Early focal electroencephalogram and neuroimaging findings predict epilepsy development after aneurysmal subarachnoid hemorrhage.

INTRODUCTION: Seizures are a common complication of subarachnoid hemorrhage (SAH) in both acute and late stages: 10-20 % acute symptomatic seizures, 12-25 % epilepsy rate at five years. Our aim was to identify early electroencephalogram (EEG) and computed tomography (CT) findings that could predict long-term epilepsy after SAH. MATERIAL AND METHODS: This is a multicenter, retrospective, longitudinal study of adult patients with aneurysmal SAH admitted to two tertiary care hospitals between January 2011 to December 2022. Routine 30-minute EEG recording was performed in all subjects during admission period. Exclusion criteria were the presence of prior structural brain lesions and/or known epilepsy. We documented the presence of SAH-related cortical involvement in brain CT and focal electrographic abnormalities (epileptiform and non-epileptiform). Post-SAH epilepsy was defined as the occurrence of remote unprovoked seizures ≥ 7 days from the bleeding. RESULTS: We included 278 patients with a median follow-up of 2.4 years. The mean age was 57 (+/-12) years, 188 (68 %) were female and 49 (17.6 %) developed epilepsy with a median latency of 174 days (IQR 49-479). Cortical brain lesions were present in 189 (68 %) and focal EEG abnormalities were detected in 158 patients (39 epileptiform discharges, 119 non-epileptiform abnormalities). The median delay to the first EEG recording was 6 days (IQR 2-12). Multiple Cox regression analysis showed higher risk of long-term epilepsy in those patients with CT cortical involvement (HR 2.6 [1.3-5.2], p 0.009), EEG focal non-epileptiform abnormalities (HR 3.7 [1.6-8.2], p 0.002) and epileptiform discharges (HR 6.7 [2.8-15.8], p < 0.001). Concomitant use of anesthetics and/or antiseizure medication during EEG recording had no influence over its predictive capacity. ROC-curve analysis of the model showed good predictive capability at 5 years (AUC 0.80, 95 %CI 0.74-0.87). CONCLUSIONS: Focal electrographic abnormalities (both epileptiform and non-epileptiform abnormalities) and cortical involvement in neuroimaging predict the development of long-term epilepsy. In-patient EEG and CT findings could allow an early risk stratification and facilitate a personalized follow-up and management of SAH patients.

How soon should urgent EEG be performed following a first epileptic seizure?

PURPOSE: Patients with a first unprovoked epileptic seizure are often seen in emergency services. Electroencephalography (EEG) is indicated for diagnosing epilepsy, but the optimal time to perform this test has not been defined. This study aimed to determine the time interval following a seizure within which EEG has the greatest diagnostic yield. METHODS: We conducted a retrospective study of all adult patients with a first unprovoked seizure who had undergone emergency EEG (July 2014-December 2019). Data collection included demographics, seizure type, time interval to EEG study, EEG pattern identified, and the prescription after emergency assessment. An optimal cut-off point for time to EEG was obtained, and an adjusted regression model was performed to establish associations with the presence of epileptiform abnormalities. RESULTS: A total of 170 patients were included (mean age: 50.7 years, 40.6% women). Epileptiform discharges were identified in 34.1% of recordings, nonepileptiform abnormalities in 46.5%, and normal findings in 19.4%. A lower latency from seizure to EEG was associated with a higher probability of finding epileptiform discharges (median: 12.7 in the epileptiform EEGs vs. 20 h in the nonepileptiform EEGs, p < 0.001). The time interval associated with the highest probability of detecting an epileptiform EEG pattern was within the first 16 h after seizure onset: 52.1% of recordings performed before the 16-h cut-off showed these abnormal patterns compared with 20.2% performed after (p < 0.001). These findings were not related to the presence of an epileptogenic lesion in neuroimaging or to other clinical variables. The finding of epileptiform abnormalities was followed by a greater prescription of antiseizure drugs (96.4% vs. 66% in nonepileptiform patterns, p < 0.001). CONCLUSION: The diagnostic yield of EEG following a first unprovoked epileptic seizure is highest when this test is performed within the first 16 h after onset of the event.

Myoclonic epilepsy in Down syndrome and Alzheimer disease. / Epilepsia mioclónica en el síndrome de Down y en la enfermedad de Alzheimer.

INTRODUCTION: Patients with Down syndrome (DS) who exhibit Alzheimer disease (AD) are associated with age. Both diseases with a common neuropathological basis have been associated with late-onset myoclonic epilepsy (LOMEDS). This entity presents electroencephalogram features as generalized polyspike-wave discharges. METHOD: We present a series of 11 patients with the diagnosis of DS or AD who developed myoclonic seizures or generalized tonic-clonic seizures. In all cases, clinical and neuroimaging studies and polygraph EEG monitoring was performed. RESULTS: In all cases, cognitive impairment progressed quickly after the onset of epilepsy causing an increase in the degree of dependence. The most common finding in the EEG was a slowing of brain activity with theta and delta rhythms, plus intercritical generalized polyspike-waves were objectified in eight patients. In neuroimaging studies was found cerebral cortical atrophy. The most effective drug in this series was the levetiracetam. CONCLUSIONS: The association of generalized epilepsy with elderly DS represents an epiphenomenon in evolution which is associated with a progressive deterioration of cognitive and motor functions. This epilepsy has some electroclinical characteristics and behaves as progressive myoclonic epilepsy, which is probably related to the structural changes that characterize the evolutionary similarity of DS with AD. Recognition of this syndrome is important, since it has prognostic implications and requires proper treatment.

A new clinical score for the prognosis of status epilepticus in adults.

BACKGROUND AND PURPOSE: The severity of status epilepticus (SE) has an important impact in clinical outcomes. The Status Epilepticus Severity Score (STESS) is a score for predicting mortality in SE at admission. The baseline modified Rankin Scale (mRS) might be a prognostic factor for assessing the short-tem outcomes of SE. Therefore, our aim was to evaluate the effectiveness of mRS and whether its addition to the STESS improves the prediction of mortality. METHODS: Consecutive patients with SE and aged >16 years were recruited during 3 years. Receiver operating characteristic curves and a logistic regression model were developed to estimate the scores of the new score, designated as modified STESS (mSTESS), and it was subsequently compared with the STESS. RESULTS: In all, 136 patients were included. Mean age was 62.01 ± 17.62 (19-95) years, and 54% were male. The capacity of the STESS to predict mortality was 74.3% (95% confidence interval 63.8%-81.8%), whilst the capacity of the mRS to predict mortality was 65.2% (95% confidence interval 54.2%-76.2%). The logistic regression model and receiver operating characteristic curves enabled the classification of mRS as follows: 0, mRS = 0; 1, mRS = 1-3; and 2, mRS > 3. These values, when added to the other items of the STESS, resulted in the mSTESS with scores between 0 and 8 points. The capacity of the mSTESS to predict mortality was 80.1%. An mSTESS > 4 established an overall accuracy of 81.8% for predicting mortality, which was considerably higher than the overall accuracy of STESS ≥ 3 (59.6%). CONCLUSIONS: The baseline mRS was associated with high mortality risk. It is proposed to use mSTESS to improve the prediction of mortality risk in SE.

Prognosis of status epilepticus (SE): Relationship between SE duration and subsequent development of epilepsy.

UNLABELLED: In animal models, SE duration is related to epileptogenesis. Data in humans are scarce, mainly in NCSE; therefore, we aimed to study the prognosis of SE de novo and which factors may influence subsequent development of epilepsy. METHODS: We evaluated patients with SE without previous epilepsy at our hospital (February 2011-February 2014), including demographics, etiology, number of AEDs, duration of SE, mortality, and occurrence of seizures during follow-up. RESULTS: Eighty-nine patients were evaluated. Median age was 69 (19-95) years old. Among them, 33.7% were convulsive. Regarding etiology, 59 were considered acute symptomatic (41 lesions, 18 toxic-metabolic), 17 remote or progressive symptomatic, and 13 cryptogenic. The median recovery time was 24h (30 min-360 h). In-hospital mortality was 29% (n = 26). After a median follow-up of 10 months, 58.7% of survivors (n = 37) showed seizures. Subsequently, we analyzed which factors might be related to the development of epilepsy, and we found that epilepsy development was more frequent with longer SE duration (37 vs. 23 h, p = 0.004); furthermore, patients with a toxic-metabolic etiology developed epilepsy less frequently (33% vs. 67%; p = 0.022). Epilepsy was also correlated (tendency) with focal SE (p = 0.073), a lesion in neuroimaging (p = 0.091), and the use of 2 or more AEDs (p = 0.098). Regarding SE duration, a cutoff of above 24h was clearly related to chronic seizures (p = 0.014); however, combining etiology and duration, the association of longer SE and epilepsy was significant in acute lesional SE (p = 0.034), but not in epilepsy with cryptogenic or remote/progressive etiology. After a logistic regression, only a duration longer than 24h (OR = 3.800 (1.277-11.312), p = 0.016) was found to be an independent predictor of the development of epilepsy. CONCLUSION: In patients with SE, the longer duration is associated with an increased risk of subsequent epilepsy at follow-up, mainly in symptomatic SE due to an acute lesion. It is unclear if it might be the result of a more severe injury causing both prolonged seizures and subsequent epilepsy, and therefore whether more aggressive treatment in this group might avoid this possibility. Most of the patients with cryptogenic or remote/progressive SE developed epilepsy regardless of SE duration. This article is part of a Special Issue entitled "Status Epilepticus".

[Cortical spreading depolarization phenomena in patients with traumatic and ischemic brain injuries. Results of a pilot study]. / Fenómenos de despolarización cortical propagada en los pacientes con lesiones cerebrales traumáticas e isquémicas. Resultados de un estudio piloto.

OBJECTIVES: To determine the frequency and duration of cortical spreading depolarization (CSD) and CSD-like episodes in patients with traumatic brain injury (TBI) and malignant middle cerebral artery infarction (MMCAI) requiring craniotomy. DESIGN: A descriptive observational study was carried out during 19 months. SETTING: Neurocritical patients. PATIENTS: Sixteen patients were included: 9 with MMCAI and 7 with moderate or severe TBI, requiring surgical treatment. INTERVENTIONS: A 6-electrode subdural electrocorticographic (ECoG) strip was placed onto the perilesional cortex. MAIN VARIABLES OF INTEREST: An analysis was made of the time profile and the number and duration of CSD and CSD-like episodes recorded from the ECoGs. RESULTS: Of the 16 patients enrolled, 9 presented episodes of CSD or CSD-like phenomena, of highly variable frequency and duration. CONCLUSIONS: Episodes of CSD and CSD-like phenomena are frequently detected in the ischemic penumbra and/or traumatic cortical regions of patients with MMCAI who require decompressive craniectomy or of patients with contusional TBI.

Implications of starting antiepileptic treatment prior to electroencephalography in first epileptic seizures.

INTRODUCTION: This study aimed to determine whether the administration of antiepileptic drugs (AED) alters the likelihood of detecting epileptiform abnormalities in electroencephalographies (EEG) performed early after a first epileptic seizure. METHODS: We performed a retrospective, observational study including patients with a first seizure attended at our centre's emergency department between July 2014 and November 2019. We collected clinical data, as well as technical data on the acquisition and interpretation of the EEG performed within the first 72 hours after the seizure, and the factors related with seizure recurrence. RESULTS: We recruited 155 patients with a mean (SD) age of 48.6 (22.5) years; 61.3% were men. Regarding seizure type, 51% presented tonic-clonic seizures of unknown onset and 12% presented focal to bilateral tonic-clonic seizures. Thirty-nine patients (25.2%) received AED treatment before the EEG was performed: 33 received a non-benzodiazepine AED and 6 received a benzodiazepine. Epileptiform abnormalities were observed in 29.7% of patients. Previous administration of AEDs was not significantly associated with the probability of detecting interictal epileptiform abnormalities (P = .25) or with the risk of recurrence within 6 months (P = .63). CONCLUSIONS: Administration of AEDs before an early EEG following a first seizure does not decrease the likelihood of detecting epileptiform abnormalities. These findings suggest that starting AED treatment immediately in patients with a high risk of early recurrence does not imply a reduction in the diagnostic accuracy of the test.

Epileptic seizures in the emergency room: clinical and electroencephalographic findings associated with brain perfusion patterns on computed tomography.

BACKGROUND: Diagnosis of epileptic seizures, particularly regarding status epilepticus (SE), may be challenging in an emergency room setting. The aim of the study was to study the diagnostic yield of perfusion computed tomography (pCT) in patients with single epileptic seizures and SE. METHODS: We retrospectively reviewed the records of patients who followed an acute ischemic stroke pathway during a 9-month period and who were finally diagnosed with a single epileptic seizure or SE. Perfusion maps were visually analyzed for the presence of hyperperfusion and hypoperfusion. Clinical data, EEG patterns, and neuroimaging findings were compared. RESULTS: We included 47 patients: 20 (42.5%) with SE and 27 (57.5%) with single epileptic seizure. Of 18 patients who showed hyperperfusion on pCT, 12 were ultimately diagnosed with SE and eight had EEG findings compatible with an SE pattern. Focal hyperperfusion on pCT had a sensitivity of 60% (95% CI 36.4-80.2) and a specificity of 77.8% (95% CI 57.2-90.6) for predicting a final diagnosis of SE. The presence of cerebral cortical and thalamic hyperperfusion had a high specificity for predicting SE presence. Of note, 96% of patients without hyperperfusion on pCT did not show an SE pattern on early EEG. CONCLUSIONS: In acute settings, detection by visual analysis of focal cerebral cortical hyperperfusion on pCT in patients with epileptic seizures, especially if accompanied by the highly specific feature of thalamic hyperperfusion, is suggestive of a diagnosis of SE and requires clinical and EEG confirmation. The absence of focal hyperperfusion makes a diagnosis of SE unlikely.

Implications of initiating antiseizure drugs prior to the performance of EEG in first epileptic seizures. / Implicaciones de iniciar fármacos antiepilépticos previo a la realización de EEG en primeras crisis epilépticas.

INTRODUCTION: This study aimed to determine whether the administration of antiepileptic drugs (AED) alters the likelihood of detecting epileptiform abnormalities in electroencephalographies (EEG) performed early after a first epileptic seizure. METHOD: We performed a retrospective, observational study including patients with a first seizure attended at our centre's emergency department between July 2014 and November 2019. We collected clinical data, as well as technical data on the acquisition and interpretation of the EEG performed within the first 72hours after the seizure, and the factors related with seizure recurrence. RESULTS: We recruited 155 patients with a mean (SD) age of 48.6 (22.5) years; 61.3% were men. Regarding seizure type, 51% presented tonic-clonic seizures of unknown onset and 12% presented focal to bilateral tonic-clonic seizures. Thirty-nine patients (25.2%) received AED treatment before the EEG was performed: 33 received a non-benzodiazepine AED and 6 received a benzodiazepine. Epileptiform abnormalities were observed in 29.7% of patients. Previous administration of AEDs was not significantly associated with the probability of detecting interictal epileptiform abnormalities (P=.25) or with the risk of recurrence within 6 months (P=.63). CONCLUSIONS: Administration of AEDs before an early EEG following a first seizure does not decrease the likelihood of detecting epileptiform abnormalities. These findings suggest that starting AED treatment immediately in patients with a high risk of early recurrence does not imply a reduction in the diagnostic accuracy of the test.

Epilepsy in patients with malignant middle cerebral artery infarcts and decompressive craniectomies.

UNLABELLED: Patients with malignant middle cerebral artery (MCA) infarctions who have undergone craniectomy are susceptible to the development of vascular epilepsy. Our objective was to study the factors that might influence the occurrence of seizures in this group of patients. MATERIALS AND METHODS: All patients who developed malignant MCA infarction and had undergone decompressive craniectomy in our center between November 2002 and January 2014 were evaluated. In the subsequent follow-up, we evaluated the clinical outcomes and attempted to identify the factors that were related to the occurrence of seizures. RESULTS: We evaluated a total of 80 patients. The median time at which the craniectomy was performed was 40.5h after the stroke. Seizures occurred in 47.5% of all patients. The mortality rate within the first week was 16%, and of those who survived 53.7% developed seizures; 9% of these seizures were acute symptomatic, and 44.8% were remote. The median onset of remote seizures was seven months, and the majority of these were motor seizures with generalization. Notably, the patients with seizures exhibited longer delays from stroke to craniectomy, greater involvements of the temporal lobe and a higher rate of post-craniectomy recanalization of the occluded artery. Regarding the timing of the surgeries, a significantly greater proportion of those who underwent surgery more than 42h after the stroke developed epilepsy (p=0.004). Logistic regression revealed that only prolonged delay (>42h) independently predicted the development of epilepsy (OR 5.166; IC 95% 1.451-18.389; p=0.011). CONCLUSIONS: More than half of patients with malignant MCA infarcts who underwent decompressive craniectomy developed epilepsy. The occurrence of seizures in these patients was related to the delay to the performance of the craniectomy.

[Usefulness of the EEG recording in the diagnosis of cyclosporin A-induced encephalopathy]. / Utilidad del registro EEG en al diagnóstico de encefalopatía asociada a ciclosporina A.

INTRODUCTION: Cyclosporine A is one of the immunosuppressors most frequently used to prevent transplant rejection. Neurotoxicity is one of the complications often associated with it. These complications include acute encephalopathy, lethargy, confusion state, tremor, headache, motor disorders, visual changes and epileptic crises amongst others, even when blood levels are at what are considered to be 'therapeutic' levels. CLINICAL CASES: We present the EEG anomalies found in 3 transplant patients (two liver transplants and on double lung transplant) to whom cyclosporin A had been given and who presented with status epilepticus. The EEG recordings showed paroxystic discharges of focal onset in the temporo-occipital areas. They were mainly correlated with the clinical findings of oculomotor and eyelid disorders. CONCLUSION: The topography of the neurophysiological findings supports--as do the other clinico-radiological findings--localization preferably to the posterior areas of cerebral dysfunction associated with cyclosporin A. Although the physiopathological origin of the encephalopathy of patients treated with cyclosporin A seems to correspond to multiple factors, we wish to point out the diagnostic usefulness of the identification of EEG changes localized to the temporo-occipital areas in the recognition of the neurotoxic syndrome in these patients.

Diagnosis of epileptic syndrome after a new onset seizure and its correlation at long-term follow-up: longitudinal study of 131 patients from the emergency room.

This study aims to demonstrate the reliability of the diagnosis of epilepsy after a new onset seizure, supported by a detailed anamnesis and the complementary tests accessible at the emergency room (ER), such as CT-scan and video-EEG. It was a prospective study including 131 adult patients (55% males, medium age 52.42 (±21.5)[16-98] years-old, follow-up 25.22 (±13.69)[12-31] months). In half of cases we could not identify any predisposing factor. Within the first 72 h, patients were included into an epileptic syndrome according to the ILAE 1989 classification, if possible. Thereafter, they were followed-up in the outpatient clinic of the Epilepsy Unit, where seizure recurrence was recorded and further diagnostic examinations were performed. 94.1% of patients initially diagnosed of epilepsy were confirmed as epileptics, and up to 57% of patients could be classified into a particular syndrome from the ER. Conversely, 44.6% of patients with the initial diagnosis of isolated seizure and one third of patients with non-epileptic seizures developed recurrence, switching their initial diagnosis to epilepsy. Both CT-scan and early EEG demonstrated its usefulness evaluating the risk of recurrence after a new onset seizure (Positive predictive value 78% and 88%, respectively). Epileptiform activity was a predictor of seizure recurrence (p<0.05), independently to the moment where the EEG was performed. According to our results, it is realistic to perform the diagnosis of epilepsy after a new onset seizure, although many patients still need further specific examinations, or seizure recurrence, to be diagnosed.