Aripiprazole for acute mania in an elderly person.

New-onset bipolar disorder is rare in the elderly. Symptom profile is similar to that in young adults but the elderly are more likely to have neurological co-morbidities. There are no case reports of elderly mania being treated with aripiprazole, an atypical antipsychotic. A 78-year-old gentleman presented to us with symptoms suggestive of mania of 1 month's duration. He had similar history 3 years ago and a family history of postpartum psychosis in his mother. There were no neurological signs on examination and work-up for an organic etiology was negative except for age-related cerebral atrophy. He improved with aripiprazole and tolerated the medications well. The use of psychotropic medications in the elderly is associated with side-effects of sedation, increased cardiovascular risk, and greater risk of extra-pyramidal side-effects. The use of partial dopaminergic antagonists like aripiprazole may be useful in the balancing of effects and side-effects.

Mania commonly affects young adults during their most productive period of life. The age at onset of mania may vary from as young as 5 years to 50 years or older, becoming rarer with advancing age; with the mean age at onset being 30 years.[1] Of all the new-onset bipolar disorders, only 6–8% occurs in those above 60 years.[2] When it occurs in the elderly, secondary causes like silent cerebral infarcts are often found.[3] The elderly mania patient also shows more neurological signs than usually seen in young adults.[4] In treatment of mania in the elderly, choosing an appropriate psychotropic is important due to poor tolerability of drugs in this group. There are no clear guidelines for the management of bipolar disorder in the elderly because most of the trials comparing aripiprazole with lithium[5] or haloperidol[6] involved young adults. This case report describes an unusually late onset of bipolar disorder in an elderly man and discusses the differential diagnosis and treatment aspects in this case.

CASE REPORT

A 78-year-old person, retired as school teacher with no history of any substance abuse or medical history. He had been suffering from bilateral knee pain diagnosed as osteoarthritis for the last 20 years and was not on any steroids. He presented with 1-month duration of altered behavior characterized by excessive psychomotor activity, emotional lability, increased self-confidence, excessive talkativeness, decreased need for sleep, and increased sense of energy level. There were a few occasions when he misrecognised his daughter as his wife who had passed away 6 months ago. On examination, he was an elderly obese person weighing 92 kg with BMI >27. His vitals were stable and no focal deficits could be found on neurological examination. Mental status examination revealed increased irritability, increased psychomotor activity, and increased self-confidence and authoritativeness. No cognitive impairment could be detected except for inattention and distractibility. His Mini Mental Status Examination score was 28/30. No abnormal involuntary movements were noticed. Neurological examination did not reveal rigidity or other extra-pyramidal symptoms. There were no frontal release reflexes. He did not have any perceptual abnormalities or delusions. He had impaired personal judgment and lacked insight.

He had similar behavior 3 years ago, diagnosed and treated as mania in the same hospital. There was positive family history in the form of his mother having had symptoms suggestive of postpartum psychosis. Investigations including HIV, VDRL, serum vitamin B12 level, TFT, EEG, routine hemogram, serum electrolytes, blood urea, and serum creatinine were normal. ECG revealed no abnormalities, except for a prolonged corrected QT interval (QTc) of 486 msec. His CT brain [Figure 1] showed cortical atrophy, especially pronounced in the temporal and frontal areas. The periventricular regions in the frontal lobe showed mild hypodensity suggestive of small vessel ischemic disease. There was bilateral basal ganglia calcification. There were no infarcts in any region. He didn′t fulfill international consensus criteria for behavioral variant of Frontotemporal Dementia (FTD).[7]

Figure 1

CT brain shows frontal cortical atrophy (top left), with frontal subcortical white matter hypodensities (top right). Widened Sylvian fissures suggestive of temporal pole atrophy and basal ganglia calcifications are also seen (bottom left). Widening of temporal horns of lateral ventricles (bottom right) is further evidence of temporal lobe atrophy

He was initiated with aripiprazole 5 mg/day because of his QTc being 486 msec. Given his age, we chose aripiprazole as it is less sedating and has lower chances of producing postural hypotension. He also required intravenous lorazepam 2 mg sos for his agitated behavior for the first 2 days. Aripiprazole was gradually increased to 15 mg, and by the end of 3 weeks he showed complete remission of his manic symptoms. At the time of admission in psychiatry ward, he scored 27 on mania severity on Young's mania rating scale (YMRS)[8] and it came down to 4 at the end of 3 weeks.

DISCUSSION

Occurrence of first episode of mania in the elderly (after 60 years age) warrants a high index of suspicion for organic causes. Co-morbid medical or neurological illness is common in such persons.[4] Sometimes, infarcts are evident only in imaging without clinical manifestations.[3] On evaluation, we did not find any obvious etiology for his mental illness, except for frontal and temporal atrophy and possible frontal sub-cortical white matter involvement. One possibility considered was that of FTD, but this was ruled out as he did not fulfill criteria for dementia and behavioral component of FTD. Bipolar disorder increases risk of dementia in the elderly.[9] It is possible that the manic episodes were the initial manifestations of FTD in this patient and this will be tested only in the follow-up. There was family history of postpartum psychosis in his mother, which is associated with a family history of bipolar disorder[10] and the index case had been diagnosed as mania 3 years ago with complete remission in the interval period. These two points and absence of any abnormalities in laboratory and clinical examination favored diagnosis of mania.

Aripiprazole has relatively high affinity for both 5-HT2A and D2 receptors similar to other atypical antipsychotics but differs from them due to its partial agonist activity at D2 and 5-HT1A receptors. Its long half-life (75 hours) allows single daily dosing.[11] Therapeutic dose range of aripiprazole advised for mania is 10–30 mg/day. It has a more favorable side-effect profile compared to typical and even atypical antipsychotics. Aripiprazole has lesser propensity to cause extra-pyramidal symptoms, an important factor in the elderly.[11] Other desirable properties are lesser chance for causing side-effects like dyslipidemia, glucose intolerance, hyperprolactinemia, postural hypotension, sedation, QT prolongation, and weight gain. Its efficacy has been proven as monotherapy in treating acute mania and in prophylaxis of bipolar disorder.[56] Hence, we chose aripiprazole for our patient in view of his already prolonged QTc interval and age of 78 years.

CONCLUSIONS

This case is unusual in that age of onset of mania is very late (75 years) and during the current second episode we could not find any organic etiology. Moreover, his condition responded well with least side-effects to aripiprazole. Hence, aripiprazole may be a safe and effective antipsychotic medication for the control of mania in the elderly.