neuro - parkinsonism Flashcards
lesion in what structure causes movement disorders?
basal ganglia
lesion in basal ganglia can cause either:
(1) dyskinesia (ie. too much movement)
or (2) akinesia/bradykinesia (eg. parkinsonism)
other than a lesion in the basal ganglia, what else may cause movement disorders?
changes in the neurotransmitters regulating the basal ganglia (especially dopamine!)
what issues with regards to dopamine can result in parkinsonism?
- dopamine deficiency
- degeneration of dopaminergic neurons
- decrease in dopamine receptor sensitivity
- imbalance of dopamine and acetylcholine
what is regulated by the basal ganglia?
- regulation of movement quantity
- learning
- emotion
what is parkinsonism?
a clinical syndrome that is characterised by:
(1) resting tremors (tremours subside with voluntary movements, and worsen with stress)
(2) lead-pipe rigidity (rigid all the time)
(3) bradykinesia (immobility)
what are some clinical presentations of bradykinesia in parkinsonism?
- postural instability! (Parkinson gait - shuffling gait with quickened and shortened steps)
- hypophonia (softer speech)
- hypomimia (slower blinking)
- decremental bradykinesia in the arm (worsens over time)
- decreased arm swinging when walking
- slower movements in general (eg. finger tapping, opening&closing of fists)
is parkinsonism the same as Parkinson’s disease?
No!
parkinsonism is a clinical syndrome.
(idiopathic) Parkinson’s disease is a CAUSE of parkinsonism.
what are the later-stage clinical presentations of Parkinson’s disease?
- autonomic dysfunction, constipation, pain
- sleep disturbances, fatigue
- mild cognitive abnormalities, dementia, depression
- increased fall risk
what is idiopathic Parkinson’s disease?
a progressive movement disorder marked by degeneration of dopamine-producing neurons of the substatia nigra
what are some causes of parkinsonism?
- idiopathic Parkinson’s disease
- wilson disease
- neuroleptic drugs (due to extrapyramidal side effect when blocks dopamine binding to D2 receptors; including: antipsychotics like risperidone, and antiemetics/anti-nausea like metoclopramide)
- infective encephalitis
- vascular parkinsonism
- parkinson-plus syndrome
what is the treatment of Parkinson’s disease?
main treatment: L-DOPA + carbidopa
also can add anticholinergics (eg. benztropine) to reuce involuntary muscle movements
why can is levodopa (L-DOPA) used instead of just dopamine?
DOPA cannot be used directly as the molecules are too large to cross the BBB
what must be added on to L-DOPA? why?
carbidopa
carbidopa inhibits DOPA decarboxylase
it also prevents the conversion of L-DOPA into DOPA in the peripheries, as carbidopa is too large to cross BBB
what are some consequences of long-term L-DOPA use?
- diminishing efficacy
- side effects ( nausea, daytime sleepiness, hallucinations/psychosis)
in view of the adverse effects of prolonged L-DOPA treatment, what is the prescription standard for young patients with Parkinson’s?
- first: prescribe dopamine agonists (eg. pramipexole)
- if needed: L-DOPA