Seizures, CSF neurofilament light and tau in patients with subarachnoid haemorrhage

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Subarachnoid haemorrhage (SAH) is a severe condition with high morbidity and mortality with an incidence of 9 per 100 000.1 The most devastating complication of SAH is delayed cerebral ischaemia (DCI). DCI is defined as new focal or global neurological deficits and new cerebral infarction on computed tomography (CT) that is not caused by rebleeding or acute hydrocephalus.2 Signs of DCI occur in about 30% of patients, typically appear between days 4 and 10 following SAH and are the major causes of morbidity and death.3 The pathophysiology of DCI is not fully understood, but intracranial arterial vasospasm probably plays a role. A major challenge in the management of SAH is early identification of DCI, thereby enabling therapeutic intervention.
Acute symptomatic seizures (ASS) have been reported to occur in 6%‐24% of SAH cases.5 Continuous EEG (cEEG) allows monitoring of patients with acute aneurysmal subarachnoid haemorrhage for detection of non‐convulsive seizures and non‐convulsive status epilepticus. Both clinical and electrographic seizures (ES) are believed to have a negative impact on the outcome.7 Continuous EEG has also been used for surveillance and early recognition of DCI.8
Significant efforts have been made to study different biomarkers as potential tools for predicting vasospasm and outcome after SAH.9 Cerebrospinal fluid (CSF) biomarkers that reflect neuronal damage have recently been studied. Neurofilament light chain protein is a cytoskeletal constituent of intermediate filaments and is thought to reflect neuronal and axonal injury when appearing in the cerebrospinal fluid (CSF). High concentrations of NFL and tau have been reported in the first days after the primary injury and extend into the period of DCI to correlate with poor long‐term outcome.11 NFL is a marker that reflects subcortical damage, while tau is more related to cortical brain injury.13
In this study, we wished to determine whether the occurrence of ASS is a clinical marker of impeding DCI and to study the association between CSF concentrations of NFL and tau and DCI in patients with acute SAH.
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