Amygdala enlargement (AE) has been reported in drug resistant lesional and non-lesional temporal lobe epilepsy (TLE). Its contribution to development of intractability of epilepsy is at best uncertain. Our aim was to study the natural course of AE in a heterogenous group of TLE patients with follow-up imaging and clinical outcomes. Methods: A prospective observational study in patients with TLE with imaging features of AE recruited from epilepsy clinics between 1994 and 2018. Demographic data, details of epilepsy syndrome, outcomes and follow up neuroimaging were extracted. Results: Forty-two patients were recruited including 19 males (45 %). Mean age at onset of epilepsy was 30.6 years and mean duration of epilepsy was 19.9 years. On MRI, 33 patients had isolated unilateral AE and eleven had AE with hippocampal enlargement (HE). Twenty (48 %) underwent temporal resections with most common histopathology being amygdalar gliosis (40 %). Engel Class IA outcome at last follow up (mean, 10 years) was 60 %.Thirty-four patients had neuroimaging follow up of at least 1 year (mean, 5 years). AE resolved in 6, persisted in 25, evolved into bilateral HS in 1, bilateral mesial temporal atrophy in 1 and ipsilateral mesial temporal atrophy in 1. Resolution of AE was associated with better seizure free outcomes (p = 0.013). Conclusions: TLE with AE is associated with favourable prognosis yet not benign. Over 50 % were drug resistant and surgical outcomes were similar to mTLE. Resolution of AE on follow up neuroimaging was associated with better seizure free outcomes.
ObjectiveTo use clinically informed machine learning to derive prediction models for early and late premature death in epilepsy.MethodsThis was a population‐based primary care observational cohort study. All patients meeting a case definition for incident epilepsy in the Health Improvement Network database for inclusive years 2000‐2012 were included. A modified Delphi process identified 30 potential risk factors. Outcome was early (within 4 years of epilepsy diagnosis) and late (4 years or more from diagnosis) mortality. We used regularized logistic regression, support vector machines, Gaussian naive Bayes, and random forest classifiers to predict outcomes. We assessed model calibration, discrimination, and generalizability using the Brier score, mean area under the receiver operating characteristic curve (AUC) derived from stratified fivefold cross‐validation, plotted calibration curves, and extracted measures of association where possible.ResultsWe identified 10 499 presumed incident cases from 11 194 182 patients. All models performed comparably well following stratified fivefold cross‐validation, with AUCs ranging from 0.73 to 0.81 and from 0.71 to 0.79 for early and late death, respectively. In addition to comorbid disease, social habits (alcoholism odds ratio [OR] for early death = 1.54, 95% confidence interval [CI] = 1.12‐2.11 and OR for late death = 2.62, 95% CI = 1.66‐4.16) and treatment patterns (OR for early death when no antiseizure medication [ASM] was prescribed at baseline = 1.33, 95% CI = 1.07‐1.64 and OR for late death after receipt of enzyme‐inducing ASM at baseline = 1.32, 95% CI = 1.04‐1.66) were significantly associated with increased risk of premature death. Baseline ASM polytherapy (OR = 0.55, 95% CI = 0.36‐0.85) was associated with reduced risk of early death.SignificanceClinically informed models using routine electronic medical records can be used to predict early and late mortality in epilepsy, with moderate to high accuracy and evidence of generalizability. Medical, social, and treatment‐related risk factors, such as delayed ASM prescription and baseline prescription of enzyme‐inducing ASMs, were important predictors.
Objective:Since the strongest risk factor for sudden unexpected death in epilepsy (SUDEP) is frequent bilateral tonic-clonic seizures (BTCSs), our aim was to determine whether postictal hypoperfusion in brainstem respiratory centres (BRCs) is more common following tonic-clonic seizures.Methods:We studied 21 patients with focal epilepsies who underwent perfusion imaging with arterial spin labeling (ASL) MRI. Subtraction maps of cerebral blood flow were obtained from the postictal and baseline scans. We identified six regions of interest in the brainstem that contain key BRCs. Patients were considered to have postictal BRC hypoperfusion if any of the six regions of interest were significantly hypoperfused.Results:All six patients who experienced bilateral tonic-clonic seizures during the study had significant clusters of postictal hypoperfusion in BRCs compared to seven who had focal impaired awareness seizures (7/15). The association between seizure type studied and the presence of BRC hypoperfusion was significant. Duration of epilepsy and frequency of bilateral tonic-clonic seizures were not associated with postictal brainstem hypoperfusion despite also being associated with risk for SUDEP.Conclusion:Postictal hypoperfusion in brainstem respiratory centres occurs more often following bilateral tonic-clonic seizures than other seizure types, providing a possible explanation for the increased risk of SUDEP in patients who regularly experience bilateral tonic-clonic seizures.
Objective. Structural MRI is a critical component in the pre‐surgical investigation of epilepsy, as identifying an epileptogenic lesion increases the chance of post‐surgical seizure freedom. In general practice, 1.5T and 3T MRI scans are still the mainstream in most epilepsy centres, particularly in resource‐poor countries. When 1.5T MRI is non‐lesional, a repeat scan is often performed as a higher‐field structural scan, usually 3T. However, it is not known whether scanning at 3T increases diagnostic yield in patients with focal epilepsy. We sought to compare lesion detection and other features of 1.5T and 3T MRI acquired in the same patients with epilepsy. Methods. MRI scans (1.5T and 3T) from 100 patients were presented in a blinded, randomized order to two neuroradiologists. The presence, location, and number of potentially epileptogenic lesions were compared. In addition, tissue contrast and the presence of motion/technical artifacts were compared using a 4‐point subjective scale. Results. Both the qualitative tissue contrast and motion/technical artifacts were improved at 3T. However, this did not result in statistically significant improvement in lesion detection. Qualitatively, five patients had subtle lesions seen only at 3T. However, minor differences in image acquisition parameters between 1.5T and 3T scans in these cases may have resulted in greater lesion visibility at 3T in four patients. Based on a general linear model analysis, the presence of a focal abnormality on EEG was predictive of the presence of a lesion at 1.5T and 3T. Significance. Repeat MRI scanning of patients with focal epilepsy at 3T using similar scan protocols does not significantly increase diagnostic yield over scanning at 1.5T; the increased signal‐to‐noise ratio can potentially be better allocated for novel scan sequences in order to provide more clinical value.
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