Corpus striatum
Corpus striatum
1. The corpus striatum is primarily composed of which two major nuclei?
A. Globus pallidus and subthalamic nucleus
B. Caudate nucleus and putamen
C. Putamen and substantia nigra
D. Thalamus and caudate nucleus
The corpus striatum comprises the caudate nucleus and putamen; these form the major input nuclei of the basal ganglia.
2. The lentiform nucleus consists of:
A. Caudate nucleus and globus pallidus
B. Caudate nucleus and putamen
C. Putamen and globus pallidus
D. Globus pallidus and substantia nigra
Lentiform (lens-shaped) nucleus comprises the putamen (lateral) and globus pallidus (medial).
3. Which neurotransmitter is the principal inhibitory transmitter of striatal projection neurons?
A. GABA (gamma-aminobutyric acid)
B. Dopamine
C. Glutamate
D. Acetylcholine
Medium spiny neurons are GABAergic and constitute the main output projections from the striatum to pallidal and nigral targets, exerting inhibitory control.
4. In Huntington disease, which part of the striatum is earliest and most severely affected?
A. External globus pallidus
B. Caudate nucleus (especially head)
C. Subthalamic nucleus
D. Substantia nigra pars compacta
Huntington disease produces early atrophy of the caudate head and anterior putamen, causing enlargement of frontal horns and choreiform movements.
5. The lenticulostriate arteries are branches of which major cerebral artery?
A. Anterior cerebral artery
B. Middle cerebral artery
C. Posterior cerebral artery
D. Anterior choroidal artery
Lenticulostriate (perforating) arteries arise from the M1 segment of the middle cerebral artery and supply much of the striatum and internal capsule.
6. The direct (facilitatory) pathway from striatum to thalamus primarily disinhibits thalamocortical activity via which target?
A. Subthalamic nucleus
B. Internal segment of globus pallidus (GPi)
C. External globus pallidus (GPe)
D. Substantia nigra pars compacta
The direct pathway inhibits GPi (an inhibitory output), which reduces thalamic inhibition and thus facilitates movement (disinhibition of thalamocortical neurons).
7. Dopaminergic input from substantia nigra pars compacta has opposing effects on striatal pathways via which receptor types?
A. D1 receptors (direct, excitatory) and D2 receptors (indirect, inhibitory)
B. D2 receptors excitatory and D1 receptors inhibitory
C. Both D1 and D2 are inhibitory
D. Dopamine has no effect on striatal neurons
Dopamine acting on D1 receptors enhances the direct pathway, facilitating movement; on D2 receptors it inhibits the indirect pathway, also promoting movement overall. Loss of nigral dopamine in Parkinson’s reduces direct and increases indirect activity, causing hypokinesia.
8. Hemiballismus is classically caused by a lesion in which basal ganglia structure?
A. Putamen
B. Caudate head
C. Subthalamic nucleus
D. Globus pallidus internal segment
Lesions of the subthalamic nucleus (often due to lacunar infarct) reduce excitation of GPi, leading to decreased inhibition of thalamus and violent involuntary flinging movements (hemiballismus).
9. On MRI, caudate atrophy with enlargement of frontal horns is most suggestive of:
A. Parkinson disease
B. Huntington disease
C. Wilson disease
D. Normal pressure hydrocephalus
In Huntington disease, marked atrophy of caudate and putamen leads to increased size of the frontal horns of the lateral ventricles on MRI/CT.
10. Which clinical sign is most characteristic of basal ganglia (striatal) dysfunction?
A. Hyperreflexia with Babinski sign
B. Abnormal involuntary movements (chorea, dystonia) or bradykinesia/rigidity
C. Loss of vibration sense
D. Pure sensory loss
Basal ganglia disorders manifest as movement disorders — either hyperkinetic (chorea, dystonia, myoclonus) or hypokinetic (bradykinesia, rigidity) — rather than classical upper or lower motor neuron signs.
11. Which cell type in the striatum is primarily affected in Huntington disease?
A. Cholinergic interneurons
B. Medium spiny GABAergic projection neurons (especially those of the indirect pathway)
C. Oligodendrocytes
D. Pyramidal neurons
Medium spiny neurons, particularly those projecting to the external globus pallidus (indirect pathway), are vulnerable in Huntington disease, leading to early hyperkinetic movements.
12. Deep brain stimulation (DBS) for Parkinson disease commonly targets which basal ganglia structure?
A. Caudate nucleus
B. Subthalamic nucleus (or sometimes GPi)
C. Putamen
D. Thalamic reticular nucleus
DBS of the subthalamic nucleus (STN) or internal segment of globus pallidus (GPi) improves motor symptoms in advanced Parkinson disease by modulating abnormal basal ganglia output.
13. A lacunar infarct of the lenticulostriate arteries most commonly produces which syndrome?
A. Pure sensory aphasia
B. Pure motor hemiparesis (contralateral)
C. Alexia without agraphia
D. Bilateral cortical blindness
Lacunar infarcts involving the posterior limb of the internal capsule or adjacent striatum/lentiform nucleus commonly cause pure motor hemiparesis due to corticospinal fiber involvement.
14. Which metabolic disorder commonly produces T2 hyperintensity in the basal ganglia, especially putamen, on MRI?
A. Multiple sclerosis
B. Alzheimer disease
C. Wilson disease
D. Amyotrophic lateral sclerosis
Wilson disease causes copper deposition with signal changes in basal ganglia (putamen, caudate) and characteristic T2 hyperintensities; clinical features include dystonia, parkinsonism, and hepatic dysfunction.
15. A patient with prominent rigidity, bradykinesia, and resting tremor likely has degeneration of which structure affecting the striatum?
A. Loss of cholinergic neurons in nucleus basalis
B. Loss of dopaminergic neurons in substantia nigra pars compacta leading to reduced striatal dopamine
C. Demyelination of corticospinal tracts
D. Lesion of dorsal columns
Parkinsonian features arise from degeneration of substantia nigra pars compacta, reducing dopamine input to the striatum and causing overactivity of the indirect pathway and reduced movement.
16. Which statement about corticostriatal projections is correct?
A. Cortical areas project topographically to the striatum (sensorimotor to putamen; associative to caudate)
B. Corticostriatal fibers arise only from motor cortex
C. Corticostriatal projections are primarily inhibitory
D. There are no cortical inputs to the striatum
Corticostriatal projections are glutamatergic and topographically organized: sensorimotor cortex projects to putamen, associative/limbic areas to caudate and ventral striatum.
17. Which clinical feature is more typical of putaminal than caudate lesions?
A. Severe cognitive and behavioral change early
B. Prominent motor symptoms such as dystonia and parkinsonism
C. Pure amnesia
D. Visual agnosia
Putamen has stronger sensorimotor connectivity and lesions often manifest with motor abnormalities (dystonia, parkinsonism), whereas caudate involvement more affects cognition and behavior.
18. A hyperkinetic movement disorder characterized by brief, irregular, nonrhythmic movements that flow from one body part to another is called:
A. Chorea
B. Parkinsonian tremor
C. Restless legs syndrome
D. Hemiballismus
Chorea consists of rapid, irregular movements that can be seen in basal ganglia disorders like Huntington disease and rheumatic chorea.
19. Which drug class increases synaptic dopamine by inhibiting dopamine reuptake and is sometimes used to treat Parkinsonian symptoms?
A. GABA agonists
B. Monoamine oxidase B (MAO-B) inhibitors and dopamine reuptake inhibitors
C. Glutamate antagonists only
D. Cholinesterase inhibitors
MAO-B inhibitors (e.g., selegiline) preserve dopamine by reducing breakdown; some agents also inhibit dopamine reuptake. These increase dopaminergic tone and help parkinsonian symptoms.
20. A lesion primarily affecting the anterior limb of the internal capsule near the head of the caudate would most likely produce which deficit?
A. Pure sensory loss in the ipsilateral limb
B. Isolated visual field defect
C. Cognitive/behavioral changes (frontal executive dysfunction) and possible mild motor deficits
D. Complete hemianopia
The anterior limb of internal capsule carries frontopontine and thalamocortical fibers; lesions near caudate head commonly produce frontal-subcortical cognitive and behavioral changes with subtle motor signs rather than pure sensory or visual deficits.
Combintion of which of the following is designated the corpus striatum
[A] Putamen and the globus pallidus
[B] Lentiform nucleus and caudate nucleus
[C] Putamen and the caudate nucleus
[D] Lentiform nucleus and the globus pallidus
Basal ganglia
Basal ganglia, for clinical purposes considered to comprise the
- Caudate nucleus
- Putamen
- Globus pallidus (GPi)
- Subthalamic nucleus
- Substantia nigra
| Basal ganglia | |
| 1 | Caudate nucleus |
| 2 | Putamen |
| 3 | Globus pallidus (GPi) |
| 4 | Subthalamic nucleus |
| 5 | Substantia nigra |
| 6 | lentiform nucleus – putamen and the globus pallidus are collectively termed the lentiform nucleus |
| 7 | corpus striatum – Combination of lentiform nucleus and caudate nucleus is designated the corpus striatum. |
1. What structures form the corpus striatum?
The caudate nucleus and lentiform nucleus (putamen + globus pallidus).
2. Which artery primarily supplies the corpus striatum?
The lenticulostriate branches of the middle cerebral artery (MCA).
3. What is the main function of the corpus striatum?
Regulation of voluntary motor control, procedural learning, and habit formation.
4. Which neurotransmitter is primarily inhibitory in the corpus striatum?
Gamma-aminobutyric acid (GABA).
5. Which neurotransmitter is excitatory in basal ganglia pathways?
Glutamate.
6. What is the role of dopamine in corpus striatum function?
Modulates motor activity via D1 (direct pathway activation) and D2 (indirect pathway inhibition) receptors.
7. Damage to the corpus striatum causes what movement disorders?
Chorea, dystonia, and parkinsonism.
8. Which disease is classically associated with degeneration of the caudate nucleus?
Huntington’s disease.
9. How does the corpus striatum connect to the motor cortex?
Through thalamic relay via the direct and indirect basal ganglia pathways.
10. What imaging finding is seen in acute infarct of the corpus striatum?
Restricted diffusion on MRI (DWI sequence) in lenticulostriate territory.
| No. | Corpus striatum:Questions | Answer |
|---|---|---|
| 1 | What structures form the corpus striatum? | Caudate nucleus and lentiform nucleus (putamen + globus pallidus). |
| 2 | Which artery primarily supplies the corpus striatum? | Lenticulostriate branches of the middle cerebral artery (MCA). |
| 3 | Function of corpus striatum? | Regulation of voluntary motor control, procedural learning, and habit formation. |
| 4 | Primary inhibitory neurotransmitter? | GABA. |
| 5 | Primary excitatory neurotransmitter? | Glutamate. |
| 6 | Dopamine’s role? | Activates direct pathway (D1) and inhibits indirect pathway (D2) to modulate movement. |
| 7 | Disorders from corpus striatum damage? | Chorea, dystonia, parkinsonism. |
| 8 | Disease with caudate degeneration? | Huntington’s disease. |
| 9 | Connection to motor cortex? | Via thalamic relay through basal ganglia pathways. |
| 10 | MRI finding in acute infarct? | Restricted diffusion in lenticulostriate territory on DWI. |
| 11 | Which part of corpus striatum receives cortical input? | Caudate nucleus and putamen. |
| 12 | Main output nuclei? | Globus pallidus interna and substantia nigra pars reticulata. |
| 13 | Clinical sign of lenticulostriate artery stroke? | Pure motor hemiparesis. |
| 14 | Basal ganglia circuit with movement suppression? | Indirect pathway. |
| 15 | Basal ganglia circuit with movement facilitation? | Direct pathway. |
| 16 | Histology: cell type dominant in striatum? | Medium spiny neurons (GABAergic). |
| 17 | Which neurodegenerative disease affects putamen in early stages? | Wilson’s disease. |
| 18 | Function in procedural learning? | Stores and automates repetitive motor tasks. |
| 19 | Common toxic cause of striatal injury? | Carbon monoxide poisoning. |
| 20 | Which side of the body is affected if left corpus striatum is damaged? | Contralateral (right) side. |
Corpus striatum
