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MHD2 Block 2 - Neuro > Thalamus, internal capsule and basal ganglia > Flashcards

Thalamus, internal capsule and basal ganglia Flashcards

1
Q

What are the divisions of the diencephalon?

A

Epithalamus (contains pineal gland)
Dorsal thalamus
Subthalamus (contains subthalamic nuclei)
Hypothalamus

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2
Q

What are the major divisions of the dorsal thalamus?

A

Anterior, medial and lateral are divided by the internal medullary lamina. The thalamic reticular nuclei is a narrow band and appears draped over the lateral thalamus

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3
Q

What are the 3 functional thalamic groups?

A

Specific/relay nuclei: well defined inputs/projections
Association nuclei
Nonspecific nuclei

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4
Q

What are the specific/relay nuclei?

A

Anterior, ventral anterior, ventral lateral, ventral posterior, lateral dorsal, medial and lateral geniculate

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5
Q

What is the purpose of the reticular nucleus of the thalamus?

A

Acts as a filter, modulates information to and from the thalamus

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6
Q

What major tract makes up most of the internal capsule?

A

Corticospinal tract

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7
Q

What thalamic nuclei are involved with motor actions?

A

The VA/VL nuclei relay informaiton from the basal ganglia and cerebellum to the motor cortex

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8
Q

What thalamic nuclei are involved with somatosensory information?

A

VPL relays information from the spinothalamic tract to the somatosensory cortex.
VPM relays information from the trigeminal tract to the somatosensory cortex

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9
Q

What thalamic nuclei are involved with auditory sensation?

A

Medial geniculate relays information from CN VII (through the inferior colliculus) to the auditory cortex

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10
Q

What thalamic nuclei are involved with vision?

A

Lateral geniculate relays information from the optic tract to the visual cortex

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11
Q

What artery supplies the thalamus?

A

The posterior cerebral artery gives off thalamic branches

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12
Q

What is the primary function of the anterior thalamus?

A

Language and memory

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13
Q

What is the primary function of the lateral thalamus?

A

Motor and sensory

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14
Q

What is the primary function of the medial thalamus?

A

Vigilance, arousal, memory

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15
Q

What is the primary function of the posterior thalamus?

A

Higher visual funciton

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16
Q

What structures make up the striatum?

A

Caudate, putamen and nucleus accumbens

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17
Q

What structures make up the lenticular nucleus?

A

Putamen and globus pallidus

18
Q

Describe the circuitry of the basal ganglia

A

A loop of excitatory and inhibitory signals:

The thalamus excites the cortex, which excites the striatum, which inhibits the GPi and SNr, which inhibit the thalamus.

19
Q

How do the basal ganglia affect LMN function?

A

No direct connection

LMNs are influenced by the BG through the cerebral cortex

20
Q

What neurotransmitter is involved with cortical input to the striatum?

A

Glutamate: excitatory neurotransmitter

21
Q

What neurotransmitter is involved with output from the BG via the GPi and SNr?

A

GABA: inhibitory neurotransmittor

22
Q

Describe the direct pathway of the basal ganglia

A

The striatum receives excitatory input from the association cortex and SNpc.
Striatum inhibits the GP from inhibiting the VA/VL of the thalamus, thus allowing VA/VL to excite the premotor cortex to initiate movement.

23
Q

What receptor is involved with the SNpc input to the striatum?

A

D1: dopamine receptor

24
Q

Describe the indirect pathway of the basal ganglia

A

The Striatum receives inhibitory input from the SNpc, which causes a transient inhibition of the GPe. Inhibited GPe leads to increased subthalamic nuclei activity, which strimulates the GPi. GPi can then decrease activity of the VA/VL leading to decreased movement.

25
Q

What changes are seen in the BG motor circuits in Parkinson’s disease?

A

Dopaminergic signalling from the SN is lost which leads to decreased excitation of the direct pathway and increased activity of the indirect pathway. This leads to decreased excitation of the motor cortex, and thus less movement.

26
Q

What changes are seen in the BG motor circuits in Huntington’s disease?

A

The inhibitory input of the striatum on the GPi is lost, which leads to decreased activity of the indirect pathway. This results in decreased inhibition of the VA/VL and thus increased excitation of the motor cortex presenting as chorea.

27
Q

What disease is associated with hypokinesia/akinesia?

A

Parkinsonism

28
Q

What disease is associated with hyperkinesia?

A

Huntington’s disease

Choreoathetosis, hemiballismus

29
Q

What are the etiologies of basal ganglia disorders?

A

Infarct, hemorrhage, tumor
Degenerative disorders
Medication side effects

30
Q

What class of drugs can cause hyperkinesia?

A

Dopamine agonists can cause chorea, dystonia

31
Q

What class of drugs can cause hypokinesia?

A

Dopamine antagonists can cause parkinsonism

32
Q

What are the primary clinical signs of parkinsonism?

A

Resting “pill rolling” tremor
Rigidity
Bradykinesia
Loss of postural reflexes (falls)

33
Q

Describe the parkinsonian gait

A

Stooped posture with shuffling and propulsive gait
Lack of armswing
Turns with multiple small steps

34
Q

What are the secondary (non-gait related) signs of parkinsonism?

A 
Hypophonic speech
Autonomic dysfunction
Micrographia
Masked facies (expressionless)
Stooped posture
35
Q

What are rare disorders that may mimic Parkinson’s disease?

A

Progressive supranuclear palsy
Multiple system atrophy
Dopamine antagonist side effects
Manganese/CO poisoning

36
Q

Describe the pathology of Parkinson’s disease

A

Gross pallor of the SN due to loss of pigmented (dopaminergic) neurons

37
Q

Describe the histologic findings of a patient with Parkinson’s disease

A

Lewy bodies: eosinophilic intraneuronal cytoplasmic inclusions, which are accumulations of alpha synuclein

38
Q

What are the drug therapies for Parkinson’s disease?

A

Anticholinergics have weak affect
Amantidine (enhances release of dopamine)
L-dopa (dopamine precursor) with Carbidopa

39
Q

What role does carbidopa play in Parkinson’s disease treatment?

A

Prevents the peripheral catabolism of L-dopa before it enters the brain, thus increasing the effect of L-dopa

40
Q

What is the surgical treatment of Parkinson’s disease?

A

Pallidotomy to stop excessive inhibitory output of the GPi

STN stimulator: implanted electrode that repeatedly fires to inhibit the STN

41
Q

Pathogenesis of Huntington’s disease

A 
Autosomal dominant (trinucleotide repeats of gene on c4)
Symptoms onset between 35-40 yrs old
Causes choreoathetosis, behavioral changes and dementia due to atrophied caudate

MHD2 Block 2 - Neuro (26 decks)

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