Neurocognitive Disorders Flashcards
delirium
disturbed attention, awareness, orientation;
has a physical cause (e.g., drugs, infection);
acute onset; usually reversible;
meds: Haldol, benzos
Alzheimer’s Disease (AD)
80% of major NCDs, increased risk for women, progressive onset and decline;
Early sxs: decreased memory, apathy, depression;
Later sxs: confusion, bx change, judgment problems, gait/motor problems;
Abnormalities: amyloid plaques, neurofibrillary tangles, neuronal damage throughout cortex esp. hippocampus + amygdala, LOW ACH
neurocognitive disorders (NCDs)
-decline in 1 or more: memory/learning, attention, EF, language, perceptual-motor, or social cognition
-MAJOR if deficits interfere w/ independence in everyday activities; MILD if not
vascular NCD
-from strokes; abrupt onset
-10-15% of major NCD in older adults but younger onset than AD
-impaired judgment and ability to make plans
NCD with Lewy Bodies
-like Alzheimers plus visual hallucinations + sleep issues
-PD-like muscle rigidity and gait
-from abnormal accumulations of protein alpha-synuclein
NCD due to Parkinson’s
-low dopamine; tx is L-Dopa
-NCD happens later in PD progression in ~40% of pts
-slowing of processing speed and EF
-same protein clumps as Lewy Bodies, in the substantia nigra (basal ganglia)
NCD due to Huntington’s Disease (Chorea)
-HD is a fatal genetic condition (50% chance if a parent has it)
-sxs emerge ages 30-50; personality and mood changes (e.g., irritability, apathy, disinhibition)
-progressive decline in memory, lack of reasoning
-choreiform movements (frequent jerking of pelvis, trunk, limbs) + writhing + facial grimaces
-LOW ACH, LOW GABA; EXCESS DA
-basal ganglia involved
frontotemporal NCD
changes in personality and bx (e.g., judgment, temper, disinhibition/poor impulse control), difficulty w/ language
NCD due to HIV
-cognitive, motor (e.g., weakness, poor coordination), and bx/mood changes
-memory, attention, language issues
-apathy, withdrawal, amotivation, inappro affect, mood swings
NCD due to Creutzfeldt-Jakob Disease
-rare, degenerative, fatal brain disorder
-from an infectious misfolded protein in the brain
-rapid progression (4-6 mos from onset to death)
-muscle coordination probs, personality change, memory, judgment, vision
hydrocephalus
accumulation of cerebrospinal fluid (CSF) in the brain’s ventricles, can be from over-production or poor absorption of CSF`
-urinary incontinence, unsteady gait
-can s/t be corrected/reversed w/ a shunt
NCD from TBI
-nature/extent of impairment depends on the injury
-posttraumatic (retrograde) amnesia, memory impairment, some EF disturbance, attention, mood regulation, aggression, apathy
-closed-head injuries typically –> loss of consciousness, whereas open-head injuries do not
-recovery 2-3 yrs, but bulk of recovery in 6-9 mos
concussion/postconcussion syndrome
-headache, dizziness, fatigue, poor concentration, memory deficit, irritability, anxiety, hypochondriacal concern, sensitivity to noise and light
-retrograde amnesia for events just before/during the TBI
-psych and physical sxs heal in same time period
-fx damage (as opposed to structural)
contusion
more serious than concussion, bleeding/bruising of the brain
-contrecoup bruising beneath point of impact and on the opposite side (freq. frontal or temporal lobes)
-cerebral swelling
-localized, structural damage
-frontal lobe syndrome: lack of foresight/concern, probs with EF, irresponsible, loss of insight
-temporal lobe syndrome: irritability, hostility
Korsakoff’s Syndrome
-alcohol-induced major NCD, amnestic-confabulatory type
-anterograde amnesia: difficulty forming new memories (also may have retrograde amnesia)
-confabulation, lack of insight, limited spontaneous conversation, probs w/ EF, disorientation, apathy, labile irritability