What is the likely diagnosis and management for a 5-year-old patient, taking levetiracetam (levetiracetam), who experienced a possible seizure or syncopal event triggered by overheating, characterized by tonic posturing, pallor, and bradycardia, with subsequent weakness and EEG findings of rhythmic intermittent delta-theta slowing?

Diagnostic Assessment of Episode 2

This episode is most consistent with reflex (vasovagal) syncope triggered by overheating, not a seizure, despite the patient being on levetiracetam. The clinical features strongly favor a syncopal mechanism over epileptic activity.

Key Clinical Features Supporting Syncope

Prodromal and Triggering Factors

• Clear vasovagal trigger present: Overheating from multiple layers on a warm day plus hot chocolate consumption creates classic conditions for reflex syncope 1
• Sitting position at onset: Vasovagal syncope commonly occurs while sitting or standing, whereas seizures can occur in any position 1
• Pallor observed: This is a hallmark feature of syncope due to peripheral vasoconstriction and reduced cardiac output, not typical of seizures 1

Event Characteristics

• Bradycardia noted: Even if uncertain due to parental anxiety during counting, the suspicion of bradycardia strongly suggests a cardioinhibitory component of reflex syncope 1
• Tonic posturing for 30 seconds: While this might seem seizure-like, brief tonic movements occur in syncope due to cerebral hypoperfusion and develop after loss of consciousness, not before 1
• Arms outstretched: This tonic posture in syncope occurs after the patient has slumped, as a result of brain ischemia 1
• No vocalization: Absence of vocalization is consistent with either diagnosis but does not favor seizure 1

Post-Event Features

• Immediate hunger upon regaining consciousness: This is characteristic of syncope recovery, not the post-ictal state of seizures 2
• Near-recurrence when sitting up to eat: This orthostatic intolerance with near-syncope when assuming upright posture is pathognomonic for vasovagal syncope and would not occur after a seizure 1
• Weakness and fatigue for 30 minutes: Post-episode fatigue occurs in both syncope and seizures, making this feature non-discriminatory 1

Why This Is NOT a Seizure

Absence of Seizure-Specific Features

• No epileptic aura: No epigastric rising sensation, unusual smell, or other focal seizure symptoms that would suggest temporal lobe involvement 1, 2
• Wrong duration for absence seizure: The 30-second duration is too long for typical absence seizures (which last 5-15 seconds) and absence seizures do not have prodromal symptoms 2
• No post-ictal confusion: The patient was immediately oriented and hungry, not confused or drowsy in the typical post-ictal manner 1, 2
• No post-ictal muscle pain: Absence of muscle aching argues against tonic-clonic seizure activity 1

EEG Findings Do Not Support Active Epilepsy

• Rhythmic intermittent delta-theta slowing in P8-O2: This focal posterior slowing is nonspecific and can represent normal developmental variation, prior injury, or metabolic effects 3
• EEG performed 10 days post-event: A normal interictal EEG cannot rule out epilepsy, but the absence of epileptiform discharges (spikes, sharp waves) makes active seizure disorder less likely 2, 3
• No mention of epileptiform activity: The absence of spike-wave discharges, polyspikes, or other epileptiform patterns is significant 2

Critical Diagnostic Pitfall

The tonic posturing is the misleading feature here. Many clinicians incorrectly assume that any tonic-clonic movements indicate seizure activity. However, syncope-induced convulsive movements are common and occur in approximately 12-90% of syncopal episodes 1. The key distinguishing feature is that in syncope, these movements:

• Are brief (typically <15 seconds) 1
• Start after loss of consciousness 1
• Are not followed by post-ictal confusion 1

Levetiracetam Considerations

• Patient is already on levetiracetam: If this were a breakthrough seizure, it would suggest inadequate seizure control requiring medication adjustment 4, 5
• Levetiracetam has limited efficacy for absence seizures: If this were absence epilepsy, levetiracetam would be a suboptimal choice, with only 26% of children achieving seizure freedom 5
• Potential for paradoxical aggravation: Levetiracetam can occasionally worsen absence seizures, though this typically manifests as increased frequency, not isolated events 6

Recommended Management Approach

Immediate Actions

• Cardiovascular evaluation takes priority: Given the bradycardia, pallor, and clear vasovagal trigger, cardiac assessment is more appropriate than escalating antiepileptic therapy 1
• Tilt table testing: Consider formal autonomic testing if recurrent episodes occur, though not urgently needed for a single event 1
• Do not increase levetiracetam: Escalating antiepileptic medication for what appears to be syncope would be inappropriate and expose the patient to unnecessary side effects 4, 5

Counseling and Prevention

• Educate on vasovagal triggers: Avoid overheating, ensure adequate hydration, recognize prodromal symptoms 1
• Teach counterpressure maneuvers: Physical maneuvers (leg crossing, muscle tensing) can abort vasovagal episodes 1
• Immediate supine positioning: At first sign of symptoms, lie down with legs elevated to prevent full syncope 1

When to Reconsider Seizure Diagnosis

• If events occur without clear triggers (especially from sleep) 1, 2
• If true post-ictal confusion develops (not just fatigue) 1, 2
• If epileptiform discharges appear on repeat EEG 2, 3
• If events increase in frequency despite trigger avoidance 5, 6