6. Movement disorders Flashcards
what is the source of dopamine in the midbrain?
substantia nigra pars compacta
what is the striatum made of?
caudate nucleus and putamen
what is the role of the striatum?
receives input from the substancia nigra pars compacta and the cortex
what are the two parts of the globus pallidus?
internal and external segment
what is the lentiform nucleus formed from?
putamen and globus pallidus
what is the basal ganglia made up of?
SNc, striatum, caudate nucleus, putamen, globus pallidus, lentiform nucleus, subthalamic nucleus
what is the role of the basal ganglia?
communicates with the motor cortex via the thalamus. increasing thalamic activity causes increased cortical activity and vice versa. role in reinforcing appropriate movements and removing inappropriate
what do direct pathways do?
reinforces appropriate movements so excites the motor cortex
what do indirect pathways do?
edits out inappropriate movements so inhibitory to motor cortex
how does dopamine facilitate movement?
exciting the motor cortex - excites direct pathway by stimulating D1 receptors on striatal neurones taking part in direct pathway, inhibits indirect by activating inhibitory D2 receptors
what does the basal ganglia regulate?
ipsilateral motor cortex
what is parkinson’s disease caused by?
degeneration of dopaminergic neurones in the SNc
what are the signs and symptoms of parkinson’s disease?
tremor (may be due to dysfunction of indirect pathway which would normally supress unwanted movements)
rigidity (lack of coordination between agonist and antagonists)
bradykinesia (due to loss of cortical excitation)
hypophonia (bradykinesia of larynx and tongue)
decreased facial movements (bradykinesia of face)
micrographia (bradykinesia in hands)
dementia (possible progression)
depression (as basal ganglia have role of in cognition and mood)
what is the presentation of huntington’s chorea?
autosomal dominant
onset at 30-50
hyperkinetic features - increased movement as loss of inhibition on thalamus
what is huntingtons caused by?
loss of inhibitory projections from striatum to GPe