10: Movement Disorders- Dodge Flashcards
rhythmic, oscillating movement of body part
tremor
clumsiness, instability, imbalance or lack or coordination with voluntary movements
ataxia
movements appear disjointed, unsteady giat, falls
involuntary muscle spasms
dystonia
can be generalized or focal (writer’s cramp, torticollis)
repetitive, purposeless, involuntary movements
tardive dyskinesia
grmacing, lip-smaking, rapid arm/leg movements
prolonged exposure to antipsychotics, neuroleptics
impaired ability of rapid alternating movements
dysdiadochokinesia
non-repetitive jerking movements of limbs, face or truk
chorea
most common tremor disorder
essential tremor : involuntary rhythmic, oscillatory movements
kinetic (tremor with movement of body part) or postural (tremor when body part held against gravity)
risk factors for essential tremor
lead, beta-carboline alkaloids
D3 receptor gene variant possibly associated with familial essential tremor
diagnosis of essential tremor
rule out other disorders that may mimic essential tremor
check thyroid function, ceruloplasmin (to exclude Wilson’s disease especially in pt less than 40 yo)
if caused by disease process… NOT an essential tremor
DD for tremor
hyperthyroidism PD Enhanced physiologic tremor Wilson's Disease (dysfunction of copper with deposition) Medications
what medications might cause a tremor?
amiodarone
beta agonists
lithium
theophylline (Asthmatics)
treatment for tremor (symptom management)
***propranolol (beta blocker)
primidone (GABA effect)
Todd’s syndrome (alice in wonderland syndrome)
characterized by migraines in children that cause micro/macropsia, teleopsia (far away), pelopsia (close)
pathophysiology of PD
loss of dopaminergic neurons in sunstantia nigra
neurons die and degenerate
imbalance in DA:Ach in striatum –> improper signalling pathway for cortical motor commands
possibly related to alpha-synuclein; defective degradation leads to increased alpha-synuclein in nigrostriatal neurons
what is MPTP?
precursor to MPP+ (neurotoxin that destroys dopaminergic receptors in substantia nigra)
*** 4 cardinal signs of PD
- bradykinesia
- resting tremor 4-6 Hz
- Cogwheel rigidity
- postural instability
combination medication =
sinemet
levodopa (crosses the BBB to act as dopa precursor) + carbidopa (inhibits the peripheral degradation of levodopa by inhibiting dopa decarboxylation)
most effective medication for PD
levodopa/carbidopa
- does not stop progression
- on/off
- motor complications (dyskinesia, choreoathetotic, dystonic)
- does not stop freezing, instability, autonomic dysfunction
- high prtn diets can effect absorption
dopamine agonists
first gen
- bromocriptine
second gen
- ropinirole
- pramipexole
- rotigotine
advantages and disadvantages of dopamine agonists
- good monotherapy early PD, not a long term monotherapy
- no interference with diet prtn or aa
- less motor complications, possibly protective
- does no stop progression
- does not stop freezing, instability, autonomic dysfunction
MAO-B inhibitors
selegiline
rasaligine
inhibit dopamine metabolism in brain
anticholinergics
triheyphendiyl
benztropine
when dopamine decreases, cholinergic effects predominate
used for tremor
adverse effects - dry mouth, urinary retention, altered mental status
COMT inhibitors
entacapone
tolcapone
increases duration of levodopa by inhibiting metabolism of levodopa by COMT
NOT monotherapy - adjunctive with levodopa/carbidopa to decrease wearing off
hepatotoxic (tolcapone)
antiviral agents
amantadine
unknown MOA
surgical options
ablation - thalamotomy, pallidotomy
deep brain stimualtion - placed with sterotactic approach with MRI or CT
restorative - fetal human/porcine nigral transplant
