He had epilepsy, which was diagnosed by a neurologist when he was 12 years old. He had been on antiepileptic medicine for several years and had no seizure activity. Based on the clinical investigation and brain magnetic resonance imaging (MRI) performed at the age of 12 years, the neurologist made the diagnosis of DWM. His MRI scan showed an absent left cerebellar hemisphere and a severely dysplastic right cerebellar hemisphere and vermis with large retro-cerebellar cerebrospinal fluid (CSF) cyst and supratentorial ventriculomegaly (VM) with thinning of the corpus callosum along with a dysmorphic right hippocampus with a suggestion of right temporal lobe atrophy (Figure 1).
There was no family history of psychiatric illness nor of alcohol or drug use. His early developmental history indicated that he was born at 24 weeks of gestation with a birth weight of 1.4 kg. The postpartum period was complicated by Neonatal Intensive Care Unit (NICU) admission, the need for intubation, and the occurrence of intraventricular hemorrhage. He had febrile convulsions and chronic pulmonary illness, and underwent surgery at the age of 3 years for patent ductus arteriosus. Despite the difficulties mentioned above, he graduated from high school through a special needs support educational program.
The patient was a young gentleman. He was wearing a casual dress, looked suspicious, and was uncooperative during the interview. He was nervous and asked to leave the room and avoided answering questions. The patient had minimal eye contact. His speech was clear, slow, but with a low tone and volume, with delayed but relevant responses. He appeared irritable, and his affect was labile while being reactive only when talking about his interests. He became defensive when asked about his anger outbursts. He seemed to have insight into his behavior but did not admit to taking responsibility. He denied death wishes, suicidal ideation, homicidal ideation, and abnormal perceptions and obsessions. No overt delusions were observed during assessment.
His neurological and general physical examinations were unremarkable. Blood investigations, including complete blood count testing, blood chemistry, and thyroid function, showed results within the normal range, and his electrocardiogram (ECG) was normal. He was referred for a neurologist review and repeat electroencephalography, which showed abnormal epileptiform discharges in the left posterior parietal region.
His presentation was evaluated by a neurologist, and an agreement was reached regarding the diagnostic formulation of intermittent explosive disorder. His behavior was managed through a multidisciplinary approach that included medical, nursing, and psychological therapy, and family support. A plan to switch his antiepileptic medicine to sodium valproate and low-dose antipsychotic medication was agreed upon. The involvement of nursing and occupational therapists to assess his need for support and monitoring of his medication at home was agreed upon. His medications were adjusted to gradually withdraw topiramate and introduce sodium valproate and a small dose of risperidone; psychoeducation was provided. His follow-up was carried out at home, and he showed recovery within a few weeks of discharge, with a significant reduction in his aggressive behavior and improved mental state; he was followed and assessed again at 6 months and after a year, and he continued to show stable mental state and behavior.