Movement Disorders

Question 1

What is the clinical syndrome of Parkinsonism?

Answer 1

1) Bradykinesia *** (must have)
2) Lead pipe rigidity
3) Tremors

Question 2

How are UMN lesion rigidity and Parkinsonism rigidity different and why?

Answer 2

UMN: Clasp knife
- some agonists > antagonists → resistance varies depending on position of joint

Parkinsonism/Extrapyramidal: Lead pipe
- both agonist and antagonistic muscles rigid → joint is tight/rigid regardless of position

Question 3

What is “cogwheel rigidity”?

Answer 3

Lead pipe rigidity + tremor

Question 4

How does bradykinesia present in parkinsonism?

Answer 4

1) Hypomimia
- mask-like faces + paucity of blinking

2) Hypophonia

3) Decremental bradykinesia
- reduced arm swing walking
- micrographia
- progressive reduction in amplitude of movements

4) Festinant gait
- reduced stride + paradoxically exaggerated tremor

Question 5

What is a festinant gait?

Answer 5

Rapid, small steps, done in an attempt to keep the center of gravity (COG) in between the feet while the trunk leans forward involuntarily and shift the COG forward

Question 6

In which condition are intention tremors seen?

Answer 6

Cerebellar lesions

Question 7

In which condition are resting tremors seen?

Answer 7

Parkinsonism
- better with movement

Question 8

What type of tremor is a postural tremor?

Answer 8

Benign essential

Question 9

What are 5 causes of Parkinsonism?

Answer 9

1) Idiopathic
2) Neuroleptic medication (anti-dopaminergics)
3) Parkinson plus syndromes
4) Wilson’s disease
5) Infective encephalitis
6) Vascular Parkinsonism

Question 10

Why should metoclopramide be avoided in a patient with Parkinson disease?

Answer 10

Blocks dopamine receptors → exacerbate parkinsonism symptoms

Must use peripherally active anti-emetics (Eg. domperidone/odansetron)

Question 11

How does Wilson’s disease cause Parkinsonism?

Answer 11

Defect in biliary Copper excretion → Copper deposited in basal ganglia of the brain

Question 12

How is Wilson’s disease diagnosed?

Answer 12

1) Low levels of caeruoloplasmin (copper transporter)
2) High urine copper levels
3) Kayer Fleishcher rings in eyes
4) Parkinsonism and Liver issues

Question 13

How is Wilson’s disease treated?

Answer 13

Penicillamine
- sequestered copper

Question 14

How is progressive supranuclear palsy different from lewy body dementia and multiple systems atrophy?

Answer 14

Progressive Supranuclear Palsy:
- Parkinsonism + eye movement abnormalities

Lewy body dementia:
- Parkinsonism + lilliputian hallucination + cognitive deficits

Multiple systems atrophy:
- Parkinsonism + autonomic failure/cerebellar disease

Question 15

Which infection is associated with parkinsonism?

Answer 15

Japanese encephalitis

Question 16

What is Parkinson Disease?

Answer 16

Neurodegenerative condition characterised by asymmetric parkinsonism and apoptosis of dopaminergic nigro-striatal neurons

Question 17

What are the clinical manifestations of Parkinson’s disease?

Answer 17

Motor:
1) Decremental bradykinesia
2) Hypophonia
3) Hypomimia
4) Micrographia
5) Festinant gait
6) Pill-rolling tremor
7) Lead pipe/cogwheel rigidity

Non-motor:
1) Depression
2) Psychiatric
3) Dementia
4) Mild cognitive impairment
5) Sleep/fatigue/REM sleep disorder
6) Dysautonomia
7) Constipation
8) Sialorrhoea
9) Pain
10) Anosmia

Question 18

What are 3 brain areas implicated in Parkinson’s disease?

Answer 18

1) Meso-cortical dopaminergic pathways
- mood/motivation

2) Nigro-strial pathways
- movements

3) Locus coerulus
- noradrenergic
- mood

4) Dorsal raphe nuclei
- serotonergic
- mood
- sleep

Question 19

How is Parkinson’s disease treated?

Answer 19

1) Conservative:
- OT/PT/Support groups

2) Surgical:
- deep brain stimulation

3) Pharmacological
a) Motor symptoms:
- L-dopa
- MOAi/COMTi
- Dopamine agonist
b) Non-motor symptoms
- Citalopram → depression
- Rivastigmine → dementia
- Quetiapine → psychosis
- Botulinum toxin → sialorrhoea
- Amantadine → dyskinesia

Question 20

What are 4 neural pathways that involve dopamine and their associated diseases?

Answer 20

1) Mesocortical → schizophrenia
2) Mesolimbic → schizophrenia
3) Nigro-striatal → parkinson disease
4) Tubero-infundibular → hyperprolactinemia

Question 21

Why should dopamine not be given in patients with parkinson’s disease?

Answer 21

1) Cannot cross BBB
2) Stays in peripheral ciculation → AEs eg.HBP/↑HR

Question 22

Why give carbidopa with L-dopa when it inhibits the conversion of levodopa to dopamine?

Answer 22

Carbidopa cannot cross BBB → prevent peripheral conversion of L-DOPA to Dopamine
→ limits peripheral side effects

Question 23

What are 4 AEs of L-dopa?

Answer 23

ST:
1) Nausea
2) ↑daytime sleepiness
3) Dyskinesia
4) Impulse control disorders
5) Psychosis/hallucinations

LT:
6) On-off phenomenon
7) “freezing”
8) Dyskinesia

Question 24

What are 4 forms of hyperkinesia?

Answer 24

1) Myoclonus
- instantaneous muscle contraction

2) Tics
- worse during anxiety/suppressible to certain extent
- basal ganglia dysfunction
- Typified by Tourette syndrome

3) Tremor
- rhythmic sinusoidal oscillatory movements

4) Choreoathetosis
- irregular jerky/twisty movements

Question 25

What are 4 forms of tremors?

Answer 25

1) Pharm (eg. ß-agonists)
2) Endocrine (eg. hyperthyroidism)
3) Essential
4) Cerebellar
5) Dystonia
6) Parkinsonism

Question 26

What are 5 causes of choreoathetosis?

Answer 26

1) Pharm (eg. L-DOPA)
2) Genetic (eg. Huntington’s disease)
3) Post-infectious (ge. Sydenham’s)
4) Autoimmune (eg. Lupus)
5) Stroke
6) Pregnancy

Question 27

What is Sydenham’s chorea?

Answer 27

Post-Strep pyogenes infection chorea