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Mohammed T. Abou-Saleh

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PREVENTION IN LATE-LIFE MENTAL DISORDERS 781Nonetheless, there are some interesting possibilities developing aswe learn more about oxidative and inflammatory processes,apoptotic mechanisms, hormonal correlates and genetic factors indisease. One possible example is the area of vascular depression.Several different lines of evidence are now supporting theconclusion that one form of late-onset depression has acerebrovascular etiology 29 . Trials of vascular agents could useincident depression as outcomes.Genetic ModelsThe genetics of mental disorders is an area of expanded activity 30 .Notably, several genes are now implicated in different forms ofAlzheimer’s disease. At present, the genetic correlates of mentaldisorders are not sufficiently specific to be used for purposes ofpopulation screening. It is entirely conceivable, however, thattrials directed at delaying onset of disease, or directed atminimizing excess disability, could be launched using some ofthis genetic information as a basis for subject selection.Clinical ModelsCo-morbidity is one of the hallmarks of mental disordersthroughout the life course. In late-life mental disorders, themost frequently observed co-morbidities are physical illness andbrain disease. This provides a possible opportunity for preventiveinterventions; we present a few examples.Visual impairment is common among older people; there is ahigh frequency of depression among older persons with impairedvision, and the depression is more strongly predictive of disabilitythan is the vision loss 31 . The vision clinic would seem to be anappropriate location for the development of programs orientatedto the prevention of depression in older patients. Similarly,aggressive intervention in depression has the potential forminimizing disability and optimizing function. This latter pointis supported by a broad range of studies demonstrating thatdepression compromises the outcome of rehabilitation in stroke,Parkinson’s disease, heart disease, pulmonary disease andfractures 32 . Research has also demonstrated that treatment ofdepression can significantly improve outcome of treatment andrehabilitation for the co-morbid physical illness or condition 33,34 .Complex programmatic interventions have been shown to haveefficacy in the area of prevention as well. Ray et al. 19 , for example,show how an intervention directed at safety with appropriate useof wheelchairs, psychotropic drugs and provision for transfer andambulation, has a significant impact on the reduction of falls innursing homes. In the outpatient setting, multidisciplinarycomprehensive assessment resulted in significant improvementsin the detection of depression and cognitive impairment andresulted in substantially reduced risk for nursing home placement35,36 .Psychosocial ModelsBereavement is perhaps the prototypical psychosocial risk factorin late-life mental disorders 37 . Considerable research has beendevoted to the exploration of bereavement-related depression,complicated grief, traumatic grief and similar constructs 38–40 .Itisentirely conceivable that preventive interventions for those withcomplicated grief could have major impact on both mental andphysical health. It is also conceivable that greater understandingof the correlates and predictors of complicated or traumatic griefmay lead to the design of earlier-stage interventions, directed atmodifying the likelihood of developing the risk factor in the firstplace. Interventions directed toward risk factors, rather thantoward disorders, may be properly considered to be primaryprevention.CONCLUSIONIn this chapter we have presented the broad parameters of aprogrammatic approach to prevention in late-life mental disorders.There is no established approach to prevention researchthat could be easily adapted to meet the needs of the field.Approaches to prevention need to be based in the deepfoundation of knowledge in treatment and services research.They must be built upon improved models of etiology,pathophysiology and risk. A new approach to prevention holdsthe promise to be a significant development for the field. We haveno doubt that success is achievable.REFERENCES1. Mrazek P1, Haggerty RI, eds. Reducing Risks for Mental Disorders:Frontiers for Preventive Intervention Research. Washington, DC:National Academy Press, 1994.2. Gruenberg EM. The failure of success. Health Soc Milbank MemorialFund Qu 1977; 55: 3–23.3. Kramer M. The rising pandemic of mental disorders and associatedchronic diseases and disabilities. Acta Psychiat Scand 1980; 62(suppl285): 382–97.4. Burns B. Prevention of mental disorders in old age. In CopelandJRM, <strong>Abou</strong>-<strong>Saleh</strong> MT, Blazer DG, eds, Principles and Practice ofGeriatric Psychiatry, 1st edn. Chichester: Wiley, 1994; 1011–16.5. Gordon R. An operational definition of disease prevention. PublHealth Rep 1983; 98: 107–9.6. National Advisory Mental Health Council. Priorities for PreventionResearch at NIMH. NIH Publication No. 98-4321. Bethesda, MD:NAMHC, 1998.7. Kraemer HC, Kazdin AE, Offord DR et al. Coming to terms with theterms of risk. Arch Gen Psychiat 1997; 54: 337–43.8. Schneider LS. Pharmacological considerations in the treatment of latelife depression. Am J Geriat Psychiat 1996; 4(suppl 1): S5l–65.9. American Psychiatric Association. Practice guidelines for thetreatment of patients with Alzheimer’s disease and other dementiasof late life. Am J Psychiat 1997; 154(suppl): 1–39.10. Small GW, Rabins PV, Barry PV et al. Diagnosis and treatment ofAlzheimer’s disease: consensus statement of the AmericanAssociation for Geriatric Psychiatry, the Alzheimer’s Association,and the American Geriatrics Society. J Am Med Assoc 1997; 278:1363–71.11. Lebowitz BD, Pearson IL, Schneider LS et al. Diagnosis andtreatment of depression in late life: consensus statement update. JAm Med Assoc 1997; 278: 1186–90.12. Reynolds CF, Frank E, Kupfer DI et al. Treatment outcome inrecurrent major depression: a post hoc comparison of elderly(‘‘young-old’’) and midlife patients. Am J Psychiat 1996; 153:1288–92.13. Nemeroff CB, De Vane CL, Pollock BG. Newer antidepressants andthe cytochrome P450 system. Am J Psychiat 1996; 153: 311–20.14. Paulsen JS, Caligiuri MP, Palmer B et al. Risk factors for orofacialand limbtruncal tardive dyskinesia in older patients: a prospectivelongitudinal study. Psychopharmacology 1996; 123: 307–14.15. Katz IR, Jeste DV, Brecher M et al. Comparison of risperidone andplacebo for psychosis and behavioral disturbances associated withdementia: a randomized, double-blind trial. J Clin Psychiat 1999; 60:107–115.16. Lohr LB, Lavori P. Editorial: whither vitamin E and tardivedyskinesia? Biol Psychiat 1998; 43: 861–2.17. Adler LA, Edson R, Lavori P et al. Long-term treatment effects ofvitamin E for tardive dyskinesia. Biol Psychiat 1998; 43: 868–72.18. Laghrissi-Thode F, Pollock BG, Miller MC et al. Double-blindcomparison of paroxetine and nortriptyline on the postural stabilityof late-life depressed patients. Psychopharm Bull 1995; 31: 659–63.

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