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Flashcards in neuro disorders Deck (18):

Degenerative disorders

alzheier's disease
multiple sclerosis
amyotrophic lateral sclerosis


char of degenerative disorders (neuro)

progressive decline over decades (not solely d/t age

-fewer are rapid (months or years)


dementia is a...
where does dementia present in r/t what

l/o neural fx
presents in varying unrelated disorders


alzheimers disease (AD)

type of dementia (64% of all dementia)
progressive and irreversible
incidence inc w age (>65))

inc 2x with every 5yrs from 65-75 the incidence is 10-15%, >85 48%


etiology of AD

~90% idiopathic (sporadic form)
apolipoprotein E gene? (implicated but unsure how)
~10% familial (genetic)


what is APP how is it involved in AD
chr 21

amyloid precursor protein gee. in type 2 DM when amyloid deposits it indicates damage

PS1-pre senelin 1 and 2

chr 21-if Downs pts lived long enough theyd likely dev AD


patho of AD

atrophy of cerebral cortex
prominent sulci and slender gyri

amygdala and hippocampus affected (both are in temporal lobe)

sensory cortex unaffected


where are amygdala and hippocampus. what are they. what do they do

theyre both in the temporal lobe. they are nuclei. they are a collection of special ganglion. these groups of ganglion have several types of connections to brain allowing response to env
hippocampus is beneath floor of ventricles fx is memory retention


lesions of AD

1. neuritic plaques
deposits of amyloid protein
2. neurofibrillary tangles (more of a problem
resistant to breakdown
persist after necrosis
fibrous proteins in cytoplasm (this will change the shape of the cell)
dec ACH


how does the brain compensate for the loss in mass of the brain w AD

w the tissue dec in mass the ventricles will inc in size


mnfts of AD

insidious onset
stage based progression over ~10yr


mnft of mild AD (when does this last from

memory problems (often diff to detect as it could be from aging. usually detected by those around person not person themself)
-careless work habits
-familiar routine is manageable eg self care


moerate AD mnfts (when does this occur)

-decline in cognition
-language problems (speech and speech reception, comprehension)
1. they will repeat words *repetitive speech*
2. paraphasias-use of words int he wrong context
-some motor disturbance (usually w use of daily objects.) not all of these will present in all indiv
-problems w ADLs


severe ADmnfts.

-severe mental impairment
-minimal voluntary movement
-no self care
-rigid, flexor posturing (hands clenched, elbows bent)


Dx of AD

very diff to Dx
-no definitive test
-clinical presentation (detailed hx) person may present w 6-12mo depression beforehand
-exclude dementia from other causes
-EEG,CT, MRI, labs (also will look at HIV, syphilis, infarcts in brain)


what labs are looked at to make AD Dx

CBC for anemia, CRP, dec B12, lytes


what is an EEG

electroencephlogram-radiographic image of brain which meas fx


Tx of AD and dementia

no cure
-behavioural and env manipulations (eg safety)
-glutamate receptor blocker (in CNs glutamate is stimulatory. it enhances NTM fx. One aspect of AD may be a buildup of this drug eg Memantine $)
-Acetylcholinesterase inhibitors (this inc fx of Ach)
-low dose antipsychotics