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Mohammed T. Abou-Saleh

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474 PRINCIPLES AND PRACTICE OF GERIATRIC PSYCHIATRYorganic illness, rather than an idiopathic cause). These researchersdescribe manic symptoms that were secondary to drugs, infection,neoplasia, epilepsy and metabolic disturbances. The patients intheir study had a later onset of symptoms (average age of onset 41years) and fewer family members with affective illness than iscommonly reported in the literature describing bipolar subjects.Stasiek and Zetin 43 have updated Krauthammer and Klerman’soriginal study with additional organic causes of manic symptoms.These authors again emphasize the importance of looking for anorganic cause of mania when there is a negative family history foraffective disorder or a later onset to the bipolar disorder.Neurological disease, particularly cerebrovascular disease, isalso associated with secondary late-life mania 44–46 . Neuroimagingof manic geriatric patients has shown differences in the basalganglia morphology and the putamen volume when compared tocontrol subjects 47,48 .McDonald et al. demonstrate a correlation between bipolardisorder and subcortical hyperintensities, as evidenced onmagnetic resonance images in patients with the onset of manicsymptoms after the age of 50 years 49,50 . Only two of the 10 patientsin this study had a family history of affective disorders 49 . Thesignificance of subcortical hyperintensities has been debated,although they are thought to result from a focal loss of brainparenchyma, due to ischemia from any cause including hypertension,vasculopathy, atherosclerosis or thromboembolism 51 .Finally, Yassa et al. 52 find a low incidence of organic factorsprecipitating mania in an elderly population. However, seven oftheir 10 geriatric bipolar patients demonstrated a stressful event inthe 6 month period prior to their manic episode. None of thesepatients had a family history of affective disorders.AFFECTIVE DISORDERSIn summary, there is evidence from family studies and chromosomallinkage studies that manic depressive illness is transmittedgenetically and may have more than one mode of genetictransmission. There is also evidence from clinical studies thatthere may be a different etiology for bipolar disorder, which hasan onset early in life, compared to those which begin in olderadults. Late-onset mania is more often associated with organicprecipitants and, as in other types of mania, may be closelyassociated with stressful events. Patients with an earlier onset totheir symptoms more often have a family history of affectivedisorder. Clinically, patients who present with manic symptomsafter the age of 50 years should be given careful consideration foran organic cause to their symptoms, particularly if there is noevidence of affective disorders in other family members.REFERENCES1. Mendlewicz J, Rainer JD. Adoption study supporting genetictransmission in manic-depressive illness. Nature 1974; 268: 327–9.2. Bertelson AA. Danish twin study of manic-depressive disorders. InSchou M, Stromgren E, eds, Origin, Prevention and Treatment ofAffective Disorder. London: Academic Press, 1979; 227–39.3. Gershon ES, Hamovit J, Guroff JJ et al. A family study ofschizoaffective, bipolar I, bipolar II, unipolar, and normal controlprobands. Arch Gen Psychiat 1982; 39: 1157–67.4. Wender PH, Kety SS, Rosenthal D et al. Psychiatric disorders in thebiological and adoptive families with affective disorders. Arch GenPsychiat 1986; 43: 923–9.5. Tsuang MT, Faraone SV. The Genetics of Mood Disorders. Baltimore,MD: Johns Hopkins University Press, 1990.6. Leonhard K, Korff I, Shulz H. Unipolar proband temperaments in thefamilies of monopolar and bipolar psychoses. Psychiat Neurol 1962;143: 416–34.7. Roglev M. Application of polygenic threshold models in the etiologyof affective disorders. 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BioPsychiat 1997; 42:115–22.21. Chandy KG. Isolation of a novel potassium channel gene hsKCa3containing a polymorphic CAG repeat: a candidate for schizophreniaand bipolar disorder? Mol Psychiat 1998; 3(1): 32–7.22. Craddock N. Expanded CAG/CTG repeats in bipolar disorder: nocorrelation with phenotypic measures of illness severity. Biol Psychiat1997; 42(10): 876–81.23. Guy C. No association between a polymorphic CAG repeat in thehuman potassium channel gene hKCa3 and bipolar disorder. Am JMed Genet 1999; 88(1): 57–60.24. Gershon E. Bipolar illness and schizophrenia as oligogenic diseases:implications for the future. Biol Psychiat 2000; 47(3): 240–51.25. Shulman K, Post F. Bipolar affective disorder in old age. Br JPsychiat 1980; 136: 26–32.26. Stone K. Mania in the elderly. Br J Psychiat 1989; 155: 220–4.27. Petterson U. Manic-depressive illness: a clinical, social and geneticstudy. Acta Psychiat Scand 1977; 269(suppl): 73–80.28. Winokur G. The Iowa 500: heterogeneity and course in manicdepressiveillness (bipolar). Comp Psychiat 1975; 16: 125–31.29. Carlson GA, Kotin J, Davenport YB et al. Follow-up of 53 bipolarmanic-depressive patients. Br J Psychiat 1974; 124: 134–9.30. Angst J, Baastrup P, Grof P et al. The course of monopolardepression and bipolar psychosis. Psychiat Neurol Neurochir (Amst)1973; 76: 489.31. Mendlewicz J, Fieve RR, Rainer JD et al. Manic-depressive illness: acomparative study of patients with and without a family history. Br JPsychiat 1972; 120: 523–30.32. James NM. Early- and late-onset bipolar affective disorder: a geneticstudy. Arch Gen Psychiat 1977; 34: 715–17.33. Taylor M, Abrams R. Manic states: a genetic study of early and lateonset affective disorders. Arch Gen Psychiat 1973; 28: 656–8.34. Gershon ES, Mark A, Cohen N et al. Transmitted factors in themorbid risk of affective disorders: a controlled study. J Psychiat Res1975; 2: 283.35. Perris C. 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