L5 Parkinson's disease and atypical Parkinsonism Flashcards
what is hypokinetic, hyperkinetic
hypo - too little movement
hyper - too much movement
what are features of parkinsonism
akinesia
rigidity
tremor
postural abnormality
what is the lifetime risk of PD
what % of cases start below 40
1 in 40
5%
what are early non motor features of PD
olfactory loss, REM sleep behaviour disturbance
constipation
what is the core feature of PD and what does it encompass
akinesia
encompasses bradykinesia (slowness of movement), poverty of movement, progressive fatiguing and decrement of repetitive movement difficulty with initiating movement
what is the Hz range of a tremor
3-6 Hz tremor in hands
sometimes 6-10 Hz postural tremor
what does early postural insatbility suggest
atypical parkinsonian condition
what pathology is affected in PD
- loss of dopaminergic neurons from the substantia nigra
- accompanied by presence of Lewy bodies - intracytoplasmic eosinophilic inclusion bodies - which stain with antibody to alpha-synuclein
what is the treatment of PD
- symptomatic
- medical treatment aims to increase the amount of dopaminergic transmission in the brain
- surgical treatment aims to improve the disordered messages from the diseased basal ganglia
how is levodopa given and why?
given together with a peripheral dopa-decarboxylase inhibitor, enzyme so
stops the breakdown of levodopa in the periphery. helps to prevent side effects such as nausea, increases central availability
what is levodope+benserazide =
levadopa+carbidopa =
=co-beneldopa (Madopar)
co-careldopa (Sinemet)
what is a side effect of levodopa
long term use associated with development of dyskinesias anf fluctuations
what are dopamine agonists give examples
drugs that directly stimulate dopamine receptors
bromocriptine, pergolide, cabergoline, roprinirole, pramipeoxle (oral), apomorphine (subcutaneous)
what are side effects of dopamine agonists
hallucinations, nausea, faintness, sleepiness
what are other drugs used in PD
MAO-B inhibitors : selegiline, rasagiline
COMT inhibitors: entacapone, opicapone
amantadine (reduces dyskinesia)
anticholinergics (sometimes used for tremors but too many side effects
what has replaced surgical operation in pd
stimulation of subthalamic nucleus
what causes drug induced parkinsonism, and what drugs were used where
- caused by dopamine blocking or depleting drugs
- neuroleptic drugs used in psychiatric practice and anti emetic drugs such as metoclopramide are common offenders
- effects reversible
how is toxic parkinsonism MPTP caused and what does it do in primates
used by drug abusers
in primates selectively kills nigral neurons (used to create an animal model of parkinsonism but without lewy )
what is post-encephalitic parkinsonism
- Von Economo’s disease
- occurred as a pandemic of post infectious parkinsonism in the 1920s
- features are hypersomnolence and psyhciatric disturbance, followed by parkinsonism
- infective agent not been identified
what is vascular pseudo-parkinsonism
- blocks blood vessels
- patients with small vessel cerebrovascular disease
- lower body
- no rest tremor or upper limb akinesia
- marche a petit pas, wide-based gait, freezing
- Dementia, UMN signs, postural instability common
what happens in progressive supranuclear palsy
- supranuclear vertical gaze palsy (atrophy of midbrain)
- early falls
- bulbar failure (problems with speech and swallowing in brainstem)
- axial rigidity
- pyramidal signs
multiple system atrophy
MSA-P/MSA-C
parkinsonism, poorly levodopa responsive, for a cerebellar syndrome PLUS autonomic failure:
urinary incontinence
erectile dysfunction
postural hypotension (bp not maintained when standing up)
striatonigral degeneration, sporadic olivopontocerebellar atrophy, Shy-Drager syndrome
what happens in Dementia with lewy bodies (initial symptoms)
symptoms - executive function, attention, visuospatial disorder
-parkinsonism, visual hallucinations, REM sleep behaviour disorder, sensitivity to neuroleptics
