Can the presenting symptoms resembling seizures in a patient with subarachnoid hemorrhage (SAH) due to ruptured aneurysm be attributed to decortication or decerebration posture caused by sudden increased intracranial pressure (ICP) rather than a true seizure?

Seizure-Like Episodes in SAH: Distinguishing True Seizures from Posturing

Yes, many "seizure-like" episodes at SAH presentation are not true epileptic seizures but rather decorticate or decerebrate posturing from sudden ICP elevation, and this distinction is clinically critical because it fundamentally changes management priorities. 1

The Core Problem: Diagnostic Uncertainty

The American Heart Association explicitly acknowledges that "a large number of seizure-like episodes have been associated with aneurysmal rupture. It is unclear, however, whether all these episodes are truly epileptic in origin." 1 This statement from the 2009 guidelines remains highly relevant because:

• While up to 26% of SAH patients experience "seizure-like episodes," more rigorous modern studies using EEG monitoring suggest the true seizure incidence is only 7.8% to 15.2% 1
• The majority of early "seizures" occur before medical presentation (when no EEG confirmation is possible), and in-hospital seizures are actually rare when prophylactic anticonvulsants are given 1
• This discrepancy strongly suggests that many witnessed episodes at ictus are actually posturing phenomena from acute ICP spikes rather than epileptic activity 1

Pathophysiologic Distinction

Posturing from Sudden ICP Elevation

• Aneurysm rupture causes instantaneous ICP elevation that can transiently exceed mean arterial pressure 2
• This acute pressure wave can produce decorticate (flexor) or decerebrate (extensor) posturing that mimics tonic-clonic activity 2
• The posturing is a direct mechanical/pressure effect on brainstem and cortical structures, not epileptic discharge 3

True Epileptic Seizures

• Actual seizures in SAH are associated with specific risk factors: middle cerebral artery aneurysms, thick subarachnoid clot burden (Hijdra scale >21), subdural hematoma, intraparenchymal hemorrhage, cortical infarction, and hydrocephalus 1, 4
• True seizures typically occur later (average 18 days post-SAH for nonconvulsive seizures) rather than at the moment of rupture 1

Clinical Algorithm for Differentiation

At Presentation (Witnessed "Seizure-Like" Episode):

Assume posturing from ICP crisis until proven otherwise if the patient presents with:

• Sudden onset at moment of "worst headache" 5
• Brief loss of consciousness (53% of SAH cases) 5
• Rapid return to baseline or persistent depressed consciousness 1
• No post-ictal confusion typical of true seizures 1

Consider true seizure more likely if:

• Episode occurs minutes to hours after headache onset (not simultaneous) 1
• Patient has high-risk features: MCA aneurysm, thick SAH clot, subdural hematoma, intraparenchymal hemorrhage 1, 4
• Witnessed rhythmic clonic activity rather than sustained posturing 1

Diagnostic Confirmation

For patients with fluctuating neurological examination, depressed mental state, ruptured MCA aneurysm, high-grade SAH, ICH, hydrocephalus, or cortical infarction, continuous EEG monitoring is reasonable to detect true seizures (Class 2a recommendation). 1

This is critical because:

• 19% of stuporous/comatose SAH patients have nonconvulsive seizures on continuous EEG 1
• These occur an average of 18 days post-SAH, not at presentation 1
• All such patients in one series died, indicating severe underlying pathology 1

Management Implications

If Posturing from ICP Crisis (Most Likely at Presentation):

1. Prioritize ICP management over antiseizure medications 3
2. Secure airway if GCS ≤8 5
3. Maintain systolic BP <160 mmHg to prevent rebleeding 5
4. Consider urgent CSF diversion if hydrocephalus present 1
5. Emergent aneurysm securing (highest rebleeding risk in first 24 hours at 3-4%) 5

If True Seizure Suspected with High-Risk Features:

In patients with aSAH and high-seizure-risk features (ruptured MCA aneurysm, high-grade SAH, ICH, hydrocephalus, cortical infarction), use of prophylactic antiseizure medication may be reasonable to prevent seizures (Class 2b recommendation). 1

However, avoid phenytoin specifically—it is associated with excess morbidity and mortality (Class 3: Harm recommendation). 1 Phenytoin burden is independently associated with worse cognitive function at 3 months. 1

If Witnessed Seizure at Presentation:

In patients who present with seizures, treatment with antiseizure medications for ≤7 days is reasonable to reduce seizure-related complications in the perioperative period. 1

Beyond 7 days, continued antiseizure medications are not effective for reducing future SAH-associated seizure risk in patients without prior epilepsy. 1

Critical Pitfalls to Avoid

1. Do not reflexively treat all "seizure-like" episodes at SAH presentation with long-term antiseizure medications—this exposes patients to medication toxicity (23.4% adverse drug effect rate) without proven benefit if the episode was actually posturing 6

2. Do not use routine prophylactic antiseizure medications in patients without high-risk features—this is not beneficial (Class 3: No Benefit recommendation) 1

3. Do not assume a witnessed tonic episode at ictus predicts late epilepsy—onset seizures/posturing are not predictive of late epilepsy; instead, cortical infarction and thick hemorrhage are the true risk factors 6

4. Do not delay aneurysm securing to obtain EEG confirmation—rebleeding risk (3-4% in first 24 hours) far exceeds seizure risk and is the immediate mortality threat 5

Bottom Line for Clinical Practice

The witnessed "seizure" at SAH presentation is more likely acute posturing from ICP crisis than true epileptic activity. Manage the ICP crisis and secure the aneurysm emergently rather than focusing on antiseizure prophylaxis. Reserve continuous EEG monitoring and targeted antiseizure treatment for high-risk patients (MCA aneurysm, thick clot, ICH, hydrocephalus, cortical infarction) who develop concerning episodes after the acute phase. 1, 4