Neuroscience 210

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Anonymous
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Neuroscience 210
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2010-04-13 00:13:13
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dementia and AD lecture
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dementia, alzheimers disease
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  1. Dementia definition
    Global deterioration of the intellectual function in the face of unimpaired consciousness

    heterogeneous, more than memory involved, organized thinking, abstract thinking, insight, judgement
  2. Evaluating Dementia
    • - General medical history
    • - General neurological history
    • - Neurobehavioural history
    • - Psychiatric history
    • - Toxic, nutritional and drug history
    • - Family history
    • - Objective examination
    • - physical
    • - neurological
    • -neuropsychological
  3. Comprehensive assessment of mental state
    • Bedside Tests: MMSE and MOCA
    • - Level of consciousness, ie. alert, drowsy, stuporous, etc.
    • - Orientation: time, place, person • Memory: remote, recent, immediate (3 object recall)
    • - Attention and concentration (serial 7’s, digit span)
    • - Knowledge, insight
    • - Language: - fluency, comprehension, repetition, object naming, tests for apraxia, reading, writing
  4. Clinical signs of DM
    frontal release signs, indicative of disfunction in frontal lobe, symptoms reflect which parts of cortex involved

    • 1. pout reflex--when lips are struck with a hammer a pout is observed
    • 2. glabellar reflex--person can't inhibit blinking in response to stimulation (tapping between eyes)
    • 3. grasp reflex--hand closes when palm stroked
    • 4. palmo mental reflex--scratch on palm induces sudden contraction of chin
  5. Parts of the brain
    • Anterior--frontal or premotor
    • - behavioural changes/loss of inhibition, antisocial behaviour, irresponsible
    • - frontotemporal dementias, Huntingtons

    • Posterior--parietal and temporal lobe
    • - disturbance of cognitive function (memory and language) without changes in behaviour
    • - AD
  6. Rapidity of course of intellectual deterioration
    • AD--longest course, many years to go from acute to subacute to chronic condition
    • Normal pressure hydrocephalus--months to years
    • CJD--months,
    • encephalitis--weeks
  7. Types of dementia
    • 1. Degenerative--degeneration of nerve cells, leads to cognitive disfunction
    • - e.g. AZ, lewy body, Tauopathies (frontotemporal), HD, PD, Wilsons (abnormal amounts of copper)
    • 2. Cerebrovascular
    • - vascular dementia, multi-infarct, CNS vasulitis
    • 3. Structural
    • - normal pressure hydrocephalus, brain tumor, head injury, subdural hematoma
    • 4. Infections
    • - CJD, neurosyphilis, HIV, Herpes simplex encephalitis
    • 5. Toxic/metabolic
    • - drug induced, alcoholism, toxins, heavy metals, deficiences, hypothyroidism
    • 6. immune disorders and cancer
    • - lupus
    • 7. Depression
  8. AD definition
    • irreversible, progressive brain disease that slowly destroys memory and thinking skills
    • - originally thought to be for middle, younger people ,discovered later that it was associated with age
  9. Human brain
    • 100 billion neurons
    • 100 trillion connections between these neurons

    neurons communicate with each and carry out metabolism, and repair themselves --AZ disrupts these
  10. AD facts
    • most common cause of dementia
    • 7-9% of people of 65 have it, 35% of people over 85
    • 4.5 mil in US and Canada have it
    • 40% of total health care costs associated with neurological diseases

    AD affects the surrounding families as well
  11. Clinical features
    • Symptoms--
    • - impairment of memory and attention, language, and communication
    • - judgement, personality changes , depression, visuo-spatial disorientation

    • Signs--
    • - motor and gait disturbances, extrapyramidal signs (poverty of movement, bradykinesias), sphincters, seizures

    • occurrence-
    • - usually late 50s or later

    • etitiology-
    • -- familial forms--10% of cases, earlier onset, have susceptibility genes
    • -- sporadic--unknown cause, majority of cases
  12. Neuropathology of alzheimers
    • -cortical atrophy
    • -synaptic and neuronal loss
    • -Neurofibrillary tangle (NFTs) with paired helical filaments
    • -abnormal microtubules associated proteins
    • -tau proteins
    • -neuritic plaques with amyloid core
    • -amyloid angiopathy
  13. Plaques and tangles
    -hallmarks of AD

    • plaques
    • - dense deposits of protein and cellular material that accumulates outside and around nerve cells
    • - amyloid precurser protein are embedded in the membrane, and are important for neuronal growth, survival and repair.
    • - enzymes (secretase) cut the APP, frees beta amyloid, which tend to stick together which form the plaques

    • tangles
    • --twisted fibres that build up insides the nerve cell
  14. Neurotransmitter abnormalities
    • - decreased Ach in the cortex and hippocampus
    • - Ach lives in basal forebrain nuclei, there is a net loss of Ach in the brain

    • Treatments
    • - trials to see if just giving more Ach worked--didn't
    • - trials using Ach agonists--also didn't work, side effects
    • - now--drugs that inhibit break down of Ach, but not a great fix because neural structures are still breaking down
  15. Symptomatic drugs for AD
    • Cholinergic drugs
    • - cholinesterase inhibitors (Aricept, Exelon, Reminyl)

    • Noncholinergic drugs
    • - possible treatments--amyloaid vaccine, secretase inhibitors, antiamyloid agents
    • - unproven treatments--estrogens, NSAIDs, vasodilators, propentofylline
  16. Symptomatic drugs for AD and imaging
    • Cholinergic drugs
    • - cholinesterase inhibitors (Aricept, Exelon, Reminyl)

    • Noncholinergic drugs
    • - possible treatments--amyloaid vaccine, secretase inhibitors, antiamyloid agents
    • - unproven treatments--estrogens, NSAIDs, vasodilators, propentofylline

    Imaging--PET scans, injection with a compound that can cross BBB and stick to amyloid
  17. Dementia with Lewy bodies
    • - fluctuating cognition with pronounced variation in attention and alertness (e.g. can be good one day and not the next)
    • - visual hallucinations
    • - Parkinsonian features (difficulty with movements)
    • - treatment with cholinesterase inhibitors, atypical antipsychotics

    - loss of pigmented neurons in the Substantia nigra in PD and Dementia with lewy bodies
  18. Frontotemporal dementia (Pick' disease)
    more behavioural changes, personality changes

    • - more common in females and at a younger age than AD
    • - focal frontal and temporal loba atrophy
    • - disinhibition, apathy, perseveration, mental rigidity and affective symptoms
    • - Tau pathology most frequently observed
    • - Familial forms--gene on Chromosome 17
    • - no curative treatment
  19. Vascular Dementia
    • accounts for 10-15% of dementias
    • occurs stroke by stroke with progressive loss of function
    • clinical features of stroke profile--hyptertension, diabetes
    • can occur with neurodegenerative dementia
    • CT scan can show multiple areas of cerebral infarction

    treatment of risk factors to lower risk

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