8B: Dementia Flashcards
Mild cognitive impairment (MCI)
transition stage between the mild cognitive decline of normal aging and the more serious problems of dementia; about 50% progress to
dementia.
Dementia
progressive decline in cognitive function due to damage or disease in the body beyond what might be expected from normal aging
Delirium
the acute, common symptomatic manifestation of early brain dysfunction, for
any reason; rapid, fluctuating course; may be hyperactive or hypoactive
delirium (positive symptoms)
symptoms that include increased activity/thought (hyperactive); examples include: agitation, hallucination, combativeness,
delusions, disorganized thought
delirium (- symptoms)
Negative symptoms - symptoms that include decreased activity/thought
(hypoactive); examples include: flat affect (no emotion), little speech, lack of
motivation, inability to converse or focus attention or follow a command
Normal pressure hydrocephalus (NPH)
It is important to rule out NPH when
considering a diagnosis of dementia. NPH is a chronic type of communicating
hydrocephalus in which the increase in intracranial pressure due to increased
cerebrospinal fluid (CSF) reaches a somewhat stable point with only slightly increased
intracranial pressure and no headache or loss of consciousness in the patient. However,
the brain tissue becomes quite compressed, leading to cognitive issues resembling
dementia.
Early AD
initial mild problems with learning, memory (esp. more recently
learned facts/info), planning, language problems (shrinking vocabulary, decreased
word fluency), problems with fine motor tasks (apraxia)
Moderate AD
memory problems now interfere with work or social life, Personality changes, problems recognizing family or friends, more apparent
problems with language (comprehension/production), inability to perform activities of daily living, urinary incontinence, impaired long-term memory,
wandering, sundowning, labile affect, delusional misidentification syndromes
(Capras, Fregoli)
Severe AD
much of cortex is atrophied; loss of ability to communicate, recognize people, care for self, single-word language use, extreme apathy and
exhaustion, bedridden until death from complications (e.g., pneumonia)
Activities of daily living (ADLs)
routine activities that people tend do every day
without needing assistance. There are six basic ADLs: eating, bathing, dressing, toileting,
transferring (walking) and continence.
Wandering
for Alzheimer’s patients, this specifically refers to the patients wandering away/escaping from their home
Sundowning
Alteration (worsening) in behavior in sync with circadian rhythm, cooccurs with wandering; may common from fatigue and/or lower light levels
Labile affect
excessive displays of emotion, or expressed emotions that do not match
the situation (laughing at the funeral of a loved one)
Plaques
Occur in Alzheimer’s disease. Plaques are formed when ‘sticky’ protein pieces
called beta-amyloid clump together. Beta-amyloid comes from a larger protein found in
myelin. Plaques may block cell-to-cell signaling at synapses and may also activate
immune system cells, which leads to inflammation and cell death. There also may be
some associated amyloid-related mechanism that prunes neuronal connections.
EXTRACELLULAR
Tau protein
the intracellular transport system is organized in orderly parallel strands
somewhat like railroad tracks; the tau protein helps the tracks stay straight.
Neurofibrillary tangles
Occur in Alzheimer’s disease. Tau protein collapses into twisted strands called tangles, which cause the intracellular cell-transport-system tracks fall apart and disintegrate. Transport of nutrients and other essential supplies across the cell body and axons is interrupted. INTRACELLULAR
Acetylcholinesterase inhibitors
molecules that block the breakdown of the
neurotransmitter acetylcholine
NMDA receptor antagonist
a molecule that acts on the glutamatergic system to block overstimulation of NMDA receptor (which has a role in long term
potentiation)
Antibody-based immunotherapies
use antibodies and other immune
modulation to target plaques/tangles for clearance
BACE inhibitors
novel drug class that interrupts Aβ production (= stop plaque formation); current clinical trials not going well
Dementia with Lewy Bodies (DLB)
dementia characterized by fluctuating cognition
with great variations in attention and alertness from hour to hour, recurrent visual
hallucinations, and the motor features of parkinsonism. Lewy bodies are clumps of
proteins in neurons
Fronto-Temporal Lobar Dementia (FTLD)
heterogeneous dementia disorders
associated with atrophy in the frontal lobes and temporal lobes, with sparing of the
parietal and occipital lobes. Symptoms include personality changes, problems with
executive function and language problems with naming or fluency
Lewy bodies
a name for the abnormal protein clumps seen inside cells in cases of Dementia with Lewy Bodies.
Fronto-temporal dementia (frontal and temporal lobes)
Personality changes, disinhibition, apathy, repetitive behavior
Semantic dementia (anterior temporal lobes)
Progressive problems with naming
Progressive non-fluent dementia (Left Broca’s area)
Quiet, trouble with word production; Also called ‘primary progressive aphasia
Posterior Cortical Atrophy (PCA)
a dementia with initial prominent visual symptoms such as problems with visual field defects, contrast sensitivity, color discrimination, and feature recognition of complex objects, acalculia (loss of math skills), and little initial decline in memory (previously was called visual variant Alzheimer’s disease)
Vascular/Multi-Infarct Dementia (secondary dementia)
a dementia with symptoms including problems with recent memory, wandering, shuffling walk, loss of bladder or bowl control, emotional
lability, difficulty with instructions, and problems handling money; major risk factors
include high blood pressure, high cholesterol, and diabetes
Dementia Pugilistica (chronic traumatic encephalopathy) (secondary dementia)
a severe form of chronic
traumatic brain injury from repeated concussions, resulting in declining mental ability, problems with memory, parkinsonism, tremors, lack of coordination, speech problems,
unsteady gait, and inappropriate or explosive behavior
Wernicke’s Encephalopathy (secondary dementia)
the abrupt onset of encephalopathy (brain disorder), ophthalmoplegia (eye paralysis), and ataxia (loss of coordination) induced by thiamine deficiency, usually from extreme dietary deficiency, often associated with chronic alcoholism; reversible with thiamine treatment. Compare to irreversible Korsakoff’s
syndrome
