Abstract
We report the case of a 16-year-old girl who presented to the psychiatric inpatient facility with elevated and labile mood, poor sleep, bizarre delusions of sexual nature and disinhibited and disorganized behaviour present for several days. The alteration in her mental state had started with low mood and withdrawal from friends and family about 7 weeks prior to this. At school she had been inserting phrases of no relevance in between essays, laughing at the principal and mumbling to herself which was radically different to her premorbid personality of being a quiet, hard-working polite person.
She had been born at 32 weeks of gestation and had had mild left-sided weakness at birth which had then delayed the age at which she had walked independently although her academic performance had been unaffected prior to this. There was no history of recreational drug or alcohol use and no family history of mental illness. The family was close-knit and very supportive.
On mental state examination she was an average built casually dressed girl who looked her stated age. She was lying in bed, calling out inappropriate and odd phrases and claiming that she had superpowers. Her affect was incongruent and rapidly fluctuating. Her attention was short-lived and speech was tangential with bizarre themes. Her blood tests were unremarkable and a computed tomography (CT) scan of the brain showed a borderline nonspecific atrophic appearance.
During this admission while on olanzapine she had developed tachycardia and hypertension and neuroleptic malignant syndrome was excluded. She was diagnosed with bipolar affective disorder (BPAD) and was started on sustained release (SR) lithium 450 mg BD and olanzapine 2.5 mg nocte after which her mental state stabilized although she had developed residual coarse tremors in her upper limbs.
Two weeks after her discharge the patient was readmitted due to recurrence of symptoms which did not coincide with her menstrual cycle and occurred despite being adherent to the medication regime. She was stabilized and discharged with Lithium SR 450 mg mane and 900 mg nocte and Olanzapine 10 mg nocte.
Two weeks later the patient presented for the third time with a 1-day history of loss of sleep and was distressed as a result of hearing voices asking her to kill herself. She was trialled on sodium valproate as well which soon had to be ceased due to excessive sedation.
During this time her mental state had deteriorated but cessation of olanzapine and intensive nursing care produced an immediate improvement in levels of orientation, physiological stability and mental alertness. The manic symptoms were controlled by continuation of lithium and blood levels were monitored to exclude toxicity. The frequency of relapse with increasing severity and the development of tremors and parkinsonian side effects to olanzapine which persisted despite cessation required a reassessment and a follow up neurological consultation.
An MRI of the brain with contrast showed patchy but extensive white matter changes indicative of an acute demyelinating process without involvement of the basal ganglia.
During this time a review of the events leading up to the first episode were discussed in detail with the family who then gave a history of transient paraesthesia in the left lower limb before the appearance of low mood which had preceded the mania and the psychosis. An MRI of the lumbosacral spine done previously had been unremarkable. Wilson's disease was excluded through blood tests, slit lamp examination of the eye and a liver biopsy. A lumbar puncture, however, showed intrathecal immunoglobulin synthesis confirming the likelihood of multiple sclerosis.
The patient had been stabilized on lithium SR at 450 mg BD. She has been attending part-time school successfully and will continue to be monitored by the neurology team who will discuss further treatment modifying options including the possibility of interferon and steroids.
Over the years, the high preponderance of psychiatric symptoms in patients with multiple sclerosis [1,2] has led to the suggestion that this disease should be considered in the differential diagnosis of patients being seen for psychiatric complaints especially when neurological deficits co-exist with mania and psychosis [3–5].