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CLINICAL PRACTICE GUIDELINES
Guidelines Abstracted from the American Academy of Neurology's Dementia Guidelines for Early Detection, Diagnosis and Management of Dementia

1. Early Detection: Determine whether screening different groups of elderly individuals with mild cognitive impairment in a general and specialty practice would be beneficial in detecting dementia.
2. Diagnosis: Update 1994 practice parameters for diagnosis of dementia.
3. Management: Define and investigate key issues in the management of dementia.

1. Early Detection: Options for early detection of dementia included assessment of general cognitive screening instruments, brief focused screening instruments, neuropsychologic batteries, and informant-based instruments.
2. Diagnosis: Formulations that are widely used in North America (e.g., National Institute of Neurologic, Communicative Disorders and Stroke - AD and Related Disorders Association (NINCDS-ADRDA) Work Group, Diagnostic and Statistical Manual, 3rd edition, revised (DSM-IIIR), and the Diagnostic and Statistical Manual, 4th edition (DSM-IV) were considered for their reliability for diagnosing dementia. Diagnostic formulations and clinical criteria were examined for their ability to reliably diagnosis prevalent dementias (e.g., Alzheimer's disease, vascular dementia, dementia with Lewy bodies, frontotemporal dementia and prion disease). Laboratory tests (e.g., structural imaging, quantitative imaging, functional neuroimaging, genetic biomarkers, CSF and other biomarkers) were examined to determine if specific tests improved the accuracy of clinical diagnosis of dementing illnesses.
3. Management: Options that were evaluated included pharmacotherapy to improve cognitive symptoms in Alzheimer's disease, patients with mixed dementias and ischemic vascular dementias. Also pharmacotherapy used to treat behavioral disturbances, educational interventions, interventions to improve functional performance, nonpharmacologic interventions for problem behaviors, Alzheimer's special care units and interventions for caregivers were evaluated.

1. Evidence provided by one or more well designed, randomized, controlled clinical trials, including overviews (meta-analyses) of such trials
2. Evidence provided by well designed observational studies with concurrent controls (e.g., case control or cohort studies)
3. Evidence provided by expert opinion, case series, case reports, and studies with historical controls

Standard	Principle for patient management that reflects a high degree of clinical certainty (usually this requires Class I evidence that directly addresses the clinical questions, or overwhelming Class II evidence when circumstances preclude randomized clinical trials).
Guideline	Recommendation for patient management that reflects moderate clinical certainty (usually this requires Class II evidence or a strong consensus of Class III evidence).
Practice Option	Strategy for patient management for which the clinical utility is uncertain (inconclusive or conflicting evidence or opinion).

• Patients with mild cognitive impairment should be recognized and monitored for cognitive and functional decline due to their increased risk for subsequent dementia. General cognitive screening instruments, which include the Mini-Mental State Exam, Kokmen Short Test of Mental Status, 7-Minute Screen, and Memory Impairment Screen, are useful for the detection of dementia when used in patient populations with increased prevalence of cognitive impairment (Guideline).
• Brief cognitive assessment instruments that focus on limited aspects of cognitive function (i.e., Clock Drawing Test, Time and Change Test) may be considered when screening for dementia (Practice Option).
• Neuropsychiatric batteries (i.e., Neuropsychologic Battery, Mattis Rating Scale, Halifax Mental Status Scale, and Fuld Object Memory Test), particularly those that emphasize memory function, should be considered useful in identifying patients with dementia when administered to a population at increased risk of cognitive impairment (Guideline).
• Interview-based techniques (i.e., Blessed Roth Scale, Clinical Dementia Rating, Informant Questionnaire on Cognitive Decline in the Elderly) may be considered in identifying patients with dementia, particularly in populations at increased risk for cognitive impairment (Practice Option).

• The DSM-IIIR definition of dementia, which is identical to the DSM-IV definition, is reliable and should be used routinely (Guideline).
  
  

• The NINCDS-ADRDA criteria for the diagnosis of probable AD or DSM-IIIR criteria for DAT should be routinely used (Guideline).
• The Hachinski Ischemic Index may be of use in the diagnosis of cerebral vascular disease in dementia (Practice Option).
• The consortium for Dementia with Lewy-bodies diagnostic criteria may be of use in clinical practice (Practice Option).
• The Consensus diagnostic criteria for frontotemporal dementia may be of use in clinical practice (Practice Option).
• Clinical criteria for Creutzfeldt-Jakob disease should be used in rapidly progressive dementia syndromes (Guideline).

• Structural neuroimaging with either a noncontrast CT or MR scan in the routine initial evaluation of patients with dementia is appropriate (Guideline).
• Linear or volumetric MR or CT measurement strategies for the diagnosis of AD are not recommended (Guideline).

• SPECT cannot be recommended for routine use in either initial or differential diagnosis (Guideline).
• PET imaging is not recommended for routine use in the diagnosis of dementia (Guideline).

• Genetic testing for suspected AD, DLB and CJD is not recommended (Guideline).
• Testing for tau mutation or AD gene mutations is not recommended for routine evaluation in patients with FTD (Guideline).

• No CSF or other biomarkers are recommended for routine use in diagnosis AD (Guideline).
• The CSF 14-3-3 protein is recommended for confirming or rejecting the diagnosis of CJD in clinically appropriate circumstances (Guideline).

• Cholinesterase inhibitors should be considered in patients with mild to moderate AD (Standard), although studies suggest a small average degree of benefit.
• Vitamin E (1000 I.U. PO BID) should be considered in an attempt to slow progression of AD (Guideline).
• Selegiline (5 mg PO BID) is supported by one study, but has less favorable risk-benefit ratio than Vitamin E (Practice Option).
• There is insufficient evidence to support the use of other antioxidants, anti-inflammatories, or other putative disease-modifying agents specifically to treat AD because of the risk of significant side effects in the absence of demonstrated benefits (Practice Option).
• Estrogen should not be prescribed to treat AD (Standard).

• Some patients with unspecified dementias may benefit from ginkgo biloba, but evidence-based efficacy data are lacking (Practice Option).

• There are no adequately controlled trials demonstrating pharmacologic efficacy for any agent in ischemic vascular (multi-infarct) dementia.

• Antipsychotics should be used to treat agitation or psychosis in patients with dementia where environmental manipulation fails (Standard). Atypical agents (e.g., risperidone, olanzepine, and quetiapine) may be better tolerated compared with traditional agents (e.g., haloperidol) (Guideline).
• Selected antidepressants (i.e., tricyclics, Mao-B inhibitors, and SSRIs) should be considered in the treatment of depression in individuals with dementia with side effect profiles guiding the choice of agent (Guideline).

• Short-term programs directed toward educating family caregivers about AD should be offered to improve caregiver satisfaction (Guideline).
• Intensive long-term education and support services (when available) should be offered to caregivers of patients with AD to delay time to nursing home placement (Guideline).
• Staff of long-term care facilities should receive education about AD to reduce the use of unnecessary antipsychotics (Guideline).

Interventions other than education for patients and caregivers

• Behavior modification, scheduled toileting, and prompted voiding should be used to reduce urinary incontinence (Standard).
• Graded assisitance, practice, and positive reinforcement should be used to increase functional independence (Guideline).
• Low lighting levels, music, and simulated nature sounds may improve eating behaviors for persons with dementia, and intensive multimodality group training may improve activities of daily living, but these approaches lack conclusive supporting data (Practice Options).

• Persons with dementia may experience decreased problem behaviors with the following interventions: music, particularly during meals and bathing (Guideline); walking or other forms of light exercise (Guideline).
• Although evidence is suggestive only, some patients may benefit from the following (Practice Options):
  • Simulated presence therapy, such as the use of videotaped or audiotaped family members
  • Massage
  • Comprehensive psychosocial care programs
  • Pet therapy
  • Commands issued at the patient's comprehension level
  • Bright light, white noise
  • Cognitive remediation

• Although definitive data are lacking, the following environments may be considered for patients with dementia (Practice Options):
  • Special care units (SCU) within long-term care facilities
  • Homelike physical setting with small groups of patients as opposed to traditional nursing homes
  • Short-term, planned hospitalization of 1 to 3 weeks with or without blended inpatient and outpatient care
  • Provision of exterior space, remodeling corridors to simulate natural or home settings, and changes in the bathing environment

• The following interventions may benefit caregivers of persons with dementia and may delay long-term placement (Guideline):
  • Comprehensive, psychoeducational caregiver training
  • Support groups
• Additional patient and caregiver benefits may be obtained by use of computer networks to provide education and support to caregivers (Practice Option), telephone support programs (Practice Option), and adult day care for patients and other respite services (Practice Option).

COMMENTARY

As always, applying clinical guidelines in practice requires specific knowledge of a particular patient's needs and consummate medical judgment. To put these guidelines into perspective, the Clinical Practice Committee solicited the following commentary from Dr. Peter Whitehouse.

As a geriatric neurologist, I welcome the publication of the synopsis of the American Academy of Neurology (AAN) guidelines (Petersen et al, 2001; Knopman et al, 2001;Doody et al, 2001) on early recognition, diagnosis, and management of dementia in this issue of JAGS (reference, 2003). As a participant in the process, I must disclose my bias towards their usefulness and also recognize the hard work that went into this process by all involved. As the first section outlines, the development of these guidelines was carefully conducted and their scope and values extend across medical and psychosocial aspects of care. It is perhaps remarkable that only the highest level of evidence, i.e. "standards", supports four of the recommendations. It is expensive to generate high quality evidence through randomized controlled studies. Such evidence often depends on industry support, which can bring certain biases. Evidence-based studies are appropriate foundations for guidelines but to be helpful to practitioners, the data needs to be interpreted by experts and complimented by the opinions in areas where little good trial evidence is available. As the studies of complementary and alternative and psychosocial interventions demonstrate particularly well, there are major challenges to conducting randomized control studies on complex integrative therapies. We will never be able to afford, conduct and/or interpret all the controlled studies needed to make the treatment of dementia based solely on highest qualities of evidence.

The quality of guidelines themselves is related to the inclusiveness of the development process and the intensity of the search for information. Moreover, the financial support and orientation of the sponsoring organizations such as pharmaceutical companies, health care organizations, federal agencies, as well as professional associations, should be considered as potential sources of bias. In my non-randomized experience, a point of contention between geriatricians and neurologists is often the value of neuroimaging (either generally or in specific ways). The recommendations of the AAN guidelines are conservative. Only non-contrast CT (or MRI) is recommended. My own view is that a non-contrast CT is appropriate in most cases but may even be excessive depending on the type of practice. During my career I have dutifully ordered a CT on patients who have not had a previous examination for at least the last year prior to visiting me. As a result, I have received a constant barrage of readings of variably judged atrophy and differently interpreted white matter changes. Had I to develop my particular, admittedly rather tertiary, practice over again, I could have saved a lot of money by ordering fewer scans. I would like to see more research-based guidelines concerning the costs and benefits of neuroimaging in patients who have had well-established typical progressive courses.

Efforts to market, and sometimes justify, more expensive neuroimaging and other diagnostic tests for dementia will continue. Recently, a proposal has been made to the Committee on Medicaid and Medicare Services that positron emission tomography for diagnosis of dementia should be reimbursed. Although rational (but unconvincing to me) arguments about sensitivity and specificity, as well as health economics can be made, there is a fundamental difficulty with all such approaches to diagnosing dementia and particularly AD. It is the difficulty that geriatricians face every day. Where does aging stop and dementia begin? How many senior moments does dementia make? How does the almost ubiquitous mild memory impairment found in old and not so old patients fit in our diagnostic process? Is this pre-dementia or early dementia? The AAN guidelines are the best attempt to address the "diagnosis" of Mild Cognitive Impairment. They specifically do not advocate general population screening but suggest that if a physician or other health care professionals has any suspicion of cognitive impairment or decline, then mental status testing should be conducted. However, be it a physician's opinion based mental status testing or a positron emission scan, any diagnosis of a progressive dementia like AD, represents an arbitrary cut point on a continuum of neuro-cognitive dysfunction. Before the term Mild Cognitive Impairment, we had such conditions as benign senile forgetfulness, aging-associated memory impairment and aging-related cognitive decline. All threshold scores on a continuum that would allow one to differentiate normal aging on one hand and AD on the other are arbitrary. Whether we call MCI of the amnesic type early AD or pre AD is a semantic/political decision and not primarily a scientific one.

These guidelines for practicing clinicians address this issue of dementia detection as early recognition. Certainly early recognition of reversible forms of dementia is desirable, although it is difficult to know how many cases of hypothyroidism or Vitamin B12 deficiency really present as dementia without other noticeable physical symptoms or signs. There is little evidence that early treatment with cholinesterase inhibitors is somehow better early in the disease although studies in MCI are underway. Any adult should be given the advice to consider legal and financial issues related to the possibility of developing cognitive impairment in old age, as it is so common. Thus, the push to recognize dementia early should be considered in the context of the motivations of those encouraging early recognition, the benefits of identifying truly reversible forms of dementia, and the advantages and disadvantages of labeling someone with a degenerative process like AD early.

Labeling the extreme of normal age related cognitive impairment as a discrete terrifying disease, namely AD, raises questions about the value of medicalizing age-related changes. Is the terror of AD worse that the actual state? If we accept some cognitive changes as "normal" but still worthy of remediation, perhaps we can think differently about ways to improve cognitive deterioration of any kind. Drugs may improve my memory or that of someone diagnosed (labeled) with AD but the right computer support or community learning environment may help us both as well. We may never develop a biomarker for dementia that categorically differentiates AD from non-disease. The only definite marker of AD is a socio-marker, i.e. a diagnosis by a physician. Let us be sure we know what and who we are labeling and for what purpose. Several epidemiological studies have shown that education and perhaps ongoing intellectual and physical activities may help people prevent age-related cognitive deterioration. Although interpretations of these case-controlled studies are fraught with difficulties, the advice to keep mentally and physically active is probably wise, regardless of the scientific support for such an assertion. Moreover, it is worthwhile to consider developing educational interventions to prevent age-related cognitive deterioration. For example, we (National Institute on Aging Cooperative Study) are currently conducting with an NIH funded primary prevention study to examine the possibility that reading books about memory training and learning in community settings, might actually delay the development of cognitive deterioration (particularly if people act on the advice in the books). Moreover, my colleagues and I in Cleveland have developed the world's first explicitly intergenerational public school to provide an educational environment that is supportive to learners of all ages, including those with various age-related cognitive challenges (Whitehouse et al., 2000).

In conclusion, the AAN guidelines will be valuable to clinicians faced with an older individual facing cognitive changes, but we must remember that there is much more to addressing the aging mind than the early recognition, diagnosis, and management of dementia. Recognizing that some degree of age-related cognitive change is practically ubiquitous and preserving and enhancing our cognitive vitality through a variety of means will help us practice our geriatrics more wisely.

Knopman DS, DeKosky ST, Cummings JL,et al. Practice parameter: Diagnosis of dementia (an evidence-based review) Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2001;56:1143-1153.

Doody RS, Stevens JC, Beck C, et al. Practice parameter: Management of dementia (an evidence-based review) Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2001;56:1154-1166.

JAGS, 2003 reference to this issue…

Whitehouse PJ, Bendezu E, FallCreek S, et al. Intergenerational Community Schools: A New Practice for a New Time. Educ Gerontol, 2000; 26:761-770.

This AGS Abstracted Guideline was abstracted from Practice parameter: Early detection of dementia: Mild cognitive impairment (an evidence-based review) Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2001;56:1133-1142, Practice parameter: Diagnosis of dementia (an evidence-based review) Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2001;56:1143-1153, Practice parameter: Management of dementia (an evidence-based review) Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2001;56:1154-1166. On behalf of the AGS Clinical Practice Committee, Samuel C. Durso, MD, Lisa Gwyther, MSW, Bernard Roos, MD and Martin Gorbien, MD abstracted the guideline and Peter J. Whitehouse, MD, PhD provided the Commentary. Address correspondence and reprint requests to: American Geriatrics Society, The Empire State Building, 350 Fifth Avenue, Suite 801, New York, NY 10118, Fax: 212-832-8646, info.amger@americangeriatrics.org.