.png)
Multiple sclerosis is a chronic demyelinating disease of the central nervous system. Demyelinating diseases also can cause almost every psychiatric disorder like other central nervous system diseases. In this case report, we are going to discuss a 19-years-old multiple sclerosis patient, who had a diagnosis of bipolar affective disorder after a psychotic depressive episode. The patient was 19-years-old male. Approximately 7 months ago, he had been diagnosed multiple sclerosis after admitting to a neurology clinic due to numbness and loss of sensation in the face and inability to look both lateral sides. His complaints regressed after several neurology polyclinic controls. Then he had been taken to a neurology polyclinic by his relatives because of reluctance, insomnia, feeling of inappropriate guilt, worthlessness, uncontrollable crying spells, refuse to eat or drink complaints, which he was suffering for 10 days. In the control MR, there had been demyelinating plaques at C6 region of cervical medulla spinalis; callosal, pericallosal and periventricular multiple demyelinating plaques in white matter at supratentorial region; several demyelinating millimetric plaques in the brain stem. However, he had been said to be stable in terms of neurology and he was referred to our psychiatry clinic. His biochemistry results and neurological examination was normal; he was hospitalized to our clinic and diagnosed with major depression with psychotic features. In his mental state examination, there was decreased self-care. He wasn’t making eye contact. His mood was depressive, affect was restricted. His speech rate and ease of conversation were decreased and there was latency in response. He was describing auditory hallucinations and visual hallucination. His speed of thinking and associations was decreased. Persecutory ideas of reference were present. HAM-D score was found 24. Paroxetine 20 mg/day, lorazepam 1 mg/day, amisulpiride 200 mg/day was ordered. At the end of the second week, psychomotor retardation and vegetative symptoms were dramatically improved. The patient, whose HAM-D score was decreased to 12, mood symptoms and psychotic symptoms regressed, discharged from hospital with paroxetine 30 mg/day and amisulpiride 300 mg/day at the end of the third week. His state at first polyclinic control was stable; however, in his second control, there was euphoric mood, increased libido, decreased need for sleep, increased energy and activity, logorrhea, increased money spending. He was hospitalized again with pre-diagnose of bipolar affective disorder manic episode and paroxetine doses were lowered and then totally stopped gradually. In multiple sclerosis, bipolar affective disorder episodes can be the first sign of the disease. Also, it can be seen as a concurrent diagnose or can be occurred as a side effect of medication used in order to treat multiple sclerosis. Multiple sclerosis and bipolar affective disorder co-occurrence is a well-known but little clarified situation. In our case, there was a bipolar affective disorder, which was occurred after multiple sclerosis. Although there is no way to tell if it was secondary to MS or they were two comorbidities, concomitance of MS and mood disorders incidence in literature suggests that MS might cause mood disorders.