Abstract
The effects of status epilepticus on the orexin/hypocretin system have yet to be investigated. The present study aimed to assay orexin-A/hypocretin-1 in the cerebrospinal fluid (CSF) of patients after generalized convulsive status epilepticus (GCSE). The study groups included 20 GCSE patients, 24 patients diagnosed with epilepsy but remaining in remission (ER), and 25 normal controls (CTR). Diagnostic lumbar puncture was performed in GCSE patients within 3–10 days of seizure cessation, as well as in the ER and to CTR subjects. Among all GCSE patients, the outcome was graded according to the modified Rankin Scale (mRS) at 1-month follow-up. Orexin-A levels were measured in unextracted CSF samples, using a commercial radioimmunoassay. There was a significant overall difference in median CSF orexin-A concentrations between GCSE, RE, and CTR patients (p < 0.001). The lowest concentrations were noted in the GCSE group compared to ER (p < 0.001) or CTR (p < 0.001). CSF orexin-A levels in GCSE patients inversely correlated with clinical outcome as assessed on the mRS at 1-month follow-up (r = −0.55; p = 0.1). In conclusion, CSF orexin-A levels may serve as a biomarker of increased turn-over of the peptide or post-SE neuronal damage, and implicates the orexin system in the pathogenesis of SE.
Highlights
Generalized convulsive status epilepticus is a medical emergency with a complex pathophysiology
The current study focused on orexin-A concentrations in patients with generalized convulsive status epilepticus in relation to clinical outcomes, in order to shed more light on the complex pathophysiology of status epilepticus (SE) and the orexin system involvement
These results suggest that cerebrospinal fluid (CSF) orexin-A might be a useful prognostic biomarker for SE patients
Summary
Generalized convulsive status epilepticus is a medical emergency with a complex pathophysiology. The fundamental principle involves the failure of endogenous mechanisms to terminate a seizure This failure can occur because of excessive abnormal excitation or from a loss of endogenous inhibitory mechanisms. These maladaptive changes allow a single seizure to transform into status epilepticus and contribute to the self-perpetuating nature and pharmaco-resistance of the disorder [1]. We reported lowered concentrations of orexin-A cerebrospinal fluid in patients suffering from repetitive generalized seizures [9]. This finding might suggest that orexin-A could serve as a biomarker in patients suffering from uncontrolled prolonged seizures
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