Movement Disorders Flashcards

1
Q

List the components of the basal ganglia.

A

Substantia nigra pars compacta (+ pars reticularis)
Striatum (caudate nucleus + putamen)
Globus pallidus (interna + externa)
Subthalamic nucleus

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2
Q

How does the basal ganglia communicate with the motor cortex?

A

Communicates via the thalamus. Changes in thalamic activity are mediated by the basal ganglia. For example increased thalamic activity leads to increased cortical excitation.

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3
Q

What is the function of the basal ganglia?

A

Role in reinforcing appropriate movements and inhibiting / removing inappropriate movements.

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4
Q

How does the basal ganglia act to reinforce appropriate movements and inhibit inappropriate movements?

A

Two pathways in the basal ganglia.

  1. Direct pathway reinforces appropriate movements by sending excitatory projections via the thalamus to the motor cortex.
  2. Indirect pathway edits out inappropriate movements by sending inhibitory projections via the thalamus to the motor cortex.
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5
Q

How does dopamine act at D1/D2 receptors to facilitate movement?

A

Dopamine excites the motor cortex by stimulating D1 receptors on striatal neurons in the direct pathway.
Dopamine inhibits the motor cortex by stimulating D2 receptors on striatal neurons in the indirect pathway.

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6
Q

If the substantia nigra pars compacta (SNc) was affected unilaterally where would signs be observed?

A

Signs of increased or decreased thalamic activity (depending on the condition) would be seen on the contralateral side to the problem. This is because the basal ganglia regulate the ipsilateral motor cortex, which then decussates as it descends down the corticospinal tract.

(most of the time the problem is bilateral so signs would be more symmetrical)

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7
Q

What is the principle pathophysiological mechanism underlying Parkinson’s disease?

A

Degeneration of dopaminergic neurons in the SNc, which removes dopamine driven influence on movement via both the direct and indirect pathways.

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8
Q

What signs and symptoms would you see in a patient with Parkinson’s disease?

A
Tremor
Rigidity (cogwheeling)
Micrographia
Hypophonia
Depression
Bradykinesia / Akinesia 
Dementia
Shuffing gait
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9
Q

Describe the aetiology of Huntington’s disease.

A

Autosomal dominant, progressive disorder
Onset around 30-50yo
Associated with loss of inhibitory projections from the striatum to GPe = too much movement.

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10
Q

What signs and symptoms would you see in a patient with Huntington’s disease?

A
Chorea (dance-like movement) 
Dystonia (overactive antag//agoinsts)
Loss of coordination 
Cognitive decline 
Behavioural disturbances
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11
Q

What is hemiballismus?

A

A rare movement disorder characterised by unilateral explosive movements. It can be caused by damage to the subthalamic nucleus (possibly after a lacunar infarct) which normally inhibits the thalamus via GPi.

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12
Q

How does the cerebellum communicate with the CNS?

A

Communicates via cerebellar peduncles.

  1. Superior cerebellar peduncle connects to the midbrain
  2. Middle cerebellar peduncle connects to the pons
  3. Inferior cerebellar peduncle connects to the medulla
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13
Q

Why might cerebellar lesions such as a tumour lead to hydrocephalus?

A

The cerebellum sits above the fourth ventricle. A lesion might compress or block the ventricle leading to reduced drainage and an accumulation of CSF.

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14
Q

What is the role of the cerebellum?

A

Uses sensory information to decide upon the most appropriate SEQUENCE of movements to perform an action. Works together with the basal ganglia to elicit appropriate movements in the appropriate sequence.

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15
Q

If the cerebellum was injured unilaterally where would cerebellar signs be observed?

A

Signs would be seen on the ipsilateral side of the body. Cerebellum projects to the contralateral motor cortex. When the corticospinal tract decussates it passes back to the side of the body the cerebellum is injured on.

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16
Q

What are the signs of cerebellar disease, and why do they occur?

A

DANISH
Dysdiadochokinesia - problem sequencing pronation-supination-pronation…
Ataxia - problem sequencing lower limb muscle contractions
Nystagmus - malcoordination of extraocular muscles.
Intention tremor
Slurred speech - malcoordination of laryngeal and tongue muscles
Hypotonia