P2D122: Acute Cerebellar Ataxia After COVID-19 Infection in a 3-year-old Female

Introduction: Acute cerebellar ataxia (ACA) presents as a loss of balance and coordination, usually following an infectious process. Post-viral cases of ACA have been described. COVID-19 has been an identified etiology of ACA, but there have been few documented case studies. In our case study, we discuss a 3-year-old female affected by ACA after COVID-19 infection.

Case Description: A previously healthy 3-year-old female presented with an unsteady gait. Sixteen days prior, she tested positive for COVID-19 and developed symptoms of malaise and daily fevers up to 104°F. The day prior to presentation, she complained of dizziness and developed an unsteady gait. She was also intermittently “talking like a baby.”
On presentation, her vitals were within normal limits. On physical exam, she had an abnormal broad based stance and was unable to take a step without falling. She had a positive Rhomberg sign and normal sensation, flexion and extension in all extremities. She had no dysarthria, aphasia, or dysmetria on finger to nose testing. Bicep reflexes were 2+, and patellar reflexes were initially 1+ but were difficult to obtain on subsequent exams due to patient cooperation.
On laboratory examination, her erythrocyte sedimentation rate and c-reactive protein were elevated to 120 mm/hr and 1.23 mg/dL, respectively. Complete blood count showed mild normocytic anemia and thrombocytosis. Her white blood count (WBC) was normal, but she had 12% monocytes on her differential. Ferritin was elevated. Electrolytes, renal function, and urine drug screen were unremarkable. She had a positive COVID-19 PCR 2 weeks prior to presentation.

A lumbar puncture was done, and cerebrospinal fluid (CSF) was clear with 10 WBC; differential revealed 76% lymphocytes, 21% monocytes and 3% macrophages. Glucose and protein were normal. Meningitis/encephalitis panel and CSF culture were negative.
An MRI Brain W WO was relatively normal with nonspecific scattered FLAIR hyperintensities. MRI lumbar spine and EEG were normal.
She was discharged after 5 days. One month after hospital discharge, she was seen in neurology clinic; symptoms had resolved. Neurological exam was normal. Repeat MRI one month later was unchanged.

Discussion: ACA typically presents in children following an acute infection, so it is reasonable that COVID-19 is an etiology of ACA. This patient’s abrupt onset of neurological symptoms warranted an in-depth evaluation to rule out other causes of ataxia. Once ACA is diagnosed, treatment is largely supportive, and patients typically recover.

Conclusion: This case expands on the clinical manifestations of COVID-19 in children. With a growing number of cases of COVID-19 since the start of the pandemic, there potentially could be more cases of ACA. It is important to keep ACA in the differential diagnosis when working up a child for new-onset ataxia.