Psychosomatics 41:446-447, October 2000
© 2000 The Academy of Psychosomatic Medicine
Steroid-Induced Mania in Poststroke Patient Involving the Right Basal Ganglion and Right Frontal Region
Kathleen Franco, M.D., and
Humayun Chughtai, M.D. , Department of Psychiatry, Consultation-Liaison, The Cleveland Clinic Foundation, Cleveland, Ohio
Key Words: Poststroke • Steriods • Mania
TO THE EDITOR: Patients are frequently referred to the psychiatric consultation-liaison service after developing a mood disorder secondary to steroids. Poststroke patients also have been observed to exhibit manic symptoms, but these are less frequent than symptoms of depression. This article reports the case of a 59-year-old man with a preexisting lesion involving the right basal ganglion and right frontal region who later developed mania after the initiation of steroids. The purpose of this report is to describe a possible correlation between the risk for steroid- induced mania and the location of the stroke. We searched MEDLINE and reviewed literature for evidence that patients with right side basal ganglion and right frontal lesions may be more prone to develop a mood disorder secondary to steroids.
Case Report
Mr. A. is a 59-year-old White man who was admitted to the hospital for cardiac transplantation. His history included two coronary artery bypass grafts, 3 years apart, for severe coronary artery disease. In addition, Mr. A. was diagnosed with diabetes mellitus II and hypercholesterolemia. He had never been diagnosed or treated for depression but he had "felt low" before transplantation. Poor appetite, low energy, lack of interest in hobbies, and early and middle insomnia were reported retrospectively.
Thirty-eight days after transplantation, a psychiatric consultation was requested for "behavioral problems." Mr. A.'s wife reported her "normally quiet" husband was now "talking nonstop" and sleeping only 3 to 4 hours each night. Mr. A. acknowledged feeling "on top of the world" and having energy to spare. He had noted his mind was racing and had "trouble catching up" to his thoughts. He had recently spent excessively on phone calls, unlike his frugality of the past. In addition, he was now " hearing God's voice" as well as getting personalized messages from the television.
Mr. A. and his wife could not recall any family members with a psychiatric illness, but they did note that his father would seem blue at times and elated or hyperactive at others. To their knowledge there had never been any treatment or hospital admission.
For more than 30 years Mr. A. had been happily married and worked steadily as an auditor. His wife also had an excellent position and they were financially secure.
Current medications included the following: prednisolone (20 mg qd), azathioprine (100 mg qd), cyclosporine (125 mg bid), enalapril (5 mg bid), acyclovir (400 mg tid), and omeprazole (20 mg qd).
Mr. A. was well-groomed and cooperative but was circumstantial and loose in his associations. During the examination, he was experiencing auditory hallucinations of God's voice speaking to him (Folstein Mini Mental State Exam = 30/30).
His differential diagnosis on Axis I was bipolar affective disorder–manic subtype or affective disorder secondary to steroids and cyclosporine.
Assessments: Complete blood count, urinalysis, complete metabolic profile, and thyroid stimulating hormone were normal. Electrocardiogram demonstrated sinus tachycardia with short PR interval, right axis deviation (QT/QTC 344/450 ms). On magnetic resonance imaging (MRI) there was evidence of a slit-like area of high signal intensity in the right basal ganglia, representing a remote infarct or residual of a small hemorrhage. There were also patchy areas of abnormal high intensity in the right frontal region.
An intriguing part of Mr. A.'s evaluation was the signal hyperintensities (SHs) or subcortical leukoencephalopathy/white matter lesions, visualized on T2-weighted MRI. Generally lesions of this type are adjacent to small vessels and are associated with hypertension, diabetes, and arterioscleroses, particularly in older patients. Localization of SHs in periventricular white matter, subcortical grey matter (basal ganglia), and deep white matter are more frequent than expected in bipolar patients.1 Additionally it is well-known that patients can exhibit disinhibition syndromes ranging from mildly inappropriate social behavior to full-blown mania from lesions to specific brain areas.2
Starkstein3 examined patients with bipolar disorder, both mania and depression (n=7), and patients with mania only (n=12). Five of the 7 patients in the group with both manic and depressive episodes had lesions restricted to the subcortical areas of the right hemisphere. In contrast, 11 of 12 patients with mania had only lesions restricted to right cortical areas. These findings suggest that subcortical mechanisms in the right hemisphere may play a role in poststroke bipolar syndromes, whereas cortical mechanisms may play a role in unipolar mania.
Robinson4 reported that a greater number of manic patients had right hemisphere lesions involving either cortical or limbic areas (orbitofrontal cortex, basotemporal cortex, or subcortical nuclei that is, head of the caudate or thalamus). Another study that used positron emission tomography with 18- fluorodeoxy-glucose to study metabolic abnormalities examined three patients with mania after right basal ganglia strokes. The term diaschisis, meaning that a brain lesion causes a distant effect, is helpful in envisioning how hypometabolic deficits in the right basotemporal cortex might lead to a secondary mania.5
In summary, both Mr. A.'s own past and family history hinted at unconfirmed cyclothymic disorder. Steroids and cyclosporine were necessary for posttransplant care. The MRI identified earlier right-sided frontal and basal ganglion lesions. It is possible that the right-sided lesions had no impact or that they were associated with a prior but mild bipolar diasthesis. Whether SHs increased Mr. A.'s risk for mania is only speculative but should be assessed in future patients.
REFERENCES
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M Botteron KN, Figiel GS, Wetzel MW, et al: MRI abnormalities in adolescent bipolar affective disorder. J Am Acad Child Adolesc Psychiatry 1992; 31:258–261[Medline]
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Starkstein SE, Robinson RG: Mechanism of disinhibition after brain lesions, J Nerv Ment Dis 1997; 185:108–114
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Starkstein SE, Fedoroff JP, Berthier MD, et al: Manic depressive and pure manic states after brain lesions. Biol Psychiatry 1991; 29:149–158[Medline]
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Robinson RG: Neuropsychiatric consequences of stroke. Ann Rev Med 1997; 48:217–229[CrossRef][Medline]
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Videbech P: MRI findings in patients with affective disorder: a meta analysis. Acta Psychiat Scand 1997; 96:157–168[Medline]
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