Parkinsons Flashcards
tremors worse on movement
essential drug induced hyperthyroid dystonic exaggerated physiological tremor
tremors worse at rest
Parkinson’s
inattention tremor
cerebellar
main symptoms of PD
resting tremor
bradykinesia
rigidity
postural and gait instability
clinical features of PD
quiet voice small hand writing stooped posture reduced or absent arm swing when walking freezing of gait shuffling gait fatigue REM sleeping pattern, act out dreams - strong predictor of developing PD change of sense of smell and taste lack of facial expression
later on in progression: postural hypotension - meds visual hallucinations constipation depression and anxiety saliva drooling - impaired swallow causing pooling, saliva also becomes thicker pain in back memory problems
cause of PD
unclear
interaction between genes and environment initiate a process causing deterioration of the substantia nigra
loss of dopaminergic neurones and this causes loss of DA
stages of PD
1) pre-diagnosis, no overt motor symtoms
2) diagnosis/maintenance: drug treatment commenced with a good response, no motor complications
3) complex - may be development of dyskinesias, unpredictable on/off motor problems and neuropsychiatric issues such as cognitive impairment and psychosis
4) palliative - poor drug response and the development of PD dementia predominate. Motor symptoms are eclipsed by multiple complications. Swallowing can be impaired. Discussions about end of life care, PEG if appropriate. Cognitive impairment and dementia are common in advanced in PD
management of PD
can’t cure, aim to control symptoms and treat thing such as constipation and depression
Levodopa - precursor of dopamine (dopamine can’t cross the BBB), increases levels of dopamine in the brain often given with carbidopa to prolong its half-life and increase efficiency
SE: efficiency decreases over time, postural hypotension, nausea/GI upset, dyskinesias psychosis, compulsive behaviours
response to levodopa makes diagnosis of idiopathic PD much stronger
Dopamine agonists: pramipexole and ropinirole
useful in younger patients that you down want to start L-dopa yet due to its decreased efficiency over time
fewer side effects than L-DOPA: nausea, hallucinations, drowsiness
MAO-B inhibitors: selegilene
inhibits MAO-B selectively
MAO-B metabolises dopamine
so helps increase level of dopamine in the brain
used widely with L-DOPA and helps reduce the dose of L-DOPA needed, in turn this reduces the SE and increases the long term effectiveness of L-DOPA
SE: postural hypotension, AF
main features of idiopathic PD
asymmetry of clinical signs
tremor and bradykinesia
management: levodopa or dopamine
diagnosis of PD
refer to specialist for assessment untreated (once drug treatment is commenced this changes clinical signs and diagnosis can be more challenging)
Bradykinesia and at least one of the following:
rigidity,
resting tremor
postural instability
three of more required for diagnosis definite of PD: unilateral onset resting tremor progressive disorder asymmetry affecting side of onset most excellent response to levodopa severe levodopa induced chorea clinical course for over ten years
key priorities for newly diagnosed patients
referral to expert
diagnosis and expert review
regular access to specialist nursing care
assess to physiotherapy for gait re-education, improvement of balance and flexibility etc.
access to OT for work, home, care and leisure activities and improvement of personal self-care activities such as eating and drinking
access to speech and language therapy
key features of dementia with lewy bodies
triad of dementia, Parkinsonism and visual hallucinations
fluctuations in alertness
key features of vascular Parkinsonism
predominant lower body sings
tremor less common
rigidity especially lower limbs and lack of facial expression
drug induced Parkinsonism
history of Dopamine blocking drugs e.g. antipsychotics, metoclopramide
symmetrical rigidity and lack of facial expression
