Cognitive disorders Flashcards
What is delirium? DSM Dx?
waxing/waning changes over the course of a day:
- change in level of consciousness with reduced ability to focus, sustain, or shift attention
- change in cognition or development of a perceptual disturbance
tends to be worse at night “sun-downing”
how does delirium differ than dementia in terms of onset, course, alertness, prognosis, and EEG changes?
Both have memory impairment, cognitive changes, and behavioral problems
DELIRIUM onset: rapid (hrs-days) course: waxing/waning alertness: hypo- or hyper-active prognosis: reversible EEG: changes: generalized slowing or fast waves
DEMENTIA onset: slow (months-years) course: stable decline alertness: stable prognosis: irreversible EEG: no changes
how does delirium differ than psychotic disorders in terms of perceptual changes and level of consciousness?
DELIRIUM
perceptual changes: visual hallucinations
level of consciousness: waxing/waning
PSYCHOTIC d/o
perceptual changes: auditory hallucinations, delusions
level of consciousness: alert
2 typical sx of delirium
visual hallucinations
short attention span
What is diagnostic of all patients with delirium?
EEG - generalized slowing or fast waves
Which psychotropic Rx can be used to treat the agitative symptoms of delirium? Which ones do you want to avoid and why?
anti-psychotics: haloperidol
want to avoid benzodiazepines because they will often cause, prolong, or exacerbate the delirium!
typical and atypical anti-psychotics have a black box warning. what is it?
increases mortality in the elderly
what is dementia? DSM?
impairment of memory and other cognitive functions without an alteration in the level of consciousness; progressive and irreversible
requires the development of MULTIPLE cognitive deficits:
- memory impairment
- cognitive ∆s (aphasia, apraxia, agnosia, changes in executive functioning)
causes significant impairment in social/occupational functioning
decline from previous level of functioning
two most common forms of dementia
alzheimers (cortical atrophy and enlarged ventricles) vascular dementia (deep WM lacunar infarcts)
others: lewy body dementia Pick/Fronto-temporal dementia HIV-associated dementia Huntington Disease Parkinson Disease Creutzfeldt-Jakob Disease (CJD) Normal Pressure Hydrocephalus
work-up for reversible causes of dementia
CBC electrolytes TFT VDRL/RPR B12/folate Brain CT/MRI
what causes reversible dementia?
hypothyroidism
The mental status exam can be used to assess dementia. What value is suggestive of dementia?
< 25
pathophysiology of Alzheimers disease - 2
decreased ACh due to
- loss of noradrenergic neurons in the basal ceruleus
- decrease in choline acetyltransferase (req’d for ACh synthesis)
results in gradual + progressive decline in cognitive functions (esp memory and language), personality changes, mood swings, paranoia, and ultimately death
In Alzheimers disease, what are the functional symptoms that are the last to go?
motor and sensory systems
treatment for Alzheimers disease - 2
the disease is characterized by decreased ACh, therefore it is logical to use Rx that increases ACh, such as
- Cholinesterase inhibitors (AChEi) - tacrine, donepezil, rivastigmine, galantamine
- NMDA antagonists - memantine
justification for using high potency antipsychotics in patients with alzheimer’s. Downsides to using this?
why should you avoid low-potency antipsychotics?
high potency antipsychotics can help with aggression, hostility, violence, but can increase EPS and increase risk of CVA (stroke)
low potency antipsychotics can result in anticholinergic and orthostatic side effects
alzheimers susceptibility genes
APO34
adults with down syndrome are at risk of developing…?
alzheimers disease
what is vascular dementia caused by?
microvascular disease that produces multiple small infarcts -> accumulation of these infarcts will result in a step-wise deterioration/loss of function into dementia
risk factors of vascular dementia?
stroke DM HTN APOe4 male sex
third most common form of dementia and its cause
lewy body dementia - lewy bodies and lewy neurites (alpha-synuclein aggregates)
5 main clinical manifestations of lewy body dementia
waxing and waning, but progressive cognitive decline visual hallucinations Parkinsonism sensitivity to neuroleptics REM sleep behavior disorder
pathological causes of pick disease/frontotemporal dementia (FTD)
subsequent clinical manifestations?
marked atrophy of frontal/temporal lobes due to neuronal loss, microvacuolization, and astrocytic gliosis in cortical layers
profound changes in personality and social conduct:
- disinhibited verbal, physical, and sexual behavior
- echolalia, overeating, oral exploration of inanimate objects
- poor insight about behavioral problems
- lack of emotional warmth, empathy, or sympathy
pick disease/frontotemporal dementia (FTD)
anticholinergic Rx and antidepressants have consistently shown to improve behavioral sx but not cognition
what causes HIV-associated dementia?
risk factors?
infections due to neutropenia and direct effect of the virus on the cells
risk factors: duration of illness, low CD4 counts, high viral loads
clinical manifestations of of HIV-associated dementia
rapid decline in all aspects: depression, social functioning (apathy, withdrawal), memory and cognition, concentration, behavior, motor ability and pscyhomotor retardation
one is the one function that is usually preserved in HIV-associated dementia?
language
when is the average age of onset for huntington’s disease? symptoms?
what other psychiatric comorbidities is usually associated with huntington’s?
35-50 - choreiform movements, muscular hypertonicity, depression, psychosis
alcoholism and suicide (high rates)
pathological cause of huntington’s disease
how is the diagnosis made? 2
trinucleotide CAG repeats on chromosome 4
genetic testing + MRI (caudate atrophy)
treatment for huntington’s disease?
none
what is lilliputian hallucinations? In what disease does it normally occur in?
associated sx?
sensations that objects appear very small
temporal lobe epilepsy
associated sx: strange smells, lip smacking, temporary loss of consciousness
pathological cause of Parkinson’s disease
loss of dopaminergic neurons in the Substantia Nigra (which provides dopamine input to the basal ganglia) –> Parkinsonism (bradykinesia, cogwheel rigidity, resting tremor, masklike facies, shuffling gait, dysarthyria)
senile plaques and neurofibillary tangles
decrease choline acetyltransferase
what do most parkinson’s patients suffer from?
depression - >50%
What is Creutzfeldt-Jakob Disease? What are some of the symptoms?
rapidly progressive degenerative disease caused by accumulation of prions ->
- early on: personality changes, immature behavior, paranoia
- rapidly progressive dementia
- myoclonus (sudden spasms of muscles)
How is Creutzfeldt-Jakob Disease diagnosed?
1) rapidly progressive dementia
2) EEG - peridoic generalized sharp waves
3) at least 2 of the following:
- myoclonus
- cortical blindness (loss of vision due to occipital cortex damage)
- ataxia, (extra)pyramidal signs
- muscle atrophy
- mutism
Potentially reversible cause of dementia? what causes this?
normal pressure hydrocephalus - idiopathic or secondary to obstruction of CSF reabsorption sites due to trauma, infection, hemmorhage
what do you see on MRI in patients with normal pressure hydrocephalus?
enlarged ventricles with increased CSF pressure
clinical manifestations of normal pressure hydrocephalus?
Wet = urinary incontinence Wobbly = gait disturbance (first) Wacky = dementia, mild with insidious onset
treatment of normal pressure hydrocephalus?
ventroperitoneal shunt
