What is the management and treatment approach for a pediatric patient presenting with cerebellar manifestations 3 days after an upper respiratory tract infection (URTI)?

Management of Pediatric Cerebellar Manifestations Post-URTI

In a young child presenting with cerebellar signs 3 days after a URTI without extracerebellar neurological symptoms (no altered consciousness, focal weakness, or cranial nerve deficits), watchful waiting is the recommended initial approach, with neuroimaging reserved for clinical deterioration. 1

Initial Clinical Assessment and Risk Stratification

Distinguish between acute cerebellar ataxia (ACA) and acute cerebellitis (AC):

• ACA typically presents with isolated cerebellar signs (ataxia, dysmetria, nystagmus) following viral illness, representing a benign post-infectious syndrome 1
• AC presents with cerebellar signs PLUS signs of increased intracranial pressure (headache, vomiting, altered consciousness), representing true cerebellar inflammation with potential for life-threatening complications 2, 3

Key clinical features to assess immediately:

• Presence of headache, vomiting, or drowsiness suggests AC rather than benign ACA 2, 3
• Isolated ataxia with normal mental status and no vomiting favors benign ACA 1
• Age >3 years with symptoms >3 days duration increases yield of significant imaging findings 1
• Extracerebellar signs (somnolence, encephalopathy, focal motor weakness, cranial nerve involvement) mandate urgent neuroimaging 1

Neuroimaging Decision Algorithm

For children with isolated cerebellar signs, recent viral illness, negative urine drug screen, and NO extracerebellar symptoms:

• Watchful waiting is appropriate without immediate imaging 1
• Reserve imaging for clinical deterioration 1

Immediate MRI brain (preferred over CT) is indicated when:

• Headache, vomiting, or altered consciousness accompany ataxia (suggests AC) 2, 3
• Any extracerebellar neurological signs are present 1
• Age >3 years with symptoms persisting >3 days 1
• Clinical deterioration during observation 1

MRI is superior to CT because it identifies 63.9% of abnormalities versus 29.3% for CT, and CT misses posterior fossa pathology 1. However, CT can identify acute hemorrhage, hydrocephalus, and cerebellar edema if MRI is unavailable 1

Treatment Based on Diagnosis

For Benign Acute Cerebellar Ataxia (Isolated Cerebellar Signs)

Supportive care only:

• Adequate hydration 4
• Rest during symptomatic period (typically 5-7 days for viral URTI) 4
• Acetaminophen or ibuprofen for discomfort 5
• Gradual return to activities as symptoms improve 4
• No specific pharmacologic treatment required 6

For Acute Cerebellitis (Cerebellar Signs + ICP Signs)

Immediate interventions:

• High-dose intravenous corticosteroids (dexamethasone is most commonly used) 2, 7, 3
• Fourteen of 15 patients in one series received IV and/or oral steroids 3
• Intravenous immunoglobulin (IVIG) was used in 8 of 15 cases in combination with steroids 3

Neurosurgical consultation if:

• Obstructive hydrocephalus develops (present in 26.6% of AC cases) 3
• Tonsillar herniation is present (occurs in 73.3% of AC cases) 3
• External ventricular drain or decompressive surgery may be required 2, 7

Diagnostic Workup

Laboratory evaluation:

• Cerebrospinal fluid examination if AC suspected: typically shows elevated leukocytes and protein 7
• Viral serologies: Mycoplasma pneumoniae, influenza A, cytomegalovirus, varicella zoster virus, Epstein-Barr virus 3, 8
• Urine drug screen to exclude toxic ingestion 1
• Consider anti-GQ1b IgG antibody if ophthalmoplegia and areflexia present (Miller-Fisher syndrome) 1

EEG consideration:

• Should be considered in all patients with undiagnosed encephalopathy to rule out non-convulsive status epilepticus 1

Follow-Up and Prognosis

For benign ACA:

• Most cases resolve completely within 1-3 weeks 6
• No specific follow-up imaging required if clinical recovery is complete 6

For AC:

• Neurological sequelae occur in approximately 27-33% of cases 3, 6
• Follow-up MRI at median 12 months shows persistent cerebellar cortical T2-hyperintense changes in 92% and cerebellar atrophy in 75% 3
• Residual symptoms may include ataxia, dysmetria, memory difficulties, dysarthria, or tremor 3
• Pathological MRI/CT findings at admission correlate with neurological sequelae 6

Critical Pitfalls to Avoid

Do not dismiss headache and vomiting as simple viral symptoms when they accompany ataxia—this triad suggests AC requiring urgent MRI and treatment 2, 3

Do not delay neuroimaging in children with extracerebellar signs, as 86% of children with significant neuroimaging pathology had additional focal neurological findings 1

Do not assume normal CT excludes serious pathology—MRI is significantly more sensitive for posterior fossa abnormalities 1

Do not withhold corticosteroids in confirmed AC—early steroid treatment may increase chance of recovery, as evidenced by absence of fatalities in treated series 3

Do not forget to consider Miller-Fisher syndrome (Guillain-Barré variant) if ophthalmoplegia and areflexia accompany ataxia 1

Do not miss varicella-associated arterial stroke, which accounts for up to one-third of pediatric arterial strokes and can present with mean delay of 3 months (range 1 week to 48 months) after VZV infection 1