HICU 7 - Subarachnoid Hemorrhage (SAH) and EEG

Subarachnoid Hemorrhage (SAH) Overview

• Aneurysmal subarachnoid hemorrhage and seizures/cerebral ischemia are covered
• The role of continuous EEG in detection of seizures, ischemia, and prognostication is detailed

Key Facts

• SAH only accounts for 3% of all strokes
• SAH results in 27% of stroke-related years of potential life lost before age 65
• Continuous EEG (cEEG) is necessary for detecting nonconvulsive seizures (NCS)
• NCS are common in SAH patients and often associated with nonconvulsive status epilepticus (NCSE)
• cEEG is a valuable tool for detecting cerebral vasospasm and delayed cerebral ischemia (DCI)
• Periodic discharges, NCSE, nonreactive background, and the absence of normal sleep architecture lead to poor SAH outcomes

Epidemiology

• The incidence of aneurysmal SAH (aSAH) ranges from 2 to 21 per 100,000 persons
• Aneurysmal SAH accounts for 3% of all strokes, but 27% of stroke-related years of potential life lost before age 65
• The chance of a patient surviving aneurysmal SAH has increased by 17% to around 65%
• Risk factors for aneurysmal SAH include hypertension, smoking, family history, and cocaine use

Intracranial Aneurysms

• Rupture of intracranial aneurysms accounts for ~80% of nontraumatic SAH
• Intracranial aneurysms are acquired lesions that develop predominantly at branching points of the anterior cerebral circulation (circle of Willis)
• Ruptured and unruptured aneurysms may be treated by endovascular coiling or craniotomy with surgical clipping

Clinical Features

• The classic presentation of aneurysmal SAH is the acute onset of severe headache that may be accompanied by seizure, loss of consciousness, or vomiting
• Focal neurological deficits, especially cranial nerve palsies, may be associated with certain aneurysm locations, elevated intracranial pressure (ICP), focal parenchymal hemorrhage, or ischemic infarction

Diagnosis

• Noncontrast head CT is rapid, widely available, and has a reported sensitivity of 90-100% for detection of SAH
• MRI or lumbar puncture may be useful in patients with a high clinical suspicion for SAH and equivocal findings on head CT
• After diagnosis of SAH, CT angiography (CTA) and catheter angiography are used to evaluate for intracranial aneurysms

Grading Scales

• The Hunt and Hess and World Federation of Neurological Surgeons grading scales are based upon features of clinical presentation and predict prognosis
• The modified Fisher grading score is a radiographic scoring system based upon the amount and distribution of subarachnoid as well as intraventricular hemorrhage and helps stratify the risk of cerebral vasospasm and delayed cerebral ischemia (DCI)

Cerebral Vasospasm and DCI

• Approximately 60% of aSAH patients have radiographic vasospasm, though only ~30% develop symptoms of cerebral ischemia
• Of the patients who survive to definitive treatment, cerebral vasospasm and DCI are the major contributors to morbidity and mortality
• The risk of cerebral vasospasm increases between Day 3 and Day 7 post-hemorrhage while the peak risk of DCI is between Days 5 and 14
• Risk factors for development of vasospasm and DCI include younger age, poor neurological grade, thick subarachnoid clot, intraventricular hemorrhage, and history of smoking
• Initial detection of vasospasm and DCI relies primarily on the clinical neurological examination and periodic serial TCD measurements of mean cerebral blood flow velocity; CTA/CT perfusion and MRI/MR angiography may aid, but the gold standard is catheter angiography

Vasospasm Treatment

• Standard detection techniques are performed infrequently
• Real-time detection and intervention are not possible using standard vasospasm detection methods
• Prophylactic use of nimodipine 60 mg every 4 hours and maintenance of euvolemia reduce the risk of poor neurological outcome from DCI
• First-line treatments for symptomatic vasospasm are noninvasive, and include volume repletion/expansion and induced hypertension
• Endovascular management of cerebral vasospasm includes balloon angioplasty and intra-arterial vasodilator (verapamil, nicardipine) administration

Seizures in SAH

• Seizures occur in 23% of SAH patients within 48 hours of SAH onset
• In-hospital seizures incidence is 2.3%; delayed seizures is 5.5%, with a latency of 7.45 months from the time of onset
• An estimated 7-8% of patients have clinical seizures at the onset of bleeding
• About 4-12% of patients develop chronic epilepsy
• Risk factors associated with the development of seizures include middle cerebral artery aneurysms, thickness of aneurysmal SAH clot, associated intracerebral hemorrhage, rebleeding, cerebral infarction, craniotomy, and poor Hunt and Hess grade
• The utility of prophylactic antiseizure drugs (ASDs) for patients with SAH isn't well established, phenytoin exposure associates with worse neurological and cognitive outcomes
• For patients without seizures, a 3- to 7-day course of prophylactic antiseizure medication other than phenytoin is a reasonable consideration

Continuous EEG for the Detection of DCI

• Continuous EEG (cEEG) has great potential for detecting and monitoring progression of DCI as it is continuous, noninvasive, and sensitive to changes
• Quantitative EEG (QEEG) parameters derived from continuous EEG are useful for detection of DCI including alpha:delta ratio (ADR), relative alpha variability (RAV), and total power and asymmetry measures
• In a study of 32 patients with low-grade aneurysmal SAH, 19 developed vasospasm, quantitative EEG demonstrated a decrease in RAV in 15 of the 19 patients, preceding TCD abnormalities by at least 2 days in the 10 patients, with positive/negative predictive values for detecting vasospasm were 76%/100%
• A 10% decrement in ADR for 6 consecutive hours can predict DCI with 100% sensitivity and 76% specificity
• ADR decrement less than 50% below baseline for 2+ consecutive hours also predicts DCI with 89% sensitivity and 84% specificity

Additional EEG Findings

• A persistent decline in ADR alongside a decrease in RAV can be useful for suggesting the development of DCI
• Epileptiform discharges as well as periodic and rhythmic patterns may also indicate risk for DCI
• Rhythmic and periodic patterns occur more commonly in patients who develop DCI
• SAH patients that develop epileptiform discharges, generalized periodic discharges, or seizures are also more likely to develop neurological deterioration and DCI

Continuous EEG for the Detection of Seizures Following SAH

• Nonconvulsive seizures (NCS) contribute to encephalopathy and coma in aneurysmal SAH patients
• The majority of aSAH patients with NCS also experience nonconvulsive status epilepticus (NCSE), which is associated with high morbidity and mortality independent of disease severity
• NCSE may be present in 8-31% of patients with persistent coma or unexplained neurological deterioration who undergo continuous EEG.
• The majority of NCS are captured within 48-72 hrs of continuous EEG hookup. 1 study showed 1/4 of seizures first detected 3 days after EEG
• Scalp EEG patterns that lie on the ictal-interictal continuum have been observed to represent intracortical seizures on depth electrodes

Continuous EEG and Prognosis Following SAH

• Clinical risk factors for poor outcome include poor clinical and radiographic grade on presentation, older age, aneurysm rebleeding, large aneurysm size, and cerebral infarction
• Presence of periodic discharges, nonconvulsive status epilepticus, as well as the absence of normal sleep architecture and reactivity are independently associated with poor neurological outcomes
• Seizure burden on continuous EEG associated with functional outcomes and cognitive impairment at 3 months
• Every hour of seizure activity on continuous EEG was associated with increased odds of disability and mortality (OR = 1.10) and reduced scores on the telephone interview for cognitive status (TICS), a global cognitive assessment

Detection of DCI

• Studies are needed to determine quantitative EEG parameters most sensitive to the initial onset of cerebral ischemia
• Differentiating quantitative EEG changes that represent ischemia from other common clinical changes, is important even if not always feasible

Quantitative EEG

• Quantitative EEG for the detection of cerebral ischemia should trigger additional diagnostic studies and more timely treatment
• Integration of QEEG for the detection of cerebral ischemia requires a multidisciplinary approach with appropriate patient selection and standardization of reporting

Proposed Recommendations for Use of Continuous EEG After SAH

• Patients without neurological improvement or with unexplained neurological deterioration should have continuous EEG to exclude NCS and NCSE
• Patients with a witnessed clinical seizure are at high risk for subsequent subclinical seizures and should undergo continuous EEG if neurological examination is normal
• Continuous EEG for the detection of DCI can be useful as a complement to the clinical neurological exam, TCD, and radiographic evaluations
• A minimum of 24-48 hours of monitoring is required to detect NCS while more prolonged monitoring is needed to monitor for DCI

Current Limitations to Widespread Application of Continuous EEG in SAH

• EEG technician availability to maintain monitoring over long periods
• The need for real-time EEG review from physicians with experience in continuous EEG interpretation