Bipolar affective disorder is a cyclic disorder of mood characterized by episodes of increased physiologic and psychological activity alternating with episodes of decreased physiologic and psychological activity.1 There may or may not be periods of normal activity between episodes. If periods of normal activity intervene, the patient may be a rapid cycler (four or more episodes of abnormality per year) or a non-rapid cycler (fewer than four episodes of abnormality per year). If periods of normal activity are absent, the patient is said to show continuous rapid cycling. Continuous rapid cycling is differentiated from a mixed affective episode by a clear switch from one affective state to another without coexistence of symptoms from each state. In addition, continuous rapid cycling involves changes in affective patients on a minute by minute, hour by hour, day by day basis for at least 1 month without intervening normal affectivity.
Continuous rapid cycling is a difficult clinical entity to treat.2 Many patients do not respond well to available pharmacologic treatment (eg, Lithium, carbamazepine, anticonvulsants, calcium channel blockers, and hypermetabolic thyroid) and become disabled. This article describes our experience using electroconvulsive therapy (ECT) for continuous rapid cycling patients unresponsive to standard pharmacologic treatment. Our initial result with a single case3 was promising, but further experience indicates the need for caution in patient selection.
We performed a retrospective review of several cycling patients who accepted ECT after other modalities had failed. Six continuously rapid cycling patients, three at Michael Reese Hospital and three at Highland Park Hospital, were offered ECT. The diagnosis of rapid cycling bipolar disorder was made in each case using the criteria of the then current DSM-III. The relative dangers were discussed and the patients chose ECT because a variety of pharmacologic treatments had failed and the disorder was uncontrolled. Bilateral ECT was adrninistered in each case; the clinician determined the number and the frequency of treatments based on the clinical course of each patient. Clinical evaluation of the patients by their psychiatrists provided the follow-up data.
The table presents the highlights of each patient's psychiatric history and treatment response.
Case 1. An 18-year-old female college freshman experienced intractable continuous rapid cycling. It was characterized by extremes of behavior ranging from wild, uncontrollable excitement to catatonic unresponsiveness changing from rninute to minute, with no one affective state lasting for more than 1 hour. There were no normal intervening days in this episode. This episode, IA, was triggered when the patient was given tricyclics during a late winter depression and did not respond to lithium, carbamazepine, phenothiazines, or butyrophenones. The lag time between the beginning of rapid cycling and the administration of ECT was 6 months. (This first episode has been more fully described.3) No chemical prophylaxis was offered between this episode and the succeeding episode, IB. Three years after her first episode, she married and soon became pregnant. Her second episode, behaviorally identical to the first, began when she delivered her first baby, and responded to 33 ECT treatments given within 1 month of delivery. She has been receiving lithium prophylaxis since and is well after 6 years of follow-up.
Highlights of the Psychiatric Histories and Treatment Responses of Six Patients With Continuous Rapid Cycling Bipolar Disorder
Case 2. An 18-year-old male college student experienced continuous rapid cycling with no intervening normal days at age 15 after a viral illness thought to be infectious mononucleosis. His observable behavior varied from a hopeless, withdrawn depressive state accompanied by suicidal attempts to an excited hyperverbal, hyperactive state in which he could derive "physical laws" explaining the universe. Lithium, carbamazepine, and valproate sodium had been tried without success. After 15 ECT treatments, his condition had improved enough that he could return to college in a distant state and even obtain an advanced degree. The lag time between establishment of rapid cycling and institution of ECT was more than 2 years. He has since regressed into a paranoid-depressive psychotic state and has refused further treatment.
Case 3. A 20-year-old man had a history of affective instability extending back to earliest childhood. No clear-cut precipitant could be found for his illness. When he was first seen, he continuously cycled from depressed to manic and back to depressed in approximately a 15-day interval. Psychotic symptoms were present. Five ECT treatments led to an improvement that lasted 1 month. A further course of 33 ECT treatments led to a remission that lasted 6 months. He has since sought megavitamin treatment without success. In this case, the lag time for institution of ECT was approximately 15 years.
Case 4. A 38-year-old married housewife reported severe depression since childhood associated with having a passive, helpless mother and an intolerable experience with a frightening, periodically violent father. In her early teens, she had experimented with multiple substances (eg, alcohol, LSD, cocaine, opiated hash, and amphetamine-like diet pills). Her rapid cycling, long depressions, and brief hypomanias with only 1 or 2 normal intervening days date from this period. In adulthood, she stopped substance abuse and experienced agitated depression with suicidal ideation interspersed with periods of intrusive rapid thinking she described as "speeding my brains out." Psychoanalytic psychotherapy, supportive psychotherapy, mood normalizers (eg, lithium, carbamazepine, verapamil hydrochloride, valproic acid, and clonazepam), and antidepressants (eg, tricyclics, monoamine oxidase inhibitors, bupropion hydrochloride, and trazodone hydrochloride) failed to control the process more than temporarily. In 1990, she had 8 ECT treatments and felt able to enjoy life for the first time. This effect was brief and the depression soon returned. It was unresponsive to selective serotonin reuptake inhibitors. An attempt at outpatient maintenance ECT was unsuccessful because of supervening memory loss. As time has passed, her hypomanias have become shorter and less deep, but her depressions have become more frequent. In this case, the lag time between onset of rapid cycling and institution of ECT was approximately 11 years.
Case 5. A 48-year-old housewife and mother of three with a stable marriage of more than 15 years suffered severe bouts of depression, each 30 to 40 days long, that left her unable to get out of bed or respond to her family. The first episode was precipitated by her first pregnancy. During this time, she had been unresponsive to tricyclic or selective serotonin reuptake inhibitor antidepressants or lithium and carbamazepine. One course of 7 and one course of 12 ECT treatments provided no significant benefit and caused an uncomfortable memory impairment. In this case, the lag between onset of rapid cycling and institution of ECT was 23 years. She remains in supportive psychotherapy, which provides some comfort to her, but continues to cycle into severe depressions on a monthly basis. She is dysthymic between depressions.
Case 6. A 42-year-old married artist has experienced bipolar mood swings of frank mania and suicidal depression since she was 18 years of age. Her first episode of serious depression occurred following group criticism at a religious retreat. This reactive depression was followed by recurrent suicidal depression and frank manias cycling such that she was asymptomatic no more than 1 month each year. During her 20s, a serious suicide attempt (a jump from a fourth story window) while psychotically depressed left her physically disabled. She may have received some benefit from tricyclic and selective serotonin reuptake inhibitor antidepressants, lithium, carbamazepine, valproate sodium, and haloperidol, as well as from intensive psychotherapy, but none of these interventions protected her from extreme mood swings. She received two courses of 10 ECT treatments each that provided significant relief from depression, but that were followed by relapses within 1 to 2 months. The ECT lag time was 18 years in this case. She continues in supportive psychotherapy and is currently benefiting from olanzapine.
These six cases are a small sample accumulated during 15 years by three psychiatrists in independent practice who are experienced clinicians and prescribers of medications known to be useful in the treatment of bipolar disorder. This small data set limits statistical analysis and allows for potential confoundings from the absence of a standardized treatment protocol. Medication dosage was in keeping with the accepted standards of the time.
The onset of rapid cycling in our patient sample occurred in childhood, adolescence, and young adulthood. In none of our cases did rapid cycling arise de nouveau. In the first episode of case 1, seasonal affective disorder was converted to rapid cycling by tricyclic antidepressant administration. In the second episode of case 1, delivery of the first child precipitated continuous cycling. In case 2, rapid cycling developed after a viral illness. In case 5, rapid cycling developed during the course of pregnancy. In the remaining cases, cycling seems to have gradually developed after long periods of affective instability, perhaps related to abuse of multiple substances in case 4.
Our most significant finding is the suggestion of an inverse relationship between the duration of rapid cycling and the response to ECT. Thus, case 1, treated within 6 months of the onset of illness in episode IA and within 1 month in episode IB, did better than succeeding cases. In contrast, cases 2 and 3, in which rapid cycling was present for 2 and 15 years, respectively, before ECT was initiated, had relatively brief remissions. Case 4, in which rapid cycling lasted 11 years before the institution of treatment, had no more than 1 month of improvement. Cases 5 and 6, in which there had been 23 and 18 years of cycling, respectively, before the institution of ECT, did not respond to two attempts each at ECT treatment, which had to be suspended because of supervening memory impairment.
Strikingly, only 1 of our 6 patients with rapid cycling had a lasting response to ECT. This patient received two courses of ECT within months of the establishment of an episode of rapid cycling 4 years apart. Tomitaka and Sakamoto4 reported a similar result for 10 rapid cycling patients treated "aggressively" with a lithium-carbamazepine regimen. Only the 4 who had been rapidly cycling for less than 2 years responded. The 6 who had been cycling for more than 2 years did not respond. It appears that successful treatment of rapid cycling demands quick intervention, regardless of modality.
Thus, ECT treatment of continuous rapid cycling labors under a paradox: it may be most efficacious if begun soon after rapid cycling is established, but most psychiatrists would rather exhaust pharmacologic alternatives before turning to its use. Kruger et al.2 would restrict ECT for those patients "in whom repeated pharmacotherapeutic approaches have been unsuccessful." In addition, although continuous rapid cycling is at times debilitating, at other times it is self-lirniting.5 It is with continuous rapid cycling patients that the clinical judgment of the physician is most critical. In such difficult cases, the patient and his or her family must participate in the decisionmaking process with complete knowledge of possible risks and possible benefits.
ECT was useful in our series of six rapid cycling patients if begun soon after continuous rapid cycling was established. As the length of continuous cycling increased, the efficacy of ECT appeared to decrease. This finding is important because it suggests that the longer continuous cycling lasts unimpeded, the less likely it is to be controlled by ECT. Such a finding may be supportive of the kindling hypothesis - pathology not prevented from recurring becomes fixed and independent of its original cause for its continuation.6 Other severe cases of continuous rapid cycling should be found to determine whether our results can be generalized.
1. Wolpert EA. From metapsychology to pathopsychophysiology: towards an etiological understanding of major affective disorders. In: Pollock G, Greenspan S, eds. The Course of Life: Late Adulthood, vol. 6. Madison, CT: International University Press; 1993:451-478.
2. Kruger S, Braunig P, Young LT. Biological treatment of rapid cycling bipolar disorder. Pharmacopsychiatry. 1996;26:167-175.
3. Berman E, Wolpert EA. Single case study: intractable manic-depressive psychosis in an 18 year old woman successfully treated with electroconvulsive therapy. J Nerv Ment Dis. 1987;175:236-239.
4. Tomitaka SL Sakamoto K. Definition and prognosis of rapid cycling affective disorder. Am J Psychiatry. 1994;152:1524 Letter.
5. McElroy S, Keck PL Rapid cycling. In: Dunner DL, ed. Current Psychiatric Therapy. Philadelphia: W. B. Saunders; 1993:226-231.
6. Post R. Transduction of psychosocial stress into the neurobiology of recurrent affective disorder. Am J Psychiatry. 1992;149:999-1010.
Highlights of the Psychiatric Histories and Treatment Responses of Six Patients With Continuous Rapid Cycling Bipolar Disorder