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Alzheimer disease


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Alzheimer disease made simple

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Alzheimer disease

  1. 1. 1 Alzheimer’s disease: Clinical Review By Dr. Tarek A. Gouda Professor of neurology Licensed consultant neurologist ,KSA(2009)
  2. 2. 2 Overview -Definition -CliniCal piCture anD Diagnosis -pathology -Differential Diagnosis -treatment
  3. 3. 3 INTRODUCTION - Progressive deterioration in cognitive ability in the absence of other known neurologic or medical problems. -It is the most common type of dementia (50-70% of cases of dementia) -Alzheimer’s disease is progressive and irreversible.
  4. 4. 4 History
  5. 5. 5 1- Cognitive dysfunction. e.g. memory loss. 2-Non-cognitive symptoms: - psychiatric symptoms(depression) - behavioral changes(agitation) 3- Impaired activities of daily living. What is Alzheimer’s disease..
  6. 6. 6 What is Alzheimer’s disease.. -Alzheimer’s disease is not a part of normal aging. -Memory loss is universal and is the first symptom in the majority of cases, The gradual onset of memory loss means that it may misattributed to normal ageing and is often recognized only in retrospect as the onset of Alzheimer's disease.
  7. 7. 7 DSM-IV criteria for dementia A1-memory impairment. A2-At least one of the following: - Aphasia - Apraxia - Agnosia - Disturbance in executive functioning B-The cognitive deficits in A1 and A2 each cause significant impairment in social or occupational functioning and represent a significant decline from a previous level of functioning C-The cognitive deficits do not occur exclusively during the course of delirium.
  8. 8. 8 Diagnosis Postmortem examination, psychologic testing, and brain imaging help establish three levels of diagnostic certainty: - “Definite” Alzheimer disease is reserved for autopsy-confirmed disease. -“Probable” Alzheimer disease is the highest level of clinical diagnosis if there is no associated illness. -“Possible” refers to those who meet clinical criteria for dementia but have another illness that may contribute, such as hypothyroidism or cerebrovascular disease. -Except for the mental state, the neurologic examination is usually
  9. 9. 9 Mild cognitive impairment -Individual has subjective symptoms (predominantly of memory loss) and measurable cognitive deficits but without notable impairment in activities of daily living. -Are up to 15 times more likely to develop dementia at follow-up, suggesting it may be a precursor to Alzheimer's disease. -No treatment approved by FDA for mild cognitive impairment
  10. 10. 10 Pathology of Alzheimer’s disease
  11. 11. 11 Pathology of Alzheimer’s disease
  12. 12. 12 Pathology of Alzheimer’s disease
  13. 13. 13 Pathology of Alzheimer’s disease
  14. 14. 14 Pathology of Alzheimer’s disease
  15. 15. 15 TAU HYPOTHESIS
  17. 17. 17 Pathology of Alzheimer’s disease
  18. 18. 18 Pathology of Alzheimer’s disease -Amyloid-β is a proteolytic byproduct of the transmembrane protein (APP) -In Alzheimer disease, amyloid is deposited around meningeal and cerebral vessels and in gray matter. -Although neurofibrillary tangles are not specific to Alzheimer disease, they occur first in the hippocampus; later, neurofibrillary tangles may be seen throughout the cerebral cortex.
  19. 19. 19 Stages of Alzheimer’s disease Mild Alzheimer’s disease : Forgetfulness, short term memory loss, impaired activities of daily livings. Moderate Alzheimer’s disease : Progression of cognitive deficits, further impaired activities of daily living ,emergence of behavioral and psychological symptoms of dementia Severe Alzheimer’s disease : Agitation ,altered sleep patterns ,assistance required in dressing ,feeding ,bathing ,established behavioral and psychological symptoms of dementia Very severe Alzheimer’s disease : Bed bound ,incontinent ,no speech ,basic psychomotor skills lost.
  20. 20. 20 Alzheimer’s disease and seizures -An estimated 10-20% patient with AD develop unprovoked seizures with higher rates in familial and early onset cases. -The relationship of epileptic activity to AD is of great clinical importance. It has been suggested that seizure activity is related to pathogenesis of AD.
  21. 21. 21 Alzheimer’s disease and depression For a person to be diagnosed with depression in Alzheimer's, he or she must have either :(DSM 4 Criteria) -depressed mood . OR -decreased pleasure in usual activities, along with two or more of the following symptoms for two weeks or longer: -Social isolation or withdrawal -Disruption in appetite that is not related to another medical condition -Disruption in sleep -Agitation or slowed behavior -Irritability -Fatigue or loss of energy
  22. 22. 22 Alzheimer’s disease and depression -Feelings of worthlessness or hopelessness, or inappropriate or excessive guilt -Recurrent thoughts of death, suicide plans or a suicide attempt -Medication to treat depression in Alzheimer's : Selective Serotonin Reuptake Inhibitors (SSRIs) are often used for people with Alzheimer's and depression because they have a lower risk than other antidepressants of causing interactions with other medications.
  23. 23. 23 Lewy body dementia In developed countries ,Lewy body dementia(LBD) is the second commonest cause of dementia after Alzheimer's disease. Main features include: 1-Development of dementia with features overlapping with those of Alzheimer's disease 2-Development of features of Parkinson's disease 3-Fluctuation in severity of condition on a day-to-day basis 4-Early development of visual hallucinations
  24. 24. 24 Lewy body dementia Patients with DLB are often abnormally sensitive to neuroleptic therapy, developing parkinsonism even if they have not shown such signs before drug administration.
  25. 25. 25 Vascular dementia -Historically, considered the second most common cause of dementia, accounting for about 20 percent of cases. - Stepwise deterioration. -Focal neurological signs consistent with stroke may be present. -Pure” vascular dementia may be relatively unusual; vascular changes may more commonly coexist with Alzheimer's plaques. - Most of the drugs used to treat cognitive symptoms of Alzheimer’s disease have also been shown to help individuals with vascular dementia.
  26. 26. 26 Normal pressure hydrocephalus Triad of dementia, gait apraxia and urinary incontinence Normal pressure hydrocephalus must be differentiated from patients whose ventricular enlargement is due to brain atrophy e.g. Alzheimer’s disease
  27. 27. 27 CT brain in Alzheimer’s disease
  28. 28. 28 Chronic subdural hematomas
  29. 29. 29 Frontotemporal dementia(FTD) -FTD is the fourth most common dementia (after Alzheimer disease, vascular dementia, and dementia with Lewy bodies), - Personality change occurs before any form of memory loss, unlike Alzheimer's, where memory loss typically presents first. -40% of cases of FTD are familial, but only 10% follow a clear autosomal dominant pattern.
  30. 30. 30 Frontotemporal dementia(FTD
  31. 31. 31 Causes of death -Appetite decreases , patients lose the ability to swallow, leading to poor nutrition and a high risk of aspiration pneumonia. -Aspiration, where a person's food goes "down the  wrong tube" when they swallow it, greatly increases the risk of pneumonia developing because they're not able to fully cough and clear the food out of their esophagus and then it settles into their lungs.
  32. 32. 32 Cholinesterase inhibitors .Rivastigmine 6-12 mg .Galantamine 8-24 mg Rationale: Acetylcholine is reduced in the cerebral cortex and hippocampus due to a selective loss of cholinergic neurons. Glutamate antagonist “Memantine 10-20 mg” Pharmacotherapy
  33. 33. 33 Memantine – new perspectives in dementia treatment  Memantine represents the first and only drug in a new class – NMDA receptor antagonists – for the treatment of Dementia  Memantine blocks pathological activation of NMDA receptors by excessively high synaptic levels of glutamate while preserving physiological activation required in learning and memory formation  Memantine is indicated for the treatment of moderate and severe Dementia – the first treatment approved for this indication Memantine SmPC; Danysz et al 2000
  34. 34. 34  Both cholinesterase inhibitors and memantine produce modest but identifiable improvements in activities of daily living.  Patients and their care givers often report the improvements in activities of daily living Pharmacology
  35. 35. 35 Although antipsychotic drugs consistently reduce agitated behavior, concerns have been expressed recently over the safety of both the older antipschotics (such as haloperidol) and the new generation of antipsychotics (such as risperidone, olanzapine, and quetiapine). It increase risk of stroke and mortality. WARNING
  36. 36. 36 Thank you