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Is It Alzheimer's? How to Pare Down the Possibilities Is it Alzheimer’s? How to pare down the possibilities A clinical guide to rule out other dementing diseases and rare reversible causes ccurate and early diagnosis of Alzheimer’s® Dowden dis- Health Media ease (AD) is evolving, and—although not yet Adefi nitive—is no longer one of exclusion. With a careful in-offi ce work-upCopyright and routineFor assessment personal tools, use only you can accurately identify >90% of patients with late- onset AD.1 AD is by far the most common cause of dementia in older patients. To help you make the diagnosis, this state-of-the-art article discusses: • AD’s clinical presentation and course • the role of neuropsychological tests for assessing cognitive and functional status • neuropsychiatric and medical fi ndings that differ- ORVIDAS entiate AD from other dementia causes KEN • indications for structural neuroimaging with CT 2008 © or MRI. Mehret Gebretsadik, MD Chief resident Presentation and course George T. Grossberg, MD Samuel W. Fordyce Professor Variability. AD’s gradual onset and progression are Director, division of geriatric psychiatry characterized by prominent memory loss, anomia, con- structional apraxia, anosognosia, and personality chang- Department of neurology and psychiatry es with affect deregulation, behavioral disturbance, and Saint Louis University School of Medicine distorted perception.1 Amnesia—particularly defi cits in anterograde episodic memory—is the most common presentation, but the disease course is heterogeneous and may be affected by: • patient age at onset • illness severity at diagnosis • comorbid medical and neuropsychiatric illnesses Current Psychiatry • premorbid cerebral reserves (amount of brain Vol. 7, No. 1 53 For mass reproduction, content licensing and permissions contact Dowden Health Media. 053_CPSY0108 053 12/13/07 1:19:30 PM Box 1 Biomarkers show promise to improve AD diagnosis esearchers are investigating surrogates however, among AD and other dementias. Rfor detecting Alzheimer’s disease (AD) Other possible serum, CSF, and urine markers and monitoring disease progression.5 include isoprostanes, sulfatides, oxysterols, homocysteine, apolipoprotein E, alpha 1- Alzheimer’s Serum and CSF markers. AD is viewed antichymotrypsin, 3-nitrotyrosine, and more.8 diagnosis as a series of sequential events, beginning No biomarkers are available or recommended with beta-amyloid (β-amyloid) accumulation for clinical use at this time. and progressing through a pathophysiologic cascade to cell death, transmitter defi cit, Neuroimaging. Amyloid imaging tracers and dementia. A unique biomarker may may increase the capacity of single photon be associated with each event, either in emission computed tomography (SPECT) the primary disease process of β-amyloid and positron emission tomography (PET) production and accumulation or intermediate to detect AD pathology. These tracers Clinical Point processes such as tau hyperphosphorylation, have high binding affi nity for amyloid and oxidation, and infl ammation.5,6 may enable PET/SPECT to detect amyloid Clinical assessment These biochemical markers are found deposits in vivo. has low specifi city more consistently in cerebrospinal fl uid (CSF) Amyloid radioligands are being developed than peripherally. Lower CSF β-amyloid and tested as potential clinical diagnostic in advanced stages, (especially β-amyloid 42) and higher CSF tau tools and surrogate biomarkers of antiamyloid where all dementia and tau-phosphorylated (p-tau) have been therapies. A radioligand that targets amyloid subtypes are similar found in AD patients compared with normal and neurofi brillary tangles in AD has been and disease controls.7 Some overlap exists, developed recently for use as a research tool. and comorbidities confuse the picture damage a person can sustain before reach- tently show small improvements in cogni- ing a threshold for the clinical expression tive and global function when treated with of dementia).1-3 acetylcholinesterase inhibitors (AChEIs) such as donepezil, rivastigmine, and galan- Staging illness severity. AD has 3 clinical tamine.4 Donepezil also is approved for use stages of cognitive dysfunction: in severe AD. Mild AD. An individual or close compan- Memantine is indicated for symptom- ion may notice increased forgetfulness and atic treatment of moderate-to-severe AD. word-fi nding diffi culties, a tendency to It differs in mechanism of action from the lose or misplace things, repeated question- AChEIs and is thought to inhibit cytotoxic ing, and some disorientation. Motor skills overstimulation of glutamatergic neurons.4 are intact. For moderately advanced AD, memantine Moderate AD. Cognitive decline contin- appears to be benefi cial alone or in combi- ues, memory deteriorates, and self-care nation with AChEIs. ability is markedly impaired. The indi- vidual may undergo personality changes, confuse time and place, have trouble com- Dementia assessment municating and recognizing family mem- Clinical assessment has low sensitivity for bers or friends, develop agitation, begin early-phase AD and compromised speci- to wander, and experience delusions and fi city in advanced stages, where all demen- hallucinations. tia subtypes are similar and comorbidities Severe AD. An individual with late-stage may confuse the picture. Promising sur- disease has severe impairment and can be rogate biomarkers and other diagnostic bedridden, incontinent, and unable to under- tools are being developed (Box 1),5-8 but stand or speak. Full-time care is required. defi nitive AD diagnosis still requires post- Staging informs treatment. In clinical trials, mortem histopathologic examination of Current Psychiatry 54 January 2008 patients with mild-to-moderate AD consis- the cerebral cortex. 054_CPSY0108 054 12/13/07 1:19:36 PM Box 2 Can your AD patient drive or live alone? Consider neuropsychological assessment CurrentPsychiatry.com europsychological tests disclose a degree time. Some older patients fi nd the tests Nof intellectual impairment that correlates distressing or tiring, and those with severe with functional impairment and may be dementia are incapable of participating. particularly useful for assessing: Patients’ anxiety about taking tests, poor • mild cognitive impairment when diagnosis test-taking skills, low motivation/effort, and is doubtful language, cultural, and educational variables • cases where major lifestyle changes may limit these tests’ usefulness and may infl uence be required, such as driving cessation or results. assisted-living placement. Interpret a neuropsychological evaluation These tests can examine performance in the context of other clinical data, such as across different domains of cognitive function, informant-based history of cognitive decline, including orientation, memory, attention, evidence of impairment in independent naming, comprehension, and praxis. activities of daily living, educational Clinical Point background, depression assessment, sensory Limitations. Neuropsychological tests have impairment, or factors other than dementia that Apraxia, aphasia, limitations, including cost and administration may account for impaired performance. and cortical visual Source: References 13,14 impairment may refl ect focal signs History and physical exam. Depending Neuropsychological testing. Most men- of atypical AD on the AD stage at presentation, patients tal status tests examine orientation, at- might not be a reliable source of informa- tention/concentration, learning, memory, tion. For a realistic and unbiased history language, and constructional praxis. The and evaluation, assess the patient sepa- Folstein Mini-Mental State Examination rately and obtain collateral information (MMSE)9 is the most widely used and well- from reliable informants. validated mental status test. A score of 10 In typical cases, the history guides the to 20 on the MMSE is generally considered physical/neurologic examination. Advanc- as moderate AD, and <10 is staged as se- ing age and family history are confi rmed risk vere AD.10 Other mental status testing op- factors for AD; others may include: tions include: • female gender (after age 80) • Blessed Information-Memory- • cardiovascular disease (such as Concentration (BIMC) cerebral infarcts, hypertension, elevated • Blessed Orientation-Memory- cholesterol/homocysteine, smoking, and Concentration (BOMC) diabetes mellitus) • Short Test of Mental Status (STMS) • history of head trauma, especially • Saint Louis University Mental Status with loss of consciousness. (SLUMS).11,12 Assess premorbid functioning and ex- Neuropsychological tests have limita- isting medical conditions. Apraxia, apha- tions, but they can supplement clinical sia, and cortical visual impairment may cognitive assessment by detecting milder refl ect focal signs of atypical AD; consider cases and may help answer questions other neurologic signs in the context of about a patient’s ability to drive or live clinical data. alone (Box 2).13,14 Early and accurate diagnosis of AD is challenging in patients with mixed demen- Reversible causes. If the patient is gener- tias, comorbid neurologic diseases, or atypi- ally healthy, a core of laboratory tests is cal features. Patients with these presentations recommended in the diagnostic workup may require referral to an expert clinician, (Table 1, page 56).6,15 Other options include: extensive workup, or longitudinal follow-up • CSF examination for atypical presen- Current Psychiatry before the diagnosis becomes clear. tations, such as unusually rapid symptom Vol. 7, No. 1 55
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