Parkinson's disease Flashcards
how is a clinical diagnosis of idiopathic parkinson’s disease made?
- using the Brain Bank criteria, and is based on:
- bradykinesia-slowness of voluntary movements, and reduced automatic movements, also seen as as progressive reduction in amplitude of repetitive movements
- muscular rigidity (lead pipe, cog wheel)
- resting tremor, low velocity, ‘pill rolling’, abolished by movement
- postural instability
- gait abnormality-forward flexed shuffling gait with reduced arm swing, and turning en-bloc-part. associated with falls
symptoms classically asymmetrical at presentation, but progress to involve both sides of the body, with side of onset characteristically affected worse
examples of rating scales used in parkinson’s disease assessment?
- Hoehn and Yahr
- UPDRS-unified parkinson’s disease rating scale-objectively rate motor symptoms
examples of parkinsonian plus syndromes?
- progressive supranuclear palsy (PSP)
- multi system atrophy (MSA)
- corticobasal degeneration (CBD)
- vascular (arteriosclerotic)
what is a glabellar tap?
this is a primitive reflex where the eyes shut if person tapped lightly between the eyebrows, but may normally be overcome rapidly so pt soon fails to blink
however, in some pts reflex cannot be overcome e.g. in parkinson’s
how does the tremor of idiopathic parkinson’s differ from that of benign essential tremor?
essential tremor: tremor is there all the time, not just at rest
bilateral tremor, usually affects both upper limbs
postural tremor-worse when arms are outstretched
improved by alcohol and rest
most common cause of head tremor (titubation)
essential tremor=autosomal dominant condition
management of essential tremor?
propranolol 1st line
primidone
causes of drug-induced parkinsonism?
drugs which block dopamine receptors or reduce the storage of dopamine:
prochlorperazine-typical antipsychotic, also used for N+V and labyrinthine disorders e.g. acute attacks of menieres disease-tinnitus, fluctuating SN deafness and episodic vertigo lasting mins-hrs
other 1st generation antipsychotics e.g. haloperidol
metoclopramide
px classically bilateral and rapid onset of motor symptoms, with rigidity and rest tremor uncommon
causes of parkinsonism (classic triad of bradykinesia, rigidity and resting tremor)?
- idiopathic parkinson’s disease
- parkinson’s plus syndromes
- multiple cerebral infarcts
- post-encephalitis
- wilson’s disease
- drug-induced
- toxin-induced e.g. MPTP, manganese, Cu (Wilson’s)
- trauma (pugilistic encephalopathy)
peak age of parkinson’s disease onset?
55-65yrs
how might the resting tremor of parkinsons be made more apparent?
asking pt to concentrate on something
how can the rigidity of parkinson’s be made more apparent?
get the pt to perform an action in the opposite limb e.g. moving arm up and down then drawing a circle
=contralateral synkinesis
what is the most likely diagnosis if a pt has parkinsonism worse in the leg than arms with a prominent gait abnormality and pyramidal signs?
vascular parkinsonism
non-motor symptoms of parkinson’s?
hyposmia or anosmia-may be present for many years before onset of motor symptoms depression dementia visual hallucinations mild urinary frequency and urgency dribbling saliva REM behavioural sleep disorder
LT problems in parkinson’s patients following L-DOPA treatment for around 5-10 years?
motor fluctuations:
-on-off fluctuations-rapid and unpredicatable fluctuations between on and off periods, and wearing off of the treatment before next dose is due (end of dose fading)
-dyskinesias during ‘on’ phase
-axial problems not respond to tment:
balance, speech and gait disturbance that don’t respond to tment, problems thought to be related to axonal degeneration outside SN where dopamine not the NT, can try and help with physio, OT and SALT
parkinson’s disease dementia:
-dementia occurring more than 1 yr after PD diagnosis.
where in the nervous system in the problem in parkinson’s disease?
basal ganglia: substantia nigra pars compacta-degeneration of dopaminergic neurones causing reduction of dopamine in the striatum, lewy bodies (alpha synuclein proteins) also form here.
typical features of parkinson’s disease dementia?
limb parkinsonism
visual hallucinations
frequent fluctuations in lucidity
can tx some of symptoms with antypical antipsychotics e.g. quetiapine, which are effective at reducing symptoms whilst not worsening the features of parkinson’s disease.
complications of parkinson’s disease?
falls aspiration pneumonia poor nutrition bed sores infections contractures bowel and bladder disorders pain-dystonia, akathisia, primary and central neuropathic pain
parkinson’s disease prognosis?
variable
some patients follow relatively benign course, others develop severe disability more quickly
younger age of onset tend to have shorter life spans
slowly progressive disease with mean duration of 15 years.
driving advice in parkinson’s?
pt should inform DVLA of diagnosis and insurers
investigations necessary before treatment with non-ergot derived dopamine agonist (although rarely used now)?
ESR
renal function
CXR
non-ergot derived e.g. cabergoline assoc. with risk of fibrotic reactions
how can dyskinesias assoc. with LT L-DOPA treatment be managed?
if occurring at peak dose try to reduce each dose of L-DOPA but make it more frequent so total daily dose remains the same
add on LA dopamine agonist
may try slow release or liquid L-DOPA
surgery may be needed
if happen at beginning or end of dose ca try soluble L-DOPA before meals, or add a COMT inhibitor.
what is acute akinesia?
also known as parkinson’s crisis
this is a rare but life-threatening complication of the disease with a sudden worsening of motor symptoms and severe akinesia
can be triggered by infection, GI disease, changes in treatment and surgery
often needs hosp admission
why must patients be warned about driving and operating machinery if taking a dopamine agonist e.g. ropinerole, or rotigotine patch?
patients can fall asleep suddenly so must be wary of feeling drowsy and being unsafe to drive
most common psychiatric problem in patient with PD?
depression
when does PD become clinically apparent?
not until more than 50% of dopaminergic cell activity in the substantia nigra has been lost
risk associated with abrupt withdrawal of levodopa treatment?
neuroleptic malignant syndrome:
characterised by muscualar rigidity, pyrexia, altered mental status, autonomic dysfunction-pallor, tachcardia, fluctuating BP, tremor, incontinence, excessive sweating/salivation.
results of investigations for neuroleptic malignant syndrome?
- FBC-often leukocytosis
- U+Es-maybe AKI, acidosis
- ABG
- clotting studies
- urine-myoglobinuria, drugs
- low Ca2+
- LFTs-raised transaminases
- raised LDH
- CK-raised
- CXR, cultures if suspect sepsis
- CT/MRI
- LP-raised protein, may be indicated to rule out differentials e.g. meningitis-pyrexia, altered mental status
management of neuroleptic malignant syndrome?
- A to E assessment, protect airway, may need ventilation and circulatory support
- IV fluids-rehydration
- reduce temperature-antipyretics, cooling devices
- reduce agitation-IV BZDs
- alkalinisation of urine and dialysis often needed if rhabdomyolysis and AKI
causes of mortality in neuroleptic malignant syndrome?
- respiratory failure
- cardiac arrhythmias
- CVS collapse
- AKI
- DIC
