Mania after vascular dementia in a patient with bipolar II disorder

Abstract

The frequency of mania in patients with vascular dementia is generally considered to be rare, as previous studies showed a 3.5% (6/174) and 2.2% (3/134) prevalence of mania in Alzheimer's disease.1,2 Actually, mania is a rare consequence of ischemic brain injury. For example, there were only two cases of mania among more than 500 consecutive stroke patients.3 Starkstein et al. reported an 83-year-old right-handed woman with mania and mild dementia (Mini Mental State Examination: 17/30) 2 months after a stroke in the right thalamocapsular region.4 However, the manic episode was reported to continue for only 15 days and may have been caused by tricyclic antidepressants, which were administered for her previous depressive state. We report here a case of bipolar II disorder (BP II) who presented with mania after the occurrence of vascular dementia with left fronto-temporal lobe infarction. The patient was a 64-year-old right-handed man with a 14-year history of BP II. He had a history of three hypomanic and two major depressive episodes, and had some cardiovascular risk factors for white matter intensities, including arterial hypertension, diabetes mellitus, and cardiac diseases. At the age of 62, he noticed speech disturbance (slurring), mild sensory aphasia, and slight right hemiplegia. Both magnetic resonance imaging and magnetic resonance angiography revealed moderate cortical atrophy and cerebral infarction in the left fronto-temporal lobe due to marked segmental stenosis of the left middle cerebral artery. Eighteen months after the infarction, symptoms of dementia such as severe memory impairment, severe sensory aphasia, agnosia, and disturbance in executive functioning developed. Two months later, the patient exhibited a manic episode. He scored 8 out of 30 on MMSE, although the MRI findings at this time were the same as those previously observed. Manic state lasted for about 4 months and after mania he also returned to marked symptoms of dementia as mentioned above, without affective symptoms, which has been continuing for 5 years up to the present. In this case, manic state presented after a 14-year history of BP II. Preliminary studies of the course and prognosis of BP II disorder indicate that the diagnosis is stable, as shown by the high likelihood that patients with BP II will have the same diagnosis up to 5 years later.5 Thus, it is difficult to explain how his first emergence of mania is due only to the natural course of BP II. Robinson et al. indicated that in 17 patients who developed secondary mania after brain injury there was only one patient with left hemisphere lesion, and that the mean period from the brain lesion to the onset of mania was 5.8 months.3 Considering these circumstances therefore it is also unlikely that the mania in our case was due to the cerebral infarction alone. In this case, the occurrence of mania may have been related to vascular dementia and the history of BP II. In other words, dementia may amplify mood fluctuation (i.e. worsening hypomania to mania). Interestingly, this phenomenon has occurred only once during the course of the patient's illness, as though a flame turned up high has quickly burnt itself out. Recently, some studies referred to the increased risk of developing dementia in patients with BP and the positive relationship between the risk and the number of depressive and manic episodes.6,7 Empirical research into BP in older adults will not only help to improve the care of this vulnerable and growing group, but will also inform research on the consequences and treatment of BP throughout patient's lifespan.8