Basal ganglia and cerebellum

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Last updated 1:43 AM on 9/6/26
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58 Terms

1
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Q: What are the three components of the motor system and the role of each?

A: Motor cortex (controller), basal ganglia (initiation/maintenance), cerebellum (coordination).


2
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Q: Which two motor functions does the cerebellum help with coordination for?

A: Fine motor control and balance.


3
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Q: How do the basal ganglia and cerebellum influence movement?

A: They influence the processing of motor control and modulate the output of the descending pathways without directly causing motor output.


4
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Q: List the major subcortical nuclei of the basal ganglia.

A: Caudate nucleus, putamen, globus pallidus (externa and interna), nucleus accumbens.


5
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Q: Which basal ganglia component comes from the diencephalon?

A: Subthalamic nucleus.


6
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Q: Which basal ganglia component is located in the rostral midbrain?

A: Substantia nigra.


7
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Q: Which structures make up the striatum?

A: Caudate nucleus and putamen.


8
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Q: Which arteries supply the whole basal ganglia, and from what vessel do they arise?

A: Lenticulostriate arteries, which are deep branches of the middle cerebral artery.


9
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Q: What are the 5 reasons the motor loop aspect of the basal ganglia is so important?

A: 1. regulation of upper motor neurons

  1. necessary for normal initiation of movement

  2. control of movement and automatic engagement of learned movements

  3. disruptions lead to a variety of movement disorders

  4. oculomotor loop


10
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Q: In one phrase each, what does the direct pathway do and what does the indirect pathway do?

A: Direct promotes movement; indirect prevents movement.


11
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Q: What controls cortical input and output, and what is its baseline state?

A: The thalamus (except for olfaction), which is always "on" and under chronic inhibition.


12
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Q: What does the direct pathway do to thalamic inhibition, and what is the net result?

A: It suppresses the inhibition of the thalamus, leading to more cortical output.


13
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Q: What does the indirect pathway do to thalamic inhibition, and what is the net result?

A: It enhances the inhibition of the thalamus, leading to less cortical output.


14
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Q: Why does basal ganglia damage not produce paralysis?

A: There are no motor neurons in the basal ganglia.


15
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Q: Unilateral basal ganglia damage produces signs on which side?

A: Contralateral.


16
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Q: Which movement disorders d/t basal ganglia damage are classified as hypokinetic?

A: Parkinson disease and drug induced disorders (for example, neuroleptics, MPTP).


17
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Q: Which movement disorders d/t basal ganglia damage are classified as hyperkinetic?

A: Hemiballismus, Huntington's disease, Tourette's syndrome, and tardive dyskinesia.

18
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Q: What is the defining pathological loss in Parkinson's disease?

A: Loss of dopamine cells in the substantia nigra.


19
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Q: What is the classic pathological feature of Parkinson's disease?

A: Lewy bodies.


20
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Q: How does loss of dopamine input affect the two pathways, and what is the consequence?

A: Less activity of the direct pathway and more activity of the indirect pathway, resulting in decreased movement.


21
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Q: What are the motor features of Parkinson's disease?

A: Rest tremor, bradykinesia (slowness of movement), rigidity, and gait imbalance.


22
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Q: What are the non-motor features of Parkinson's disease?

A: Autonomic dysfunction (orthostatic hypotension, constipation, sexual dysfunction), cognitive impairment, sleep disorders, and depression/anxiety.


23
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Q: What are the three symptom categories of Huntington's disease?

A: Chorea (involuntary writhing movements), cognitive impairment and dementia, and psychiatric disorders.


24
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Q: What is the pathology of Huntington's disease and its functional result?

A: Loss of caudate nucleus neurons that participate in the indirect pathway, resulting in excess movement (hyperkinetic).

25
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Q: Where is the lesion in hemiballism, and what is the clinical presentation?

A: Lesion in the subthalamic nucleus, producing involuntary, wild, flailing limb movements contralateral to the damage.

26
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Q: How do subthalamic nucleus lesions produce hyperkinetic movement?

A: STN lesions cause decreased stimulation of the GPi within the indirect pathway and consequently disinhibition of the thalamus, resulting in hyperkinetic movements of the hemichorea-hemiballism spectrum.


27
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Q: Why is the cerebellum called a "comparator"?

A: It compares what you intend to do with what actually happens.


28
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Q: List the key functions of the cerebellum.

A: 1. Regulation of balance, posture and muscle tone;

  1. coordination of voluntary movements including timing and force of the different muscle groups required for a specific movement

  2. motor learning through trial and error

  3. cognitive function

  4. eye movements.


29
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Q: What connects the two cerebellar hemispheres, and what are the surface folds called?

A: The vermis, a thick bundle of fibers; the surface is extensively folded into folia.


30
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Q: Is cerebellar control of the body ipsilateral or contralateral?

A: Ipsilateral.


31
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Q: From where does the cerebellum receive information, and where does it send information?

A: It receives from a variety of sources including spinal and vestibular pathways, and sends information to the cortex via the thalamus.


32
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Q: What are the three ways the cerebellum can be subdivided?

A: By lobes, by regions/zones, and by functional areas.


33
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Q: Name the three anatomical lobes of the cerebellum.

A: Anterior lobe, posterior lobe, and flocculonodular lobe.


34
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Q: Which fissure separates the anterior from the posterior lobe?

A: The primary fissure.


35
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Q: Which fissure separates the cerebellum from the flocculonodular lobe?

A: The posterolateral fissure.

36
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Q: What defines Chiari malformation?

A: Herniation of the cerebellar tonsils through the foramen magnum.


37
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Q: What are the three phylogenetically defined cerebellar regions?

A: Vestibulocerebellum, spinocerebellum, and cerebrocerebellum.


38
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Q: Vestibulocerebellum: anatomy, input, functions, and characteristic deficit?

A:

anatomy โ€” Flocculonodular lobe

input โ€” input from vestibular nuclei

function โ€” functions are eye movements, balance, and posture

deficit โ€” deficit is nystagmus/eye movement abnormality.


39
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Q: Spinocerebellum: anatomy, input, functions, and characteristic deficit?

A:

anatomy โ€” Vermis and intermediate zone

inputโ€” input from the spinal cord

functions โ€” functions are motor coordination allowing error correction and muscle tone

deficit โ€” deficit is postural instability.


40
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Q: Cerebrocerebellum: anatomy, input and output, functions, and characteristic deficit?

A:

anatomy โ€” Lateral portions of the hemispheres

inputโ€” input from cortex via pons/output to thalamus

functions โ€” functions are fine motor control, planning, adjusting movements, and motor learning

deficit โ€” deficit is limb ataxia.


41
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Q: What deficit results from damage to all parts of the cerebellum?

A: Gait problems, that is ataxia.


42
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Q: Which artery supplies the posterior lobe of the cerebellum?

A: Posterior inferior cerebellar artery (PICA).


43
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Q: Which artery supplies the flocculonodular lobe?

A: Anterior inferior cerebellar artery (AICA).


44
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Q: Which artery supplies the anterior lobe?

A: Superior cerebellar artery (SCA).

45
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Q: What are the two main divisions of the cerebellum and the role of each?

A: Cerebellar cortex, the input center; deep cerebellar nuclei, the input and output center.


46
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Q: Name the three layers of the cerebellar cortex from superficial to deep.

A: Molecular layer, Purkinje cell layer, granular layer.


47
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Q: What does the molecular layer contain?

A: Mainly dendrites and axons.


48
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Q: What is the significance of the Purkinje cell layer, and what controls it?

A: It is the sole output of the cerebellar cortex to the deep nuclei, and it is controlled by climbing fibers.


49
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Q: What does the granular layer contain?

A: Axons of Purkinje cells, climbing fibers, and mossy fibers.


50
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Q: What do the cerebellar peduncles do?

A: They carry white matter tracts to and from the rest of the brain.


51
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Q: Superior cerebellar peduncle: connection and traffic?

A: Connects to the midbrain; mainly output to thalamus and cortex.


52
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Q: Middle cerebellar peduncle: connection and traffic?

A: Connects to the pons; input from motor cortex.


53
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Q: Inferior cerebellar peduncle: connection and traffic?

A: Connects to the medulla; mainly input from spinal cord and inferior olivary nucleus.


54
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Q: Cerebellar deficits occur on which side relative to the lesion, and which way does the patient sway or fall?

A: Deficits are ipsilateral to the lesion, and the patient sways or falls toward the site of the lesion.


55
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Q: What two types of asynchrony does cerebellar damage produce?

A: Space (accuracy of movement) and time (coordination).


56
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Q: What other deficits result from cerebellar damage?

A: Difficulty with balance, difficulty in motor learning, and cognitive linguistic impairments whose role is poorly understood.


57
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Q: What is dysdiadochokinesia?

A: Inability to rapidly alternate movements.


58
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Q: What is dysmetria?

A: Inaccuracy in range and direction of movement.