Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Neuro > Movement disorders > Flashcards

Movement disorders Flashcards

(103 cards)

Start Studying
1
Q

Classic features of Parkinson’s

A

TRAP

Tremor (resting)
Rigidity
Akinesia
Postural instability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How to diagnose PD?

A

Clinical diagnosis - history, exam, response to medications

MRI to exclude other causes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Risk factors for PD

A 
Male
Age >60
Family history
Heavy metal exposure
Pesticides
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What’s the goal of treatment in PD?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How does PD usually start?

A

Unilateral involvement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

AEs of MAO B inhibitors

A

Nausea and headache most common
Confusion and hallucinations
Depression

Beware of drug interactions with ADs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

AEs of amantadine

A

Livedo reticularis
Confusion
Nightmares

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

AEs of anticholinergic therapy

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

Caution in age >65

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A

DA agonist - younger people. Avoid >70yo.

DA replacement - older people

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

List 4 DA agonists

A

Pramipexole
Rotigotine (patch; bypasses oral absorption)
Ropinirole
Cabergoline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What’s dopamine dysregulation syndrome?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Complications of DBS

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

CI to DBS

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What is duodopa?
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
26
Who should be considered for duodopa?
``` Advanced PD Severe dyskinesia Motor on off fluctuations Dysphagia Unpredictable response to oral medications ```
27
With what therapy must melanoma be ruled out?
Duodopa
28
AE of duodopa
Neuropathy | Surgical complications such as peritonitis, abdominal pain, displacement of tube into stomach
29
What is apomorphine?
Continuous subcut infusion of dopamine agonist Via portable infusion pump Decreases dyskinesia and off time
30
Who would be suitable for apomorphine?
Advanced PD Can't tolerate dopamine Dyskinesia
31
AE of apomorphine
``` Nausea hypotension Subcut nodules Pain, bleeding at needle site Autoimmune haemolytic anaemia Sleep attacks/Drowsiness +/- driving restrictions ```
32
When is botox used in PD?
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
33
List non-motor symptoms of PD
``` 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
34
How to differentiate between PD-dementia and DLB?
PD-dementia - dementia typically occurs about a year after the onset of PD symptoms DLB - dementia occurs concurrently or prior to onset of PD
35
List motor symptoms of PD
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)
36
List 3 Parkinson's Plus syndromes
- Multisystem atrophy (MSA) - Progressively supranuclear palsy - Corticobasal degeneration
37
Which drugs can cause parkinsonism?
Dopamine antagonists - antipsychotics, metoclopramide, CCB, AEDs
38
How does drug induced parkinson's differ from idiopathic PD?
Symptoms usually bilateral
39
Do symptoms resolve after stopping offending agent in drug induced parkinson's?
Not always | Symptoms can persist for long periods of time
40
List predictors of benign course in PD
Younger age of onset Female Tremor predominant
41
List predictors of poor prognosis in PD
``` Male Late age of onset Gait and balance issues Dementia Bradykinesia as an initial symptom Poor response to levodopa ```
42
List 3 clinical syndromes of multiple system atrophy?
MSA with predominant cerebellar ataxia (MSA-C) MSA with parkinsonism (MSA-P) Shy-Drager syndrome
43
Mean age of onset for MSA
50-60 years old
44
Clinical features of MSA | Hint: think of the subtypes
- Akinetic-rigid parkinsonism - Autonomic failure - orthostatic hypotension - Urogenital dysfunction - erectile dysfunction, urinary frequency, urgency, incontinence, incomplete bladder emptying - Cerebellar ataxia - Pyramidal signs
45
Which symptoms happen first in MSA?
Urogenital symptoms followed by orthostatic hypotension
46
How to diagnose MSA?
Clinical diagnosis | Lack of response to levodopa (but 30-50% have transient benefit and so can be mistaken as idiopathic PD)
47
How does corticobasal degeneration present?
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
What do you expect to find on neuroimaging in corticobasal degneration?
Normal CTB MRIB initially Later you get asymmetrical cortical atrophy affecting predominantly the posterior frontal and parietal regions, and dilatation of the ventricles
49
How do you diagnose corticobasal degeneration?
Clinical diagnosis
50
Rx corticobasal degeneration
No treatments to delay progression Treatments mainly aimed at providing symptom relief In those with clinical parkinsonism, can trial levodopa
51
Medial survival from onset of symptoms with corticobasal degeneration is ...
6-8 years
52
What are the 2 most common phenotypes of progressive supranuclear palsy?
Richardson syndrome (classic form of PSP) PSP-Parkinsonism
53
How does Richardson syndrome (PSP) present?
Presents as disturbance of gait, resulting in fall Slowing of vertical saccades Other common features dysarthria, dysphagia, rigidity, frontal cognitive abnormalities, sleep disturbance
54
How does PSP-parkinsonism present?
Unilateral limb symptoms including tremor Moderate initial response to levodopa May be confused with idiopathic PD
55
How to diagnose PSP?
Clinical diagnosis
56
When to be suspicious of PSP?
New onset neurologic, cognitive, or behavioural deficits in absence of other identifiable cause in patients ≥40 years of age
57
List the core clinical features of PSP
Postural instability Oculomotor deficits especially vertical gaze palsy Akinesia/parkinsonism Frontal lobe impairments including speech and language problems, and behavioural change
58
Why do we use carbidopa?
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
Dopamine is broken down by ...
MAO and COMT Hence we use MAO B inhibitors - rasagiline, selegiline and COMT inhibitor - entacapone
60
Only medication that has evidence against psychosis in PD is...
Clozapine D1/2 and NA antagonist But serious side effects so not used much clinically. Instead we use quetiapine.
61
Depression in PD Rx
TCA - nortriptyline Pramipexole helps depression (Alsu use SSRI, mirtazapine but no trials show evidence)
62
Dementia in PD Rx
Ach inhibitor Rivastigmine Donepezil (insufficient evidence) Not approved in Australia but we use it
63
REM sleep behaviour disorder in PD Rx
Amitriptyline | Clonazepam
64
Rx DLB
Levodopa - May exacerbate cognitive and behavioural disturbance Antipsychotics - Can exacerbate extrapyramidal side effects Ach inhibitors Antidepressants
65
Essential tremor Presentation Age of onset
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
What's essential tremor plus?
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
Rx essential tremor
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
Multiple system atrophy 2 main phenotypes Other features
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
MSA | Median age of onset
54 years
70
MSA pathology
Alpha-synucleinopathy
71
MSA MRI findings
MSA-P = putaminal rim MSA-C = hot cross bun sign in the pons
72
MSA treatment
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
Progressive Supranuclear palsy clinical features
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
MRI PSP
Hummingbird sign - midbrain atrophy
75
PSP pathology
Tauopathy
76
PSP treatment
Levodopa - may respond initially but doesn't last Amantadine
77
Corticobasal degeneration presentation
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
What is corticobasal degeneration?
When symptoms are seen in PSP, AD, FTD but they don't have all the features
79
Pathology corticobasal degeneration
Tauopathy
80
Corticobasal degeneration treatment
BOTOX for dystonia
81
Huntington's disease presentation
``` Chorea form movements of limbs and torso Cognitive impairment Mood disturbance - depression, suicide Psychosis Oculomotor dysfunction ``` Can present quite young with parkinsonian features
82
Median age of onset in Huntington's disease
35-44
83
Explain anticipation in Huntington's disease
CAG trinucleotide repeats of huntington gene on chromosome 4 >37 repeats: symptomatic Anticipation = greater number of repeats, earlier onset Autosomal dominant
84
Huntington's disease pathology
Affects GABAergic neurons in basal ganglia | Gross caudate atrophy
85
Huntington's disease treatment
Chorea - tetrabenazine, risperidone, olanzapine Parkinsonian features - levodopa Antidepressants Antipsychotics and mood stabilisers
86
What's tardive dyskinesia?
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
Hemiballismus - unilateral violent flinging movement of limbs Where is the lesion?
Contralateral subthalamic nucleus, but other areas of the basal ganglia can be involved
88
What's tourette syndrome?
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
Tourette syndrome treatment
Habit reversal training - most effective Tetrabenazine, risperidone -if habit reversal training doesn't work ADHD - clonidine OCD - SSRI
90
What's dystonia?
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
Common forms of dystonia
Cervical dystonia Blepharospasm - constant blinking Writer's cramp
92
Dystonia treatment
Levodopa Clonazepam Trihexyphenidyl DBS, Botox
93
Fragile X associated tremor/ataxia syndrome presentation
``` Intention tremor Ataxia Parkinsonism Peripheral neuropathy Autonomic disturbance Cognitive impairment Mood disorder ```
94
Fragile X associated tremor/ataxia syndrome pathology
CGG triplet repeat (55-200) in FMR1 gene (>200 Fragile X) X linked autosomal dominant
95
Wilson's disease presentation
Dysarthria, dystonia, tremor, rigidity, chorea, ataxia Behavioural, cognitive and mood disturbance Liver disease
96
Wilson disease pathology
Autosomal recessive Disorder of copper metabolism
97
Wilson disease diagnosis
Low serum ceruloplasmin High urinary copper Kayser-Fleischer rings around iris High copper on liver biopsy (gold standard)
98
Wilson's disease treatment
Chelating agents - Penicillamine or trientene plus zinc Parkinsonism - levodopa Antipsychotics Antidepressants Liver transplant
99
Restless legs syndrome | secondary causes
``` AED Pregnancy Iron deficiency ESKD Peripheral neuropathy ```
100
Restless leg syndrome treatment
Treat secondary cause Dopamine agonist - pramipexole Levodopa Pregabalin, gabapentin, opioids
101
Restless leg syndrome presentation
Constant urge to move legs
102
Normal pressure hydrocephalus triad
Gait disturbance Cognitive impairment Urinary dysfunction
103
Normal pressure hydrocephalus triad treatment
Ventriculoperitoneal shunt

Neuro (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions