neurocognitive disorders

refering to a decline in cognitive function that may range from mild-severe and can sometimes be reversible, including: memory loss, dec attention span, difficulty problem solving, visuospatial difficulties, behavioral changes, learning/retention problems, and judgement/reasoning problems

cognitive impairment

main types of cognitive impairment

dementia and delirium

characterized by an alteration of attention, consciousness, and cognition w reduced ability to focus, sustain, or shift attention

delirium

who is often affected by delirium

high prevalence in elderly, inpatient settings, really sick pts

delirium sx

develops fast and can fluctuate

perceptual disturbances (visual hallucinations most common, sometimes auditory)

reduced ability to focus or maintain attention

marked decicity of short term memory and recall

anxiety

irritability

psychomotor restlessness

sundowning

causes of delirium

drugs/alc (either being on them or being in withdrawal from them)

infection (esp UTIs)

neurologic disease (alzhimers, parkinsons)

metabolic disturbances (hypo/hyperglycemia, electrolyte imbalances)

meds

delirium risk factors

underlying brain disease (dementia, stroke, parkinsons disease)

old age (esp in hospitals and nursing homes)

sensory impairment (blind/deaf pts)

a phenomenon when pts have mild/moderate delirium at night, most common in pts w preexisting dementia

sundowning

sundowning sx

inc confusion/disorientation, agitation/mood swings, hallucinations, paranoia, difficulty sleeping, worsened by hospitilizations, sensory deprivation (leave a lamp on for them to help them sleep), and meds

what is the HALLMARK of delirium

distractibility

delirium clinical presentation

distractibility

disorganized or tangential speech (never getting back to the point)

drowsy/lethargic

semi-comatose

hyper-vigilance (particularly in alc/drug withdrawl)

dec cognitive functioning level (cant do normal mental activities)

dementia

perceptual disturbances (visual/auditory hallucinations)

language difficulties (esp in multilingual pts, may forget lots of words in one particular language but not other language)

hyperactive delirium signs (easiest to recognize)

restlessness/pacing

anxious

rapid mood swings

visual disturbances

resist care

hypoactive delirium signs

inactive

reduced activity

sluggish

drowsy

dazed

do not interact with caregivers/providers

mixed delirium signs

mix of hypo and hyperactive delirium that quickly switches back and forth

what should we look for/ask about when evaluating for delirium

usually will have to take hx from person besides pt (family member bringing them in) or may be evaluating them for something else and realize somethings off

ask about onset of sx

previous hx of demential/delirium

current meds

illnesses

organ failure (esp liver failure)

alc/drug use

check vitals (specifically BG and fever to see if its an infxn)

check head for possible injury

do a complete physical exam on everything else

which 2 sx must have at least one present to dx delirium

acute onset and fluctuating course AND/OR inattention

common medication causes of delirium

benzos (ex alprazolam, diazepam)

antihistamines (benadryl, atarax)

TCAs (amitriptyline)

neuroleptics (clonzapine)

parkinsons meds (levodopa and amantadine)

ANTICHOLINERGIC DRUGS (can be reversed w physostigmine)

opioids (morphone, tramadol)

sleeping aids

corticosteroids

H2 blockers (cimetidine, ranitidine)

what labs should we run for someone w delirium

urinalysis/urine culture (check for UTIs)

CBC (see high WBC if theres an infxn)

glucose

toxicology (see drug use)

vitamin B12 (for wernikes encephalopathy)

CMP, calcium, TSH/FT4, ABG

when would we need imaging to assess delirium, if ever

not needed if its from a treatable illness/injury, no evidence of trauma, no new focal neurologic signs are present and pt is arousable and able to follow simple commands

HEAD CT if unknown cause of delirium or if pt is not improving w tx of known cause delirium

if ct neg do an MRI, which is more sensitive for acute ischemic stroke, posterior fossa lesions, and white matter lesions

EEG to exclude seizures and can confirm metabolic or infectious encephalopathies

what other dx can we do to determine delirium cause

lumbar puncture mandatory if unknown cause, esp if pt has a fever

delirium tx

treat underlying

a dangerous sx of alc withdrawl that includes tremors or shakes in hands and is a medical emergency that can be life threatening

delirium tremens

delirium tremens tx

ICU admit

benzos to control agitation, prevent seizures and reduce complications rks

IV fluids for hydration and electrolyte imbalances

vit B1 to prevent wernickes encephalopathy

monitor and supportive care

a progressive decline in intellectual function with NO disturbance in consciousness, insidious onset w gradual progression and usually no precipitating event

dementia

cognitive decline but no change in level of function

dementia

dementia prevelence

1% at age 60, doubles every 5yrs and gets to 30-50% by 85, life expectance after dx is around 3-15yrs

most common cause of dementia

alzheimers

other causes of dementia

vascular dementia, frontotemporal dementia, dementia with lewy bodies

progressive dementia w insidious onset and the atrophy of the cerebral cortex linked to genetic mutations

alzheimers

pathogenesis of alzheimers

will see AMYLOID BETA PEPTIDES AND TAU PROTEIN TANGLES

complete pathogenesis unclear but some autoimmune nature (too much amyloid beta builds up plaques on neurons → triggers inflammatory reaction → immune system kills neurons)

simultaneously tau molecules assemble microtubules to support nerve cell structure (like railroad tracks) → chemical changes in neuron make the tau protein change shape → cant hold microtubules in place, tau proteins get tangled (neurofibrillary tangles) → cell dies

overall see loss of neurons and synapses in the cerebral cortex and certain subcortical regions

where will you see degeneration in the brain of a pt w alzheimers

temporal, parietal, frontal cortex, cingulate gyrus, hippocampus shrinks, ventricles grow

first and most prominent sx of alzheimers

short term memory loss

other sx of alzheimers that may vary

executive function issues, visuospatial function issues, language problems

alzheimers tx

family support/support groups, alzheimers association, small things like hiding shoes to keep them from leaving the house alone

what can cause damage to brain blood vessels and eventually may progress to vascular dementia

stroke, brain hemorrhage, narrowed or chronically damaged brain blood vessels

an abrupt onset of dementia with stepwise or progressive accumulation of defecits that depend on the location of the strokes that caused the damage

vascular dementia

what hx will pts w vascular dementia have

hx of cerebrovascular accidents

vascular dementia general sx

focal neurologic deficits, depression

vascular dementia subcortical sx

dec concentration, forgetfulness, slowed thinking

vascular dementia motor sx

abnormal gait, focal weakness, dyscoordination

what hx will pts w frontotemporal dementia have

hx of psychiatric dx (psychosis vibes)

causes of frontotemporal dementia

abnormal protein inclusions in teh cytoplasma and/or nucleoi of neuronal and/or glial cells

neuron loss, swollen neurons, loss of myelin, and astrocytic gliosis in frontal/temporal lobes, cortical and/or basal ganglia atrophy

how is frontotemporal dementia defined by

which proteins are found in the intraneural aggregates (either Tau or TAR DNA-binding protein 43)

what type of frontotemporal dementia has 50% tau aggregates and 50% TAR DNA-binding protein 43 aggregates

behavioral variant

what type of frontotemporal dementia has 70% tau aggregates and 30% TAR DNA-binding protein 43 aggregates

progressive non-fluent aphasia (speech issues) (main cause)

what type of frontotemporal dementia has 100% TAR DNA-binding protein 43 aggregates

semantic dementia

subtype of frontotemporal dementia has behavioral problems like apathy, loss of sympathy/empathy, stereotypical, compulsive or perseverative behavior, hyperorality or dietary changes or executive deficits w relative sparing of visuospatial skills and memory

behavioral variant frontotemporal dementia

subtype of frontotemporal dementia that has language impairment/deficits that impair daily functioning, with aphasia being the most prominent intially

primary progressive aphasia

a subtype of primary progressive aphasia (which is a type of frontotemporal dementia) that has impaired single word comprehension and impaired confrontation naming, with impaired object knowledge, surface dyslexia/dysgraphia, but normal repition and speech production

semantic variant primary progressive aphasia

a subtype of primary progressive aphasia (which is a type of frontotemporal dementia) that has agrammatism in production and apraxia of speech and normal single word comprehension and object knowledge but impaired comprehension of complex sentences

non-fluent variant primary progressive aphasia

an abnormal collection of alpha-synuclein protein (lewy bodies) in the anterior frontal lobe, temporal lobes, cingulate gyrus and insula

dementia with lewy bodies

clinical features of dementia with lewy bodies

hard to distinguish from parkinsons bc similar motor deficits

can have sx like alzheimers

psychiatric disturbances like visual hallucinations or fluctuating delirium

cognitive dysfxn like visuospatial and executive issues

what is the only 100% definitive dx for alzheimers

brain autopsy post mortem

what sx of dementia. will come from the shrinking of the hippocampus

short term memory loss, repeating questions or stories, diminished ability to recall recent conversations or events

what sx of dementia. will come from dysfxn in the tempo parietal junction of the left hemisphere

word finding difficulty, difficulty recalling names of people, places, objects etc, using many different pronouns and circumlocutions

difficulty with articulation, fluency, comprehension, and meaning is specifically in Brocas/Wernickes area

what sx of dementia. will come from dysfxn of the right parietal lobe

visuospatial dysfxn, poor navigation, getting lost in familiar places, impaired recognition of familiar people/places

what sx of dementia. will come from dysfxn of the frontal lobes or subcortical areas (basal ganglia/white matter)

executive function, distractibility, impulsivity, mental inflexibility, concrete thought, slowed processing speed, poor planning/organization, impaired judgement, apathy

dementia risk factors

family hx, chronic illness (vascular disease, DM), significant head injury, female (bc longer life expectancy)

ways to lower risk of dementia

education, ongoing intellectual stimulation

functions of the temporal lobe

memory, understanding, language

functions of the occipital lobe

vision

functions of the parietal lobe

perception, making sense of the world, arithmetic, spelling

functions of the frontal lobe

executive functions, thinking, planning, organizing, problem solving, emotions and behavioral control, personality

functions of the motor cortex

movement

functions of the sensory cortex

sensations

what questions do we ask when getting a hx for a possibel dementia pt

ask about risk facots, amount of decline from premorbid level of functioning, ability to be a reliable historian, evaluate speech, screen for depression, activities of daily living impacted

what do we look for in a physical exam for a possible dementia pt

do complete neuro exam, eval underlying medical illnesses, other underlying neurologic conditions, try to rule out treatable conditions, evaluate their level of self care

what eval for dementia do we do for pts over 70

quick screening, ask them to repeat 3 simple nouns, do the clock test (how well can they draw an analog clock w the proper instructed time), and then ask them to recall the 3 nouns

if there is any deficit in the quick screening do a full Mini Mental State Exam and if theres any deficit there do a full neuropsych eval

what is the goal of imaging when evaluating dementia and what do we use

goal is to rule out cerebrovascular disease, tumors, or structural abnormalities (may not actually see evidence of neurodegenerative disease)

MRI best, CT second line

what is imagine we can use to differentiate between alzheimers and frontotemporal dementia

PET scan (radiolabeled ligand for beta-amyloid)

what labs do we get for EVERY dementia pt

B12 and FT4/TSH

what labs do we get if were clinically suspicious of dementia

RPR, CBC (possible infxn), electrolytes, glucose, lipids (high cholesterol may mean stroke)

what labs do we get if were worries about alzheimers disease

CSF analysis (will see beta amyloid dec and tau protein inc)

non pharm tx for dementia

anything that can dec rate of decline (and reduce risk in normal pts) bc you CANT regain lost skills

aerobic exercise, frequent mental stimulation (coloring books, puzzles, games, little outings with others), active role in community and family life, continuing activities pt is confident in, little stuffed animals like pretend pets

first line cognitive pharm tx for alzheimers and lewy body dementia (can PROLONG capacity for independence but does NOT prevent disease progression)

cholinesterase inhibitors (donezepil, rivastigmine, galatamine)

do NOT give to frontotemporal dementia pts bc makes it worse

second line pharm tx for alzheimers (maybe lewy body dementia)

memantine (contraindicated for frontotemporal dementia)

how can we treat depression for dementia pts

SSRIs, buproprion, venlafaxine (effexor)

AVOID paroxetine bc anticholinergic effects

how can we treat insomnia for dementia pts

trazodone

AVOID antihistamines, benzos, and zolpidem (can cause delirium)

how can we treat apathy and delusions for dementia pts

apathy- methylphenidate (only select pts, can cause agitation)

delusions- risperidone, olanzapine, quetiapine

AVOID haloperidol bc bad ADRs (tardive dyskinesia, QT prolongation)

additional concerns for rapidly progressive dementia

prion disease, infections, toxins, neoplasms, autoimmune disease, jakob-creutzfeldt disease