Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Email this article to a Colleague Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to My Articles & Searches Download to citation manager Citing Articles via HighWire Citing Articles via Google Scholar Articles by Monji, A. Articles by Tashiro, N. Search for Related Content PubMed Citation Articles by Monji, A. Articles by Tashiro, N. Traumatic Brain Injury

Brain Injury-Induced Rapid-Cycling Affective Disorder Successfully Treated With Valproate

Department of Neuropsychiatry, Faculty of Medicine, Kyushu University, Fukuoka, Japan, Department of Psychiatry, Miyazaki Medical College, Miyazaki, Japan

Key Words: Traumatic Brain Injury • Valproate

TO THE EDITOR: Brain injury has been shown to precipitate secondary bipolar affective disorders. Moreover, a few reports have shown some cases of rapid-cycling affective disorders after brain injury.^1–3 Rapid-cycling affective disorder, which is defined as the occurrence of four or more affective cycles (i.e., episodes of mania and/or depression) per year, has been generally regarded as refractory to treatment and prophylaxis with lithium. Recent evidence supports the effectiveness of valproate for the treatment of both organic affective disorders and rapid cycling affective disorders.⁴ We herein report a case of brain injury-induced rapid-cycling affective disorder that was successfully treated with valproate.

Case Report

The patient, who had had no family history of psychiatric disorders, was involved in a traffic accident at 4 years of age, and he lost consciousness immediately after, suffering brain injury. Twenty days after the brain injury, a computed tomography (CT) scan showed hydrocephalus, and a ventriculo-peritoneal valve was thus implanted. After surgery, the ventricular size normalized, and he recovered consciousness about 1 month after the brain injury. About 5 months later, a generalized tonic-clonic seizure was observed, and an electroenchephalogram (EEG) showed the presence of bilateral and diffuse spike and wave forms. He thus began to be treated with valproate at that time. The ventricular-peritoneal valve was removed when he was 12 years of age. Because an EEG showed no epileptic abnormality, valproate was discontinued when he was 13 years of age. Soon after the discontinuation of valproate, the onset of rapid-cycling affective disorder was observed. The average length of the affective cycles was approximately 2 weeks. He was admitted to a psychiatric hospital for the first time at 14 years of age. An EEG showed bilateral frontal intermittent rhythmic delta activity (FIRDA), and a magnetic resonance imaging (MRI) scan revealed a mild deformity of the corpus callosum due to the old brain injury. No thyroid dysfunction was detected. Different medications (e.g., lithium, carbamazepine, antidepressants, and neuroleptics) were administered, but all proved to be therapeutically unsuccessful. His manic symptoms were controlled with lithium and/or carbamazepine in addition to neuroleptics, but he invariably became depressive immediately after the resolution of these manic episodes. His depressive episodes were highly intractable to both lithium and/or carbamazepine in addition to antidepressants. He was hospitalized for 45 days because of a manic episode at 16 years of age. Valproate (maximum dose 800 mg/d; maximum level 64 mg/L) was added to lithium and levomepromazine. His manic symptoms resolved within 1 month. An EEG showed no intermittent rhythmic delta activity at that time. Levomepromazine was discontinued before he was discharged from the hospital. Thereafter, without antidepressants, he did not develop any depressive symptoms and became euthymic for the first time in about 4 years. Lithium was discontinued 2 months after the time of discharge from the psychiatric hospital. He has since remained euthymic on valproate alone for 6 months.

Discussion

To our knowledge, there have been only two reported cases of rapid-cycling affective disorders after brain injury.^2,3 The intervals between the brain injury and the onset of rapid-cycling affective disorder of these two cases are a few days and 6 months, respectively. The occurrence of rapid-cycling affective disorders independent of brain injury in this case may thus be a possibility because an interval of 9 years between the brain injury and the onset of rapid-cycling affective disorder was observed. Nevertheless, this independence seems unlikely for the following reasons. First, the onset of rapid-cycling affective disorder was observed soon after the discontinuation of valproate, which was administered about 6 months after the brain injury, and its cessation was observed soon after the readministration of valproate. Bamrah and Johnson^l reported a case of bipolar affective disorder, the onset of which was 2 years after the head injury. Second, both an EEG and MRI scan when the patient was 14 years old suggested the presence of an organic brain lesion due to the brain injury. FIRDA has occasionally been interpreted as a sign of deep midline lesions from various etiologies.⁵ Moreover, an EEG showed no intermittent rhythmic delta activity after the readministration of valproate. Third, the patient had neither pre-injury psychiatric disorders nor a family history of psychiatric disorders. Recent reports have shown that valproate has marked antimanic and mixed-state efficacy, but minimal-to-moderate antidepressant properties in rapid-cycling affective disorders. The combination therapy of valproate and lithium is thus recommended for the treatment of rapid-cycling affective disorders.⁴ Pope et al.² described a case of rapid-cycling affective disorder after brain injury that was successfully treated with valproate added to lithium. On the other hand, this case suggests that the monotherapy of valproate may be effective for the treatment of rapid-cycling affective disorder after brain injury. Although the exact mechanisms of action for valproate have not yet been elucidated, postulated theories include an "anti-kindling" effect in the limbic system on emotion, cognition, and behavior; an enhancement of GABAergic-mediated inhibitory control; and action as a general CNS stabilizer. Whatever the mechanisms are, the therapeutic neuropsychiatric effects of valproate appear to be of quick onset, and it should be considered to be a primary pharmacological intervention for the treatment of neuropsychiatric symptoms after brain injury.

REFERENCES

1. Bamrah JS, Johnson J: Bipolar affective disorder following head injury. Br J Psychiatry 1991; 158:117–119[Abstract/Free Full Text]
2. Pope HG, McElroy SL, Satlin A, et al: Head injury, bipolar disorder, and response to valproate. Compr Psychiatry 1988; 28:34–38
3. Zwill AS, McAllister TW, Cohen I, et al: Ultra rapid cycling bipolar disorder following a closed-head injury. Brain Inj 1993; 7:147–152[Medline]
4. Freeman MP, Stoll AL: Mood stabilizer combinations: a review of safety and efficacy. Am J Psychiatry 1998; 155:12–21[Abstract/Free Full Text]
5. Kameda N, Itoh N, Nakayama H, et al: Frontal intermittent rhythmic delta activity (FIRDA) in pituitary adenoma. Clinical Electroenchephalogr 1995; 26:173–179

This article has been cited by other articles:

				E. Kim and T. J. Humaran Divalproex in the Management of Neuropsychiatric Complications of Remote Acquired Brain Injury J Neuropsychiatry Clin Neurosci, May 1, 2002; 14(2): 202 - 205. [Abstract] [Full Text] [PDF]

Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Email this article to a Colleague Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to My Articles & Searches Download to citation manager Citing Articles via HighWire Citing Articles via Google Scholar Articles by Monji, A. Articles by Tashiro, N. Search for Related Content PubMed Citation Articles by Monji, A. Articles by Tashiro, N. Traumatic Brain Injury

Get information about faster international access.

Privacy Policy

Copyright © 1999 Academy of Psychosomatic Medicine. All rights reserved.

Home | Search | Current Issue | Past Issues | Subscribe | All APPI Journals | Help | Contact Us