Journal articles: 'Manic depressive illness'

1

Lynn, David J. "Manic-Depressive Illness." Journal of Clinical Psychiatry 70, no. 3 (March 15, 2009): 435. http://dx.doi.org/10.4088/jcp.08bk04803.

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AKISKAL, HAGOP S. "Manic-Depressive Illness." American Journal of Psychiatry 148, no. 4 (April 1991): 531. http://dx.doi.org/10.1176/ajp.148.4.531.

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CROW, T. J. "Manic-Depressive Illness." American Journal of Psychiatry 148, no. 4 (April 1991): 531—a—532. http://dx.doi.org/10.1176/ajp.148.4.531-a.

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Papageorgis, D. "Manic-depressive illness." Behaviour Research and Therapy 29, no. 4 (1991): 377. http://dx.doi.org/10.1016/0005-7967(91)90087-j.

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Rothschild, Anthony J. "Manic-depressive illness." General Hospital Psychiatry 14, no. 1 (January 1992): 77–79. http://dx.doi.org/10.1016/0163-8343(92)90029-a.

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Bauer, Mark S., Gregory E. Simon, Evette Ludman, and Jurgen Unützer. "‘Bipolarity’ in bipolar disorder: Distribution of manic and depressive symptoms in a treated population." British Journal of Psychiatry 187, no. 1 (July 2005): 87–88. http://dx.doi.org/10.1192/bjp.187.1.87.

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SummaryCross-sectional analysis of 441 individuals with bipolar disorder treated at a US health maintenance organisation investigated the distribution of manic and depressive symptoms in that illness. Clinically significant depressive symptoms occurred in 94.1% of those with (hypo)mania, while70.1% inadepressive episode had clinically significant manic symptoms. DSM-unrecognised depression-plus-hypomania was over twice as prevalent as DSM-recognised mixed episodes. Depressive symptoms were unimodally distributed in (hypo)mania. Depressive and manic symptoms were positively, not inversely correlated, and their co-occurrence was associated with worse quality of life. Implications for the DSM and ICD nosological systems are discussed.

7

Coryell, William, Martin Keller, Jean Endicott, Nancy Andreasen, Paula Clayton, and Robert Hirschfeld. "Bipolar II illness: course and outcome over a five-year period." Psychological Medicine 19, no. 1 (February 1989): 129–41. http://dx.doi.org/10.1017/s0033291700011090.

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SynopsisA five year semi-annual follow-up of patients with non-bipolar (N = 442), bipolar II (N = 64) and bipolar I (N = 53) major depression tracked the courses of prospectively observed major depressive, hypomanic and manic syndromes. In all three groups, depression was much more likely in any given week than was hypomania or mania. However, during the majority of weeks, no full syndrome was present and none of the groups exhibited evidence of continuing psychosocial deterioration. Though all three groups exhibited similar times to recovery from index and subsequent major depressive episodes, both bipolar groups had substantially higher relapse rates and developed more episodes of major depression, hypomania and mania. The two bipolar groups, in turn, differed by the severity of manic-like syndromes and thus remained diagnostically stable; the bipolar II patients were much less likely to develop full manic syndromes or to be hospitalized during follow-up. In conjunction with family study data showing that bipolar II disorder breeds true, these data support the separation of bipolar I and bipolar II affective disorder.

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McKeon, Patrick, Patrick Manley, and Gregory Swanwick. "Manic-depressive illness — I: clinical characteristics of bipolar disorder subtypes." Irish Journal of Psychological Medicine 9, no. 1 (May 1992): 6–9. http://dx.doi.org/10.1017/s0790966700013823.

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AbstractThe clinical and demographic features of 100 bipolar disorder patients, who were categorised into bipolar I, bipolar II, unipolar mania and rapid cycling groups, and who were further classified on the basis of the sequence of occurrence of the manic and depressive episodes within each cycle, are compared. Bipolar I (including unipolar manic) patients, 77% of whom had a sequence of moods where mania preceded depression (Mania-Depression – normothymic Interval: M.D.I.) constituted 69% of the total sample. Six per cent were classified as bipolar II and 25% has a rapid cycling disorder. Patients who had an M.D.I. sequence of moods, whether rapid or non-rapid cycling, had a younger age of onset, a higher male:female ratio and a stronger family history of bipolar disorder than patients whose depression preceded mania (D.M.I.). Unipolar manic patients, 12% of the sample, had a comparable age of onset, a greater family history of bipolarity and more frequent hospitalisations than the bipolar I-M.D.I. group. Rapid cycling patients had a lower mean serum thyroxine concentration than the non-rapid cycling bipolar disorder patients. This study supports the rationale for distinguishing bipolar patients with an M.D.I, sequence from those with a D.M.I, pattern and rapid cyclers from non-rapid cyclers.

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Goodwin, Frederick K., and S. Nassir Ghaemi. "Understanding Manic-depressive Illness." Archives of General Psychiatry 55, no. 1 (January 1, 1998): 23. http://dx.doi.org/10.1001/archpsyc.55.1.23.

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Carroll, B. J. "Brain mechanisms in manic depression." Clinical Chemistry 40, no. 2 (February 1, 1994): 303–8. http://dx.doi.org/10.1093/clinchem/40.2.303.

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Abstract Manic depressive illness (bipolar disorder) is the mood disorder classically considered to have a strong biological basis. During manic depressive cycles, patients show dramatic fluctuations of mood, energy, activity, information processing, and behaviors. Theories of brain function and mood disorders must deal with the case of bipolar disorder, not simply unipolar depression. Shifts in the nosologic concepts of how manic depression is related to other mood disorders are discussed in this overview, and the renewed adoption of the Kraepelinian "spectrum" concept is recommended. The variable clinical presentations of manic depressive illness are emphasized. New genetic mechanisms that must be considered as candidate factors in relation to this phenotypic heterogeneity are discussed. Finally, the correlation of clinical symptom clusters with brain systems is considered in the context of a three-component model of manic depression.

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MacKinnon, Dean F., Kay Redfield Jamison, and and J. Raymond DePaulo. "GENETICS OF MANIC DEPRESSIVE ILLNESS." Annual Review of Neuroscience 20, no. 1 (March 1997): 355–73. http://dx.doi.org/10.1146/annurev.neuro.20.1.355.

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12

Kinney, D., and R. Richards. "Creativity and manic depressive illness." Science 234, no. 4776 (October 31, 1986): 529. http://dx.doi.org/10.1126/science.3764424.

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Gershon, E. S. "Genetics of manic-depressive illness." Current Opinion in Psychiatry 2, no. 1 (February 1989): 41–44. http://dx.doi.org/10.1097/00001504-198902000-00010.

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Govaerts, A., J. Mendlewicz, and P. Verbanck. "Manic-Depressive Illness and HLA." Tissue Antigens 10, no. 1 (December 11, 2008): 60–62. http://dx.doi.org/10.1111/j.1399-0039.1977.tb00753.x.

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Redfield Jamison, Kay. "Manic-Depressive Illness and Creativity." Scientific American 272, no. 2 (February 1995): 62–67. http://dx.doi.org/10.1038/scientificamerican0295-62.

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Silverstone, Trevor. "Dopamine in manic depressive illness." Journal of Affective Disorders 8, no. 3 (May 1985): 225–31. http://dx.doi.org/10.1016/0165-0327(85)90020-5.

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Anonymous. "Depressive and Manic-Depressive Illness Fact Sheet." Journal of Psychosocial Nursing and Mental Health Services 34, no. 8 (August 1996): 7. http://dx.doi.org/10.3928/0279-3695-19960801-04.

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18

Swann, Alan C. "Mixed features: evolution of the concept, past and current definitions, and future prospects." CNS Spectrums 22, no. 2 (March 7, 2017): 161–69. http://dx.doi.org/10.1017/s1092852916000882.

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Mixed states address the relationships between episodes and the course of an illness, presenting significant clinical challenges. Recurrent affective disorders were described thousands of years ago as dimensional disturbances of the basic elements of behavior, combining the characteristics of what we would now consider manic and depressive episodes. It was recognized from the beginning that combinations of depressive and manic features are associated with a severe illness course, including increased suicide risk. Early descriptions of affective disorders formulated them as systemic illnesses, a concept supported by more recent data. Descriptions of affective disorders and their course, including mixed states, became more systematic during the 19th century. Structured criteria achieved importance with evidence that, in addition to early onset, frequent recurrence, and comorbid problems, mixed states had worse treatment outcomes than other episodes. In contrast to 2000 years of literature on recurrent affective episodes and mixed states, the unipolar–bipolar disorder distinction was formalized in the mid-20th century. Mixed-state criteria, initially developed for bipolar disorder, ranged from fully combined depression and mania to the DSM–5 criteria, no longer limited to bipolar disorder, of a primary depressive or manic episode with at least three symptoms of the other episode type. The challenges involved in understanding and identifying mixed states center largely on what drives them, including (1) their formulation as either categorical or dimensional constructs, (2) the specificity of their relationships to depressive or manic episodes, and (3) specificity for bipolar versus major depressive disorder. Their existence challenges the distinction between bipolar and major depressive disorders. The challenges involved in identifying the underlying physiological mechanisms go to the heart of these questions.

19

Saugstad, Letten F. "Age at Puberty and Mental Illness." British Journal of Psychiatry 155, no. 4 (October 1989): 536–44. http://dx.doi.org/10.1192/bjp.155.4.536.

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The hypothesis of a neurodevelopmental aetiology of manic-depressive psychosis and schizophrenia is based on the relation between onset of puberty and the final regressive events in the central nervous system (elimination of 40% of neuronal synapses), and the discrepancy in body build in the two disorders which is similar to that between early- and late-maturing individuals. The marked rise in manic–depressive psychoses and decline in schizophrenia, particularly the non-paranoid categories, accompanying the decline in mean pubertal age by some four years during the past hundred years are taken as evidence that manic–depressive psychosis affects early maturers and schizophrenia particularly affects late maturers. Gender differences and social differentials accord with this theory. Redundancy of neuronal synapses characterises manic-depressive psychosis, and reduced density of synapses is a characteristic of schizophrenia, whereas ‘normality’, with optimal synaptic density, is in between.

20

Dean, C., R. J. Williams, and I. F. Brockington. "Is puerperal psychosis the same as bipolar manic-depressive disorder? A family study." Psychological Medicine 19, no. 3 (August 1989): 637–47. http://dx.doi.org/10.1017/s0033291700024235.

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SynopsisThe first degree relatives of three groups of women were interviewed; 51 women who had had an illness within two weeks of childbirth and no non-puerperal episodes (the puerperal group), 33 who had puerperal and non-puerperal episodes (the mixed group), and 19 women with bipolar manic-depressive disorder who had non-puerperal episodes only (the manic-depressive group).Over 60% of the affected relatives in all three groups had affective illnesses; in the main these were not puerperal. There were significantly more first degree relatives who had had general practitioner or hospital treatment for psychiatric illness in the puerperal group and in the mixed group than in the manic-depressive group. The puerperal patients had a better prognosis in terms of their illness (number of relapses and time on medication), work functioning and social functioning than the manic-depressive group and the mixed group. The mixed group had an earlier age of onset than the manic-depressive group and the puerperal group. The hypothesis that puerperal psychosis is the same as bipolar manic-depressive disorder was not upheld. The mixed group and the puerperal group were similar with respect to the risk in first degree relatives but differed in terms of prognosis.There were no significant differences between the groups with respect to puerperal episodes in first-degree relatives, although the rate of puerperal psychosis in the first-degree relatives of the puerperal patients was significantly greater than in the general population. The hypothesis that there is a specific genetically determined puerperal psychosis was not supported. Women who had had an illness with an onset within two weeks of childbirth (mixed and puerperal) subsequently had an illness following 36% of their childbirths. In women who had had puerperal and non-puerperal episodes (mixed) the risk was higher; over 50 % of deliveries in these women were followed by psychiatric illness.

21

Keck, Paul E., Mark A. Frye, and Michael E. Thase. "Bipolar Depression: Best Practices for the Hospitalized Patient." CNS Spectrums 12, S19 (November 2007): 4–11. http://dx.doi.org/10.1017/s1092852900015844.

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One of the most challenging clinical topics in psychiatry is the diagnosis and treatment of bipolar depression. The term mood stabilizer is frequently employed in the treatment of the hospitalized bipolar patient, although clinicians do not universally agree on a consensus definition of this term. Most clinicians would agree that a mood stabilizer refers to a medication that is effective for the acute treatment of manic, mixed, hypomanic, or depressive episodes. Many experts agree that such treatment should offer efficacy against mania, should not worsen depression, and preferably should treat depression as well. In addition, the acute effectiveness in stabilization should not be at the expense of inducing alternate mood symptoms or switching the patient into the alternate phase of illness. From a maintenance standpoint, a mood stabilizer should also prevent against future relapse or recurrence of manic, mixed, hypomanic, or depressive symptoms or episodes (Slide 1).In addition to use of mood stabilizers, there are other issues surrounding treatment of the hospitalized patient with bipolar depression, including the commonly comorbid issue of substance abuse. Hazardous drinking may more commonly occur in bipolar depression or depressive phase of illness, representing a more complex clinical picture. To facilitate understanding of this complex disorder and its appropriate treatment, this discussion centers around the case of a major depressive episode in a patient with a past history of of mania (ie, bipolar I depression or bipolar depression).

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O'MAHONY, E., A. CORVIN, R. O’CONNELL, C. COMERFORD, B. LARSEN, I. R. JONES, F. McCANDLESS, et al. "Sibling pairs with affective disorders: resemblance of demographic and clinical features." Psychological Medicine 32, no. 1 (January 2002): 55–61. http://dx.doi.org/10.1017/s0033291701004986.

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Background. As part of a collaborative linkage study, the authors obtained clinical and demographic data on 160 families in which more than one sibling was affected with a bipolar illness. The aim of the study was to identify clinical characteristics that had a high degree of familiality.Method. Data on age at onset, gender, frequency of illness-episodes and proportion of manic to depressive episodes were examined to determine intra-pair correlations in affected sibling pairs. Dimension scales were developed measuring frequency and severity of lifetime mania, depression, psychosis and mood-incongruence of psychotic symptoms; degree of familial aggregation for scores on these dimensions was calculated.Results. Sibling pairs correlated significantly for age at onset (ρ = 0·293, P<0·001); dimension scores for psychosis (ρ = 0·332, P < 0·001); and proportion of manic to depressive episodes (ρ = 0·184, P = 0·002). These findings remained significant when correcting for multiple testing. Of the other test variables; mania (ρ = 0·171, P = 0·019); incongruence dimensions (ρ = 0·242, P = 0·042); frequency of manic episodes (ρ = 0·152, P = 0·033); and frequency of depressive episodes (ρ = 0·155, P = 0·028) were associated with modest correlations but these were not significant after correction. Degree of familial aggregation was not significant for sex (κ = 0·084) or dimension scores for depression (ρ = 0·078, P = 0·300).Conclusions. Significant but modest familial resemblance has been shown for some specific features of bipolar illness, particularly age at onset and degree of psychosis. Further research may establish the extent to which these findings are mediated by genetic and/or environmental factors.

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Swann, Alan C. "Manic-Depressive Illness and Substance Abuse." Psychiatric Annals 27, no. 7 (July 1, 1997): 507–11. http://dx.doi.org/10.3928/0048-5713-19970701-12.

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24

Jamison, Kay Redfield, and Melvin G. McInnis. "Genetic studies of manic–depressive illness." Nature Medicine 2, no. 5 (May 1996): 521–22. http://dx.doi.org/10.1038/nm0596-521.

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25

De bruyn, A., P. Raeymaekers, L. A. Sandkuijl, K. Mendelbaum, J. Mendlewicz, and C. Van Broeckhoven. "LINKAGE STUDIES IN MANIC DEPRESSIVE ILLNESS." Clinical Neuropharmacology 15 (1992): 302B. http://dx.doi.org/10.1097/00002826-199202001-00585.

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26

Dubovsky, Steven L. "Calcium Antagonists in Manic-Depressive Illness." Neuropsychobiology 27, no. 3 (1993): 184–92. http://dx.doi.org/10.1159/000118978.

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27

Wulsin, Lawson, Michael Bachop, and David Hoffman. "Group Therapy in Manic-Depressive Illness." American Journal of Psychotherapy 42, no. 2 (April 1988): 263–71. http://dx.doi.org/10.1176/appi.psychotherapy.1988.42.2.263.

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Suarez, BrianK, CarolL Hampe, AlanF Wright, J. Mendlewicz, and P. Simon. "LINKAGE ANALYSIS IN MANIC-DEPRESSIVE ILLNESS." Lancet 330, no. 8554 (August 1987): 345–46. http://dx.doi.org/10.1016/s0140-6736(87)90948-2.

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29

Baron, Miron. "The Genetics of Manic Depressive Illness." Journal of Nervous and Mental Disease 177, no. 10 (October 1989): 645. http://dx.doi.org/10.1097/00005053-198910000-00019.

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30

Mendlewicz, J. "Genetic mapping of manic-depressive illness." Trends in Genetics 7, no. 1 (January 1991): 311. http://dx.doi.org/10.1016/0168-9525(91)90188-v.

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Mendlewicz, J. "Genetic mapping of manic-depressive illness." Trends in Genetics 7, no. 10 (October 1991): 311. http://dx.doi.org/10.1016/0168-9525(91)90409-j.

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MENDLEWICZ, J. "Manic depressive illness and X chromosome." Lancet 338, no. 8776 (November 1991): 1213. http://dx.doi.org/10.1016/0140-6736(91)92083-e.

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33

Schou, Mogens. "Lithium Treatment of Manic-Depressive Illness." JAMA 259, no. 12 (March 25, 1988): 1834. http://dx.doi.org/10.1001/jama.1988.03720120038032.

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Peselow, Eric D., Ronald R. Fieve, Constance Difiglia, and Michael P. Sanfilipo. "Lithium Prophylaxis of Bipolar Illness." British Journal of Psychiatry 164, no. 2 (February 1994): 208–14. http://dx.doi.org/10.1192/bjp.164.2.208.

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Using a longitudinal life-table analysis, we assessed the efficacy of lithium alone, administered within the context of a naturalistic clinical setting, by calculating the probability of patients remaining free of an affective episode (manic or depressive) over a five-year course. In addition, for those who suffered a manic or depressive relapse, we attempted to analyse the subsequent course of patients who suffered a manic/hypomanic or depressive relapse and were then restabilised on lithium plus either a neuroleptic, carbamazepine, or a benzodiazepine, or lithium plus an antidepressant. Lithium alone offered an average 83% probability against an affective relapse after one year, 52% after three years, and 37% after five years. For patients who failed on lithium alone, it appeared that combination treatment offered greater protection against subsequent affective relapse than the initial course on lithium alone.

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Zaman, R., M. Agius, and A. Hankir. "Manic-depressive illness and the artistic temperament." European Psychiatry 26, S2 (March 2011): 261. http://dx.doi.org/10.1016/s0924-9338(11)71971-x.

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IntroductionA notion exists of a special kind of relationship between poets and being “crazy”. A possible correlation between madness and genius is one of the oldest and most persistent and controvertialof cultural concepts. We decided to investigate the relationship between manic-depressive illness and the artistic temperament.MethodA review was conducted on Professor Kay Redfield Jamison's treatise Touched with Fire, Manic-depressive Illness and the Artistic Temperament.ResultsResearch strongly suggests that, compared with the general population, writers and artists show a vastly disproportionate rate of the affective disorders manic-depressive and depressive illness. Research employing systematic biographical methodology has also given strong support to a much higher rate of mood disorders in artistic populations than could be expected from chance alone. A British study revealed many overlapping mood, cognitive, and behavioral changes between hypomania and intense creative states. Many of the changes in mood, thinking, and perception that characterize the mildly manic states are highly characteristic of creative thought as well. Although it seems counterintuitive at first, melancholy has also been reported to be associated with artistic inspiration and productivity.DiscussionNot all (not even most) writers and artists suffer from major mood disorders. Likewise, most of those who have a major mood disorder are not writers or artists. However despite this, research does strongly suggest that there is a correlation between manic-depressive illness and the artistic temperament. The major resistance to an association between psychopathology, or mental illness, and creativity seems to revolve around a few central points.

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McKeon, Patrick, Patrick Manley, and Gregory Swanwick. "Manic-depressive illness — II: treatment outcome in bipolar disorder subtypes." Irish Journal of Psychological Medicine 9, no. 1 (May 1992): 9–12. http://dx.doi.org/10.1017/s0790966700013835.

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AbstractThe treatment outcome of 100 bipolar disorder patients (B.P.) was examined retrospectively to determine whether bipolar subtypes had a differential prophylactic response to lithium, carbamazepine, neuroleptics and antidepressant drugs when these treatments were given in a predetermined sequence. Sixty-eight per cent of 53 B.P.-I patients with a mania-depression-normothymic-interval (M.D.I.) sequence of mood changes had a good response to lithium, and all but one of the remainder responded with the addition of carbamazepine or an antidepressant. While only 17% of 12 unipolar manic patients achieved prophylaxis with lithium and a further 17% when carbamazepine was added, the other 66% remained normothymic when a neuroleptic was prescribed with lithium. Of the seven rapid cycling patients where depression preceded mania, 28% had a good prophylactic effect with lithium, a further 28% when a tricyclic antidepressant was added and 14% with lithium and carbamazepine. None of the 18 rapid cycling M.D.I. group had a good response to lithium, but 39% stabilised when carbamazepine was added to lithium. Twenty-eight per cent of this group failed completely to respond to any of the treatments used. Neuroleptics increased the severity and duration of depressive phases for all subtypes except the unipolar mania group.

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Kendell, R. E., J. C. Chalmers, and C. Platz. "Epidemiology of Puerperal Psychoses." British Journal of Psychiatry 150, no. 5 (May 1987): 662–73. http://dx.doi.org/10.1192/bjp.150.5.662.

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Computer linkage of an obstetric register and a psychiatric case register made it possible to investigate the temporal relationship between childbirth and psychiatric contact in a population of 470 000 people over a 12-year period resulted in 54 087 births: 120 psychiatric admissions within 90 days of parturition. The ‘relative risk’ of admission to a psychiatric hospital with a psychotic illness was extremely high in the first 30 days after childbirth, particularly in primiparae, suggesting that metabolic factors are involved in the genesis of puerperal psychoses. However, being unmarried, having a first baby, Caesarian section and perinatal death were all associated with an increased risk of psychiatric admission or contact, or both, suggesting that psychological stresses also contribute to this high psychiatric morbidity. Women with a history of manic depressive illness, manic or depressive, had a much higher risk of psychiatric admission in the puerperium than those with a history of schizophrenia or depressive neuroses, and the majority of puerperal admissions met Research Diagnostic Criteria for manic or depressive disorder. Probably, therefore, puerperal psychoses are manic depressive illnesses and unrelated to schizophrenia.

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Shulman, Kenneth I., and Mauricio Tohen. "Unipolar Mania Reconsidered: Evidence from an Elderly Cohort." British Journal of Psychiatry 164, no. 4 (April 1994): 547–49. http://dx.doi.org/10.1192/bjp.164.4.547.

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Earlier studies have failed to differentiate the unipolar manic subtype from bipolar patients with both manic and depressive episodes. This retrospective cohort study of 50 elderly manic in-patients identified six patients (12%) who met strict criteria for a course of unipolar mania. Significant differences emerged in age at onset, with a mean of 41.2 years for unipolar mania compared with 64.7 years for the others. Consequently, clinical course was significantly longer, 27.7 v. 7.4 years. Elderly patients pursuing a unipolar manic course are among the very few elderly ‘bipolars’ whose illness begins early in life. Recent neuroradiological investigations and data from geriatric studies suggest that the concept of unipolar mania is worthy of further investigation.

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Solé, Eva, Marina Garriga, Marc Valentí, and Eduard Vieta. "Mixed features in bipolar disorder." CNS Spectrums 22, no. 2 (December 29, 2016): 134–40. http://dx.doi.org/10.1017/s1092852916000869.

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Mixed affective states, defined as the coexistence of depressive and manic symptoms, are complex presentations of manic-depressive illness that represent a challenge for clinicians at the levels of diagnosis, classification, and pharmacological treatment. The evidence shows that patients with bipolar disorder who have manic/hypomanic or depressive episodes with mixed features tend to have a more severe form of bipolar disorder along with a worse course of illness and higher rates of comorbid conditions than those with non-mixed presentations. In the updated Diagnostic and Statistical Manual of Mental Disorders (5th ed.; DSM–5), the definition of “mixed episode” has been removed, and subthreshold nonoverlapping symptoms of the opposite pole are captured using a “with mixed features” specifier applied to manic, hypomanic, and major depressive episodes. However, the list of symptoms proposed in the DSM–5 specifier has been widely criticized, because it includes typical manic symptoms (such as elevated mood and grandiosity) that are rare among patients with mixed depression, while excluding symptoms (such as irritability, psychomotor agitation, and distractibility) that are frequently reported in these patients. With the new classification, mixed depressive episodes are three times more common in bipolar II compared with unipolar depression, which partly contributes to the increased risk of suicide observed in bipolar depression compared to unipolar depression. Therefore, a specific diagnostic category would imply an increased diagnostic sensitivity, would help to foster early identification of symptoms and ensure specific treatment, as well as play a role in suicide prevention in this population.

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Robinson, A. D. T. "A Century of Delusions in South West Scotland." British Journal of Psychiatry 153, no. 2 (August 1988): 163–67. http://dx.doi.org/10.1192/bjp.153.2.163.

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Two groups of patients admitted to psychiatric hospital in Dumfries were studied, drawn from the periods 1880–1889 and 1970–1979. Feighner criteria were applied to make three diagnostic categories – depression, mania and schizophrenia – and the occurrence and content of delusions were noted for each. A significant decline in the prevalence of delusional depressive illness was found between the two periods, and a similar trend was noted for delusional manic illness. In contrast, the prevalence of delusional schizophrenic illness was stable. This decline is taken to reflect a change in the phenomenology of affective illness since last century in South West Scotland. The content of delusions is also discussed.

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Linter, C. M. "Short-Cycle Manic-Depressive Psychosis in a Mentally Handicapped Child without Family History." British Journal of Psychiatry 151, no. 4 (October 1987): 554–55. http://dx.doi.org/10.1192/bjp.151.4.554.

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Diagnosis of classic psychiatric illness in mentally handicapped individuals remains difficult. Manic-depressive illness has previously been reported in both pre-pubertal and pubertal children with a mental handicap and with a family history. This paper reports a case of manic-depressive psychosis in childhood, with no family history, short-cycle mood swings and good response to lithium therapy.

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Lazarus, Arthur. "Factitious Disorder in a Manic Patient: Case Report and Treatment Considerations." International Journal of Psychiatry in Medicine 15, no. 4 (December 1986): 365–69. http://dx.doi.org/10.2190/1j1y-ap87-8w21-f0nx.

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A case of factitious disorder with physical symptoms is described in a patient with manic-depressive illness. The coexistence of factitious disorder and bipolar disorder has not been previously reported. Clinicians should search for an underlying affective disorder in patients who fabricate signs and symptoms of physical illness, since mania may simulate or contribute to the production of factitious behavior.

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Crammer, J. L. "Disturbance of Water and Sodium in a Manic-Depressive Illness." British Journal of Psychiatry 149, no. 3 (September 1986): 337–45. http://dx.doi.org/10.1192/bjp.149.3.337.

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Abstract:

Specific questioning and frequent observation of a 69 year-old woman with cyclic bipolar manic-depressive illness showed that she had disturbances of thirst, appetite, bowel and bladder function and dramatic changes in body weight, in association with different phases of her mental illness. Examination of one manic phase under constant diet and inpatient control showed cardiovascular changes, sodium retention, body weight gain, with raised aldosterone secretion but steady vasopressin. There appears to be a sub-group of manic-depressive patients with evidence of disturbed hypothalamic functions as part of their mental illness, as shown particularly by changes in water and electrolyte metabolism.

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Feier, Gustavo, Samira S. Valvassori, Gislaine T. Rezin, Márcio Búrigo, Emilio L. Streck, Flávio Kapczinski, and João Quevedo. "Creatine kinase levels in patients with bipolar disorder: depressive, manic, and euthymic phases." Revista Brasileira de Psiquiatria 33, no. 2 (March 18, 2011): 171–75. http://dx.doi.org/10.1590/s1516-44462011005000005.

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Abstract:

OBJECTIVE: Bipolar disorder is a severe, recurrent, and often chronic psychiatric illness associated with significant functional impairment, morbidity, and mortality. Creatine kinase is an important enzyme, particularly for cells with high and fluctuating energy requirements, such as neurons, and is a potential marker of brain injury. The aim of the present study was to compare serum creatine kinase levels between bipolar disorder patients, in the various phases (depressive, manic, and euthymic), and healthy volunteers. METHOD: Forty-eight bipolar patients were recruited: 18 in the euthymic phase; 17 in the manic phase; and 13 in the depressive phase. The control group comprised 41 healthy volunteers. The phases of bipolar disorder were defined as follows: euthymic-not meeting the DSM-IV criteria for a mood episode and scoring < 8 on the Hamilton Depression Rating Scale (HDRS) and Young Mania Rating Scale (YMRS); manic-scoring < 7 on the HDRS and > 7 on the YMRS; depressive-scoring > 7 on the HDRS and < 7 on the YMRS. Patients in mixed phases were excluded. Blood samples were collected from all participants. RESULTS: Creatine kinase levels were higher in the manic patients than in the controls. However, we observed no significant difference between euthymic and depressive patients in terms of the creatine kinase level. CONCLUSION: Our results suggest that the clinical differences among the depressive, manic, and euthymic phases of bipolar disorder are paralleled by contrasting levels of creatine kinase. However, further studies are needed in order to understand the state-dependent differences observed in serum creatine kinase activity.

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Kendler, Kenneth S. "Kraepelin's final views on manic-depressive Illness." Journal of Affective Disorders 282 (March 2021): 979–90. http://dx.doi.org/10.1016/j.jad.2020.12.200.

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Yildiz, Aysegul. "Phosphoinositide metabolism, lithium and manic depressive illness." Spectroscopy 16, no. 3-4 (2002): 307–16. http://dx.doi.org/10.1155/2002/535201.

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Abstract:

Physiology underlying manic depressive illness and treating effects of its most commonly used remedy – “lithium” is yet to be elucidated. Recent years of psychopharmacology research witnessed sparkling developments in our understanding of the mechanisms underlying lithium’s mood stabilizing effects. Recent data on molecular biology andin vivomagnetic resonance spectroscopy suggest that some of the initial actions of lithium may occur through the inhibition of the enzyme inositol monophosphatase (IMPase) and reduction ofmyo–inositol, which in turn initiate a cascade of events at different levels of signal transduction process and gene expression in brain; such as the effects on protein kinase C, myristoylated alenine rich C kinase substrate protein, glycogen synthase kinase 3β, B cell lymphoma–2 protein, and activator protein–I. It is likely that the enzyme IMPase other that being the key point in initiating lithium’s therapeutic effects, may also play a critical role in the physiology underlying manic depressive illness.

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Gershon, Elliot S. "Single gene findings in manic-depressive illness." Current Opinion in Psychiatry 4, no. 1 (February 1991): 51–55. http://dx.doi.org/10.1097/00001504-199102000-00012.

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Egeland, J. "Molecular-Biologic Basis of Manic-Depressive Illness." Pharmacopsychiatry 25, no. 01 (January 1992): 37–40. http://dx.doi.org/10.1055/s-2007-1014385.

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Whitney, Diane K., Verinder Sharma, and Karen Kueneman. "Seasonality of manic depressive illness in Canada." Journal of Affective Disorders 55, no. 2-3 (October 1999): 99–105. http://dx.doi.org/10.1016/s0165-0327(98)00197-9.

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Rietschel, M., M. M. Nöthen, W. Maier, M. Albus, E. Franzek, and P. Propping. "Tyrosine hydroxylase gene and manic-depressive illness." Lancet 345, no. 8961 (May 1995): 1368. http://dx.doi.org/10.1016/s0140-6736(95)92566-x.

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Journal articles on the topic 'Manic depressive illness'

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