Flashcards in 27. Extrapyramidal Disease CPC Deck (51)
how much dopamine production must be lost for pts to develop signs of Parkinsonism?
what are the components of the basal ganglia?
-striatum (caudate and putamen)
-Globus Pallidus (interna and externa)
what is a good site for DBS in parkinson's disease?
term for: Quick (“dance-like”) movements that are rapid, jerky and irregular, usually affecting muscles of the face orobuccal cavity and limbs.
Involuntary slow writhing (“worm-like”) movements flowing from one to the next, sometimes associated with chorea
a twisting movement, usually of the neck or trunk
includes a throwing or flinging movement, usually of one side, where it is called a hemibalism.
fleeting purposeless movement, however they tend to be repetitive and stereotyped, as opposed to chorea, which is random.
hyperkinesia that can come in different speeds (fast versus slow) and can be exaggerated in different positions or actions.
the opposite of dyskinesia. consists of a slowing of movement. This can manifest as slowed postural corrections to being thrown off balance or decreased facial expressiveness. It can include a type of stiffness, called rigidity, which is different than spasticity since it produces smooth resistance to passive movement. can also affect initiation of movement and patients can “get stuck”.
Decreased facial expressiveness. Is a bradykinesia of facial muscles
Increase in resting muscle tone. In parkinsonism it is consistent throughout the range of motion, unlike the “clasp-knife” effect of spasticity. When rigidity and tremor are both present “cogwheeling” results.
what are some drugs that can cause Parkinson's like symptoms?
a flinging movement of one side of the body that would result from a small stroke in the contralateral subthalamic nucleus.
most common causes of choreoathetosis?
what is the genetic pattern of Huntington's?
autosomal dominant, with complete penetrance (50% of offspring)
what does genetic anticipation mean?
the number of CAG repeats can go from 36 to 40 in a generation and the patient may be the first person who is symptomatic
how many CAG repeats will result in Huntington/s?
Clinical triad of huntington's?
chorea, dementia, behavior change (may result in problems with the law)
what drug will make Huntington's wlrse?
levodopa (given for Park)
what are some drug treatments for Huntington's?
neuroleptics, which block dopamine. (haloperidol, perphenazine)
what is the problem with chronic use of neuroleptics?
they can sensitize the system, and over time can have a reverse effect --> tardive dyskinesia
what do dopamine-depleting drugs cause, and should we use them to treat Huntington's?
cause severe depression: we shouldn't use them.
essential tremor: does it run in families? what is the age of onset?
yes. age of onset is 25-55 yrs.
how bad can essential tremor get?
tends to get worse with time: sometimes will get so bad it's hard to function.
does essential tremor tend to be unilateral or bilateral?
parkinson's is unilateral
what is affected the most with essential tremor?
upper limbs, head, voice.
what is something that we wouldn't necessarily recommend but that can help essential tremor?
what anti-epilepsy drug is NOT effective for essential tremor?
valproate: has tremor as a side effect