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
what are signs and symptoms of huntington’s chorea?
chorea (dance like movements due to increased motor cortex activation)
dystonia (uncomfortable contractions of agonists and antagonists leads to odd postures to over activity in muscle circuits and loss of coordination)
loss of coordination ^
cognitive decline and behaviour disturbances
what is hemiballismus?
a rare disorder caused by damage to the subthalamic nucleus which normally inhibits the thalamus via GPi resulting in unilateral explosive (ballistic) movements
what is a cause of hemibasillismus?
sub cortical stroke
what is the cerebellum made of?
midline vermis and two laterally placed hemispheres
what are the roles of the different parts of the cerebellum?
vermis - trunk
hemispheres - ipsilateral side of the body
how does the cerebellum communicate with the rest of the CNS?
via the cerebellar peduncles:
superior cerebellar peduncles - midbrain
middle - pons
inferior - medulla
what is a consequence of cerebellar tumours and why does this occur?
can cause hydrocephalus as it sits above the fourth ventricle
what is the role of the cerebellum?
sequencing and coordination of movements by using sensory information and deciding upon the most appropriate sequence of movements to perform the action
how do the cerebellum and basal ganglia work together?
basal ganglia decides the most appropriate movements and the cerebellum then sequences these
what inputs and outputs does the cerebellum receive?
sensory inputs from the ipsilateral spinal cord and contralateral sensory cortices
outputs are to the contralateral motor cortex
on what side would you get a cerebellar lesion presentation?
ipsilateral
its outputs are to contralateral mtoor cortex but then the due to the decussation of corticospinal pathway
https://www.getbodysmart.com/motor-system/pyramidal-tract-pathway
its a double crossing over
what are the signs of cerebellar disease?
dydiadochokinesia (difficulty with rapidly alternating mvoemnts - sup to prone to sup to prone)
ataxia(unsteady gait due to difficulty sequencing lower limb muscle contractions and loss of unconscious proprioception from lower limbs)
nystagmus (flickering eye movements due to malcoordination of extra ocular muscles)
intention tremor (tremor gets worse as target approaches)
slurred speech - dysarthria due to malcoordination of laryngeal and tongue musculature
hypotonia
