Parkingson's Disease Flashcards
Risk
Advancing age Male Caucasian >Asians and Africans rural living and farmers- pesticides Family history
Smoking and caffeine
Increased in life-long smokers
caffeine may be protective
Clinical syndrome comprising of?
Bradykinesia and at least one of
tremor
rigidity
postural instability
What causes it- general
basal ganglia
Lewy bodies and neuronal degeneration
asymmetry,sustained response to levodopa etc
Causes of Parkinsonism neurodegenerative conditions;
PD, Lewey body dementia. progressive supranuclear palsy, multiple system atrophy
Drug induced- dopamine antagonists (anti-psychotics, anti-emetics), sodium valproate, MPTP
Vascular
Metabolic- Wilsons disease
Clinical signs
asymmetric signs
movement disorder
Others; anosmia, REM sleep disorders- dream enactment, hypophonia, dysphagia, dystonia, constipation and urinary disturbance, autonomic disturbance, depression and dementia
Bradykinesia
Slow and small movement with less rhythm -slow gait with shuffling steps reduced facial expression and blinking reduced gesticulation small handwriting
PD gait
difficulty initiating
slowed pace, small steps
stooped
festinating, freezing
tremor
usually one hand and spreads
leg and jaw
Rigidity
lead pipe
cogwheel rigidity- ridgity plus tremor
Pathophsiology
Dopamine neurones from substantia nigra (brain stem) caudate and thalamus degenerate
Less dopamine in basal ganglia
Imaging
shows non-specific age related change
DaTscan - inject tracer that binds to dopaminergic neurones- reduced putamen neurones, expensive
Expensive, takes all day
Treatment
Increase production L-Dopa
Decrease breakdown COM and MOA
Dopamine agaonsuts: ropinerole
pramipexole
rotigotine (patch), apomorphine (s/c injections
L-dopa containing drugs - precursor of dopamine
MAOI-Inhibitors
COMT-Inhibitors
Objective of treatment
Increase dopaminergic stimulation to improve movement
Too much dopaminergic stimulation adverse effects:
Dyskinesia-abnormal movement
confusion
hallucinations
impulse control disorders
