psych cognitive disorders Flashcards
def of cognitive disorder
signif chang in cognition from a previous level of functioning
two main types of cognitive disorders
delirium and dementia
57 yo M with tremor, EPS, frontal dizziness, and sluggish pupillary reflexes
most likely tertiary syphilis; order VDRL and TSH
delirium lasts how long?
can last from days to weeks, and may become chronic
other terms for delirium
encephalopathy; acute organic brain syndrome; acute confusional state; acute toxic psychosis; and ICU psychosis
how common is delirium
ten to thirty percent of medically admitted patients exhibit delirium
DSM IV criteria for delirium
disturbance of consciousness, change in cognition, develips over a short period of time (hrs to days) and tends to fluctuate throughout the course of the day
treatment of delirium
orient the patient; lights on and window shades up; meds can be used symptomatically (haloperidol)
do NOT use benzos with delirium
can cause/prolong delirium
dementia
impairment of memory and other cognitive functions without alteration in the level of consciousness
msot common cause of dementia
alzheimers (50 to 70 percent)
second most common cause of dementia
vascular dementia
dsm four criteria for dementia
multiple cognitive deficits manifested by both memory impairment and one or more of aphasia, apraxia, agnosia, loss of exec functioning; deficits do not occur exclusively during delirium
alzheimers disease epi
affects women three times more commonly than men; very heritable
alzheimers mech
decrease in ach due to loss of noradrenergic neurons in the basal ceruleus and decreased choline acetyltransferase (reqd for Ach synthesis)
alzheimers genes
account for only 5% of cases; presenelin I, presenelin II, amyloid precursor protein APP; major susceptibility gene is APOe4
explanation for Alzheimers disease
amyloid cascade hypoth; exce of Abeta peptides either by overproduction or diminished clearance
postmortem findings in alzheimers disease
diffuse atrophy with enlarge ventricles and flattened sulci; senile plaques and NFTs; (plaques but no tangles correlate with severity of dementia)
treatment for alzheimers
cholinestase inhib can slow cognitive decline for 6-12 mos; also NMDA antags can be used
examples of cholinesterase inhib used in AD
Tacrine (Cognex); donepezil (Aricept); rivastigmine (Exelon); galantamine (Razadyne)
examples of NMDA antags used for AD
Memantine (Namenda)
treatment for vascular dementia
cholinesterase inhib have been shown to be successful; antihypertensive tx; tx symptoms as necessary
cause of Lewy body dementia
Lewy bodies and Lewy neurites (aggregations of alpha synuclein) in the brain, primarily in the basal gang
clinical manifestations of LBD
progressive cognitive decline; waxing and waning of cognition is core feature; VH of animals and people; paranoid delusions; parkinsonis; sens to neuroleptics; REM sleep behavior disorder is common
Difference between LBD and Parkinson disease dementia
LBD is onset of dementia within 12 mos of parkinsonism sx; dementia that begins more than 12 mos after the parkinsonism sx is classified as Parkinson disease dementia
treatment for LBD
cholinesterase inhib help improve VH; psychostimulants, levodopa/carbidopa, and dopamine agonists may improve cognition, apathy and psychomotor slowing
treatment for REM sleep behavior disorder in LBD
clonazepam
Pick disease/FTD presents when
between 45 and 65
genetics of FTD
about 25% are familial and may be assoc with mutation in the progranulin or MAPT gent
duration of illness to death in FTD
5 years
clinical manifestations of FTD
changes in personality and social conduct; disinhibited behavior; echolalia, overeating, oral exploration of objects; lack emotional warmth; poor insight; preservation fo memory, language, and spatial functions
pathology of FTD
marked atrophy of the frontal and temporal lobes; neuron loss, microvacuolization, and astrocytic gliosis in cortical layer II
treatment for FTD
anticholinergic meds and antidepressants improve behavioral sx but not cognition
most common dementia caused by infectious disease
hiv assoc dementia
what is the cuase of dementia in HIV-assoc dementia?
the infections as well as direct effects of the virus on cells
treatment for HIV-assoc dementia
HAART improves cognition and prolongs life; also psychostimulants target fatigue and psychomotor retardation
caudate atrophy
huntingtons disease
HD gene
trinuc repeat on chrom 4
treatment for HD
none
lilliputian hallucinations
sensation that objects appear very small; seen in parkinsons disease
parkinsons disease pathology
neuron loss in the substantia nigra, which provides dopamine to the basal gang
what percent of PD patients develop dementia?
30-40 percent
how is PD like AD
senile plaques and NFTs, loss of neurons, and decr choline acetyltransferase
source of CJD
a small number of patients have become infected through corneal transplants
clinical features of CJD
rapidly progressive dementia 6-12 mos after onset of sx; myoclonus is seen in most patients; basal gang and cerebellar dysfunction; personality changes; coma, death
diagnosis of CJD
rapidly progressive dementia and periodic generalized sharp waves on EEG plus at least two of: myoclonus, cortical blindness, ataxia, pyramidal, or EPS; muscle atrophy, mutism
NPH
enlarged ventricles with incr CSF pressure; gait distubrance; urinary incont; dementia
cause of NPH
can be idiopathic or secondary to obstruction of CSF reabsorption sites due to trauma, infx, or hemorrhage
treatment of NPH
relieve pressure with shunt; of the clinical triad, dementia is least likely to improve
most common finding in delirum
impairment in recent memory
dementia with cogwheel rigidity and resting tremor
LBD or PD
dementia plus diminished position and vibration sensation plus megaloblasts on CBC
vit B12 def
dementia plus tremor plus abnormal LFTs plus kayser-fleisher rigns
wilson disease; check ceruloplasmin
dementia plus diminished position and vibration plusArgyll robertson pupils
neurosyph; do CSF VDRL
delirium timing of symptoms
usually worse at night, whereas in dementia the sx are stable throughout the day
EEG changes
fast waves or generalized slowing seen in delirium; not seen in dementia
senile plaques and NFTs
not unique to Alzheimers; also seen in Down syndrome and normal aging
a stroke to the frontal lobe
can lead to sx of schizophrenia, bipilar I disorder, and depression
FTD leads to a more rapid progression to death than in alzherimers dementia
right
prion diseases besides CJD
kuru; Gertmann-Straussler syndrome, fatal familial insomnia, and bovine spongiform encephalopathy (mad cow disease)
the three Ws of NPH
wobbyl, wet and wacky
