmal, large amplitude,
flinging/throwing movements of the arm/leg
1. Hyperkinetic ﴾ dyskinetic ﴿ disorders
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36. Myoclonus
• sequence of repeated, often nonrhythmic, brief shock-like jerks due to
sudden involuntary contraction or relaxation of one or more muscles
Chorea
• ongoing random-appearing sequence of one or more discrete involuntary
movements or movement fragments.
Athetosis
 slow, continuous, involuntary writhing movement that prevents
maintenance of a stable posture
 represents a form of slow chorea
Dystonia
involuntary sustained or intermittent muscle contractions that cause twisting
and repetitive movements, abnormal postures, or both.
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37.  Some disorders associated with lesions of the basal ganglia
are:
1. Lesions of the subthalamic nucleus produce contralateral
hemiballismus
2. Small unilateral lesions of the anteroventral portion of the
caudate cause contralateral choreoathetosis .
3. Unilateral lesions of the globus pallidus may cause
contralateral hemidystonia, hemiparkinsonism, or tremor,
whereas bilateral globus pallidus lesions may cause dystonia,
parkinsonism, abulia, or akinesia .
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38. 4. Lesions of the substantia nigra result in parkinsonism.
5. Unilateral Lentiform nuclei hemorrhages or lacunar infarcts
may present with sudden falling to the contralateral side while
sitting, standing, or walking – ‘’like a falling dog’’
6. Ventral basal ganglia lesions – schizophrenia and affective
disorders.
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39. Thalamus
• The thalamus (meaning “inner chamber” or “meeting place” in
Greek) is an important processing station in the center of the
brain.
• Nearly all pathways that project to the cerebral cortex passes
via synaptic relays in the thalamus.
• It is often thought of as the major sensory relay station.
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inner chamber” or “meeting place

41. • They represent the largest portion of the diencephalon.
• Other diencephalic structures are ;
 The epithalamus (pineal and habenular complex)
 The subthalamic nucleus
 and the hypothalamus.
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42. • The thalamus is divided into a medial nuclear group, lateral
nuclear group, and anterior nuclear group by a Y-shaped
white matter structure called the internal medullary lamina.
• Nuclei located within the internal medullary lamina itself are
called the intralaminar nuclei.
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44. Landmarks of the thalamus
o Medially:
 third ventricle
o laterally:
 Internal capsule and basal ganglia
o Dorsal
 Forms floor of lateral ventricle
o Ventral
 continuous with sub thalamic nuclei
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45. • Three main
categories of
thalamic nuclei:
1. Relay nuclei
2. Intralaminar
nuclei
3. Reticular nucleus
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46. Relay nuclei
• Most of the thalamus is made up of relay nuclei, which
receive inputs from numerous pathways and then project to the
cortex.
• Relay nuclei receive massive reciprocal connections back from
the cortex.
SPECIFIC THALAMIC RELAY NUCLEI
• These specific relay nuclei lie mainly in the lateral thalamus.
• All sensory modalities, with the exception of olfaction, have
specific relays in the lateral thalamus en route to their primary
cortical areas.
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47. Anterior nuclei
• lies between the arms of this Y-shaped structure.
• it is related to emotion and memory function.
• It receives input from the hippocampus through the fornix.
• Output - cingulate gyrus
• Lesions of the anterior nucleus are associated with loss of
memory and impaired executive function.
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48. Medial nuclei
• lies on the medial side of the internal medullary lamina.
• It sends or receives projections from the amygdala, limbic
systems, hypothalamus, and prefrontal cortex.
• has functions related to cognition, judgment, affect, olfaction,
emotions, sleep and waking, executive function, and memory.
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49. Lateral nuclear group
• Divided into the dorsal tier
and the ventral tier.
• Serve as specific relay
stations between motor and
sensory systems.
• The dorsal tier nuclei
consist of the lateral dorsal
and lateral posterior nuclei
and the pulvinar.
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50. • The ventral tier of the lateral nucleus are true relay nuclei,
connecting lower centers with the cortex and vice versa.
• VPL and VPM nucleus are the major sensory relay nuclei.
• The VL receives input from the basal ganglia and cerebellum
then projects to the motor and supplementary motor areas.
• The VA nucleus also receives projections from the globus
pallidus and the substantia nigra then projects primarily to the
premotor cortex.
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51. • The VL and VA nucleus coordinates the motor system.
• Pulvinar nucleus
 Input – other thalamic nuclei, geniculate bodies, superior
colliculus
 Output – peristriate area and posterior parietal, cingulate
and prefrontal areas
 Function – visual attention and cortical attention for
language related tasks for left hemisphere
visuospatial tasks for right hemisphere
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53. Intralaminar Nuclei
• Their main inputs and outputs are from the basal ganglia.
• The caudal intralaminar nuclei include the large
centromedian nucleus and are involved mainly in basal ganglia
circuitry.
• The rostral intralaminar nuclei have an important role in
relaying inputs from ARAS to the cortex, maintaining the
alert, conscious state.
• It also have input and output connections with the BG.
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54. Reticular Nucleus
• The reticular nucleus forms a thin sheet located just lateral to
the rest of the thalamus and just medial to the internal.
• The reticular nucleus is the only nucleus of the thalamus that
does not project to the cortex.
• it receives inputs mainly from other thalamic nuclei and the
cortex and then projects back to the thalamus.
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57. Major imputes and outputs
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58. Vascular Supply of the Thalamus
• The blood supply to the thalamus comes primarily via
thalamoperforating arteries of the posterior communicating
and posterior cerebral arteries.
• The anterior choroidal artery supplies the lateral geniculate
body.
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61. Clinical correlates
• The arterial territory responsible for a thalamic ischemic
infarct may be inferred from the clinical findings;
1. Paramedian Territory
• clinical triad of somnolent apathy, memory loss, and
abnormalities of vertical gaze.
• Bilateral medial thalamic infarcts account for the
behavioral syndrome.
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62. • Due to embolic occlusion of the top of the basilar artery or
local atheroma at the origin of the PCA;
1. Transient LOC or somnolence
2. Behavioral changes
3. Recent memory loss
4. Vertical gaze and convergence disorders
5. Contralateral hemiataxia
6. Delayed action tremor
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63. Thalamogeniculate Territory
• Ischemia in this causes some of the components of the classic
thalamic syndrome described by Dejerine and Roussy.
• All these findings occur on the side of the body contra lateral
to the lesioned thalamus.
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64. 1. Hemianesthesia
2. Transient slight hemiparesis
3. Hemiataxia
4. Hemiataxia–hypesthesia
syndrome
5. Lack of nonvolitional
utilization of the
contralateral body.
6. Dysequilibrium
7. Choreoathetoid movements
8. Athetoid posture (“thalamic
hand”)
9. Paroxysmal pain (thalamic
pain)
10. Homonymous hemianopia
(often due to simultaneous
medial occipital infarction)
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65. Territory of the Posterior Choroidal Arteries
• These vessels supply mainly the lateral geniculate body,
pulvinar, posterior thalamus.
• The most common clinical manifestations infarction of this
area include:
1. Homonymous quadrantanopia
2. Decreased optokinetic nystagmus
3. Hemisensory loss
4. Mild hemiparesis, accompanied by sensory loss
5. Transcortical aphasia
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66. Thalamic hemorrhages
• Common sites of hypertensive h’ge
• Prominent sensory deficits
• Contralat. Hemiplegia or hemiparesis
• Aphasia after h’ge into dominant thalamus
• Homonymous visual field defects
• Ocular dysfunction
• Prognosis depends on amount and site of bleeding
 ant. and dorsal types: usually benign
posteromed. and posterolat. types: poor prognosis
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67. Clinical Manifestations of Lesions in the
Thalamus
1. Because of the smallness lesions of the thalamus involve
several of the nuclei and several of the functional regions are
usually affected with neighboring areas of the brain as well.
2. Except for sensory deficits, unilateral thalamic lesions result
in transient deficits.
• Bilateral or Unilateral with compression to other side causes
coma or akinetic mutism .
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68. Disturbances of Alertness
• Infarction bilateral Paramedian artery
– Transient Somnolence or coma
– Prolonged coma if mid brain tegmentum involved
– Oculomotor paresis
– Day time somnolence and abnormal sleep, but REM sleep
is normal, suggesting that the medial thalamus lesion
• Pure thalamic involvement have very small reactive pupil(
diencephalic pupils), and Akinetic mutism .
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69. Autonomic disturbance
• Due to Paramedian thalamic lesions
• Kleine-Levin syndrome, which is characterized by
o episodes of somnolence,
o hyperphagia,
o impaired recent memory
o hypersexual behavior
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70. Disturbances of Mood and Affect
• Lesions of the paramedian region
 Apathy, disinterest, and a lack of drive
• bilateral medial thalamic damage
 Partial Klüver-Bucy syndrome,
 Chronic amnesia, distractibility, hyperorality, affective
dyscontrol, and a socially inappropriate behavior.
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71. • Right thalamic lesions
 A manic-like state with disinhibition and affecting speech.
• DM and anterior nucleus lesion gives schizophrenia.
Memory disturbance
 Bilateral or unilateral anterior or DM nucleus lesion
 Transient or permanent impairment of recent memory.
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72. • Bilateral anterior nucleus without DM nuclei lesion
 Permanent amnestic syndrome
 Korsakoff amnesia
• A unilateral left polar thalamic infarction
 Pure amnesia
• Left thalamic lesion – mainly affect verbal memory
• Right non dominanat thalamic lesion – affects visuospatial
tasks (nonverbal memory).
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73. Thalamic amnesia
 Anterograde verbal
 Retrograde visual
 Preserved motor learning
 Disorientation to time
 Confabulation, or falsification of memory
 Prosopagnosia
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74. Sensory disturbance
 Thalamic lesions may cause sensory loss, often accompanied
by paresthesias and pain.
 PARESTHESIAS AND PAIN
 Lesions in the ventral posterior lateral nucleus
 Contra lateral paresthesias that lack “objective” sensory loss.
• “thalamic midline split,”
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75. Thalamic pain
• Called Dejerine–Roussy syndrome.
• Contralateral unpleasant or excruciatingly painful sensation.
• Contra lateral hemi body sensory loss to all modalities, with
occasional facial sparing.
• It is generally accompanied by hypesthesia to cutaneous
stimuli and cold but not to heat.
• Appear at the time of the injury or when the sensory loss
begins to improve.
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76. SENSORY LOSS
• Usually contra lateral to the lesion.
• Occur in the distal portion of the limbs and the face than the
mid line.
• All sensory modalities are involved mainly primary sensory
modalities are affected.
• Hemiparesis if internal capsule is involved.
• Due to VPL and VPM nuclei lesions.
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77. Motor Disturbances
POSTURAL DISTURBANCES
• lesions of the ventral lateral and postral lateral nuclei
• unable to stand or even sit, despite normal strength of the
limbs when tested against resistance (thalamic astasia).
• Motor neglect- neglect to use limbs.
• Fall backward or toward the side contralateral to the lesion.
• contralateral hypotonia, reduction of emotional expression,
and transient neglect.
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78. References
• Dejongs neurologic examination 8th edition.
• Brazis localization in clinical neurology 7th edition.
• H. Blumenfeld neuroanatomy through clinical cases
2nd edition.
• Snells clinical neuroanatomy,7th edition.
• Atlas of neuroanatomy and neuro physiology
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