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Delta Med - Neurology > Neurology 1(B) - Movement Disorders > Flashcards

Neurology 1(B) - Movement Disorders Flashcards

1
Q

What are the Dx criteria for Restless leg syndrome?

A

Urge to move legs accompanied by unpleasant sensations
Worse when inactive
Partially or totally relieved by movement
Circadian rhythm - worse in evening or night than day

Associated and supporting features: FHx, dopa response, PLMS

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2
Q

What is the classification of restless leg syndrome?

A 
Primary
Secondary
 - Fe deficiency
 - ESRD
 - Pregnancy
 - DM
 - RA
 - PD
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3
Q

What are treatment options in RLS?

A 
Improve sleep hygiene
Avoid exacerbating factors - caff, EtOH, SSRIs, dopamine blockers, TCAs
Levodopa
Dopamine agonists (Pramipexole)
Gabapentin (CBZ, valproate)
Opiods
Tramadol
BDZ
Irone, Mg, clonidine
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4
Q

What are dopamine related Sx in PD?

A

Fluctuations, involuntary movements, neuropsychiatric
Motor disability
Reduced on and off

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5
Q

What are non-dopamine related Sx in PD?

A 
anosmia
Depression
personality change
Lethargy, pain
REM SBD
Balance, gait, swallowing, speech
Mood
Sleep, pain
Cognition
Autonomic
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6
Q

What are exogenous risk factors for PD?

A 
Well water
rural environment
non-smoking
pesticide/herbicide exposure
minor head trauma
Positive FHX - greatest RF
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7
Q

What is the mechanism of nigral cell death in PD?

A

induced mitochondrial respiratory failure and oxidative stress in nigral neurons

  • ox stress, free rad formation
  • mito dysfunction
  • excitotoxic damage
  • protein mishandling
  • inflammation
  • cell death, apoptosis

4-12% loss/year, 10x normal
4-6y presymptomatic period

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8
Q

What are levodopa associated disabilities in PD?

A

Motor fluctuations - 10%pa (80% by 10y)

  • wearing off, end of dose, subtle psychomotor
  • on-off, random, brittle, sudden increased magnitude
  • assoc involutnary movements, pain, akathesia, mood, autonomic

Dyskinesias

  • variable disability
  • peak dose, off phase, dystonia, diphasic
  • vary between pts but remain consistent for all patients

Neuropsychiatric toxicity - 60%

  • major dose limiting effect
  • common in later disease, elderly, cognitive impairment
  • correlates with LB density in amygdola, parahippocampus, inferior temporal cortex

Reduced response

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9
Q

What features of parkinsons are not responsive to levodopa?

A

falls, instability, gait disturbance
Swallowing, speech disturbance
cognition - concentration, attention, memory
Depression, anxiety
sleep disturbance
incontinence, hypersalivation, constipation
fatigue, pain

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10
Q

What are predictors for cognitive impairment in AD?

A

Attention, working memory, reduced processing speed are features, similar to AD

Predictive factors:

  • age
  • age at disease onset
  • duration of disease
  • akinetic-rigid disease pattern
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11
Q

What is the congnitive profile in PD?

A 
dysexecutive syndrome
impaired attention
memory -free recall difficulties
visuospatial dysfunction
behavioural and personality changes
language and praxis generally preserved
less often - amnestic syndrome with early language involvement
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12
Q

What are core Dx features of Dementia with lewy bodies?

A

Cognitive decline (70%)
fluctuation in cognition/attention
visual hallucinations
motor parkinsonism (95% eventually)

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13
Q

What are other clinical features of DwLB?

A

age of onset 75y
duration 7 years
rate of decline 4 MMSE/year

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14
Q

What are features of levodopa?

A 
gold standard treatment of PD
95% response rate
honeymoon period
increased survival - 9 to 14y
no clinical evidence of neurotoxicity
low acute SE profile
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15
Q

What are examples of dopamine agonists?

A

Ergoline agonists - bromocriptine, pergolide, cabergoline

Pramipexole

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16
Q

What are features of dopamine agonist monotherapy?

A

less powerful control of motor symptoms
lower risk for developing dyskinesias or motor fluctiations
pramipexole has antidepressant action

as adjunct to levodopa - improves motor control, reduces off time, and limits need for levodopa

17
Q

What are risks of ergot derived dopamine agonists?

A

Fibrosis!
thickening retraction and stiffening of heart falves, due to high affinity to 5-HT(2B) - expressed in heart valves, mediate mitogenesis and proliferation of fibroblasts
mod severe valvular regurgitation in 23% pergolide, 28% cabergoline
cumulative dose effect

18
Q

What are features of non-ergot derived agonists of dopamine?

A

Pramipexole - significant reduction in off hours on levodopa, lower fluctuations in dyskinesias vs levodopa
effective, delayed motor complications c.f. levodopa

19
Q

What are significant AEs associated with pramipexole?

A 
somnolescence
nausea or vomiting
dizziness
hypotension
involuntary movements
hallucinations
fatigue
confusion
rash
Impulse control disorders!
20
Q

What are features of rotigoline?

A

Transdermal dopamine agonist patch
effective in early and late disease
not affected by food or gastric emptying

21
Q

What are features of impulse control disorders?

A

complex behaviours related to aberrent or excessive dopamine receptor stimulation - pathological gambling, hypersexuality, compulsive shopping or eating

Caused by dopamine agonists, not by entacapone.

Levodopa does cause punding at high doses

22
Q

What are RFs for Impulse control disorders?

A

Younger age, males
Dopamine agonists - dose related pramipexole > ropinirole > pergolide
Premorbid novelty seekins, risk taking, alcohol abuse, pathological gambling
FHx

23
Q

What are features of entacapone?

A

COMT inhibitor - prevents extracerebral metabolism of levodopa
doubles the t1/2 of levodopa
increases bioavailability by 35%
useful in moderate flucuations

SEs: discolouration, diarrhoea, increased levodopa SE, postural hypotension, neuropsychiatric, dyskinesia, nausea

24
Q

What is selegiline?

A

MAOB inhibitor

  • effective as symptomatic monotherapy
  • efficacious as adjunct to levodopa, mild effect
25
Q

What are neuroleptics which can be considered in neuropsychiatric toxicity?

A

quetiapine/olanzapine/clozepine

26
Q

What are features of apomorphine?

A

potent receptor agonist
S/C injection (improved dyskinesias with infusion)
nausea inhibited by domperidone pretreatment
rapid and reliable response
dyskinesias issue with intermittent injection

27
Q

What are features of duodopa?

A

delivered by PEGJ tube - bypasses stomach
improved on time, reduced dyskinesias
>50% reduction in off time, increased on time without dyskinesias in 90%
Need to have resistant motor fluctiation, no active neuropsychiatric features and no major cognitive dysfucntion, age

28
Q

What is the role of thalamic DBS?

A

drug resistant tremor, dominant limb

29
Q

What is the role of pallidal DBS?

A

dyskinesias

30
Q

What is the role of subthalamic DBS?

A

resistant fluctuations, severe off phase disability

31
Q

What are possible pathological mechanisms of parkinson’s disease?

A

Aberrant or increased alpha synuclein?

  • Alpha synuclein
  • DJ1

Impaired protein degradation

  • Parkin (PARK2)
  • UCH-L1

Energy failure - mitochondrial function or increase in ROS

  • Pink 1
  • DJ 1
32
Q

What are examples of parkinson’s plus syndromes?

A 
Multi system strophy
Progressive supranuclear palsy
Vascular, cerebrovascular disease
Alzheimer's disease
Cortico-basal degeneration
Dementia with lewy bodies
Postencephalitic parkinsonism
Post-traumatic
Toxic - Mn, MPTP, CO, Cyanide, Carbon Disulphide
Wilson's disease
FTD with parkinsonism
33
Q

What are clinical red flags for Parkinson’s plus syndromes?

A

Rate of decline - wheelchair sign
Early falls and instability, especially backwards
Early autonomic symptoms
No response to levodopa at adequate doses
Pure lower half parkinsonism - vasc, NPH etc.
Absence of tremor, jerky postural or action tremor
early marked speech and swallowing dysfunction
early cognitive dysfunction
stridor, apraxia, myoclonus, neck flexion

34
Q

What systems are involved in MSA?

A

extrapyramidal
autonomic
cerebellar
corticospinal

Glial cytoplasmic inclusions are specific to MSA

35
Q

How can MSA be differentiated from PD?

A

(25% have pure parkinsonism, with 50% levodopa response - however asymmetrical, no rest tremor)

Otherwise:

  • poor initial l-dopa response
  • autonomic failure
  • speech and bulbar dysfunction
  • early falls
  • progression (50% wheelchair at 5y)
  • preserved cognition
  • no neuropsychiatric toxicity
PLUS:
sleep apnoea 40%
stridor 30%
anterocollis 15%
myoclonus 30%
atypical response to levodopa - facial dyskinesias, no motoric response
36
Q

What is the pathology of MSA?

A

neuronal loss, gliosis
oligodendroglial cytoplasmic inclusions > neuronal cytoplasmic inclusions > intranuclear inclusions
striatonigral and olivopontocerebellar systems
spinal cord - intermediolateral colum and onuf’s nucleus

37
Q

What are the 6 classical features of progressive supranuclear palsy?

A

akinetic-rigid syndrome - bradykinesia, tremor uncommon
supranuclear gaze palsy (mandatory)
frequent falls in 1st year, postural instability
increased axial tone - neck hyperextension
pseudobulbar palsy
subcortical dementia, frontal lobe signs

38
Q

What is the pathology of PSP?

A

neuronal loss, gliosis, neurofibrillary tangles, neuropil threads, tufted astrocytes
pallido-subthalamic complex, Substantial nigra, superior colliculus, periaqueductal grey, red nucleus, pretectal areas
tau positive glial inclusions

MRI - generalised, brainstem (midbrain) atrophy

39
Q

What are features of corticobasal degeneration syndrome?

A

Parkinsonism - rigidity
Other motor - myoclonus, dystonia, pyramidal signs, bulbar dysfunction
Cortical sensory and motor features - cortical sensory loss, apraxia
Gaze palsy
Dementia - typically late, early pick’s like

Delta Med - Neurology (2 decks)

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