Recurrent Mania Research Articles

The madness of King George III: a psychiatric re-assessment

This research, based on a study of King George III's medical records and of contemporary diaries of his courtiers and equerries, further confirms the considerable doubt on the claim of Richard Hunter and Ida Macalpine that the King suffered from recurrent attacks of acute porphyria.The present study examines the above records from a psychiatric viewpoint, together with some additional reports, to re-assess the nature of the King's maladies. It concludes that he suffered from recurrent mania (four episodes), with chronic mania and possibly a degree of fatuity during the last decade of his life.This is in agreement with previous reports that he suffered from manic-depressive psychosis.

Recurrent Mania With Psychosis Following Acute Alteration of Thyroid Status in a Girl With Hyperthyroidism After Craniospinal Irradiation

Recurrent Mania With Psychosis Following Acute Alteration of Thyroid Status in a Girl With Hyperthyroidism After Craniospinal Irradiation

Costs of bipolar disorder.

Bipolar disorder is a chronic affective disorder that causes significant economic burden to patients, families and society. It has a lifetime prevalence of approximately 1.3%. Bipolar disorder is characterised by recurrent mania or hypomania and depressive episodes that cause impairments in functioning and health-related quality of life. Patients require acute and maintenance therapy delivered via inpatient and outpatient treatment. Patients with bipolar disorder often have contact with the social welfare and legal systems; bipolar disorder impairs occupational functioning and may lead to premature mortality through suicide. This review examines the symptomatology of bipolar disorder and identifies those features that make it difficult and costly to treat. Methods for assessing direct and indirect costs are reviewed. We report on comprehensive cost studies as well as administrative claims data and program evaluations. The majority of data is drawn from studies conducted in the US; however, we discuss European studies when appropriate. Only two comprehensive cost-of-illness studies on bipolar disorder, one prevalence-based and one incidence-based, have been reported. There are, however, several comprehensive cost-of-illness studies measuring economic burden of affective disorders including bipolar disorder. Estimates of total costs of affective disorders in the US range from $US30.4-43.7 billion (1990 values). In the prevalence-based cost-of-illness study on bipolar disorder, total annual costs were estimated at $US45.2 billion (1991 values). In the incidence-based study, lifetime costs were estimated at $US24 billion. Although there have been recent advances in pharmacotherapy and outpatient therapy, hospitalisation still accounts for a substantial portion of the direct costs. A variety of outpatient services are increasingly important for the care of patients with bipolar disorder and costs in this area continue to grow. Indirect costs due to morbidity and premature mortality comprise a large portion of the cost of illness. Lost workdays or inability to work due to the disease cause high morbidity costs. Intangible costs such as family burden and impaired health-related quality of life are common, although it has proved difficult to attach monetary values to these costs.

Seasonality and affective disorders: a report from North India

Case records of the patients with major affective disorders (ICD-10 criteria), seen over a 5 year period in a busy clinic in North India were examined for Seasonal Affective Disorder (SAD) as per DSM-III-R criteria. In addition, seasonality of episodes of all affective disorders was also studied. Around 5.67% of the cases ( n=44) retrospectively met the DSM-III-R criteria of SAD and predominant pattern was that of summer depression ( n=18). There was also a consistent pattern of seasonal mania either in conjunction with seasonal depression ( n=18) or in form of seasonal recurrent mania ( n=11). None of the cases of depression showed any atypical vegetative features. In cases not meeting criteria for SAD ( n=731), there was a trend for peaks for depressive episodes in winter followed by a smaller peak in summer months while manic episodes had peaks towards rainy and winter months. As compared to seasonal patterns of affective disorders in temperate zones, there was a general trend for opposite patterns of seasonality in SAD as well as in non-SAD. The findings are discussed in context of the climatic conditions of North India.

An Unquiet Mind: A Memoir of Moods and Madness

Kay Redfield Jamison Picador, £15.99, pp 220 ISBN 0330 346 504 An Unquiet Mind is a landmark in the history of writing about manic depressive illness. Kay Redfield Jamison, professor of psychiatry at Johns Hopkins University and coauthor of arguably the foremost scientific book on manic depressive illness, has “come out” and described her own lifelong battle against recurrent mania and depression. I recently saw the book displayed in an airport lounge bookstall in Minneapolis where it was rated number 10 in the non-fiction bestsellers list for Minnesota. Not many good books written by …

Maintenance ECT for treatment of recurrent mania

Maintenance ECT for treatment of recurrent mania

Manic episode, thyroid gland function and lithium.

This paper addresses the issue of (recurrent) mania in relation to an increased T4-value, whether or not influenced by lithium. Lithium has an anti-TSH-effect on the thyroid gland by inhibiting the intracellular enzyme adenylate cyclase. This might cause hypothyroidism. Moreover, lithium is also known to have a direct stabilizing effect on (behavioral manifestations) of dopamine receptor supersensitivity. The hypothesis regarding the relation between thyroid function and affective disturbances is that the altered thyroid function may cause a change in the availability of the central dopamine receptors. Dopamine is known to be able to cause a manic state. TSH and TRH are also involved in this mechanism. It is, therefore, very likely that an increased thyroid function, whether or not caused by discontinuation of lithium-therapy, could induce a (recurrent) mania.

Subclinical hypothyroidism in recurrent mania

Treatment of cyclic mood disorders wim thyroid extracts has been reported by Gjcssing (1938). The relationship between recurrent psychotic depression and hypothyroidism was first reported by Libow and Durell (1965b). In a longitudinal study of manic-depressive psychosis, elevated thyroid-stimulating hormone (TSH) values were observed in early phases of hypomania or depression (Dewhurst et al 1969). The resulting hypothesis of increased TSH levels in (otherwise eethyroid) bipolar patients with a rapid-cycling course of illness or affective relapse was supported by further studies (Wehr and Goodwin 1979; O'Shannick and EIlinwood 1982; Cowdry et ai 1983; Roy-Byrne et al 1984; Tollefson et al 1985), and several other investigations showed that thyroid hormones augment the efficacy of tricyclic antidepressants (Prange et el 1969; Goodwin et al 1982). After the successful treatment of rapid-cycling women with daily 500 ~g of levothyroxine (Stancer and Persad 1982), thyroid hormones were suggested to be helpful if antidepressants, lithium, carbamazepine, or neuroleptics failed (Extein et al 1982; Leibow 1983; Joffe et ai 1984; Bauer and Wbybrow 1986). This article tries to prospectively correlate variables of thyroid activity with clinical ratings in a manic-depressive patient over a period of more than 2 years.

Course of bipolar disorder in eastern India

The life course of affective episodes was determined for 95 consecutively admitted patients from eastern India fulfilling RDC criteria for definite mania during the current episode, using SADS-L interviews. There was a significantly greater frequency of manic compared to depressive relapses. Presentation as recurrent mania was very common. The total numbers of affective and manic episodes were significantly higher among those with recurrent mania and in cases where the first illness episode was manic.

Limbic lesions in a patient with recurrent mania

Limbic lesions in a patient with recurrent mania

Lithium carbonate: effects on sleep patterns of normal and depressed subjects and its use in sleep-wake pathology.

The effects of lithium carbonate on sleep patterns have been investigated both acutely in normal and depressed subjects and chronically in depressed subjects. In normal subjects receiving lithium for two weeks total sleep time did not vary, REM sleep decreased and REM sleep latency increased. In depressed subjects, either on short therm therapy or on long term therapy stages 3 and 4 increased, REM sleep decreased, REM latency increased and REM activity/time spent asleep (an index of REM intensity per minute of sleep) decreased. Plasma lithium levels were negatively correlated with REM sleep percentage and positively correlated with REM sleep latency. Besides, it has been shown in one paper that short term therapy with lithium caused small but significant delays in the sleep-wake circadian rhythm. These effects are of interest in view of polygraphic sleep abnormalities found in affective disorders and possible circadian disturbances accounting for these abnormalities. Indeed lithium might act in correcting spezial sleep abnormalities and/or circadian disturbances. In addition to its predominant use for the prophylaxis of recurrent mania and depression, lithium carbonate has been proposed and tried in the prophylactic treatment of abnormally prolonged sleep episodes featuring the Kleine-Levin syndrome.

Down's Syndrome with Mania

Sovner et al (1985) proposed that the presence of Down's Syndrome (DS) precludes the possibility of concomitant mama, and this is not a new claim, since Earl (1961) had stated that neither cyclothymia nor manic-depressive psychosis occurred in the mentally retarded. While Sovner et al conceded that cases of mania in individuals with DS may simply have gone unrecognised or unpublished, they felt this to be unlikely. However, lest this suggestion enter the canon, we present a previously unreported case of a young adult with both DS and recurrent mania.

Hazards and adverse effects of lithium.

Recognized in Roman times for their calming effects by the Greek physician Seranus Ephesios, Li+ salts have only recently been used to treat mania. During the 18oos, Li+ was used with little success to treat urinary calculi and gout, and Li+ bromide salts were employed briefly as hypnotic and antiepileptic agents later in that century. In 1949, Australian John Cade reported profound antimanic effects of Li+ salts in an explosive, chronically ill patient (1). Unfortunately, however, at about the same time in the US, Li+ was introduced as a salt substitute, used in large quantities, and caused numerous adverse effects, including death, due to inadvertent Li+ poison­ ing. After that, Li+ rapidly fell into disrepute in America. Fortunately, the subsequent recognition that routine monitoring of serum levels allows Li+ to be used safely enabled Li+ to take its rightful place as a cornerstone in the treatment of mood disorders. In 1970, the Food and Drug Administration officially approved the use of Li+ for treating acute mania and as prophylaxis against recurrent mania. The lifetime incidence of major affective disorder in the general population is between 10 and 20% (2), and it is estimated that four billion US dollars have been saved as a direct result of the therapeutic benefits of Li+ (3).

Social and psychological support adjunctive to lithium therapy: a critical review.

As lithium therapy becomes more and more widely used for the treatment and control of recurrent mania and depression, the question of whether or not therapeutic outcome may be enhanced by the provision of supportive psychotherapy or other adjunctive social measures has gained in importance. Reports of psychological and social support given to patients receiving lithium therapy are reviewed critically and the question is raised as to the economics of providing such non-pharmacological back-up as a routine concomitant of lithium therapy. Some consideration is given to the psychological mechanisms that are likely to be associated with lithium therapy procedures and that might be exploited by the psychotherapist.

Effects of lithium carbonate on sleep

LITHIUM carbonate is now widely used for the treatment of mania,ls2 the prophylaxis of recurrent mania and depression2-4 and, to an extent, in the treatment of selected depressed patients. 5- 7 There is a clear trend towards the increased use of lithium for more patients and for longer periods of time.s Since depressed and manic patients have a significant sleep disturbance and. as it has been suggested that there may be significant associations between these sleep changes and both the clinical syndromes and the antidepressant drug effects,s-13 it seemed important to determine the effect of lithium on sleep (both acutely and chronically). Further, if lithium, which is now being used chronically for many patients, were to adversely affect sleep, then these patients may experience long-term sleep alterations of unknown implications. It is also of interest to determine what, if any, are the correlations between lithium’s therapeutic and prophylactic effects and its influence on the disturbed sleep pattern of these patients. Depressed patients (as a group) have a reduction in total sleep time, more awakenings during the night and less stage 4 sleep. 11, 14- 21 In addition, Mendels and Hawkins17,22 have reported that depressed patients take longer to fall asleep and wake significantly earlier in the morning and have increased amounts of stage 1 sleep. Reports on the amount of stage 1 REM sleep obtained by depressed patients are conflicting. Some studies report a reduction in REM sleep during depression, *I48 17* 20, 23-25 others report normal or even slightly increased REM sleep time with depression26p 27 with an earlier REM sleep onset1s,26 and an increase in phasic REM sleep elements such as eye movements. l s Later reports by MENDELS et aLa 2s* 3o likewise reflect a relatively high percentage of REM sleep as well as a pressure to achieve REM sleep in some (but not all) depressed patients. Two previous studies31* 32 of the effects of lithium carbonate on sleep offer apparently contradictory results, although the different findings may be a function of the dose administered and the subjects studied. BREBBIA et al. 31 administered 750 mg/24 hr lithium carbonate for 8 days to three control subjects and to three manic patients with plasma levels ranging between 0.34 and 0.46 mEq/l. The plasma levels are below those regarded as being in the therapeutic or prophylactic range. 2,8 They reported no uniform change in sleep pattern associated with the drug. KUPFER et al.,32 on the other hand, reported a significant increase in delta wave sleep (stages 3 and 4 combined) and a significant decrease in stage 1

Treatment and Prophylaxis of Manic States with a Carbonic Anhydrase Inhibitor

Considering the similarity of the change in electrolyte distribution after the administration of lithium preparations and of carbonic anhydrase inhibitors, we have made an attempt of the treatment and prophylaxis of manic states with benzanilamide, a carbonic anhydrase inhibitor. The following conclusions are tentatively drawn: (1) Benzanilamide, at the oral dosage of 1,000-2,000 mg/day, may have anti-manic effects, though the potency seems to be somewhat weaker than that of lithium preparation. (2) Benzanilamide may well prevent from the manic episodes in a patient exhibiting frequent relapses. (3) Benzanilamide may be superior than lithium preparation in the prophylactic use to recurrent mania, since the former develops much less adverse reactions and can be used more safely than the latter.

Case of Melanotic Alveolar Sarcoma of Liver, Characterised by Rapidity of Growth and Abnormal Weight

M. D—, æt. 30, servant, was admitted to the Limerick Asylum on April 28th, 1910, from the Limerick Prison, suffering from recurrent mania with delusions. This woman was tried at the Connaught Winter Assizes, held in Limerick in December, 1909, for the manslaughter of her illegitimate infant by throwing it into the fire, and was sentenced to nine calendar months' imprisonment with hard labour.

A Case of Recurrent Mania

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Clinical Cases

Annie P., æt. 35 years, had been an inmate of Rainhill Asylum for 12 years. She was subject to attacks of recurrent mania, in the intervals between which she would be quiet, orderly, and rational; the attacks usually lasted some months, and were attended with great restlessness and loquacity, but not with much incoherence. She was at these times very mischievous and destructive, and was indeed a very troublesome patient — generally appearing to have a very good notion of what she was about, and seeming to commit many of her destructive acts on purpose to give trouble, though this apparent capacity for self-restraint was doubtless illusory. In April, 1883, she had been for upwards of 18 months in a maniacal condition, which attack had thus been not only unusually prolonged, but had also been in some respects exceptionally severe. On May 1st following she did not appear very well, but exhibited at that time no special symptoms beyond a little mental dulness and some delay in responding to questions. These symptoms gradually increased, and though there were no physical signs of disease, patient called out at times when moved; she took her food fairly well, but had to be fed, and her bowels were freely relieved after medicine. At 2.15 p.m., on the 5th inst., a great change was observed in her; her face was noted to be livid, conjunctivae insensitive to touch, pupils much dilated, being each about 6 mm., and did not respond to light; respirations slow; pulse 80, full; temp. about 95° (the index did not rise at all, and the thermometer did not register lower); limbs flaccid; plantar reflex, very slightly marked, as also were the knee jerks. She was, in fact, deeply comatose, and presented all the symptoms of cerebral hæmorrhage, a diagnosis of which was, with some confidence, made. Two drops of croton oil were given, and an enema, but neither had any effect. At 5 p.m., in addition to deepening coma, there was distinct drawing of the angle of the mouth to left. The eyes were directed straight forwards, or with a very, slight external deviation in each. At 10 p.m. every muscle in the extremities appeared absolutely flaccid, and the reflexes were completely abolished. Pupils as before. Respirations irregular, with mucous rattling in throat. Pulse 110, bounding. Temp, about 95° (the index, as before, would not rise at all). 11.45 p.m., died.