Basal Ganglia Flashcards

1
Q

Describe function of following connections of basal ganglia:
1. Cortical
2. Between nuclei
3. Brain sten

A
  1. Inhibits excessive activity of motor cortical area (4&6), inform basal ganglia about program & intention of movement
  2. Control intrinsic activity
  3. Regulation of muscle tone & body posture
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2
Q

Describe caudate circuit & its function

A

Sensory & motor association areas —caudate nucleus—globus pallidus—thalamus—supplementary motor, premotor & prefrontal areas
F, cognitive control of sequences of motor movements. This subconciously determines within seconds patterns of movement which will be used together to achieve a goal.

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3
Q

Describe putamen circuit & its function

A

Premotor, supplementary motor & somatosensory areas —putamen—globus pallidus—thalamus—primary motor & premotor areas
Execute learned patterns of movement

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4
Q

Enumerate connections of basal ganglia to brain stem

A

Reticular formation, red nucleus, vestibular nucleus

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5
Q

Mention neurotransmitters in basal ganglia

A

Cerebral cortex release glutamate on corpus striatum
Intrastriatal interneurons release Ach
Substantia nigra release dopamine on corpus striatum
Coprus striatum release GABA on substantia nigra
Basal ganglia release NE, ecephalin & Serotonin on brain stem

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6
Q

Describe effect of stimulatiry & inhibitory circuits

A

Stimulatory, facilitate muscle activity especially at beginning if voluntary movement like rising from sitting or beginning to walk
Inhibitory, inhibit unwanted muscle activity

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7
Q

Describe the direct pathway

A

Cortical fibers stimulates striatum by glutamate, striatum inhibits to GPi (GABA, inhibitory), which disihibits the thalamus & thalamic projections excite motor neurons.
This functions to maintain ongoing motor activity

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8
Q

Describe the indirect pathway

A

Cortical input to stiatum in excitatory (glutatmate), striatum inhibits GPe (GABA, inhibitory) thus the subthalamic nuclei are released from GPe inhibition thus cause increased GPi activity which inhibitsvthe thalamus & the net effect is cortical inhibition & suppression of muscle activity.

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9
Q

Effects of dopamine & acetylcholine

A
  1. Dopamine in nigrostriatal fibers activates direct pathway (D1) & inactivates indirect pathway (D2) thus facilitatory to movement.
  2. Acetycholine is present in balance with dopamine to facilitate the movement
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10
Q

What happens with degeneration in the dopamine releasing neurons?

A

Decreased activity of direct pathway & increased activity of indirect pathway, thus hypokinesia & slow voluntary movements take place, known as parkinsonism.

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11
Q

Mention functions of basal ganglia

A
  1. Regulation of muscle tone
  2. Role in voluntary movements
  3. Automatic associated movements
  4. In lower animals, BG is highest motor center
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12
Q

Describe role of BG in muscle tone

A

Caudate is stimulatory, lentiform is inhibitory there is net inhibition.
It decreases the activity of alpha motor neurons through decreasing the activity of motor cortex
It decreases the activity of gamma motor neurons through stimulation of inhibitory reticular formation

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13
Q

Describe role of BG in voluntary movements

A

There are no direct descending tracts from basal ganglia, but it affects voluntary movements by extra-pyramidal tracts
1. Storage of programs of some learned voluntary movements in putamen circuit, lesion results in motor apraxia
2. Planning of motor activity through caudate circuit
3. Provision of postural background for the fine voluntary movements, adjust muscle tone of proximal muscles via ventro-medial pathways to facilitate more regulated fine skilled actions

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14
Q

Causes of chorea

A

Lesion in the caudate nucleus & degenrenation of GABA releaseing striatal fibers to GPe leading to decreased activity of indirect pathway:
1. As a complication of rheumatic fever, but no dementia
2. Congenital (Huntington’s chorea) = progressive dementia

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15
Q

C/P of chorea

A
  1. Hypotonia & pendular knee jerk
  2. Involuntary movements: sudden semipurposeful movements
  3. Dancing movements of arms, legs, face, head & trunk, increase by emotions decrease by sleep
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16
Q

Mention causes of athetosis

A

Lesion of lentiform nucleus mainly globus pallidus (degeneration of GABA releasing neurons which project to thalamus)

17
Q

C/P of athetosis

A
  1. Hyoertonia
  2. Involuntary movements = slow twisting movements. Involving distal parts, snake-like movements. Increase by emotions decrease by sleep.
18
Q

Cause of hemiballismus

A

Lesion in subthalamic nuclei, when glutamate decreases in it, it can’t carry out its normal function in exciting GPi which becomes inhibited

19
Q

C/P of Hemiballismus

A
  1. Hypertonia
  2. Involuntary movements: attacks of rapid violent movements. Involving half of body that may cause loss of balance, may be fatal due to respiratory muscle spasm.
20
Q

Causes of parkinsonism

A
  1. Idiopathic due to unknown neurotoxin or oxidation reactions with free radical generation
  2. Viral encephalitis, vascular, trauma, poison
  3. Drug-induced by antipsychotics, antiemetics, reserpine, tetrabenazine, methyldopa
21
Q

Describe C/P of parkinsonsim

A
  1. Rigidity
  2. Static tremors
  3. Akinesia
  4. Postural deficits & tendency to frequent fall
  5. Cognitive impairment as depression
22
Q

Describe rigidity of parkinsonism

A

Stiffness of muscle during movement. In both flexor & extonsor but f is more.
Alpha rigidity
Mechanism: net effect of basal ganglia is inhibitory so its lesion causes increased excitability of motir neurons

23
Q

Describe static tremors of parkinsonism

A

Involuntary, regular rapid movements disappear during sleep exaggerated by fatigue & emotions, diminished by voluntary movement.
It may be due to oscillatory discharge (on & off) of globus pallidus interna & thalamic nuclei leading to alternative activation & inactivation of cortical motor areas

24
Q

Describe manifestations of parkinsonian akinesia

A
  1. Difficulty in initiating voluntary movement, no automatic subconscious movements
  2. Difficulty in buttoning shirt & necktie before shirt
  3. Mask face & no blinking, staring look
  4. Monotonous slow slurred speech
  5. Shuffling gait with trunk bent forward
25
Q

Mechanism of akinesia in parkinson

A
  1. Increased thalamo-cortical inhibition is associated with decreased activity of supplementary motor area, due to loss of planning & programming functions of BG
  2. The increased muscle tone & rigidity interferes with initiation of movement. All lead to avoidance to do any movement as simplest acts require great mental effort.