Parkinsonism and parkinsons disease Flashcards

1
Q

CST/pyramidal tract leads to what kind of features

A

UMN - pyramidal weakness, spasticity

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2
Q

basal ganglia leads to what kind of symptoms [extra pyramidal]

A

hyperkinetic - dystonia, tics, myoclonus, chorea, tremor

hypokinetic - parkinsonism, parkinsons disease

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3
Q

cerebellum leads to what kind of symptoms

A

nystagmus
ataxia
intention tremor

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4
Q

what is the parkinsonian syndrome

A

rigidity, akinesia/bradykinesia and resting tremor

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5
Q

what is dystonia

A

prolonged muscle spasms and abnormal posture

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6
Q

what is chorea - ballismus

A

fragments of movements flow irregularly form one body segment to another causing a dance like appearance
ballismus: if amplitude of these movements is large

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7
Q

what motor symptoms does PD present with

A

tremor, muscle rigidity, akinesia, rest tremor and gait and postural impairment

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8
Q

what are motor features in PD divided into

what does a certain course have on the prognosis

A

tremor dominant - with relative absence of other motor symptoms

non-tremor dom - such as akinetic - rigid syndrome and postural instability gait disorder

mixed

tremor dom - slower rate of progression and less functional disability

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9
Q

clinical non motor features of PD

when are they common and what are they associated with

A

olfactory dysfunction, cognitive impairment, psychiatric symptoms, sleep disorders, autonomic dysfunction, pain and fatigue

common in early PD and before the onset of motor features and assoc with reduced health related quality of life

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10
Q
when is PD usually diagnosed 
how long can non motor symptoms be present before motor onset 
how is progression of PD worsened
what is the honeymoon phase 
advanced stages characterised by what 
late stage PD
A

with the onset of motor symptoms

more than a decade

worsening of motor features

initially ^ responds to symptomatic therapies (honeymoon phase)

emergence of complications of long term symptomatic treatment

resistent motor and non motor features, postural instability, freezing of gait, falls, dysphagia, speech dysfunction

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11
Q

after 17 years of disease what happens

after 20 years

A

80% have gait freezing and falls, 50% report choking

dementia occurs in 83% of patients

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12
Q

what is rapid eye movement sleep behaviour

A

abnormal or disruptive behaviour which occur during rapid eye movement sleep and are often related to dream enactment

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13
Q

how is rapid eye movement disorder diagnosed

A

overnight polysomnography to document REM sleep without atone and to rule out mimics such as obstructive sleep apnoea, seizures

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14
Q

what is the treatment for rapid eye movement disorder

A

clonazepam or melatonin at bedtime

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15
Q

PD with RBD (rapid eye movement sleep behaviour disorder) has a disease subtype of what

A

characterised by more severe autonomic dysfunction, gait impairment and dementia

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16
Q

what do individual with isolated RBD have

A

increase risk f developing a neurodegenerative condition

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17
Q

in parkinsons disease what do sections through the brainstem show
pigment loss correlates
what is a neurohistological hallmark of PD

A

loss of normal dark black pigment in the substantia nigra and locus coeruleus

with dopaminergic cell loss

Lewy bodies

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18
Q

M:F ratio of risk for PD
other risk factor
what does early onset dictate

A

M: F 3:2
age greatest risk factor
<40 - genetic cause likely

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19
Q

what do symptomatic treatments do

A

enhance intracerebral dopamine concentrations or stimulate dopamine receptors

20
Q

give symptomatic drugs

A

levodopa
dopamine agonists
monoamine oxydase type B inhibitors
amantadine

21
Q

when is treatment initiated in PD

A

when symptoms cause disability or discomfort aiming to improve function and QOL

22
Q

what responds to treatment early in the disease

A

bradykinesia and rigidity

23
Q

what are MAO B inhibitors for

whats needed for more severe symptoms

A

only moderately effective

levodopa and dopamine agonists

24
Q

how does tremor respond to treatment

A

inconsistently responsive esp in lower doses to dopamine replacement therapy
anticholinergics, trihexyphenidyl or clopazine can be effective for tremor

25
Q

SE of dopamine agonists and levodopa

A

nausea, daytime somnolence and oedema

26
Q

SE of dopamine agonists

A

impulse control disorders such as pathaoligcal gambling, hyper sexuality binge eating compulsive spending

27
Q

who should dopamine agonists be avoided in

A

history of addiction
OCD
impulsive personality
elderly with cognitive impairment as it can be associated with hallucinations

28
Q

SE of levodopa

A

long term use is associated with motor complications such dyskinesia and motor fluctuations

29
Q

give the 4 long term complications of dopaminergic therapy for PD

A

motor fluctuations
non motor fluctuations
dyskinesia - involuntary choreiform or dystonic movements
drug induced psychosis - hallucinations, illusions, delusions

30
Q

pharma stuffs to reduce dopamine fluctuations

A

add a dopamine agonist
add a MAO B inhibitor
add a COMT inhibitor

31
Q

other ways of managing the long term complications of dopaminergic therapies

A

stable levodopa - carbidopa gel
sub cut infusion of apomorphine
non - dopaminergic treatments such as amantadine and clozapine

32
Q

how is psychosis in PD managed

A

with clozapine

alternat quetiapine

33
Q

visual hallucinations and delusions in PD patients with dementia

A

rivastigmine

34
Q

depression assoc with PD

A

treated with anti depressants

35
Q

the clinical syndrome of parkinsonism - motor symptoms

A

bradykinesia
rest tremor
rigidity
postural and gait impairment

36
Q

what is bradykinesia

how can it be assessed

A

slowness of movement with progressive loss of amplitude or speed during attempted rapid alternating movement of body segments - hypomimia, hyophonia, micographia

asking the px to perform some repetitive movements as quickly and as widely as possible or global assessment to spontaneous movements

37
Q

resting tremor is what
when does it vanish and reappear
frequency
hand tremor and PD

A

involuntary
active moment and reappears after a few sec when arms held outstretched
3-6Hx
hand tremor not typical for PD

38
Q

rigidity is what
how to distinguish rigidity from spasticity owing to UMN lesion
rigidity and resting tremor leads to what
positive froments test is what

A

increased muscle tone

no increase with higher mobilising speed

cog wheel rigidity

rigidity increases in examined body segment by voluntary movement of other body parts

39
Q

describe postural and gait impairment

A
stopped posture 
slow 
shuffling steps 
decreased arm swing 
slow turning with multiple small steps 
freezing
40
Q

investigations for PD

A

rule out hypothyroidism, anaemia
structural brain imaging
PET, DAT
positive levodopa or SC apomorphine challenge

41
Q

red flags in PD ( a lot of them)

A
symmetrical symptoms 
severe axial or lower limb involvement 
frequent falls 
fast disease progression 
eye movement disorder
tics, myoclonus, chorea
pyramidal or cerebellar dysfunction 
bulbar or psuedobulbar features
parietal associate sensory disturbances
apraxia 
severe cognitive deterioration or psychosis 
marked autonomic dysfunction
42
Q
what is vascular parkinsonism 
rest tremor?
other signs?
levodopa response 
ix
A

parkinsonism in lower limbs

rest tremor uncommon

spasticity, hemiparesis, pseudo bulbar palsy

poor levodopa response

structural brain imaging

43
Q

drug induced parkinsonism
tremor
presence of what
treatment

A

symmetrical
coarse postural tremor
orolingual dyskinesia, akathisia

gets better a few months after drug withdrawel

44
Q
essential tremor describe 
seen at rest?
genetic and onset
responds to what
hand tremor
A
symmetric, postural higher frequency up to 12 Hz
infrequently observed at rest 
autosomal dom - 15 years
alcohol responsiveness 
hand tremor is present is mild
45
Q
multi system atrophy is a common cause of what 
when 
triad of what 
signs 
levodopa response 
MRI
A

degenerative parkinsonism
60/70s

dysautonomia, cerebellar features and parkinsonism

severe dysarthria, dysphonia, marked antecollis, inspiratory sighing, orofacial dystonia

suboptimal and short-lived response in 1/3

cerebellar and pontine atrophy - hot cross bun sign

46
Q

progressive supra nuclear palsy is what
signs
leveodopa

A
symm akinetic rigid syndrome with predominant axial involvement 
gait and balance impairment 
vertical gaze supranuclear palsy
retrocollis
staring 

no respose

47
Q
FXTAS when 
genetic
symptoms 
progression 
milder in who
MRI
dx
children can have what
A

> 50

abnormal number of CGG repeats in the FMR1 gene

cerebellar gait ataxia, postural/intention tremor, parkinsonism, dysautonomia, cognitive decline, peripheral neuropathy

slow disease progression

in females often POF and menopause

MRI with T2 hyper intensities in the middle cerebellar peduncles

confirmation by molecular testing

children may have classical fragile X syndrome