Optic Nerve Topography in Multiple Sclerosis Diagnosis: The Utility of Visual Evoked Potentials.

OBJECTIVE: To assess the added value of the optic nerve region (by using visual evoked potentials [VEPs]) to the current diagnostic criteria. METHODS: From the Barcelona clinically isolated syndrome (CIS) cohort, patients with complete information to assess dissemination in space (DIS), the optic nerve region, and dissemination in time at baseline (n = 388) were selected. Modified DIS (modDIS) criteria were constructed by adding the optic nerve to the current DIS regions. The DIS and modDIS criteria were evaluated with univariable Cox proportional hazard regression analyses with the time to the second attack as the outcome. A subset of these patients who had at least 10 years of follow-up or a second attack occurring within 10 years (n = 151) were selected to assess the diagnostic performance. The analyses were also performed according to CIS topography (optic neuritis vs non-optic neuritis). RESULTS: The addition of the optic nerve as a fifth region improved the diagnostic performance by slightly increasing the accuracy (2017 DIS 75.5%, modDIS 78.1%) and the sensitivity (2017 DIS 79.2%, modDIS 82.3%) without lowering the specificity (2017 DIS 52.4%, modDIS 52.4%). When the analysis was conducted according to CIS topography, the modDIS criteria performed similarly in both optic neuritis and non-optic neuritis CIS. CONCLUSION: The addition of the optic nerve, assessed by VEP, as a fifth region in the current DIS criteria slightly improves the diagnostic performance because it increases sensitivity without losing specificity.

Cortical Spreading Depression Phenomena Are Frequent in Ischemic and Traumatic Penumbra: A Prospective Study in Patients With Traumatic Brain Injury and Large Hemispheric Ischemic Stroke.

PURPOSE: Spreading depolarization (SD) phenomena are waves of neuronal depolarization, which propagate slowly at a velocity of 1 to 5 mm/minute and can occur in patients with ischemic or hemorrhagic stroke, traumatic brain injury, and migraine with aura. They form part of secondary injury, occurring after spreading ischemia. The purposes of this study were to describe the frequency and characteristics of SD phenomena and to define whether a correlation existed between SD and outcome in a group of patients with TBI and large hemispheric ischemic stroke. METHODS: This was a prospective observational study of 39 adult patients, 17 with malignant middle cerebral artery infarction and 22 with moderate or severe traumatic brain injury, who underwent decompressive craniectomy and multimodal neuromonitoring including electrocorticography. Identification, classification, and interpretation of SDs were performed using the published recommendations from the Cooperative Study on Brain Injury Depolarization group. The outcomes assessed were functional disability at 6 and 12 months after injury, according to the extended Glasgow outcome scale, Barthel index, and modified Rankin scale. RESULTS: Four hundred eighty-three SDs were detected, in 58.9% of the patients. Spreading depolarizations were more common, particularly the isoelectric SD type, in patients with malignant middle cerebral artery infarction (P < 0.04). In 65.21% of patients with SDs on electrocorticography, the "peak" day of depolarization was day 0 (the first 24 hours of recording). Spreading depolarization convulsions were present in 26.08% of patients with SDs. Patients with more SDs and higher depolarization indices scored worse on extended Glasgow outcome scale (6 months) and Barthel index (6 and 12 months) (P < 0.05). CONCLUSIONS: Evidence on SD phenomena is important to ensure continued progress in understanding their pathophysiology, in the search for therapeutic targets to avoid additional damage from these secondary injuries.

Is Spreading Depolarization a Risk Factor for Late Epilepsy? A Prospective Study in Patients with Traumatic Brain Injury and Malignant Ischemic Stroke Undergoing Decompressive Craniectomy.

OBJECTIVE: Spreading depolarizations (SDs) have been described in patients with ischemic and haemorrhagic stroke, traumatic brain injury, and migraine with aura, among other conditions. The exact pathophysiological mechanism of SDs is not yet fully established. Our aim in this study was to evaluate the relationship between the electrocorticography (ECoG) findings of SDs and/or epileptiform activity and subsequent epilepsy and electroclinical outcome. METHODS: This was a prospective observational study of 39 adults, 17 with malignant middle cerebral artery infarction (MMCAI) and 22 with traumatic brain injury, who underwent decompressive craniectomy and multimodal neuromonitoring including ECoG in penumbral tissue. Serial electroencephalography (EEG) recordings were obtained for all surviving patients. Functional disability at 6 and 12 months after injury were assessed using the Barthel, modified Rankin (mRS), and Extended Glasgow Outcome (GOS-E) scales. RESULTS: SDs were recorded in 58.9% of patients, being more common-particularly those of isoelectric type-in patients with MMCAI (p < 0.04). At follow-up, 74.7% of patients had epileptiform abnormalities on EEG and/or seizures. A significant correlation was observed between the degree of preserved brain activity on EEG and disability severity (R [mRS]: + 0.7, R [GOS-E, Barthel]: - 0.6, p < 0.001), and between the presence of multifocal epileptiform abnormalities on EEG and more severe disability on the GOS-E at 6 months (R: - 0.3, p = 0.03) and 12 months (R: - 0.3, p = 0.05). Patients with more SDs and higher depression ratios scored worse on the GOS-E (R: - 0.4 at 6 and 12 months) and Barthel (R: - 0.4 at 6 and 12 months) disability scales (p < 0.05). The number of SDs (p = 0.064) and the depression ratio (p = 0.1) on ECoG did not show a statistically significant correlation with late epilepsy. CONCLUSIONS: SDs are common in the cortex of ischemic or traumatic penumbra. Our study suggests an association between the presence of SDs in the acute phase and worse long-term outcome, although no association with subsequent epilepsy was found. More comprehensive studies, involving ECoG and EEG could help determine their association with epileptogenesis.

Does continuous electroencephalography influence therapeutic decisions in neurocritical care?

OBJECTIVES: In the neurocritical care unit (neuro-ICU), the impact of continuous EEG (cEEG) on therapeutic decisions and prognostication, including outcome prediction using the Status Epilepticus Severity Score (STESS), is poorly investigated. We studied to what extent cEEG contributes to treatment decisions, and how this relates to clinical outcome and the use of STESS in neurocritical care. METHODS: We included patients admitted to the neuro-ICU or neurological step-down unit of a tertiary referral hospital between 05/2013 and 06/2015. Inclusion criteria were ≥20 h of cEEG monitoring and age ≥15 years. Exclusion criteria were primary epileptic and post-cardiac arrest encephalopathies. RESULTS: Ninety-eight patients met inclusion criteria, 80 of which had status epilepticus, including 14 with super-refractory status. Median length of cEEG monitoring was 50 h (range 21-374 h). Mean STESS was lower in patients with favorable outcome 1 year after discharge (modified Rankin Scale [mRS] 0-2) compared to patients with unfavorable outcome (mRS 3-6), albeit not statistically significant (mean STESS 2.3 ± 2.1 vs 3.6 ± 1.7, p = 0.09). STESS had a sensitivity of 80%, a specificity of 42%, and a negative predictive value of 93% for outcome. cEEG results changed treatment decisions in 76 patients, including escalation of antiepileptic treatment in 65 and reduction in 11 patients. CONCLUSION: Status Epilepticus Severity Score had a high negative predictive value but low sensitivity, suggesting that STESS should be used cautiously. Of note, cEEG results altered clinical decision-making in three of four patients, irrespective of the presence or absence of status epilepticus, confirming the clinical value of cEEG in neurocritical care.

Tumor-associated status epilepticus: A prospective cohort in a tertiary hospital.

INTRODUCTION: Tumor-associated status epilepticus (TASE) follows a relatively benign course compared with SE in the general population. Little, however, is known about associated prognostic factors. METHODS: We conducted a prospective, observational study of all cases of TASE treated at a tertiary hospital in Barcelona, Spain between May 2011 and May 2019. We collected data on tumor and SE characteristics and baseline functional status and analyzed associations with outcomes at discharge and 1-year follow-up. RESULTS: Eighty-two patients were studied; 58.5% (n = 48) had an aggressive tumor (glioblastoma or brain metastasis). Fifty-one patients (62.2%) had a favorable outcome at discharge compared with just 30 patients (25.8%) at 1-year follow-up. Fourteen patients (17.1%) died during hospitalization. Lateralized period discharges (LPDs) on the baseline electroencephalography (EEG), presence of metastasis, and SE severity were significantly associated with a worse outcome at discharge. The independent predictors of poor prognosis at 1-year follow-up were SE duration of at least 21 h, an aggressive brain tumor, and a nonsurgical treatment before SE onset. Lateralized period discharges, super-refractory SE, and an aggressive tumor type were independently associated with increased mortality. CONCLUSIONS: Status epilepticus duration is the main modifiable factor associated with poor prognosis at 1-year follow-up. Accordingly, patients with TASE, like those with SE of any etiology, should receive early, aggressive treatment.