Dementia Management


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Mohamed Shehata,MD Assistant Professor of Medicine Baylor College of Medicine Houston TX


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Dementia Management :

Dementia Management ABCDE Presentation Mohamed Shehata,M.D Clinical Assistant professor of Medicine Baylor College of Medicine Houston. TX. USA

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Definition Types Etiology Diagnosis Management Prognosis Care giver burden resources


Definition Dementia is a clinical syndrome in which multiple cognitive domains—including memory, language, spatial skills, judgment, and problem solving—are impaired to a disabling degree


Causes A) REVERSIBLE: 1-Metabolic:hepatic ,uremic encephalopathy Hypothyroidism, hyperthyroidism, Vit . b12,Folate 2-Vascular: Stroke 3-Neuro: seizure,NPH 4-Infectious: Fungal,bacterial,Viral,Syphilis,HIV,Lyme,CJD 5-Toxic: Drug effects,ETOH 6-Traumatic: post traumatic and sequale 7-Psychiatric: acute or chronic psychosis 8-Neoplastic:meningeal carcinomatosis



Normal Pressure Hydrocephalus:

Normal Pressure Hydrocephalus Diagnosis: Clinically by triad of Dementia, gait abnormality and urinary incontinence Imaging C.T and MRI with increased ventriculo -cortical ratio ( unreliable and could be late sign) Treatment: surgical by peritneo-ventricular shunt.

Cortical vs sub cortical :

Cortical vs sub cortical Some diseases that cause subcortical patterns of dementia lead to earlier gait, balance, and swallowing difficulties than occur with most causes of cortical dementia. Subcortical signs: extrapyramidal syndromes slowing of thought and movement (psychomotor slowing ).). Subcortical dementias are primarily found in progressive supranuclear palsy, Parkinson disease with dementia, Huntington disease, and the small-vessel form of vascular dementia.

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. The defining clinical signs of cortical dementia are aphasia (impaired language), apraxia (impaired movement programming), and agnosia (impaired recognition)—the three “ A”s Cortical signs characterize Alzheimer dementia and the frontotemporal lobar degeneration syndromes of primary nonfluent aphasia, and frontotemporal dementia (with and without motoneuron disease

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Mixed patterns of dementia characterize cortical basal ganglionic degeneration and dementia with Lewy bodies.

Vascular Dementia:

Vascular Dementia 2 types” A-large vessel territory infract. B-Small vessel disease

Dementia with Lewy Bodies:

Dementia with Lewy Bodies Characterized by: - Dementia,Parkinsonism,Visual halluciantion,REM sleep disorder. Ususally starts with, perceede or within one year of parkinsonism onset Extrapyramidal symptoms are worse by antipsychotics, and dementia worse with dopamenergic agents

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40% of cases of parkinsonism Subcortical type dementia impaired learning and memory, psychomotor slowing, constructional apraxia, and more profound visuospatial impairment than in similarly staged patients with Alzheimer dementia.


Pathology Lewy bodies are intracytoplasmic inclusions composed of α- synuclein . Lewy bodies are concentrated in the catecholaminergic nuclei of the brainstem ( substantia nigra , locus ceruleus , and dorsal motor nucleus of the vagus nerve ), the amygdala, entorhinal cortex, and neocortex .

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Substantia nigra neurons with intracytoplasmic inclusions ( arrow ) of aggregated α- synuclein ( Lewy bodies).


Management similar to those described for Alzheimer dementia. Dopaminergic medications can potentially create or worsen psychotic symptoms, particularly visual hallucinations in vulnerable patients. Quetiapine has a low risk of producing parkinsonism and, unlike clozapine, is not associated with hematologic toxicity

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Parkinsonism itself may require treatment with dopaminergic medications that may exacerbate hallucinations. REM sleep behavior disorder may be mistakenly reported by a caregiver as nocturnal hallucinations.

Clinical Description and Diagnosis of Alzheimer Dementia:

Clinical Description and Diagnosis of Alzheimer Dementia Slowly progressive terminal illness Can be staged into Mild,moderate and severe according to symptoms. Impairment at 1-Memory(recent) 2-cognition (planning , aphasia, apraxia, agnosia ) 3-Sensory 4-motor

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the National Institute of Neurological and Communicative Disorders and Stroke–Alzheimer’s Disease and Related Disorders Association (NINCDS-ADRDA) use the following categorization criteria: Possible Alzheimer dementia—Patient’s course is marked by atypical features or coincident, potentially confounding comorbidities. Probable Alzheimer dementia —There are multiple domains of functionally disabling impairment, including memory loss. Definite Alzheimer dementia— Brain tissue on autopsy confirms the diagnosis in a patient with clinically probable Alzheimer dementia.

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There are no widely used biomarkers for Alzheimer dementia, so the goal of the clinical evaluation remains the exclusion of nondegenerative causes. -All patients with suspected Alzheimer dementia should undergo the tests mentioned previously for patients with dementia (imaging studies, blood tests) in addition to other tests specific to the patient’s medical history

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. Imaging findings of generalized or medial temporal atrophy are common but nonspecific for Alzheimer dementia. - fluorodeoxyglucose positron emission tomographic scanning (reduced cerebral glucose metabolism in posterior cingulate, parietal, and temporal cortices is characteristic of Alzheimer dementia

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Other tests not routinely performed and considered optional at this time include assessment for the apolipoprotein E (APOE) genotype (the e4 allele implies greater likelihood of Alzheimer dementia in a patient with cognitive impairment);); and CSF analysis for amyloid beta (A β) amino acids 41-42 (lower levels imply Alzheimer dementia) and phospho -tau (higher levels imply Alzheimer dementia).

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The two hallmark neuropathologic lesions that define Alzheimer dementia are the neuritic amyloid plaque and the neurofibrillary tangle, both of which are generally found in increasing numbers with increasing disease severity

Photomicrograph of the neuropathologic findings of Alzheimer dementia:

Photomicrograph of the neuropathologic findings of Alzheimer dementia Left , neuritic amyloid plaques (Campbell-Switzer stain). Right , neurofibrillary tangles ( Gallyas stain).

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The most common cause of ementia . Alzheimer dementia accounts for more than half of all cases and increases in frequency with advancing age

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The prevalence of severe dementia from all causes in patients older than 60 years is estimated at 5% and in those older than 85 years between 20% and 50%. The lifetime risk of developing Alzheimer dementia is estimated to be between 12% and 17%

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Besides age, APOE status is the second most important risk factor for Alzheimer dementia. In both familial late-onset Alzheimer dementia and sporadic cases, presence of the APOE e4 allele increases risk, whereas presence of the e2 allele decreases risk.

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The lifetime risk of Alzheimer dementia in persons without a family history increases from 9% in those without an APOE e4 allele to 29% in those with one copy of the allele. APOE e4 homozygotes make up roughly 2% of the population, and approximately 80% to 90% of them are estimated to develop Alzheimer dementia in their lifetimes. APOE genetic testing is available but not generally recommended for asymptomatic individuals because of the current absence of effective disease-modifying therapy

Progression of Alzheimer Dementia:

Progression of Alzheimer Dementia The mean time from the diagnosis of probable Alzheimer dementia until death is approximately 6 years. Multiple staging schemes of dementia severity between MCI (CDR score = 0.5) and death can be most simply summarized as mild (CDR score = 1.0 ) moderate (CDR score = 2.0 ) severe (CDR score = 3.0).

Mild dementia:

Mild dementia Disability in some normal daily activities misplacing items in inappropriate places , becoming lost in familiar places, having difficulty with simple financial transactions (being unable to make change), and experiencing mild deterioration in personal care. Most tasks are completed correctly most of the time, and patients may deny they have a problem ( anosognosia ).


Moderate-stage Characterized by more severe impairment of -Cognitive skills Language (naming, spelling), Basic daily activities (preparing meals, managing household finances ). Delusional thinking is also characteristic, with stealing and infidelity as two prevalent themes. Patients at this stage cannot generally make a successful pretense of normalcy and require supervision, even if they continue to deny that anything is wrong.

Severe dementia :

Severe dementia require assistance with all basic activities of daily living including dressing, bathing, personal hygiene, and eating. Urinary and bowel incontinence develops during this stage. Affected patients are more frankly aphasic (fluent aphasia), agnosic (failure to recognize familiar people and places), and apraxic (inability to write or dress) in addition to having memory loss .

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Alzheimer dementia is best treated with the primary therapeutic modality of caregiving, with the physician largely providing assistance to the caregiver . In this context, pharmacotherapy and lifestyle adjustments can be used. There are six major categories of pharmacotherapy to consider in any patient with Alzheimer dementia.


Prevention There are as yet no proven pharmacologic or other primary prevention therapies for Alzheimer dementia

Intellectual Decline:

Intellectual Decline Two classes of drugs have been approved by the U.S. Food and Drug Administration ( FDA : 1- acetylcholinesterase inhibitors . Donepezil, galantamine , and rivastigmine approved for the treatment of mild to moderate Alzheimer dementia. activities of daily living, and functioning treatment goals focus on delaying the worsening of these features, although a minority of patients can actually show temporary partial improvement ..

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2- N-methyl-D-aspartate receptor antagonist Memantine is approved as treatment for the moderate to late stages of Alzheimer dementia . After a full therapeutic trial of a medication from one class, there is some evidence to suggest that modest additional benefit may be obtained by adding a medication from the other class

Behavioral Decline:

Behavioral Decline AZ related Psychosis : agitation (particularly sundowning ), paranoid delusions, and hallucinations (typically, but not exclusively, visual and more common in patients with dementia with Lewy bodies than Alzheimer dementia). No approved agents FDA but atypical antipsychotic agents, such as quetiapine , are widely used in patients with parkinsonism, for example, because they are less likely to cause or exacerbate extrapyramidal syndromes than are older agents.

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Two recent studies showed no efficacy of such agents in patients with dementia when used in either a community-based setting or a subspecialty practice. Because the dosages used in both studies were considered by many subspecialists too low to be conclusive, the use of these agents continues. The FDA requires a black box warning label on the use of atypical antipsychotic agents in the treatment of dementia because of the roughly 1.6-fold increased risk of mortality they pose (

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Older typical antipsychotic drugs, such as haloperidol, pose an even higher risk of parkinsonism, tardive dyskinesia, and death in patients with Alzheimer dementia. All antipsychotic agents should be avoided in patients with prolonged QT intervals because of the risk of torsades de pointes and ventricular tachycardia.

AZ related depression:

AZ related depression Drugs with anticholinergic properties, such as tricyclic antidepressants , should be avoided in the treatment of depression in patients with Alzheimer dementia because of the risk of exacerbating confusion . Selective serotonin reuptake inhibitors (SSRIs) are preferred and can sometimes also help ease agitation. However, SSRIs may occasionally precipitate rapid eye movement (REM) sleep behavior disorder (body or limb movements during REM sleep) in patients with an underlying Lewy body–related disorder. Trazadone , is widely used although randomized controlled trials of this drug are lacking.

AZ realted Anxiety:

AZ realted Anxiety Buspirone or an SSRI may be tried initially to treat anxiety in patients with Alzheimer dementia. If not effective, a low-dose atypical antipsychotic medication (as described earlier) might be considered

AZ related Sleep Disorders:

AZ related Sleep Disorders A) simple sleep hygiene ( reduced daytime sleep, and increased daily physical activity …….. etc ) short-acting sedative-hypnotic Antihistamines , may have adverse effects on cognition and so are not recommended.

REM sleep behavior disorder :

REM sleep behavior disorder Clonazepam( cognition, falls) Melatonin.

Obstructive sleep apnea:

Obstructive sleep apnea Occasionally associated with cognition impairment. Can be confused with MCI Dx : sleep study Treatment as OSA

Other Commonly Associated Disorders:

Other Commonly Associated Disorders Urinary incontinence: due to overflow and spastic bladder can be diff. by PVR scan Overflow Rx by frequent toileting plan Spastic RX by anticholinergic meds as Oxybutynin at lowest doses

Abrupt Decline:

Abrupt Decline With associated illness as UTI, PNA, meds SE, periop. Trial of Haldol decreased periop. delirium duration

Lifestyle Changes:

Lifestyle Changes Home safe environment Safe return home program for wandering Driving Gun ownership Placement Caregiver Burden

Wrap up:

Wrap up AZ: chronic,terminal,progressive illness Stages: Mild,moderate,severe RX: Nonpharm+Pharm End of life issues,placement,care giver burden, local organizations and societies for support.

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