S7 - Movement Disorders

Question 1

outline the anatomy of the basal ganglia

what are the main areas called ?

general role of the basal ganglia ?

Answer 1

substantia nigra

striatum - caudate and putamen

leniform neucleus - putamen and globus pallidus

the subthalmic neucleus

the basal ganglia - communicate with the motor cortex via the thalamus - increased thalamic activity will cause increased cortical activity and vice versa

Question 2

what is the normal function of the basal ganglia ?

what does it enable and inhibit ?
with what chemical does it cause this action ?

Answer 2

o Normal function

reinforcing appropriate movements and
removing inappropriate movements.

Direct pathways reinforces appropriate movements (excitatory to motor cortex)

Indirect pathway edits out inappropriate movements (inhibitory to motor cortex)

Dopamine facilitates movement by exciting the motor cortex

Basal ganglia regulate ipsilateral motor cortex, hence if SNc is affected unilaterally (rare) there will be contralateral signs due to decussation of the corticospinal tract

Question 3

explain using a diagram from the lecture how the indirect and direct pathways of the basal ganglia work to prove you understand it

Answer 3

this could be an exam q

Question 4

what has gone wrong to cause parkinsons disease ?

Answer 4

Parkinson’s disease
Caused by degeneration of dopaminergic neurones in SNc
Therefore have lost the dopamine-driven facilitation of
movement via both pathways

Question 5

signs and symptoms of Parkinsons disease

Answer 5

Symptoms and signs:
• Tremor (unclear mechanism, but may be related to
dysfunction of indirect pathway which would normally
suppress unwanted movements)

• Rigidity

• Bradykinesia (best understood mechanism. Slow
movements due to loss of cortical excitation)

• Hypophonia (quiet speech = bradykinesia of larynx and
tongue)

• Decreased facial movement / mask-like facies
(bradykinesia of face)

• Micrographia (small handwriting = bradykinesia in hands)
• Dementia

• Depression (basal ganglia also have a role in cognition
and mood)

Question 6

outline the disease huntingtons chorea

Answer 6

Huntington’s chorea

Autosomal dominant, progressive disorder

Early onset around 30-50 years old

Early stages associated with loss of inhibitory projections from striatum to GPe
• This leads to hyperkinetic features (increased movement as the brakes have been taken off the thalamus)

Question 7

signs and symptoms of huntingtons chorea

Answer 7

Features

• Chorea (dance-like movements due to increased motor
cortex activation)

• Dystonia (uncomfortable contractions of agonists and
antagonists leading to odd posture)

• Loss of co-ordination (similar to above presumably)
• Cognitive decline and behavioural disturbances (related to role of basal ganglia in higher metal functions)

Question 8

outline Hemiballismus

Answer 8

o Hemiballismus

Rare disorder

Can be caused by damage to subthalamic nucleus which
normally inhibits the thalamus via GPi

Can be caused by sub-cortical stroke (lacunar infarct)

Causes unilateral explosive (‘ballistic’) movements

Question 9

outline the anatomy of the cerebellum

Answer 9

• Cerebellum
o Anatomy
Midline vermis and two laterally placed hemispheres

Vermis deals with trunk, hemispheres with the ipsilateral side of the body

Communicates with the rest of the CNS via the cerebellar peduncles (different to the cerebral peduncles!)

• Superior cerebellar peduncle connects to midbrain
• Middle cerebellar peduncle connects to pons
• Inferior cerebellar peduncle connects to medulla

Sits above the fourth venricle
• Cerebellar lesions (e.g. tumours) can cause
hydrocephalus

Question 10

use the diagram and show what is destoryed and the consequence of huntingtons, hellibelismus and parkinsons

Answer 10

do it - exam q

Question 11

functions of the cerebellum

Answer 11

Normal functions

However, has a clear role in the sequencing and co-ordination of movements

Uses sensory information to decide upon the most appropriate sequence of movements to perform an action

Works with basal ganglia which decide most appropriate movements. Cerebellum then sequences these movements.

Hence, cerebellum has profuse sensory inputs from
proprioceptive neurones and the sensory cortices

Cerebellum receives sensory input from ipsilateral spinal cord and contralateral sensory cortices. Its outputs are to
contralateral motor cortex. Hence, ipsilateral signs of cerebellar
damage due to decussation of corticospinal pathway

Question 12

outline sings of cerebellar disease (6 signs)

mnemomic : DANISH

Answer 12

o Signs of cerebellar disease

Dysdiadochokinesia
• Difficulty with rapidly alternating movements

Ataxia
• Unsteady gait as a result of difficulty sequencing lower
limb muscle contractions as well as loss of unconscious
proprioception from lower limbs

Nystagmus
• Flickering eye movements due to malcoordination of
extraocular muscles

Intention tremor
• A tremor that worsens as a target is approached

Slurred speech (dysarthria)
• Caused by malcoordination of laryngeal and tongue
musculature

Hypotonia
• Unclear mechanism

Question 13

explain using diagrams Basal Ganglia Laterlisation

Answer 13

unilateral basal G damage - contralateral effects - explain why w/diagram

however mostly bilateral as its degenerative

Question 14

explain using diagrams Cerebellar Laterlisation

Answer 14

cerebelar damage - ipsilateral signs

spinocerebellar pathways project ipsilateraly to the cerebellar hemisphere

pontine neucli deccusate - so cortical input to cerebellum is contralateral

cerebelar hemispehre then talks to the contralteral cortex - then tell corticolspinal pathways to move the contralteral side - which means its the ipsislteral side

dont need to rember just explain this with the diagram