An 8-year-old boy was referred to our hospital for subacute stroke. Three days prior, he fell and hit the right side of his head on a coffee table. He seemed fine immediately after, but the following 2 days, he had right facial weakness, difficulty concentrating, and was doing and saying things that did not make sense. His mother brought him to the pediatrician, who ordered magnetic resonance imaging (MRI) which revealed new large infarction of the left caudate and putamen. He was started on aspirin 81 mg daily and admitted to our hospital. On exam, he had significant executive function and concentration errors, while constructions were intact. He had some choreiform movements on the right with mild hyperreflexia distally in the right leg and positive right Babinski. Computed tomography angiogram was negative for dissection; repeat MRI (Figure 1) with MR angiography (MRA) and MR venography (MRV) demonstrated restricted diffusion within the left caudate, anterior lentiform nucleus, anterior limb of the internal capsule, and deep white matter of the frontal lobe consistent with acute infarct, but no evidence of dissection or venous thrombosis. His past medical history was remarkable only for mild anxiety and an itchy rash 1 month earlier that did not look like varicella. His family history was remakable for a pulmonary embolism in his mother following cardiac ablation for Wolff-Parkinson-White and a maternal grandfather with multiple strokes starting at age 56; there was no known family history of mental health issues. Echocardiogram and electrocardiogram were unremarkable. His prothrombotic workup was remarkable only for mild anemia with mean cell volume of 78 fL and hemoglobin of 11.8 GM/dL; heterozygosity for the PAI 14G gene variant, and homozygosity for the MTHFR 1298C gene variant, with normal homocysteine. His alertness and concentration improved during his 3-day hospitalization, and he was discharged home on aspirin, iron, and folate with outpatient rehabilitation.
However, after discharge home, his family noted severe anxiety, depression, impulsivity, aggression, hyperactivity, trouble with concentration, mouthing objects, restlessness, and no remorse for his actions. He was fighting, biting, kicking, punching, and spitting at family members. He lost interest in toys and only wanted to watch television. He was unable to return to school and was started on homebound instruction. He was started on cyproheptadine for decreased appetite, guanfacine for poor attention, and as-needed hydroxyzine for anxiety by his pediatrician. He returned to the hospital a month and a half post discharge with chest pain, but was discharged the next day when no cardiac pathology was found. At his follow up stroke clinic exam 2 months post discharge, he was uncooperative, and his insight and judgment appeared poor. He was referred urgently to psychiatry clinic, where he was diagnosed with a personality change due to cerebrovascular accident and combined type attention-deficit/hyperactivity disorder, specifically disinhibited and aggressive features. The mother quit her job to stay home and care for him.
Over the next year, multiple medications were tried and discontinued by the pediatrician and psychiatry clinic. Cyproheptadine was stopped because it did not help. The initial guanfacine did not help. Amphetamine sulfate caused headaches. He became suicidal on atomoxetine. His aggression worsened on extended-release guanfacine. Atomoxetine was retried at a lower dose, but he became aggressive on that, and security was called to psychiatry clinic. Risperidone helped behavior, particularly rage outbursts, but caused weight gain and was sedating, so the dose was readjusted multiple times. Low dose methylphenidate was added approximately 16 months post discharge, and that helped impulsivity and inattention. In addition to medication, he received individual counseling and family counseling. The family was noticing definite improvements by 1 1/2 years post discharge; then, he developed worsening anxiety and depression and an eye-blinking tic. Counseling, which had been stopped when he improved, was restarted. He was switched from short-acting to extended-release methylphenidate. Clonidine was added to help the tic and anxiety. He was weaned off risperidone, then it was restarted, and fluoxetine was added when he became anxious in school. At his last follow up, 3 years post stroke, he was doing well on aspirin, clonidine, dexmethylphenidate, and fluoxetine and was feeling back to his old self. However, he still got anxious in large crowds, and his family reported he acted like a younger child in the mornings until he got his morning medications.
The behavior symptoms had a significant impact on the child's family due to the disruption of the behavioral symptoms. His motor symptoms had resolved much faster than the psychiatric symptoms and were barely noticeable after a few months. The mother finally returned to work 3 1/2 years after his stroke.