Movement Disorders Flashcards

1
Q

What is the Parkinson’s triad?

A

Bradykinesia
Tremor
Rigidity

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2
Q

What causes Parkinson’s disease?

A

The degeneration of dopamine producing neurons in the brain

  • Degeneration of substantia nigra
  • Lewy body deposition in neurons
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3
Q

How does Parkinson’s disease present?

A

Parkinsonism
(triad, shuffling gait, masked face, postural instability)

Neurocognitive disturbance
(depression, dementia)

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4
Q

What are the aims of Parkinson’s disease treatment?

A

Increase dopamine signalling and control symptoms

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5
Q

What is considered to be the best treatment for Parkinson’s disease? How does it work?

A

Levodopa

Levodopa crosses the BBB and is converted to dopamine

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6
Q

What is levodopa administered with and why?

A

Cabidopa

Blocks peripheral effects of levodopa (arrhythmia)

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7
Q

Patient with longstanding Parkinson’s disease presents with dyskinesia.

What is dyskinesia and why has it occurred?

A

Abnormal, uncontrolled movement

Patient likely prescribed levodopa. Levodopa has a good response initially but this wears off and it can cause dyskinesia.

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8
Q

Name an adjuvant therapy used to treat Parkinson’s disease which

  • increases dopamine signalling
  • helps control symptoms
A

Monoaine oxidase B inhibitor (rasagiline): increases dopamine signalling by inhibiting the breakdown of dopamine

Benztropine: an anticholinergic which controls symptoms by lowering ACh levels (which are usually high in Parkinson’s due to the abnormal dopamine levels)

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9
Q

Name an monoamine oxidase B inhibitor. What are its indications in Parkinson’s disease?

A

Adjuvant therapy with levodopa

First line in young patient where levodopa induced dyskinesia is a concern

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10
Q

What is the difference between Parkinson’s disease dementia (PDD) and Lewy body dementia?

A

Dementia late feature of PDD

Dementia early/first feature of Lewy body dementia

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11
Q

What are the characteristics of Lewy body dementia?

A

Dementia
Parkinsonism
Visual hallucination

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12
Q

What are the characteristics of Multiple System Atrophy?

A

Parkinsonism
Autonomic dysfunction
Cerebellar dysfunction

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13
Q

What might be seen on MRI in multiple system atrophy?

A
Putamen atrophy
Pons atrophy (hot cross bun sign)
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14
Q

What are the characteristics of progressive supranuclear palsy?

A

Parkinsonism
Dementia
Difficulty moving eyes

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15
Q

What might be seen on MRI in progressive supranuclear palsy?

A

Midbrain atropy (hummingbird sign)

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16
Q

What are the characteristics of vascular Parkinsonism?

A

Slow progression
Gait disturbance predominated
Lower body affected more

Possibly in patient with poor cardiovascular health or history of strokes

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17
Q

How can you distinguish vascular Parkinsonism from other causes?

A

SPECT scan

18
Q

What drugs can cause Parkinsonism?

A

Antiepileptics
Antipsychotics
Antiemetics
Lithium

19
Q

What is the commonest action tremor?
How does it present?
How do you treat it?

A

Essential tremor

Slow progressing action tremor over years

Propranolol

20
Q

What is ‘enhanced physiological tremor’? What can cause it?

A

Exaggeration of the physiological tremor which occurs with contraction

Stress, fatigue, exercise, caffeine

21
Q

Tremor worsening on approaching a target.

Diagnosis?
Part of brain injured?

A

Intention tremor

Cerebellum

22
Q

What are the clinical signs of a psychogenic tremor?

A

Abrupt onset tremor starting in arms and spreading to head/legs. May have changing characteristics.

(psychogenic tremor not a disgnosis of exclusion)

23
Q

What is on orthostatic tremor?

A

Leg/trunk tremor on standing up

24
Q

What is the commonest cause of a tremor at rest?

A

Parkinson’s disease

25
Q

What are the characteristics of a Parkinsonian tremor?

A

Unilateral initially
4-6 Hz
Pill rolling

26
Q

Tremor at rest, movement which worsens on approaching a target.

Diagnosis?
Part of brain injured?

A

Holmes (rubral) tremor)

Cerebellum

27
Q

What non neurological causes are there for tremor?

A

Hyperthyroidism
Hypoglycaemia
Alcohol withdrawal
Drugs

28
Q

What is dystonia and what causes it?

A

Spasming and abnormal posturing

Co-contraction of agonist and antagonist muscles

29
Q

Clinical name for dystonia affecting: eyes (blinking) and neck (twisting)?

A

Eyes: blepharospasm
Neck: cervical torticollis

30
Q

How do you manage

  • acute dystonia?
  • focal dystonia?
  • generalised dystonia?
A

Acute: antihistamine (diphenhydramine) or anticholinergic (benzatropine)

Focal: botox

Generalised: levodopa

31
Q

What inheritance pattern does Huntington’s disease show?

A

Autosomal dominant with genetic anticipation (condition worsens as it passes down the generations)

32
Q

What causes Huntington’s disease?

A

Excess CAG repeats on huntingtin gene forms excess huntingtin protein which forms neurotoxic protein aggregates in neurons

33
Q

Describe the presentation of Huntington’s disease.

A

Early: personality change, depression, clumsiness, abnormal eye movements

Late: chorea, rigidity and dementia

34
Q

What medications can be given to Huntington patients to:

  • stop disease progression?
  • relieve symptoms?
A

Stop progression: none

Symptom relief: tetrabenazine

35
Q

What is Synenham’s chorea?

A

Self limiting chorea in 5-15 year old girls caused by rheumatic fever.
Associated with behavioural disturbance and OCD

36
Q

What is Tourette’s syndrome and how does it present?

A

Neurodevelopmental disorder causing tics

Simple and complex vocal/phonic tics (blinking often first tic) which worsen with stress

37
Q

What condition is Tourette’s syndrome associated with?

A

ADHD

38
Q

How do you treat Tourette’s syndrome?

A

Psychosocial interventions

Rispiradone (+ clonidine if ADHD) if psychosocial interventions fail

39
Q

How do you treat restless leg syndrome?

A

Prampipexole (dopamine agonist)

40
Q

What is chorea?

A

continuous, spontaneous and random jerky movements

41
Q

What is myoclonus?

A

sudden brief ‘shock-like’ movement caused by muscular contraction/inhibition

42
Q

What is hemibalism and what causes it?

A

flinging movement of limb

cerebrovascular lesion of subthalamic nucleus