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Motor System and Movement disorders: Basal ganglia and cerebellum
Terms in this set (47)
What are the components of the basal ganglia and what are there functions?
Caudate nucleus (receive efferent from motor cortex)
Putamen (receive efferents from motor cortex)
Subthalamic nucleus (receive efferents from motor cortex)
Substantia nigra (pars compacta) that is a relay center
Globus pallidus (External) that is a relay center
Globus pallidus (internal) that afferents to motor cortex via thalamus
Substantia nigra (pars reticularis) that afferents to motor cortex via thalamus
What is the function of basal ganglia?
Motor-movement selection and action
Oculomotor-decisions about eye movements and spatial attention; fast eye movement
Executive-moves you toward your goals
Behavioral flexibility and control-social function and filtering information that is important and unimportant
What are the motor function of the basal ganglia?
Send inhibitor input to thalamus (thalamus excites cortex) that helps coordinate appropriate initiation, scaling and termination of movements.
Results in smooth, controlled motor output (appropriate start and stop) that is important for motor learning
Sends inhibitor input to brainstem motor centers such as the Pedunculopontine nucleus (PPN) and midbrain locomotor center
Pedunculopontine nucleus (PPN)
controls reticulospinal tract for postural muscle activity
Midbrain locomotor center
Control reticulospinal tract for rhythmic actions (walking, running)
What are the positive clinical manifestations of basal ganglia pathology?
Less inhibition leads to hyperkinesia that leads to
1) Increased muscle tone-rigidity that is like a lead-pipe or cog wheel
2) Resting tremor
3) Dyskinesia- movement disorders like chorea (rapid, jerky movements), Athetosis (slow, writhing movements) and ballismus (violent, flinging movements)
What are the negative clinical manifestations of basal ganglia pathway?
Greater inhibition leads to hypokinesia that leads to
1) Akinesia-difficulty initiating movement
2) Bradykinesia- slowed movements
3) Poor postural adjustments - flexion posture
What is the cause of Parkinson's disease
Damage to dopamine-producing neurons of substantia nigra (pars compacta) that causes decreased inhibition of output nuclei (Globus pallidus (internal) and substantia nigra (pars reticularis) which leads to them creating greater inhibition on motor cortex (hypokinesia)
PPN cells die and create less inhibition to RST leading to less inhibitation of postural muscle and less excitation of rhythmic motor actions
What are the symptoms of Parkinson's disease
Akinesia, bradykinesia (hypokinesia)
Flexion posture, abnormal postural reflex (hypokinesia)
Rigidity, resting tremor (hyperkinesia)
What is the clinical treatment of Parkinson's disease?
Dopamine Precursor (levodopa) that crosses the blood-brain barrier
Physical therapy for range of motion, improved ambulation and motor performance
What causes Huntington Disease?
Degernation of striatl nuclei (putamen an dcaudate) that results in hyperactivity due to effects at basal ganglia
Affects of other cerebral neurons leading to death, dysphagia, aspiration pneumonia, cardiopulmonary dysfunction, pressure injury/infection)
Chorea and/or athetoid movements are common
What causes hyperkinesia in Huntington's disease?
Loss of basal ganglia inhibition of thalamus and PPN as there is increased inhibition of globus pallidus from corpus striatum so the thalamus over-excites the cortex and the PPN creates greater inhibition of RST so there is a loss of control of postural movements
Hyperkinesia that results from lesion of subthalamic nucleus
Loss of excitation from subthalamic nucleus to globus pallidus that causes a loss of inhibition to the thalamus causing violent flinging movements
Athetoid-type (writhing) movements of the face and tongue
Side effect of some anti-psychotic drugs
Anti-dopamnergic effects on CNS (loss of inhibition of thalamus)
Perinatal brain injury that can manifest with spasticity and dyskinesia
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