Arteritis and Large Vessel Occlusive Strokes in Children After COVID-19 Infection.

We describe 2 previously healthy children who suffered disabling arterial ischemic strokes because of acute intracranial large vessel occlusion within 3 to 4 weeks of coronavirus disease 2019 (COVID-19) infection. Both children presented from communities with high COVID-19 case rates in the Southwest United States. An 8-year-old American Indian girl experienced severe iron deficiency anemia requiring blood transfusion and presented with bilateral middle cerebral artery (MCA) distribution strokes 3 weeks later. She underwent emergent mechanical thrombectomy of the left MCA with successful clot retrieval but experienced reocclusion of that artery 5 hours after intervention. She also had evidence of cerebral arteritis on catheter angiography and vessel wall imaging, and clot pathology revealed recently formed, unorganized platelet- and fibrin-rich thrombus with sparse clusters of erythrocytes, degenerated histiocytes, few eosinophils, and rare neutrophils. A 16-year old African American boy demonstrated evidence of arteritis on brain magnetic resonance angiography and serological markers of cardiac and renal injury accompanied by positive lupus anticoagulant antibodies. The children described in this report express clinical features inconsistent with focal cerebral arteriopathy, including elevated markers of systemic inflammation in both bilateral MCA strokes in one case and multiple organ system dysfunction in the other case. Neither patient fulfilled criteria for multisystem inflammatory syndrome in children, given absence of fever. These cases illustrate that systemic postinfectious arteritis with cerebrovascular involvement may complicate COVID-19 infection in previously healthy school-aged children, and their presentations may overlap but not fulfill criteria for multisystem inflammatory syndrome in children or focal cerebral arteriopathy.

Juvenile Huntington disease exacerbated by methylphenidate: case report.

The authors describe the case of an 8-year-old boy, otherwise healthy, who presented with symptoms consistent with attention-deficit hyperactivity disorder (ADHD) and was started on a trial of methylphenidate. Within 4 weeks, he experienced a rapid decline in fine motor skills, with dysarthria, intention tremor, motor impersistence, and diffusely increased tone. Symptoms persisted despite cessation of methylphenidate. At that time, a paternal history of Huntington disease was disclosed. Molecular analysis revealed an expansion in CAG repeats to 75 copies, within the range characteristic of juvenile Huntington disease. This report raises the possibility that use of dopaminergic agonists in patients with a family history of Huntington disease may lead to clinical exacerbation of motor symptoms and/or unwitting diagnosis in an unprepared family.