Chapter 8_Neurocognitive Disorders (NCDs) Flashcards
What are the six cognitive domains that can be affected by NCDs?
learning and memory, language, complex attention, perceptual motor skills, social interaction, and executive function
What is another way to think of delirium?
Acute brain failure. It is a medical emergency associated with high mortality; it often goes unrecognized
aka toxic/metabolic encephalopathy, acute organic brain syndrome, acute confusional state, acute toxic psychosis, ICU psychosis
Risk factors for delirium
- advanced age
- polypharmacy (including psychotropic meds like benzos and anticholinergics)
- limited mobility
- history of previous delirium
- male gender
- severe or terminal illness
- alcohol use
- malnutrition
- pain
- preexisting cognitive impairment/depression
- multiple medical comorbidities
What are the 5 categories of delirium?
- substance intoxication delirium
- substance withdrawal delirium
- medication-induced delirium
- delirium due to another medical condition
- delirium due to multiple etiologies
delirium+hemiparesis or other focal neuro signs
dx and test?
CVA or mass lesion
head ct/brain MRI
delirium +elevated bp+papilledema
dx and test?
hypertensive papilledema
head ct/brain MRI
delirium + dilated pupils + tachycardia
substance intoxication
UDS
delirium+fever+nuchal rigidity+photophobia
meningitis
LP
delirium+tchycardia+tremor+thyromegaly
thyrotoxicosis
Free TSH, T3, T4
How does delirium present?
- deficits in attention and awareness
- cognitive deficits develop acutely over hours to days
- symptoms fluctuate throughout course of the day (usually worse at night)
- deficits in recent memory/language abnormalities/perceptual disturbances (usually visual)
- differing degrees of psychomotor activity
Three types of delirium based on psychomotor activity?
- mixed type (most common): activity remains stable at baseline or fluctuates rapidly between hyper and hypo
- hyopactive (most likely to go undetected): decreased activity; lethargy/drowsiness
- hyperactive: agitation, mood lability, uncooperativeness; often seen in drug withdrawal or toxicity
How does delirium show up on EEG?
generally manifests are diffuse background slowing on EEG
exception: DELIRIUM TREMENS; FAST ACTIVITY on EEG
What are some useful labs for evaluating a patient with delirium?
fingerstick blood glucose, pulse ox, ABG, ECG, UDS, blood alcohol level, therapeutic drug levels, hepatic panel, thyroid hormone level, chest xray, head CT/MRI, EEG, LP
Treatment for delirium
TREAT UNDERLYING CAUSE
can give haloperidol for agitation
When to use benzos to treat delirium?
ONLY FOR ALCOHOL OR BENZO WITHDRAWAL!
do not use for anything else because they can worsen delirium via disinhibition or oversedation
Difference between mild and major NCDs
Patients with major NCDs require assistance with IADLS, while patients with minor NCDs do not
Cognitive impairment with stepwise increase in severity + focal neurologoical signs
vascular dx
head ct/brain MRI
cognitive impairment + cogwhell rigidity + resting tremor
Lewy body disease/Parkinsons
clinical dx
cognitive impairment + gait apraxia + urinary incontinence + dilated cerebral ventricles
Normal pressure hydrocephalus
Head CT + brain MRI
cognitive impairment + fatigue + cold intolerance + coarse hair + constipation
hypothyroidism
TSH, free T4
Cognitive impairment + paresthesias + diminished position and vibration sensation + megaloblasts on CBC
Vitamin B12 deficiency
Serum B12
Cognitive impairment + tremor + Kayser-Fleischer rings + abnormal LFTs
Wilson’s dx
cerumoplasmin
Cognitive impairment + diminished position and vibration sensation + Argyll Robertson Pupils (accomodation response present, but no light)
Neurosyphillis
CSF FTA-ABS and VDRL
A good quick screening test useful for delirium?
Mini Mental State Exam (MMSE)
What are the components of MMSE?
Orientation, registration (naming objects), attention (DLROW), recall (3 objects within 5 minutes), language (repetition, comprehension, writing)
What is the most underlying cause of major NCD?
Alzheimer’s disease
Clinical manifestations of Alzheimer’s
gradual progressive decline
primary domains affected: memory, learning, language
-motor and sensory symptoms seen late in course of dx, death within 10 years of dx
Etiologies of Alzheimer’s (name 2)
- accumulation of beta amyloid plaques and intraneuronal tau protein tangles
- 1% autosomal dominant single gene mutation (amyloid precursor protein) = early onset
down syndrome = higher risk for developing early onset AD
What is the only way to dx Alzheimer’s
postmortem pathological exam of the brain
Cure/treatment for Alzheimer’s
no cure yet :(
What are treatment options for AD?
- cholinesterase inhibitors (i.e denopezil) can slow deterioration
- NMDA receptor antagonist can provide modest benefit
- agitation and aggression treated with antipsychotics
- supportive care with caregiver
Danger of antipsychotics in patients with dementia?
Black box warning - increased risk of death/mortality
Second most common cause of NCD after AD?
vascular disease aka vascular cognitive impairment
How does cognitive decline happen in vascular disease?
- large/small vessel strokes in cortical or subcortical structures respectively
- microvascular disease affecting periventricular white matter
Risk factors for vascular disease?
hypertension DM smoking obesity hyperlipidema atrial fib old age
How to treat vascular cognitive impairment?
No cure/effective treatment
Try to manage risk factors and prevent strokes
symptomatic management
Classical presentation of vascular NCD?
stepwise loss of function corresponding with microinfarcts
Pathologic features of Lewy body disease (LBD)
pathologic aggregrations of ALPHA-SYNUCLEIN and Lewy neutrites in the brain (primarily basal ganglia)
Core features of LBD
- waxing and waning attention/alertness
- visual hallucinations (vivid, gnomes, dwarves)
- development of EPS after cognitive symptoms
What are some secondary/suggestive features of LBD?
REM sleep behavior disorder - violent movements during sleep in response to dreams
Antipsychotic sensitivity
Treatment for LBD?
- cholinesterase inhibitors for cognitive/behavioral symptoms
- quatiapine or clozapine for psychotic symptoms (low dose, watch out for EPS or NMS)
- levodopa for parkinsonism
- melatonin for REM sleep disorder
Pathology seen in frontotemporal degeneration (FTD)?
Marked atrophy of the frontal and temporal lobes
What are the two variants of FTD?
Behavioral - DISINHIBITED behavior (sexual, verbal, physical), overeating/sucking on objects, lack of emotional warmth, apathy, decline in social/executive function
language- difficulties in speech and comprehension
T/F: Most patients with FTD also have significant deficits in learning/memory and perceptual motor function
FALSE. relative sparing of learning/memory and pereceptual motor function
How to treat behavioral symptoms of FTD?
Serotonergic meds may help reduce disinhibition, anxiety, impulsivity,
What is the most common infectious agent known to cause NCD?
HIV!
How to treat NCD due to HIV?
HAART may be beneficial
psychostimulants to treat symptoms
Genetic pathology of Huntingtons disease?
trinucleotide CAG repeats in huntingtin (HTT) protein on chromosome 4
autosomal dominant
Triad of clinical manifestations in Huntington’s
Motor - chorea, bradykinesia
cognitive - decline in executive function (precedes motor symptoms)
psychiatric - depression, apathy, irritablity, obsessions, impulsivity, INCREASED SUICIDE RISK
How to dx?
Family hx of HD or genetic testing showing increased CAG repeats
How to treat movement symptoms and psychiatric symptoms of HD?
movement - tetrabenazine
psych - atypicals
Parkinson’s is due to depletion of ….. in the basal ganglia
DOPAMINE
Motor signs of Parkinson’s
cogwhell rigidity, in bloc turning, postural instability, bradykinesia, resting tremor, masked faces
Cognitive and psychiatric manifestations of Parkinsons
executive dysfunction, visuospatial impairments, depression, anxiety, personality cahnges, visual hallucinations, paranoid delusions (either from dx itself or meds)
cognitive decline appears AFTER motor symptoms
Which two symptoms are required for PD dx?
presence of bradykinesia and tremor/rigidity
How to treat PD?
motor symptoms with carbidopa-levodopa and or dopamine agonists (watch out for psychosis!)
cholineserase inhibitors for cognitive symptoms
quetiapine and clozapine useful in psychotic symptoms (don’t use other antipsychotics because of EPS)
A form of subacute spongiform encephalopathy caused by proteinaceous infectious particles
PRION DISEASE (CJD)
Diagnosis of prion disease?
- RAPID PROGRESSIVE COGNITIVE DECLINE
- at least 2: MYOCLONUS, visual/cerebellar signs (ataxia, nystagmus, hypokinesa)
- supportive findings on EEG (sharp wave complexes, lesions in putamin/caudate nucleus on MRI, or 144-3-3- protein in CSF
Any treatment for prion disease?
Nope, Most die in a year. poor raibon
Pathology of normal pressure hydrocephalus?
enlarged ventricles on imaging with localized CSF pressure but normal opening pressures on LP
Etiology of NPH?
idiopathic or secondary to CSF obstruction due to infetion (meningitis) or hemorrhage (subaarachnoid or intraventricular)
Manifestations of NPH?
Wobbly - gait disturbance (first)
Wet - urinary incontinence
Wacky - cognitive impairment (insidiious), executive dysfunction; least likely to improve
How to treat NPH?
VP shunt may improve symptoms
