parkinsons Flashcards

(93 cards)

1
Q

define parkinsons

A

chronic, progressive neurodegenerative conditions that occurs secondary to loss of dopaminergic neurones within substania nigra

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2
Q

what is parkinsonism?

A
  • Parkinsonism: bradykinesia and at least one of: resting tremor, rigidity, postural instability
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3
Q

who is more at risk of parkinson’s?

A

Epidemiology: 1.5x more common in men
- One of the most common neurological disorders  lifetime risk of 2.7%
- Peaks between ages of 55-65yrs and has slowly progressive onset

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4
Q

what does the basal ganglia do?

A

Physiology: basal ganglia are involved in movement  helps start and fine tune movement by motor cortex
- Functions of basal ganglia: inhibition of muscle tone, coordinated/ slow/ sustained movement, suppression of useless patterns of movement, initiation of movement

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5
Q

what causes parkinson’s?

A

Aetiology: idiopathic
- Very small proportion (2-3% of the cases) are causes by monogenic causes – single gene variant causing disease
- Majority of cases are linked to complex interaction between genetics and environment

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6
Q

when may parkinson’s present?

A

PD may not be apparent until a substantial number of neurones have been lost within substania nigra (around 50-80%)

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7
Q

what is the direct pathway within basal ganglia and what does it do?

A

Direct pathway: mostly stimulatory pathway: shorter pathway and mostly off and linked to D1 receptors
- Activation of direct leads to a series of neural connections through basal ganglia and eventually leads to initiation of movement
- dopamine that is released from substania nigra via dopaminergic neurones are able to activate the direct pathway via D1  leading to generation of movement

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8
Q

what is the indirect pathway in the basal ganglia and what does it do?

A

indirect pathway: mostly an inhib pathway – a longer and linked to D2 receptors
- activation is essential to inhib muscular tone to prevent unnecessary movement
- dopamine released from substania nigra via dopaminergic neurones are able to inhib the inhibitory pathway  generation of movement

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9
Q

how is dopamine involved within parkinson’s?

A

dopamine: acts on direct and indirect pathway to permit movement generation
- this process is finely tuned and provides coordinated movement
- PD: issue with initiation of movement

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10
Q

how may the symptoms present in PD?

A

Symptoms: unilateral symptoms at onset with gradual onset that develop into bilateral signs
- Motor symptoms
- Non motor complications: depression, dementia, sleep disturbances, autonomic dysfunction causing ill-health

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11
Q

what are the three main features of PD?

A

Classic features: bradykinesia, resting ‘pill rolling’ tremor and cogwheel rigidity

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12
Q

what shows bradykinesia?

A
  • Bradykinesia: general slowing of voluntary movements, reduced arm swing, reduction in the amplitude with repetitive movements
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13
Q

what indicates a tremor?

A
  • Tremor: can be induced by distraction, pill rolling movement:
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14
Q

describe pill rolling tremor

A

rubbing grains of sand in between finger and thumb

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15
Q

how may rigidity present?

A
  • Rigidity: increase resistance to passive movement, cogwheel due to superimposed tremor
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16
Q

apart from the classic three symptoms seen within PD, what other symptoms/ features may be seen?

A
  • Expressionless face – parkinsonian mask
  • Micrographia – small writing
  • Soft voice
  • Drooling of salvia
  • Shuffling gait – festinating gait
  • Glabellar tap:
  • Depression
  • Bowel and bowel symptoms: urgency, incontinence, constipation
  • Sleep disorder
  • Sexual dysfunction
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17
Q

what is glabellar tap?

A

repeated tapping of forehead and associated with persistent blinking

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18
Q

how is the diagnosis of PD made?

A

Diagnosis: clinical judgement made by bradykinesia and another major feature of parkinsonism
- UK parkinson’s disease society (PDS) brina bank diagnosis criteria

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19
Q

what are the 4 steps involved in the parkinson diagnosis?

A
  1. identification of features
  2. identify exclusion criteria
  3. identification supporting PD
  4. absence of red flags
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20
Q

what signs identify parkinsons?

A
  • Bradykinesia + (muscular rigidty/ postural instability/ resting tremor) - one of the three as well as bradykinesia
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21
Q

what need to be excluded within PD diagnosis?

A
  • Repeated strokes and stepwise progression
  • Head trauma – history
  • Definite encephalitis
  • Sustained remission
  • Unilateral features after 3 years
    oculogyric crisis
    antipyschotic/ dopamine depleting drugs
    other atypical neuro features
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22
Q

what is oculogyric crisis?

A

form of dystonic movement characterised by paroxysmal, conjugate and typically upward deviation of eyeball which can occur for hours to seconds  usually acute

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23
Q

what supports parkinsons - need 3 of these points?

A
  • Progressive disorder, unilateral disorder, resting tremor
  • Persistent asymmetry
  • Excellent response to levodopa
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24
Q

what neuro red flags need to be out ruled for PD diagnosis?

A
  • Rapid development of gait impairment, early bulbar dysfunction, non -progressive motor symptoms, reps dysfunction, early severe autonomic dysfunction
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25
what is parkinson plus syndrome?
group of conditions that may get mistaken for parkinsons - They affect wider area and can cause more complex disease
26
what are parkinson plus syndrome examples?
MSA dementia with Lewy Body progressive supranuclear palsy corticobasal degeneration
27
what is MSA and how is it different to parkinsons?
- MSA: mutli system atrophy – adult onset, rapidly progressive characterised by autonomic dysfunction – severe postural hypotension, urogenital dysfunction  poor response to levodopa
28
what is PSP and how is it different to PD?
- Progressive supranuclear palsy (PSP): typically presents at 50-60yrs and characterised by vertical gae, dysarthria and cognitive decline. Tremor is rare
29
what is dementia with lewy body and how does it differentiate to PD?
- Dementia with Lewy Body (DLB): early onset dementia with <1yr has Parkinson features. May have hallucinations and fluctuating consciousness
30
what is seen within corticobasal degeneration?
- Corticobasal degen (CBD): progressive dementia, parkinsonism and limb apraxia.
31
what is apaxia?
Apraxia: problems with motor planning eg unable to wave hello
32
what investigations are needed?
- Clinical diagnosis - Neuro imaging – CT/MRI to rule out others eg cerebrovascular disease - PET: with fluorodopa to help localise dopamine deficiency within basal ganglia - Striatal dopamine transporter using 123I-FP-CIT single photon emission CT – DaTscan  differentiate Parkinsonism from essential tremor
33
what are motor complications of PD?
- Motor ‘on-off’ fluctuations- switch from dyskinesia to immobility within minutes - Dyskinesia – hyperkinetic movement due to dosing of medications - Freezing of gait – can not complete movement - Wearing off phenomenon – towards end of dose - Falls
34
what are non motor complications of PD?
- Aspiration pneumonia - Nutritional deficiency, dysphagia, weight loss - Bladder, bowel and sexual dysfunction - Pressure sores, postural hypotension - Impulse control disorders and psychosis
35
describe the tremor in Parkinson's?
1. Tremor: 4-6Hz, worse at morning (at rest), asymmetrical  can be both sides but it will be worse on dominant side, pill rolling
36
describe features of bradykinesia?
- Micrographia, spidery writing - Repetitive movements go from large – small - Face: parkinson’s mask, lack of eye blinking (serpentine stare) - Gait: slow hesitant, stooped posture, inability to stop or turn, poor arm swing - Speech: initially monotonous, as PD worsens it becomes tremulous, slurring dysarthria (due to bradykinesia, tremor, rigidity)
37
describe cogwheel rigidity
3. Cogwheel rigidity: seen in those with damage in extrapyramidal damage tracts no matter what pressure/ velocity it will not give way
38
name some conditions that can have parkinsonism?
dementia with lewy body, wilsons – build up of copper (can go into basal ganglia) drug induced parkinson plus syndromes
39
what drugs can cause parkinsonism?
- Drug induced: dopamine antagonists (anti-psychotics, metoclopramide, MPTP)
40
describe the parkinson plus syndromes
- Parkinson plus: MSA (Parkinson features + autonomic dysfunction + ataxia), PSP (slow movements + Parkinson + cant look up with eyes)
41
what features would you assess for parkinson's?
1. Observe: face, tremor (ask them to close eyes and count back) 2. Assess upper tone: demonstrate cogwheel rigidity, kinnier Wilson  distract them and lift one arm and then test tone on another 3. Repetitive hand movements: writhing, glabellar tap (tap forehead eventually you would stop blinking but in PD keep blinking) 4. Speech, get them to stand up, assess gait and turning 5. Retropulsion and anteropulsion: pulling on shoulders and they would fall in that direction
42
what is wilsons disease?
disorder of cu metabolism
43
what is low cauroplasm?
gh urinary copper and low serum copper
44
what can copper deposition do?
- Copper deposition: basal ganglia disease, liver cirrhosis, kaiser-fleischer rings, kidney disease, low IQ, cardiomyopathy
45
how would copper deposition cardiomyopathy present on an ECG?
ST segment depression T wave inversion
46
how do you treat wilsons disease?
penicillamine (copper chelating agent)
47
name some tremor differentials?
- Anxiety - Hyperthyroidism - Drugs eg B2 agonists - Cerebellar disease (intentional)  stroke, alcoholism, B12 deficient. Seen on finger to nose test - Essential tremor
48
describe an essential tremor?
- 5-8Hz - Tremor occurs when trying to adopt a posture - Shaking occasionally at rest on intention - Typically worse on upper limbs
49
what can make an essential tremor worse?
caffeine, poor sleep, stress/ anxiety
50
what can make an essential tremor improved?
alcohol
51
how can manage essential tremor?
: sleep and stress controls. Beta adrenergic antagonists  propranolol, primidone, topiramate.
52
what is chorea?
dance like (choreography)  rhythmical, non purposeful movements
53
what conditions can cause chorea?
- Basal ganglia lesion, huntingtons, sydenham’s (rheumatic fever caused by strep A), benign hereditary chorea
54
what drugs can cause chorea?
- Drug causes: levodopa, phenytoin, alcohol, oral contraceptive
55
what is athetosis?
slow moving, typically in fingers
56
what can cause athetosis?
- Causes: damage to basal ganglia (ischaemia, athetoid cerebral palsy – due to kernicterus, excess bilirubin, associated with dystonia’s)
57
what is hemiballismus?
: violent, contouring, continuous movements – usually rotational - Unilateral
58
what can cause hemiballismus?
- Secondary to infarction/ haemorrhage of contralateral subthalamic nucleus - Eg left sided stroke would cause this on right side
59
what is myoclonus?
violent, sudden jerks of single or groups of muscles
60
what can cause myoclonus?
- Causes: nocturnal, paramyoclonus multiplex
61
what is seen in neuroleptic complications?
akathisia acute dystonia chronic traditive dyskinesia
62
what is akathisia?
restless, repetitive and irresistible to move
63
what is acute dystonia?
acute muscle contractions, spasmodic torticollis (neck), trismus (in mouth), oculogyric crisis (dystonia of the eyes)
64
how is neuroleptic complications get resolved?
IV anti-muscarinics
65
what is chronic tarditive dyskinesia?
mouthing and lip smacking, grimaces, eye blinking  seen after several months of anti-psychotics
66
what drugs can cause neuroleptic complications?
anti-psychotics and some anti-emetics
67
what are tics?
idiosyncratic movements of face, neck or hands which are part of normal motor gestures
68
what can be seen as simple tics?
- Simple tics: sniffing, facial grimaces are common in childhood and may resolve
69
what is gilles de la tourettes syndrome?
multiple tics (motor and speech) - Associated with behavioural problems eg ADHD or OCD - Childhood and adolescence, more common in males - Lifelong
70
what is dystonia?
prolonged muscular contraction eg spasm
71
what are causes of dystonia?
- Causes: primary torsion dystonia, dopamine responsive dystonia,
72
what drugs can induce dystonia?
- Drug induced: metoclopramide, prochlorperazine, anti-psychotics
73
how can you distinguish between asterixis and tremor?
Asterixis: can be distinguished from tremor on the basis of prolonged absence of EMG activity during flapping  seen in hypercapnia, encephalitis
74
what signs are seen in Multi system atrophy - MSA?
autonomic dysfunction cerebellar dysfunction
75
what is seen with dementia LB?
parkinsons hallucinations, delusions REM sleep disorder fluctuating consciousness
76
what can be seen in PSP?
balance issues, mobility, frequent falls change in behaviour
77
what is PSP?
progressive supranuclear palsy
78
what is CBD?
corticbasal degeneration
79
what signs are seen in CBD?
problems recalling words, aphasia, short term memory loss
80
why is levodopa prescribed with peripheral decarboxylase inhib?
helps dopamine go in
81
what is COMT inhib?
carbidopa-levodopa
82
give an example of COMT inhib?
entacapone
83
what is the MOA of COMT inhib?
prevents dopamine breakdown
84
give an example of a dopamine agonist?
rotigotine
85
what is the risk in using dopamine agonists?
pulmonary fibrosis impulse issues
86
what can be seen within impulse issues with dopamine agonists?
addiction - internet, sex, shopping
87
give examples of monoamine oxidase-B inhib?
selegiline rasagiline
88
what is the moa of monoamine oxidase B inhib?
prevents dopmaine breakdown
89
what are the mian side effects of levodopa?
dyskinesia - excessive motor activity from too much dopamine
90
what signs are seen in dyskinesia?
dystonia, chorea, athetosis
91
what is athetosis?
writhing/ twisting of wrists
92
what can be prescribed to help in dyskinesia from excess levadopa?
amantadine
93