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mild NCD
mild cognitive impairment, focus of early intervention
major NCD (dementia)
progressive neurodegenerative condition, has different stages
reversible NCD is also called
temporary dementia
causes of reversible NCD
stroke, depression, med side effects, nutrient deficiencies, metabolic disorders
AD stage 1
no symptoms, maybe unnoticeable issues with memory and routine
AD stage 2
very mild, lose things, short term memory loss, aware of decline and may be ashamed
AD stage 3
mild cognitive decline, changes in thinking/reasoning are noticeable by others and interfere with life, may forget names/words
AD stage 4
moderate cognitive decline, forget child's bday, lose ability to shop, cook, and manage finances, may have depression
AD stage 5
moderately severe cognitive decline, lose ability for some ADLs independently, may need to go to memory care unit
AD stage 6
severe cognitive decline, SUNDOWNING, unable to recall spouse, disorientation, delusions, probably institutionalized
AD stage 7
very severe cognitive decline, terminal end stage, body starts to shut down, aphasic, unable to recognize family
AD causative factors
• neurotransmitter alterations
• plaques & tangles
• head trauma
• genetics
what neurotransmitter is involved in AD
acetylcholine decreases
how does low acetylcholine impact AD development
ACh is supposed to break down plaques and tangles, so low levels means more damage
how do cholinesterase inhibitors help AD
slow degradation of ACh
how do NMDA receptor antagonists help with AD
slow neuronal degradation
vascular NCD
blocked blood flow to brain -> neuro deterioration, more abrupt onset than AD, may have small strokes
vascular NCD factors & etiologies
hypertension, cerebral emboli, cerebral thrombosis
NCD due to parkinson's
loss of nerve cells in substantia nigra (in brain) and decrease in dopamine (causes decreased mobility), can resemble AD
NCD due to lewy bodies
similar to AD, progresses faster, often misdiagnosed as AD
second most common cause of NCD
lewy bodies, 25% of NCD cases
substance induced NCD
result of reactions to or overuse/abuse of substances
causes of substance induced NCD
alcohol, inhalants, sedatives, toxins, meds that cause anticholinergic side effects
NCD due to huntingtons
genetic disease, damages cerebral cortex and basal ganglia, usually declines into dementia and ataxia
what affects the course of NCD due to huntingtons
age of onset (juvenile onset and late onset are the shortest course)
delirium
disturbance in level of awareness and a change in cognition, develops rapidly over short period
delirium common causes
infection, electrolyte imbalance, hypoxia
delirium symptoms
distracted, rambling, impaired reasoning and goal directed behavior, disorientation to time and place
delirium autonomic manifestations
tachycardia, sweating, flushed face, dilated pupils, high BP
is delirium reversible
usually yes, resolve underlying etiology
4 types of delirium
1. substance intoxication delirium
2. substance withdrawal delirium
3. medication induced delirium
4. delirium due to another medical condition or multiple etiologies
primary NCD
disorder is directly caused by brain disease, not other illness
secondary NCD
caused or related to another disease or condition
most common NCD
Alzheimer's
aphasia
inability to speak
apraxia
impaired ability to carry out motor activities despite intact motor function
NCD due to prion disease predisposing factors
due to prion disease (duh), onset is usually between age 40 and 60, progression from diagnosis to death in 2 years, sometimes genetic components
other conditions that can cause NCD examples
hypothyroidism, brain tumor, pernicious anemia, MS, lupus
NCD diagnostics
EEG, CT, PET, MRI, lumbar puncture, blood or urine test
how do drugs help with NCD
help with cognitive impairment, agitation, aggression, hallucinations, thought disturbances, wandering, depression, anxiety, sleep