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Dementia 1. memory loss, personality change, impaired intellectual fxns 2. from dz/trauma 3. NOT part of normal aging and impact ADLs and relationships Definitions: 1. memory: store, retain, recall info and experiences; can be long/short 2. executive fxn: ability to plan, organize, sequence, or abstract info 3. attention: concentrating on one aspect of environment while ignoring other things Agnosia 1. 2. 3. 4. inability to recognize sensory input visual: can’t name common objects (eg: watch, pencil) auditory: can’t recognize sounds responsible lesions: occipitotemporal region Apraxia 1. sensory and motor systems intact, but can’t perform common actions 2. eg: brushing hair, blowing out a match 3. responsible lesions: dominant inferior parietal lobe Amnesia 1. 2. 3. 4. anterograde: can’t recall events/form new memories after an injury retrograde: can’t recall events that occurred before an injury responsible lesions: hippocampus, temporal lobe, and its connections major finding in alzheimer’s Memory in the Brain 1. 2. 3. 4. memory and recall located in hippocampus amygdala, striatum, mammillary bodies involved hippo: spatial & declarative learning amygdala: emotional memory Common Memory Disorders 1. 2. 3. 4. 5. Alzheimers: most common dementia Vascular & Lewy Body: next most common; often +Alz Benign Forgetfulness of Aging: normal cognitive changes Mild Cognitive Impairment: pre-dementia state Delirium: acute, cognitive disturbance; many causes; coexists with dementia a. characterized: decline in consciousness, loss of attention b. related to: medication, metabolic disturbance, infection Types of Dementia 1. Cortical a. Major symptoms: disturbances in memory, language, perception, function b. regions affected: temporal (medial), parietal, frontal c. Dz: Alzheimer’s, Lewy Body, Vascular dementia, frontotemporal dementia (Pick’s dz) 2. Subcortical a. Major symptoms: emotional probs, slowed motor fxn, disturbed executive fxn, less pronounced memory loss b. regions affected: thalamus, striatum, midbrain, striatofrontal c. Dz: Parkinson’s, progressive supranuclear palsy, normal pressure hydrocephalus, Huntington’s, Creutzfedlt-Jakob, chronic meningitis 3. Neurodegenerative a. primary degenerative dz process of CNS b. most common underlying cause of dementing illnesses c. Dz: Alzheimer’ 4. Other a. origin of degenerative process causing the dementing illness is outside the CNS or it is of NONorganic etiology b. eg: structural dz/trauma, vascular dz, hereditary metabolic dz, demyelinating dz, infectious dz, metabolic/nutritional dz, psychiatric dz Treatable Dementia 1. Less than 10% 2. In order to rule out reversible/treatable conditions consider: structural processes, infections, metabolic dz, nutritional def, psychiatric issues 3. Examples: a. pseudodementia from depression b. normal-pressure hydrocephalus c. thyroid hormone deficiency/excess d. thiamine def. (Wernicke-Korsakaff) e. tertiary syphilis f. pernicious anemia g. alcoholism Dementia Work-Up 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. Serum Chemistries Urinalysis CBC w/diff folate & Vit B12 Liver, renal, thyroid fxn serologic studies for syphilis (RPR) LP if +RPR EEG MRI <65 old, <2 yr hx, focal neurologic sx, nl pressure hydrocephalus signs, falls, trauma neuropsychological testing (bedside and formal) Bedside Neuropsych Testing 1. MMSE- memory and language 2. Clock Drawing- visuospatial 3. “how would you comb your hair”; “how would you blow out a match” apraxia Alzheimer’s Dz 1. 2. 3. 4. most common 5.2 million Americans 6th leading COD Characteristics: a. gradual memory loss & difficulty learning b. problems with reasoning and judgement c. loss language skills d. disorientation e. can’t perform routine tasks 5. 6. 7. 8. 9. 10. 11. 12. f. personality & behavior change later on in dz Causes: a. undetermined b. chromosomes 1, 14, 21 early onset c. chromosome 19 (ApoE4 gene) late onset d. amyloid plaques and neurofibrillary tangles Amyloid plaques: clumps “beta-amyloid” that accumulate b/n abnormal n cell axons and dendrites dense, insoluble structures a. neocortex & hippo Neurofibrillary tangles: twisted paired strands hyper-phosphorylated MT-associated protein called tau inclusion bodies from damaged neuronal MTs a. correlation b/n density of NF tangles on post mortem autopsy and measured antemortem cognitive decline ACh a. important NT in areas of brain involved in process of memory formation (hippo, cerebral cortex, amygdala) b. decreased by ~90% in Alz Dz cognitive impairment & disordered memory c. pharmacotherapy: inhibit breakdown of ACh Diagnosing a. hx b. direct exam of mental/physical status c. lab findings d. neuropsychological testing e. neuroimaging f. the only way to confirm ddx of Alz dz is via post-mortem exam (brain autopsy) Management a. nonpharmacological behavioral interventions i. behavioral interventions by care givers ii. safe/structured environment iii. active tx iv. psychotherapeutic interventions v. pastoral interventions b. cognitive enhancers i. cholinesterase-inhibitor 1. Donepezil (Aricept) 2. Rivastigmine (Exelon) 3. Galantamine (Reminyl/Razadyne) ii. Glu antagonist 1. Memantine (Namenda) c. meds for behavioral symptomatology i. antipsychotics- NO ii. antidepressants iii. mood stabilizers iv. anxiolytics v. hypnotics vi. pain meds d. education and support for caregivers i. caregiver burden counseling ii. legal services iii. medical/ancillary services iv. advocacy groups Long term Care a. sometimes the best clinical strategy to provide as much independence and functionality as possible in least restrictive environement b. challenging c. requires preparation Basic Needs in Alz Dz a. mental stimulation b. physical activity c. social engagement d. proper nutrition 13. Research on Alz Dz a. Amyloid cascade hypothesis b. Amyloid based treatment strategies c. Tau based treatment strategies d. Neuroprotective treatment strategies Benign Forgetfulness of Aging 1. 2. 3. 4. 5. 6. 7. mild loss of memory- slow to recall names/ dates adequate ADL’s and IADL’s poor performance on delayed recall tasks = most sensitive indicator verbal fluency intact vocab can increase dementia NOT normal end product of aging “mild cognitive impairment”- pre-dementia state Lewy Body Dementia 1. 2. 3. 4. 5. 6. 7. 8. 3rd most common form dementia overlap w/ Alz and PD visual hallucinations PD features prominent sensitive to antipsychotic med SE rapid evolution of dementing processes Lewy Bodies (hallmark of PD) found in brainstem, limbic system, and cortex dementia develops w/in year of PD or when comes first Parkinson’s Dz 1. 2. 3. 4. 5. 6. dementia in ½ executive function > language/ visuospatial brainstem bradykinesia = hallmark depression common drugs used to treat can induce psychosis/delirium; these need to be ruled out before ddx of dementia can be made Vascular Dementia (Multi-Infarct Dementia) 1. 2. 3. 4. 5. 2nd most common form dementia brain damage 2* stroke/ MI MRI- neuronal damage hypertension/other vascular dz overlap with Alz. Dz mixed dementia Frontotemporal Dementia 1. 2. 3. 4. 5. 6. Pick’s Dz Pick’s Bodies atrophy of frontal and temporal lobes up to 5% dementia Frontal Lobe syndrome inappropriate social behavior (disinhibition) earlier onset than other forms of dementia (~50s) ~1/2 pts have fam hx; link to mutation of tau on chrom 17 Normal Pressure Hydrocephalus 1. 2. 3. 4. classic triad: dementia, gait disturbance, urinary incontinence enlarged ventricles no elevated ICP clinical treatment: shunt placement; can lead to reversal of dementia in cases of head trauma/SAH Creutzfeldt-Jakob Dz 1. prion dz 2. symptoms: dementia, myoclonus, abnormal EEG (diffuse slowing w/ periodic sharp waves/spikes) 3. spongiform encephalopathy 4. rapidly progressive- death w/in year 5. possible transmission via tissue transplantation sx Pseudodementia 1. 2. 3. 4. 5. 6. “Dementia syndrome of depression” 5% pts may coexist w/other dementias symptoms: poor concentration, apathy, anhedonia, sleep disturbance, psychomotor retardation treatable & reversible responds to antidepressants Korsakoff’s Syndrome 1. end result of untreated/partially treated Wernicke’s Encephalopathy caused by thiamine deficiency resulting in CNS enzyme dsyfxn 2. near total inability to make new memories 3. pts confabulate responses 4. chronic alcoholism 5. treatment: thiamine replacement therapy AIDS 1. 2. 3. 4. 5. 6. 7. direct action HIV on brain subcortical > cortex bradykinesia little to no disturbance w/ language early features: forgetfulness, poor concentration, slowed thinking late features: executive dysfxn, apathy treatment: anti-virals Head Injury 1. retrograde > anterograde 2. doesn’t progress unless further trauma occurs 3. CTE, Dementia Pugilistica, Boxer’s Dementia Transient Global Amnesia 1. 2. 3. 4. 5. dramatic memory disturbance typically only once; more can happen over several years temporal & spatial disorientation orientation for person intact retro/anterograde amnesia for hours 6. anxious/distressed 7. ask same Q over & over 8. vascular insuff to midbrain (including hippo & midline thalamic projections) Psychogenic Amnesia 1. 2. 3. 4. inconsistent loss recent & remote memory relative indifference to deficits “who am I?” (disoriented to person) aka “dissociative amnesia” Huntington’s Dz 1. 2. 3. 4. 5. AD chromosome 4 excessive CAG repeats onset: 30-50 years dementia + chorea atrophy of cerebral cortex and heads caudate nuclei Subdural Hematoma 1. 2. 3. 4. reversible dementia tearing of bridging veins in subdural space symptoms: headaches, confusion, inattention, apathy, memory loss, drowsiness, coma lateralizing signs less prominent (hemiparis, hemianopsia, CN abnormalities) Delirium 1. 2. 3. 4. 5. 6. acute, disorganized mental process shifting attention, awareness, consciousness disordered thinking impaired perceptual discrimination fluctuating cognitive deficits cause: substance intoxication, substance w/drawal, infection, medical condition