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Basal Ganglia Flashcards

1
Q

What is the function of the basal ganglia?

A

Important in voluntary movements, adjusting posture

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2
Q

What makes up the striatum?

Which are motor and which are cognitive?

A

Putamen -motor

Caudate - cognitive

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3
Q

What makes up the lentiform nucleus?

A

Putamen - motor

Globus pallidus

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4
Q

What is another name for the substantia innominata?

A

Substantia nigra

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5
Q

What are the two parts of the substantia nigra?

A

Pars reticulata

Pars compacta

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6
Q

For the basal ganglia, which pathway is excitatory and which pathway is inhibitory?

And what receptors do they have?

A

Direct = D1 receptor = excitatory

Indirect = D2 receptor = inhibitory

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7
Q

If dopamine acts thru D1, what is the effect?

A

Excitatory pathway is stimulated

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8
Q

If dopamine acts thru D2, what is the effect?

A

Inhibitory pathway is inhibited

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9
Q

How does the direct/excitatory pathway of basal ganglia work?

A

SNc input —> striatum, releases GABA

GABA —> inhibits GPi

GPi cant inhibit thalamus

=increased motion

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10
Q

How does the indirect/inhibitory pathway work?

A

SNc —> striatum, releases GABA

GABA—> inhibits GPe —> activates Sub-thalamic nucleus (STN)

STN —> stimulates GPi —> GABA released and goes to thalamus

=inhibits thalamus, decreased motion

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11
Q

What is the blood supply for the basal nuclei?

A

primary from MCA - lenticulostriate As.

Also ACA and Anterior choroidal

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12
Q

What is the classic triad associated with Parkinson’s disease?

A

Tremor- pill rolling
Cogwheel Rigidity
Bradykinesia

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13
Q

What are symptoms of Parkinson’s disease?

A

Classic triad

Hypokinesia
Postural instability
Dementia
Visuoperceptive impairments 
Can affect walking (sloooow walking)
Speech affected and facial expressions
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14
Q

What is the underlying cause of Parkinson’s?

A

No dopamine via Pars Compacta** of substantia nigra

No dopamine = striatum not stimulated = no GABA released to act on Pars reticulata and GPi = thalamus still inhibited

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15
Q

What are some cause so f Parkinsonian Syndyrome?

A 
Idiopathic Parkinson’s disease
Encephalitis lethargically
Head trauma
			• Dementia pugilistica
MPTP 
			• Designer drug
CO and Manganese poisoning
Drug induced
			• Neuroleptic (dopamine blocking drugs) 
Wilson Diseae
			• Heptolenticular degeneration 
Rigidity 
• + other deficits in multiple neurodegenerative diseases
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16
Q

What are some treatments for Parkinson’s?

A

Drugs that increase dopamine or prevent its breakdown

Deep brain stimulation

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17
Q

What defect does Huntington’s Chorea result from?

A

Degeneration of neurons in striatum (mostly the putamen) that leads to decreased GABA

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18
Q

When does Parkinson’s disease start?

A

Late in life (~60/70 y.o)

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19
Q

What is the average onset of Huntington’s CHorea?

A

Progressive disease beginning at 45 y.o.

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20
Q

What is the heritability of Huntington’s?

A

Autosomal dominant HTT gene mutation - CAG Trinucleotide repeat

21
Q

What is Huntington’s chorea characterized by?

A

‣ Involuntary, jerky, and rapid movements

‣ Dementia

‣ Unsteady gait, slurred speech, trouble maintaining tongue protrusion, irregular breathing

‣ Many pts. Also diagnosed w/ depression
• Not just due to chronic illness
• Higher risk of suicide

22
Q

What are treatments for Huntington’s chorea?

A

Tetrabenazine (serotonin antagonist)

Typical antipsychotic (antagonize dopamine)

Reserpine, tetrabenazine (depleting dopamine)

23
Q

What is chorea?

A

Spontaneous rapid, jerky, arrhythmic, and involuntary movements which are purposeless, or fragments of motor programs

24
Q

What is Ballismus caused by?

A

Lesion of the CONTRALATERAL subthalamic nucleus

25
Q

What is Ballismus characterized by?

A

Flailing, flinging movement of whole extremity

26
Q

What is Ballismus related to?

A

Stroke, inflammation or tumor

27
Q

What is Athetosis?

A

Inability to sustain body part in one positions, w/ movements of a snake-like or writhing fashion

28
Q

What is Athetosis often seen with?

A

Chorea

29
Q

What characterizes Athetosis?

A

Slow, writhing, continuous movements

30
Q

What is Athetosis dcaused by?

A

Dopamine blocking drugs, or hypoxicischemic injury

31
Q

What is focal Dystonia?

What kind of pain does it cause?

A

Writer’s cramp - a persistence or fixing of posture at extreme of an athetoid movement of extremities or trunk

Not painful, just impaired ability to write bc of involuntary , sustained muscle contracture of extensor and/or flexors of hand

32
Q

What are other kinds of Dystonia seen?

A

Torticollis (cervical Dystonia)

Blepharospasm

Drug induced

33
Q

What is Sydneham’s Chorea?

A

Neurological disorder of childhood resulting form acute rheumatoid fever.

34
Q

What is the JONES criteria for syndenham’s chorea?

A
  • J = joints (arthritis)
    * <3 = heart (-carditis)
    * N = Nodules (subcutaneous)
    * E = Erythema marginatum
    * S = Sydenham’s chorea
35
Q

What is Syndenham’s chorea characterized by?

Who does it affect more?

A

rapid, irregular, and aimless involuntary movements of the arms and legs, trunk, and facial muscles

It affects girls more often than boys and typically occurs between 5 and 15 years of age.

36
Q

The basal ganglia provide feedback tot he cortex to either ___ or ____

What does this allow for?

A

Stimulate motor activity OR inhibit motor activity

Allowing for complex movements

37
Q

What is the modifier in the direct pathway?

A

Cortex activates pars Compacta to modify striatum via D1 and dopamine

Pars compacta will stimulate straitum to further release gaba to GPi and Pars Reticulata

38
Q

What is the modifier in the indirect pathway?

A

Cortex activates Pars compacta to modify striatum via D2 and dopamine

Will inhibit striatum and allow for GABA to work on GPe, allowing for STN to activate GPi and further inhibit thalamus

39
Q

What is affected to cause Wilson’s disease?

A

Globus pallidus Internus and striatum

40
Q

What does GPi do?

A

Inhibit thalamus via GABA

41
Q

What does GPe do?

A

Inhibit STN via GABA

42
Q

What 2 things inhibit the thalamus at rest?

What is this called?

A

GPi

Substantia nigra Pars reticulata

Tonic inhibition of thalamus

43
Q

How is the striatum activated during the direct pathway?

What does this allow it to do?

A

Cortex releases glutamate to striatum

Striatum releases gaba to

GPi —> can no longer inhibit thalamus
Pars Reticulata —> can no longer inhibit thalamus

44
Q

What is the role of the subthalamic nucleus during the indirect pathway?

A

Once uninhibited from GPe

STN will stimulate GPI which will then go and inhibit thalamus

45
Q

What is the skeletomotor loop?

Role of it?

A

Motor cortex —> putamen —> VA and VL

role in control of glacial, limba and musculature

46
Q

What is the Oculomotor Loop?

Role?

A

from eye field (posteiror parietal, prefrontal) —> Caudate —> VA and Medial dorsal

role in control of saccadic eye movements

47
Q

What is the associative loop?

Role?

A

from post. Parietal and middle and inferior temporal lobe —> caudate —> Va and Medial Dorsal

Role in cognition and executive behavioral functions

48
Q

What is the limbic loop?

Role?

A

from medial and lateral temporal lobes and hippocampal formation (ant. cingulate gyrus)
—> ventral striatum
—> Ventral pallidum
—> Medial dorsal and VA

Participates in the motivational regulation of behavior and emotions

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