NCD--Substance Induced, + d/t HIV, Prion, Parkinsons, Huntingtons, Other Flashcards
what are the DSM criteria for substance/medication induced Major or Mild NCD
A–> criteria are met for a major or mild NCD
B–> neurocognitive impairments do not occur exclusively during the course of a delirium and persist beyond the usual duration of intoxication and acute withdrawal
C–> involved substance or medication and duration and extent of use are capable of producing the neurocognitive impairment
D–> temporal course of the neurocognitive deficits is consistent with the timing of substance or medication use and abstinence (i.e deficits remain stable or improve after a period of abstinence)
E–> neurocognitive disorder not attributable to another medical condition and is not better explained by another disorder
what types of alcohol relayed NCDs are there
major NCD: nonamnestic-confabulatory type
major NCD: amnestic-confabulatory type
mild NCD
what are the 4 types of substances listed in the DSM for substance/medication induced Major or Mild NCD
alcohol
inhalant
sedative/hypnotic/anxiolytic
other or unknown
what is a specifier for substance/medication induced Major or Mild NCD
persistent–> neurocognitive impairment continues to be significant after an extended period of abstinence
what neurocognitive impairment is seen most predominantly in NCDs due to sedative/anxiolytic/hypnotic drugs/meds
greater disturbances in MEMORY than in other cognitive functions
NCD due to alcohol frequently manifests with a combination of what impairments
impairments in EXECUTIVE FUNCTIONING and MEMORY and LEARNING domains
what are the features of alcohol-induced amnestic confabulatory NCD (korsakoffs)
prominent amnesia (severe difficulty learning new information with rapid forgetting)
tendency to confabulate
*may co occur with signs of thiamine encephalopathy (wernicke’s) with associated features such as nystagmus and ataxia
what ocular abnormality is associated with wernicke’s encephalopathy
lateral gaze paralysis (ophthalmoplegia)
what are the more common neurocognitive symptoms related to methamphetamine use? what kind of overall NCD profile is seen in methamphetamine use
difficulties with learning and memory
difficulties with executive function
*most common neurocognitive profile approximates that seen in vascular NCD
what ocular abnormalities can be associated with methamphetamine use
evidence of vascular injury–> i.e focal weakness, unilateral incoordination, asymmetrical reflexes)
what is the rate of NCD of intermediate duration in those with hx alcohol abuse
30-40% in the first 2 months of abstinence
–> mild NCD may persist especially in those who do not achieve stable abstinence before until after age 50
is major NCD due to alcohol abuse common
no–> MAJOR NCD is rare, may result from concomitant nutritional deficits as in alcohol-induced amnestic confabulatory NCD
what is seen on MRI of individuals with chronic alcohol abuse
cortical thinning
white matter loss
enlargement of sulci and ventricles
*it is possible to observe NCDs without neuroimaging correlates however
*many of these changes reverse after period of of succesful abstinence
those with sub/med induced NCD may have deficits in what areas that are beyond that seen in many other NCDs
reduced cognitive capacity
difficulty concentrating
what are the criteria for major/mild NCD due to HIV infection
A–The criteria are met for major or mild neurocognitive disorder.
B–There is documented infection with human immunodeficiency virus (HIV).
C–The neurocognitive disorder is not better explained by non-HIV conditions, including secondary brain diseases such as progressive multifocal leukoencephalopathy or cryptococcal meningitis.
D–The neurocognitive disorder is not attributable to another medical condition and is not better explained by a mental disorder.
what pattern of NCD is seen in major/mild NCD due to HIV infection
“subcortical pattern”
–> prominently impaired EXECUTIVE FUNCTION, slowing of processing speed, problems with more demanding attentional tasks, difficulty in learning new information
–> in major NCD due to HIV, SLOWING may be prominent
major/mild NCD due to HIV infection show relatively preserved function in what cognitive areas
recall of learned information is relatively preserved
language difficulties are uncommon
what % of those infected with HIV have at least mild neurocognitive disturbance
1/3 to 1/2
*may not meet full criteria for NCD
estimated 25% meet criteria for mild NCD
estimated fewer than 5% meet criteria for major NCD
how might major/mild NCD due to HIV infection present in developing countries in which perinatal HIV transmission is common
may present as neurodevelopmental delay
what are the criteria for major/mild NCD due to Prion disease
A–The criteria are met for major or mild neurocognitive disorder.
B–There is insidious onset, and rapid progression of impairment is common.
C–There are motor features of prion disease, such as myoclonus or ataxia, or biomarker evidence.
D–The neurocognitive disorder is not attributable to another medical condition and is not better explained by another mental disorder.
what type of onset and progression would you expect for major/mild NCD due to Prion disease
insidious onset, rapid progression of impairment (i.e progression to major NCD over as little as 6 months)
what are some motor features of prion disease
myoclonus
ataxia
what is the most common spongiform encephalopathy/prion disease
sporadic creutzfeldt-jakob disease (CJD)
how do those with CJD typically present
neurocognitive deficits
ataxia
abnormal movements–> myoclonus, chorea, dystonia
startle reflex is common
what are the characteristic biomarker features of prion disease
recognized lesions on MRI with DWI or FLAIR
tau or 14-3-3 protein in CSF
characteristic TRIPHASIC waves on EEG
(family history or genetic testing for rare familial forms)
what would be seen on EEG in prion diseases
characteristic triphasic waves
what proteins would be seen in CSF in prion diseases
tau or 14-3-3 protein
what is the annual incidence of sporadic CJD
1-2 per 1 million people
what are prodromal symptoms of prion disease
fatigue, anxiety, problems with appetite or sleeping, difficulties with concentration
what is the most sensitive diagnostic test for prion diseases currently
MRI with DWI–> see multifocal gray matter hyper-intensities in subcortical and cortical regions
what is the expected onset and progression of major/mild NCD due to parkinsons disease
insidious onset
GRADULE progression of impairment
list features that are frequently present in the context of major/mild NCD due to parkinsons disease
apathy
depressed mood
anxious mood
hallucinations
delusions
personality changes
REM sleep behaviour disorder
excessive daytime sleepiness
what is the prevalence of parkinsons disease in people older than 85
3%
what % of those with parkinsons disease will develop a major NCD sometime in the course of their illness
75%
what are risk factors for development of parkinsons disease
exposure to herbicides and pesticides
RFs for development of NCD in parkinsons = older age at disease onset and increasing duration of disease
what type of neuroimaging may be helpful to distinguish lewy body vs non-lewy body dementias
dopatmine transporter scans i.e DaT scans or structural neuroimaging scans
how do you distinguish between the two lewy body dementias (parkinsons and dementia with lewy bodies)
onset and timing–> for parkinsons, motor and other symptoms must have been present for about a year before onset of cognitive symptoms
for dementia with lewy bodies, cognitive symptoms begin at the same time or shortly before motor symptoms
what are the early cognitive changes seen in huntingtons disease
executive function (rather than learning and memory)
often precede the emergence of the typical motor abnormalities of huntingtons disease
what are the typical motor abnormalities of huntingtons disease
bradykinesia and chorea
what is the genetic abnormality responsible for huntingtons disease
CAG trinucleotide repeat expansion in the HTT gene on chromosome 4
*fully penetrant, autosomal dominant (repeat length of 36 or more is invariably associated with huntingtons disease)
what psychiatric symptoms may be associated with huntingtons disease
depression
irritability
anxiety
obsessive-compulsive symptoms
apathy
psychosis–more rare
what is the average age at diagnosis of huntingtons disease
40
what is the median survival after motor symptom diagnosis of huntingtons disease
about 15 years
*psychiatric and cognitive symptoms of huntingtons disease can predate motor symptoms by as much as 15 years
what neuroimaging changes are seen in those with huntingtons disease
volume loss in basal ganglia (particularly caudate nucleus and putamen)
