What could the EEG and MRI show in a patient with a history of recent Human Rhinovirus (HRV)/Enterovirus infection and worsening neurologic symptoms?

What the Overnight EEG and Morning MRI Could Reveal

In a patient with recent HRV/Enterovirus infection and worsening neurologic symptoms, the MRI may show characteristic hyperintensities in the brainstem (particularly the posterior pons and medulla), bilateral cerebellar dentate nuclei, and potentially spinal cord gray matter changes if acute flaccid myelitis is developing, while the EEG will help identify encephalopathic changes, seizure activity, or periodic discharges that guide treatment decisions. 1, 2, 3

Expected MRI Findings in Enterovirus/HRV Neurologic Disease

Brainstem and Cerebellar Involvement

• The most characteristic MRI pattern shows T2-weighted and FLAIR hyperintensities in the posterior brainstem (pontine tegmentum, medulla oblongata), which occurs in approximately 56-71% of patients with enterovirus 71 encephalitis 2, 3, 4
• Bilateral cerebellar dentate nuclei involvement is pathognomonic for enterovirus neurologic disease and should be specifically evaluated 1, 2, 4
• Diffusion-weighted imaging (DWI) may be particularly sensitive for detecting early changes and can show restricted diffusion in affected brainstem regions 5, 2

Spinal Cord Findings

• If acute flaccid myelitis (AFM) is developing, MRI will demonstrate gray matter changes in the spinal cord, particularly affecting the ventral horn at cervical levels—this distinguishes AFM from acute flaccid paralysis (AFP), which lacks these MRI changes 1
• Enhancement along ventral nerve roots at the conus medullaris level may occur in some cases 2

Less Common but Important Patterns

• Hippocampal involvement with T2/FLAIR hyperintensity can occur, though this is unusual for enterovirus (more typical of HSV encephalitis) 2
• Leptomeningeal enhancement may be present in atypical cases 2
• Rhinovirus specifically can cause cerebellar dentate nuclei abnormalities prominent on DWI, potentially leading to cerebellar atrophy on follow-up imaging 5

Expected EEG Findings

Encephalopathy Detection

• EEG is abnormal in >80% of patients with viral encephalitis and is crucial for distinguishing organic encephalopathy from psychiatric disease 1
• Diffuse high-amplitude slow waves indicate encephalopathic changes and support the diagnosis of CNS involvement 1

Seizure Activity Identification

• EEG should identify non-convulsive seizures or subtle motor seizures, which are common in enterovirus encephalitis, particularly with brainstem involvement 1
• Myoclonic jerks (a hallmark of enterovirus 71 rhombencephalitis) may have EEG correlates 3, 4
• Temporal lobe spike-and-wave activity or periodic lateralized epileptiform discharges (PLEDs) would suggest HSV encephalitis rather than enterovirus 6

Is This Workup Sufficient?

What's Missing: Critical Diagnostic Tests

This imaging and EEG workup is NOT sufficient without concurrent CSF analysis and viral testing. 1, 7

• CSF PCR for enteroviruses is essential and should be performed on cerebrospinal fluid, as viruses like EV-D68 are rarely detectable in stool samples 1
• Respiratory samples (throat/nasopharyngeal swabs) and stool samples must be submitted in addition to CSF, as rhinovirus/enterovirus may be detectable in respiratory specimens even when CSF is negative 1, 5
• CSF analysis should include cell count (expect pleocytosis in 87% of cases), protein, and glucose 7, 4

Additional Testing Considerations

• HSV-1, HSV-2, and VZV PCR testing from CSF should be performed to exclude herpes simplex encephalitis, which requires immediate acyclovir treatment and has different MRI patterns (medial temporal lobe involvement) 6, 7
• Blood samples for enterovirus RT-PCR may be helpful, particularly if CSF cannot be obtained 1
• Serologic testing has limited acute utility but paired acute and convalescent samples can provide retrospective confirmation 6

Clinical Correlation with Imaging/EEG Findings

Severity Grading Based on Clinical-Radiologic Correlation

• Grade I disease (myoclonus, tremor, ataxia) typically shows brainstem hyperintensities without extensive involvement 3
• Grade II disease (myoclonus plus cranial nerve deficits) shows more extensive brainstem lesions 3
• Grade III disease (rapid respiratory deterioration, shock, coma) carries 14% mortality and requires immediate ICU transfer—MRI may show extensive brainstem involvement 3, 4

Warning Signs Requiring Escalation

• If MRI shows extensive bilateral brainstem involvement or spinal cord gray matter changes, immediate pediatric/adult ICU consultation is mandatory for airway protection and ventilatory support planning 7
• Progressive myoclonus, loss of doll's eye reflex, or apnea indicate impending Grade III disease with high mortality risk 3

Common Pitfalls to Avoid

• Do not assume normal MRI excludes serious enterovirus CNS disease—MRI can be normal early in the disease course, and clinical deterioration can be rapid 3
• Do not delay empiric acyclovir while awaiting test results if HSV encephalitis remains in the differential, as mortality increases significantly with treatment delays beyond 4 days 6
• Do not rely solely on CSF testing—respiratory and stool samples are critical for enterovirus/rhinovirus detection 1
• Do not miss acute flaccid myelitis—specifically request spinal cord imaging if there is any limb weakness, as gray matter changes on MRI are the defining feature 1