Dementia 2 Flashcards
AD Risk factors
increasing age, females, family history of dementia, low education, low income, low occupational status, depression, head injury, low folate/B12, high homocysteine, presence of apolipoprotein E4 allele, postop delirium, alcohol abuse
Early symptoms of AD
cognitive symptoms: trouble keeping appointments, difficulty finding words, misplacing objects
functional symptoms: diff driving, diff selecting clothes, missing appointments, problems at work
Behavioral symptoms: subtle changes in personality, social withdrawal, depression
patients with depression vs. dementia
patients with depression demonstrate less motivation during cognitive testing. express cognitive complaints that exceed measured deficits. maintain language and motor skills.
when do you image brain?
focal findings on exam. rapid onset/decline. falls/head trauma.
treatment for frontotemporal dementia
no role for cholinesterase inhibitors. careful use of atypical antipsychotics. divalproex for behavioral control. SSRIs for irritability, depression, impulsive behaviors.
pharmacotherapy for alzheimer’s disease
cholinergic therapy, NMDA receptor antagonists, investigational agents, treatment of neuropsychiatric symptoms
why do anticholinesterases work?
degeneration of basal nucleus of Meynert results in acetylcholine deficiency. this contributes to memory deficits. anticholinesterases block degradation of acetylcholine.
4 acetylcholinesterase inhibitors
Tacrine (obsolete), donepezil (approved for all stages of AD), rivastigmine, galantamine
memantine
targets excitotoxicity, which may cause neuronal damage. glutamate NMDA receptor blocker.
first approach if someone has neuropsychiatric disturbances in AD
find the trigger for disturbances and avoid them. if that doesnt work, antipsychotics, antidepressants, anxiolytics.
vascular dementia
multi-infarct dementia. cerebral amyloid angiopathy. hypertension related small vessel disease. stepwise progression. usually seen with cardiovasc risk factors
hypertensive small vessel disease and progressive cognitive impairment
arteriosclerosis of small arteris supplying deep grey and white matter. lacunar infacts. subcortical leukoencephalopathy. Subcortical dementia: cognitive slowing, impaired problem solving, visuospatial abnormalities, disturbances of mood and affect
what does hypertension particularly affect?
small vessels such as the lenticulostriate. these supply deep structures such as the basal ganglia and internal capsule
treating vascular dementia
focus on controlling cardio risk factors. max blood pressure control, statins, stop smoking, control blood sugar, mental and physical exercise, diet. treat with cholinesterase inhibitors
lewy body dementia
intracellular, fibriller deposits of a presynaptic terminal protein called alpha synuclein. sporadic disorders. parkinson’s and dementia with lewy bodies are most common
parkinson’s disease
sporadic. resting tremor, difficulty initiating movement, slowed movement, rigidity, shuffling gait, postural instability. dopaminergic deficit. responsive to L-Dopa treatment. pallow of the substantia nigra. degeneration and loss of pigmented dopaminergic neurons of substantia nigra. often contain lewy bodies.
pathogenesis of Parkinsons
mutations in alpha synuclein gene. lewy bodies are composed of fibriller aggregates of alpha synuclein. pesticide exposure may be risk factor. oxidative stress, impaired axonal transport, inhibition of oxidative phosphorylation implicated in pathogenesis
dementia with lewy bodies
sporadic, late onset. memory less frequently effected compared to AD. frontal and subcortical features (attention deficit and alertness) common. pronounced fluctuations and variations in symptoms. vivid hallucinations, delusions. sleep disorders common. acting out dreams
neuropathology of lewy body dementia
nigral pallor. significant atrophy of limbic areas. cortical type lewie bodies in frontal, temporal, and insular cortex, and in limbic areas. nigral lewy bodies. lewy neurites. Usually plaques and tangles.
lewy body dementia treatment
cholinesterase inhibitors may provide symptomatic support. trial of carbidopa/levodopa for movement symptoms. AVOID antipsychotics, as they make parkinson symptoms a lot worse. clonazepam for sleep disorders
what are first areas to show lewy bodies in LBD
amygdala and cingulate gyrus
LBD vs Parkinson dementia
LBD: onset of dementia within 12 months of parkinsonism. movement disorder usually second.
parkinson dementia: onset of dementia more than 12 months after diagnosis of parkinsons. movement disorder usually first
