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Neuro > Movement disorders > Flashcards

Movement disorders Flashcards

1
Q

Classic features of Parkinson’s

A

TRAP

Tremor (resting)
Rigidity
Akinesia
Postural instability

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2
Q

How to diagnose PD?

A

Clinical diagnosis - history, exam, response to medications

MRI to exclude other causes

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3
Q

Risk factors for PD

A 
Male
Age >60
Family history
Heavy metal exposure
Pesticides
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4
Q

What’s the goal of treatment in PD?

A

Symptomatic treatment only
Does not improve balance
Does not prevent progression of disease

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5
Q

How does PD usually start?

A

Unilateral involvement

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6
Q

List 5 main classes of PD therapy

A

1) Dopamine replacement
- Levodopa is gold standard for motor symptoms but also has the highest risk of motor complications
2) Dopamine agonist
3) MAO B inhibitors
4) Amantadine
5) Anticholinergics

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7
Q

Treatment options for mild PD

A

1) MAO B inhibitor
- Selegeline, Rasagiline
- Safinamide is a newly approved drug and is used as an adjunct to levodopa

2) Amantadine
- Monotherapy or add on
- When tremor is predominant
- Also used for management of dyskinesia

3) Anticholinergic therapy
- Benztropine, trihexyphenidyl
- Used in tremor control
- Monotherapy or add on

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8
Q

AEs of MAO B inhibitors

A

Nausea and headache most common
Confusion and hallucinations
Depression

Beware of drug interactions with ADs

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9
Q

AEs of amantadine

A

Livedo reticularis
Confusion
Nightmares

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10
Q

AEs of anticholinergic therapy

A 
Cognitive impairment
Blurred vision
Dry mouth
Constipation
Urinary retention
Dry red itchy skin

Caution in age >65

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11
Q

Rx for moderate PD - when symptoms begin to interfere with functioning

A

DA agonist - younger people. Avoid >70yo.

DA replacement - older people

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12
Q

List 4 DA agonists

A

Pramipexole
Rotigotine (patch; bypasses oral absorption)
Ropinirole
Cabergoline

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13
Q

AEs of DA agonists

A 
Nausea, vomiting
Drowsiness
Pathological gambling, compulsive sexual behaviour and spending 
Hallucinations
Confusion
Pedal oedema
Orthostatic hypotension
Rotigotine patch may cause skin irritation

Start low, go slow

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14
Q

How to stop PD medications particularly DA agonists and levodopa?

A

Don’t discontinue abruptly due to risk of withdrawal syndrome, acute akinesia or neuroleptic malignant syndrome

Withdrawal can resemble other psychostimulant withdrawal syndromes with prominent psychiatric (anxiety, panic attacks, depression, agitation, fatigue) and autonomic (orthostatic hypotension, diaphoresis) manifestations

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15
Q

Rx for advanced stage PD

A

Levodopa (gold standard) +/- MAO B inhibitor +/- DA agonist
- Always titrate with IR tablets

If ongoing issues with motor fluctuations and dyskinesia, can consider…

Deep brain stimulation

Apomine infusion

Duodopa

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16
Q

AEs of levodopa

A

Dyskinesia with prolonged use
- Motor fluctuations and dyskinesia will occur after 5-10 years. Adjuncts are available to reduce motor fluctuation.

Nausea
Headache
Confusion
Hallucinations/delusions
Dizziness
Orthostatic hypotension
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17
Q

What’s dopamine dysregulation syndrome?

A

When people get addicted and abuse dopaminergic medications especially IR form, impairing function

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18
Q

What’s punding?

A

When PD patients repeatedly do purposeless, stereotyped behaviours e.g. sorting or disassembling

Can occur after use of short-acting dopaminergic agents

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19
Q

What is dyskinesia?

A

Happens with prolonged use of levodopa. Doesn’t happen with DA agonists.
The earlier the onset of PD, the higher the risk

Involuntary movements of limbs, torso, neck and head
Usually dystonic movements and sometimes more choreiform in nature

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20
Q

Why does dyskinesia happen?

A

It is thought that as PD becomes more advanced, you lose dopaminergic neurons that store dopamine in the basal ganglia, so the individual’s response becomes dependent on plasma levels that fluctuate based on systemic absorption which is erratic

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21
Q

What’s diphasic and peak dose dyskinesia?

A

Diphasic dyskinesia affects limbs and occurs when dopamine levels rise and fall
Peak dose dyskinesia affects head and neck and occurs when dopamine levels peak

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22
Q

Who should be considered for DBS?

A 
Age <70 (not a hard rule)
Severe dyskinesia that affects QOL
On and off fluctuation
Response to dopaminergic therapy 
Good cognitive function
Tremor that can't be controlled with medication
At least 5 years of PD

Need neuropsych assessment

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23
Q

Complications of DBS

A

Surgical complications
Neuropsychiatric/behavioural issues - higher risk of suicide
Mechanical malfunction

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24
Q

CI to DBS

A

Dementia
Active psychiatric disorders
Dominant levodopa resistant motor symptoms
Structural abnormalities on MRI

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25
Q

What is duodopa?

A

Continuous levodopa carbidopia intestinal gel infusion

Through a percutaneous gastrojejunostomy tube that connects to a pump

Less “off times” and more “on” times without dyskinesia
Can titrate dose

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26
Q

Who should be considered for duodopa?

A 
Advanced PD
Severe dyskinesia
Motor on off fluctuations
Dysphagia
Unpredictable response to oral medications
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27
Q

With what therapy must melanoma be ruled out?

A

Duodopa

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28
Q

AE of duodopa

A

Neuropathy

Surgical complications such as peritonitis, abdominal pain, displacement of tube into stomach

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29
Q

What is apomorphine?

A

Continuous subcut infusion of dopamine agonist
Via portable infusion pump
Decreases dyskinesia and off time

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30
Q

Who would be suitable for apomorphine?

A

Advanced PD
Can’t tolerate dopamine
Dyskinesia

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31
Q

AE of apomorphine

A 
Nausea 
hypotension
Subcut nodules
Pain, bleeding at needle site
Autoimmune haemolytic anaemia
Sleep attacks/Drowsiness +/- driving restrictions
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32
Q

When is botox used in PD?

A

Cervical dystonia (inject into the sternocleidomastoid; risk of dysphagia)
Head tremors
Blepharospasm (involuntary movement of eyes)
Eyelid apraxia (difficulty with eyelid elevation; risk of causing ptosis and diplopia)
Sialorrhea (drooling)
Limb dystonia
Hyperhidrosis (excessive sweating)

Only lasts 12 weeks

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33
Q

List non-motor symptoms of PD

A 
Hallucinations
Cognitive decline and dementia
Disturbed sleep pattern and REM behavioural disorder
Vivid dreams
Anosmia 
Restless leg syndrome
Fatigue
Depression, anxiety, psychosis

Autonomic symptoms
Postural instability/hypotension (as a result of advanced PD or levodopa)
Constipation
Dysphagia
Neurogenic overactive bladder or underactive bladder
Sexual dysfunction

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34
Q

How to differentiate between PD-dementia and DLB?

A

PD-dementia - dementia typically occurs about a year after the onset of PD symptoms

DLB - dementia occurs concurrently or prior to onset of PD

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35
Q

List motor symptoms of PD

A

Masked facies
Decreased blink reflex due to motor slowing
Eyelid apraxia (difficulty opening eyes; usually late feature)
Hypophonia (soft speech) due to glottal rigidity
Micrographia due to bradykinesia and limb rigidity
Dysphagia due to pharyngo-oesophageal motor slowing
Excessive salivation due to decreased swallowing
Camptocormia (severe involuntary flexion of the thoraco-lumbar spine; late feature; may respond to dopamine)
Gait issues - freezing, shuffling, festinating (short and progressively more rapid steps)

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36
Q

List 3 Parkinson’s Plus syndromes

A
  • Multisystem atrophy (MSA)
  • Progressively supranuclear palsy
  • Corticobasal degeneration
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37
Q

Which drugs can cause parkinsonism?

A

Dopamine antagonists - antipsychotics, metoclopramide, CCB, AEDs

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38
Q

How does drug induced parkinson’s differ from idiopathic PD?

A

Symptoms usually bilateral

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39
Q

Do symptoms resolve after stopping offending agent in drug induced parkinson’s?

A

Not always

Symptoms can persist for long periods of time

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40
Q

List predictors of benign course in PD

A

Younger age of onset
Female
Tremor predominant

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41
Q

List predictors of poor prognosis in PD

A 
Male
Late age of onset
Gait and balance issues
Dementia
Bradykinesia as an initial symptom
Poor response to levodopa
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42
Q

List 3 clinical syndromes of multiple system atrophy?

A

MSA with predominant cerebellar ataxia (MSA-C)

MSA with parkinsonism (MSA-P)

Shy-Drager syndrome

43
Q

Mean age of onset for MSA

A

50-60 years old

44
Q

Clinical features of MSA

Hint: think of the subtypes

A
  • Akinetic-rigid parkinsonism
  • Autonomic failure - orthostatic hypotension
  • Urogenital dysfunction - erectile dysfunction, urinary frequency, urgency, incontinence, incomplete bladder emptying
  • Cerebellar ataxia
  • Pyramidal signs
45
Q

Which symptoms happen first in MSA?

A

Urogenital symptoms followed by orthostatic hypotension

46
Q

How to diagnose MSA?

A

Clinical diagnosis

Lack of response to levodopa (but 30-50% have transient benefit and so can be mistaken as idiopathic PD)

47
Q

How does corticobasal degeneration present?

A

Typically begins with cognitive impairment

Followed by progressive asymmetric movement disorder - symptoms starting in one limb with akinesia, rigidity, dystonia, focal myoclonus, ideomotor apraxia, alien limb phenomenon

48
Q

What do you expect to find on neuroimaging in corticobasal degneration?

A

Normal CTB MRIB initially

Later you get asymmetrical cortical atrophy affecting predominantly the posterior frontal and parietal regions, and dilatation of the ventricles

49
Q

How do you diagnose corticobasal degeneration?

A

Clinical diagnosis

50
Q

Rx corticobasal degeneration

A

No treatments to delay progression
Treatments mainly aimed at providing symptom relief

In those with clinical parkinsonism, can trial levodopa

51
Q

Medial survival from onset of symptoms with corticobasal degeneration is …

A

6-8 years

52
Q

What are the 2 most common phenotypes of progressive supranuclear palsy?

A

Richardson syndrome (classic form of PSP)

PSP-Parkinsonism

53
Q

How does Richardson syndrome (PSP) present?

A

Presents as disturbance of gait, resulting in fall
Slowing of vertical saccades

Other common features dysarthria, dysphagia, rigidity, frontal cognitive abnormalities, sleep disturbance

54
Q

How does PSP-parkinsonism present?

A

Unilateral limb symptoms including tremor

Moderate initial response to levodopa

May be confused with idiopathic PD

55
Q

How to diagnose PSP?

A

Clinical diagnosis

56
Q

When to be suspicious of PSP?

A

New onset neurologic, cognitive, or behavioural deficits in absence of other identifiable cause in patients ≥40 years of age

57
Q

List the core clinical features of PSP

A

Postural instability
Oculomotor deficits especially vertical gaze palsy
Akinesia/parkinsonism
Frontal lobe impairments including speech and language problems, and behavioural change

58
Q

Why do we use carbidopa?

A

Stops breakdown of levodopa into dopamine in the periphery
So more goes to CNS to act on DA receptors
Less side effects e.g. less nausea

59
Q

Dopamine is broken down by …

A

MAO and COMT

Hence we use MAO B inhibitors - rasagiline, selegiline

and COMT inhibitor - entacapone

60
Q

Only medication that has evidence against psychosis in PD is…

A

Clozapine
D1/2 and NA antagonist

But serious side effects so not used much clinically. Instead we use quetiapine.

61
Q

Depression in PD Rx

A

TCA - nortriptyline

Pramipexole helps depression

(Alsu use SSRI, mirtazapine but no trials show evidence)

62
Q

Dementia in PD Rx

A

Ach inhibitor
Rivastigmine
Donepezil (insufficient evidence)

Not approved in Australia but we use it

63
Q

REM sleep behaviour disorder in PD Rx

A

Amitriptyline

Clonazepam

64
Q

Rx DLB

A

Levodopa
- May exacerbate cognitive and behavioural disturbance

Antipsychotics
- Can exacerbate extrapyramidal side effects

Ach inhibitors

Antidepressants

65
Q

Essential tremor
Presentation
Age of onset

A

BIlateral UL symmetrical postural/action tremor ~4-12 Hz
Can also have head, voice or lower limb tremors

Bimodal distribution - 2nd and 6th decades

Improves with ETOH

66
Q

What’s essential tremor plus?

A

Characteristic tremor + mild neurological sign e.g. cognitive impairment, dystonic posturing, impaired tandem gait

And may have resting tremor

This is a little bit controversial

67
Q

Rx essential tremor

A

Beta blocker - propanol

Primodone

Topiramate

Clonazepam

DBS if not managed well on medication

Focused USS thalamotoomy - uses USS waves to burn certain areas of thalamus to stop tremor

68
Q

Multiple system atrophy
2 main phenotypes
Other features

A

Cerebellar
Parkinsonian

Other features
Orthostatic hypotension
Stridor, sleep apnoea
Dysphonia, dysarthria
Dysphagia
Jerky tremor, postural or action
Pyramidal signs e.g. brisk reflexes, extensor plantars
Antecollis (head pushes forward), camptocromia (torso is flexed at the hips), Pisa syndrome (lateral deviation of torso)
- REM sleep behaviour disorder
- Labile emotions
- Depression, anxiety
69
Q

MSA

Median age of onset

A

54 years

70
Q

MSA pathology

A

Alpha-synucleinopathy

71
Q

MSA MRI findings

A

MSA-P = putaminal rim

MSA-C = hot cross bun sign in the pons

72
Q

MSA treatment

A

Levodopa for MSA-P but can exacerbate orthostatic hypotension

Orthostatic hypotension

  • Elevate bed up to 10 degrees
  • Hydration
  • Compression stockings
  • Fludrocortisone, midodrine

Urinary dsyfunction
- Oxybutynin, solifenacin, mirabegron

73
Q

Progressive Supranuclear palsy clinical features

A

Gaze palsy - initially slowed vertical > horizontal saccades, down gaze affected first; later restricted vertical and subsequently horizontal eye movements
*overcome with doll’s eye manoeuvre

Impaired postural reflexes –> frequent falls backwards

Axial rigidity and retrocollis (head goes backwards)

EPS - bradykinesia

Dysarthria, dysphagia

Cognitive impairment

74
Q

MRI PSP

A

Hummingbird sign - midbrain atrophy

75
Q

PSP pathology

A

Tauopathy

76
Q

PSP treatment

A

Levodopa - may respond initially but doesn’t last

Amantadine

77
Q

Corticobasal degeneration presentation

A

Parkinsonism - dystonia, rigidity

Limb apraxia = ‘alien limb

Myclonus/myoclonic jerk

Cortical sensory sign - neglect, dysgraphaesthesia (can’t tell which arm when you’re touching both arms; but can tell which you touch one arm), asterognosis (can’t tell what the object is where they feel it)

Speech apraxia or nonfluent aphasia

Cognitive impairment

78
Q

What is corticobasal degeneration?

A

When symptoms are seen in PSP, AD, FTD but they don’t have all the features

79
Q

Pathology corticobasal degeneration

A

Tauopathy

80
Q

Corticobasal degeneration treatment

A

BOTOX for dystonia

81
Q

Huntington’s disease presentation

A 
Chorea form movements of limbs and torso
Cognitive impairment
Mood disturbance - depression, suicide
Psychosis
Oculomotor dysfunction

Can present quite young with parkinsonian features

82
Q

Median age of onset in Huntington’s disease

A

35-44

83
Q

Explain anticipation in Huntington’s disease

A

CAG trinucleotide repeats of huntington gene on chromosome 4

> 37 repeats: symptomatic
Anticipation = greater number of repeats, earlier onset

Autosomal dominant

84
Q

Huntington’s disease pathology

A

Affects GABAergic neurons in basal ganglia

Gross caudate atrophy

85
Q

Huntington’s disease treatment

A

Chorea - tetrabenazine, risperidone, olanzapine

Parkinsonian features - levodopa

Antidepressants
Antipsychotics and mood stabilisers

86
Q

What’s tardive dyskinesia?

A

Delayed onset of orofacial dyskinesia in context of antipsychotic use. Can come on much later even after antipsychotics are ceased.

Rx: reduce antipsychotic. Change to atypical antipsychotic.
Tetrabenazine, benztropine if above doesn’t work.

87
Q

Hemiballismus - unilateral violent flinging movement of limbs
Where is the lesion?

A

Contralateral subthalamic nucleus, but other areas of the basal ganglia can be involved

88
Q

What’s tourette syndrome?

A

Motor and vocal tics
Can be complex - yelling out rude sentences etc

Associated with ADHD, OCD, learning disorder, mood disorder

Onset 2-15 years

Ability to suppress, urge to perform

89
Q

Tourette syndrome treatment

A

Habit reversal training - most effective

Tetrabenazine, risperidone -if habit reversal training doesn’t work

ADHD - clonidine

OCD - SSRI

90
Q

What’s dystonia?

A

Sustained intermittent muscle contractions, with abnormal, often repetitive movements or postures, twisting or tremulous

Genetic, acquired or idiopathic

Can be focal (one muscle), segmental (muscles affecting next to each other), multifocal, generalised

Isolated or combined with other neuro symptoms (Parkinsonism, myoclonus)

Action specific, diurnal variation, sensory trick

91
Q

Common forms of dystonia

A

Cervical dystonia
Blepharospasm - constant blinking
Writer’s cramp

92
Q

Dystonia treatment

A

Levodopa

Clonazepam

Trihexyphenidyl

DBS, Botox

93
Q

Fragile X associated tremor/ataxia syndrome presentation

A 
Intention tremor
Ataxia
Parkinsonism
Peripheral neuropathy
Autonomic disturbance 
Cognitive impairment
Mood disorder
94
Q

Fragile X associated tremor/ataxia syndrome pathology

A

CGG triplet repeat (55-200) in FMR1 gene
(>200 Fragile X)

X linked autosomal dominant

95
Q

Wilson’s disease presentation

A

Dysarthria, dystonia, tremor, rigidity, chorea, ataxia

Behavioural, cognitive and mood disturbance

Liver disease

96
Q

Wilson disease pathology

A

Autosomal recessive

Disorder of copper metabolism

97
Q

Wilson disease diagnosis

A

Low serum ceruloplasmin
High urinary copper
Kayser-Fleischer rings around iris
High copper on liver biopsy (gold standard)

98
Q

Wilson’s disease treatment

A

Chelating agents - Penicillamine or trientene plus zinc

Parkinsonism - levodopa
Antipsychotics
Antidepressants
Liver transplant

99
Q

Restless legs syndrome

secondary causes

A 
AED 
Pregnancy
Iron deficiency
ESKD
Peripheral neuropathy
100
Q

Restless leg syndrome treatment

A

Treat secondary cause

Dopamine agonist - pramipexole
Levodopa
Pregabalin, gabapentin, opioids

101
Q

Restless leg syndrome presentation

A

Constant urge to move legs

102
Q

Normal pressure hydrocephalus triad

A

Gait disturbance
Cognitive impairment
Urinary dysfunction

103
Q

Normal pressure hydrocephalus triad treatment

A

Ventriculoperitoneal shunt

Neuro (9 decks)

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