Basal Glanglia Flashcards by Brooke Niles

Basal ganglia structures

Caudate 
Putamen
Globus pallidus 
Subthalamic nucleus
Substantia nigra

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Striatum

Caudate and putamen

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Lenticular nucleus

Putamen

Globus pallidus

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Basal ganglia function

Indirect influence on movement via the thalamus

PIE - planning, initiation, execution of movement

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Other basal ganglia functions

Postural control
Maintaining muscle tone
Production of automatic movements

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Does the basal ganglia receive sensory input?

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Basal ganglia - input nuclei

From cortex

Primarily striatum(caudate, putamen)

Also substantia nigra

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Basal ganglia - output nuclei

To thalamus

Via the globus pallidus inter us and substantia nigra

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Two pathways exist from input to output basal ganglia nuclei

Direct pathway and

Indirect pathway

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Direct pathway

net effect: thalamus excitation

Disinhibition

facilitating movement
Increased movement

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Indirect pathway

net effect: thalamus inhibition

inhibiting movement
Decreased movement

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BG inhibits the thalamus

Input to thalamus is inhibitory via globus pallidus and substantia nigra

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Normal BG output at rest

Some amount of inhibition on the thalamus

How much of thalamus is inhibited by GB determines if movement will occur or not

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BG and cortex

Cortex contributes to how much the BG inhibits thalamus via the direct and indirect pathways

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Thalamus not/less inhibited

Disinhibited = INCREASED movement

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Thalamus inhibited

Decreased movement

BG has other than news for different functions

Passes through different pathways and projects to frontal lobe and limbic system

Motor (movement), oculomotor (eye movement), prefrontal (cognitive processes), limbic (emotion and motivational drives- neurobehavioral and psych disorders)

Common movement disorders no/slow movement —> fast

Akinesia
Bradykinesia/hypokinesia
Rigidity 
Dystopia
Athetosis
Chorea
Ball is us
Tics
Myoclonus
Tremor

BG and dyskinesia

Abnormal movement caused by BG dysfunction

Akinesia
Bradykinesia
Rigidity

Rigidity

Increased, uniform resistance to passive movement of a limb throughout the entire ROM

Superimposed by rachetlike jerkiness to passive movement of a limb

Movement disorders - involuntary movements

Dystonia (sustained contractions)
Athetosis (writhing)
Chorea (rapid, irregular,jerky)
Ballismus (large amp, sudden flailing)
Tics (twitches)
Myoclonus (cyclical, spasmodic alteration in contract and relax)

Tremor

Rhythmic or semi-rhythmic oscillation movement

Resting tremor

Often seen w/ BG lesion

Obvious when limbs are at rest, decreases/stop when pt moves limbs

Parkinon’s disease

Idiopathic neurodegenerative condition caused by loss of dopaminergic neurons in substantia nigra

Parkinson’s triad

Bradykinesia, rigidity, resting tremor —> Postural instability, unsteady gait

Parkinson’s onset, progression

45-65 yo M>F Progression is gradual leading to severe disability Reasons well to LevoDopa

Which pathway more effected w/ Parkinson’s?

Direct pathway DA normally has excitatory effect on direct ath way and inhibitory effect on indirect W/ loss of DA—> underactive direct pathway, overactive indirect pathway —> no/less movement

Huntington’s disease

Autosomal dominant neurodegenerative disease Progressive - usually choreiform movement disorder, along w/ dementia and psych disturbances, ultimately lead to death Progressive atrophy of caudate nucleus and also putamen

Huntington’s onset

30-50 yo Initial symptoms: subtle chorea, behavioral disturbances Death usually occurs w/in 10-15 yr after onset

Huntington’s characterized by

Abnormalities of body movements, emotions, cognition | Tics, athetosis, dystopia posturing

Which pathway more effected - Huntington’s?

Indirect! Less/no Enk released by striatum Result is disinhibition of thalamus which produces movement