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
SE of dopamine agonists and levodopa
nausea, daytime somnolence and oedema
26
SE of dopamine agonists
impulse control disorders such as pathaoligcal gambling, hyper sexuality binge eating compulsive spending
27
who should dopamine agonists be avoided in
history of addiction OCD impulsive personality elderly with cognitive impairment as it can be associated with hallucinations
28
SE of levodopa
long term use is associated with motor complications such dyskinesia and motor fluctuations
29
give the 4 long term complications of dopaminergic therapy for PD
motor fluctuations non motor fluctuations dyskinesia - involuntary choreiform or dystonic movements drug induced psychosis - hallucinations, illusions, delusions
30
pharma stuffs to reduce dopamine fluctuations
add a dopamine agonist add a MAO B inhibitor add a COMT inhibitor
31
other ways of managing the long term complications of dopaminergic therapies
stable levodopa - carbidopa gel sub cut infusion of apomorphine non - dopaminergic treatments such as amantadine and clozapine
32
how is psychosis in PD managed
with clozapine | alternat quetiapine
33
visual hallucinations and delusions in PD patients with dementia
rivastigmine
34
depression assoc with PD
treated with anti depressants
35
the clinical syndrome of parkinsonism - motor symptoms
bradykinesia rest tremor rigidity postural and gait impairment
36
what is bradykinesia | how can it be assessed
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
resting tremor is what when does it vanish and reappear frequency hand tremor and PD
involuntary active moment and reappears after a few sec when arms held outstretched 3-6Hx hand tremor not typical for PD
38
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
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
describe postural and gait impairment
``` stopped posture slow shuffling steps decreased arm swing slow turning with multiple small steps freezing ```
40
investigations for PD
rule out hypothyroidism, anaemia structural brain imaging PET, DAT positive levodopa or SC apomorphine challenge
41
red flags in PD ( a lot of them)
``` 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
``` what is vascular parkinsonism rest tremor? other signs? levodopa response ix ```
parkinsonism in lower limbs rest tremor uncommon spasticity, hemiparesis, pseudo bulbar palsy poor levodopa response structural brain imaging
43
drug induced parkinsonism tremor presence of what treatment
symmetrical coarse postural tremor orolingual dyskinesia, akathisia gets better a few months after drug withdrawel
44
``` essential tremor describe seen at rest? genetic and onset responds to what hand tremor ```
``` 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
``` multi system atrophy is a common cause of what when triad of what signs levodopa response MRI ```
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
progressive supra nuclear palsy is what signs leveodopa
``` symm akinetic rigid syndrome with predominant axial involvement gait and balance impairment vertical gaze supranuclear palsy retrocollis staring ``` no respose
47
``` FXTAS when genetic symptoms progression milder in who MRI dx children can have what ```
>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