Objetivos: El objeto de este trabajo es describir cuatro pacientes con distonía cráneocervical (DCC) tratados con Estimulación Cerebral Profunda (ECP). Además, investigamos la eficacia del tratamiento y los predictores de la evolución quirúrgica, por medio de la revision y análisis de publicaciones previas.Métodos: Cuatro pacientes con distonía cráneocervical (DCC) fueron tratados con ECP el globo pálido interno (Gpi) o del Núcleo Subtalámico (NST). Se realizaron búsquedas en Pubmed y Medline para obtener información detallada de pacientes que fueron operados con ECP para DCC. El punto principal que señala la eficacia de este tratamiento fue el cambio en la escala de Burke–Fahn–Marsden para Distonia (Puntuación de movimiento y discapacidad, BFMDRS- M/D) luego de la cirugía. Resultados: Setenta y cinco pacientes fueron incluidos en el conjunto de datos, incluyendo 69 pacientes con Gpi-ECP y 6 pacientes con NST - ECP. El promedio temporal de seguimiento fue de 28 meses luego de la cirugía. La mejoría promedio en la puntuación de la BFMDRS-M fue de 24.5 ± 11.2 en los exámentes preoperatorios y 8.1 ± 5.7 en los postoperatorios, al momento de la última evaluación, con un promedio de mejoría del 66.9% (p < 0.001). El puntaje promedio de la BFMDRS-D score fue de 8.1 ± 4.6 en el preoperatorioy and 3.6 ± 2.5 en el postoperatorio, con un promedio de mejoría del 56.0% (p < 0.01). Se encontraron correlatos positivos entre cada uno de las puntuaciones de movimiento y discapacidad preoperatorios y en las puntuaciones de movimiento y discapacidad y en los porcentajes de mejoría postoperatoria (r = 0.247, p = 0.034; r = 0.331, p = 0.034, respectivamente).Conclusión: La ECP en los núcleos GPi/NST es un tratamiento efectivo para pacientes con DCC médicamente refractaria, incluyendo aquéllos con síntomas preoperatorios severos. La edad al comienzo de la DCC y la duración de la enfermedad no predijeron la mejoría en las puntuaciones para el movimiento.
Some recent studies suggest that some imaging-negative temporal lobe epilepsy (TLE) had significant amygdala enlargement (AE). Contradictory data were also reported in previous studies regarding the association between AE and TLE. The present study was to investigate the clinical characters of a group of TLE with AE and compare the amygdala volume of the same patient before and after antiepileptic drugs treatment by a larger sample size.This study recruited 33 mesial TLE patients with AE and 35 healthy volunteers. The clinical history, seizure semiology, electroencephalogram (EEG), fluorodeoxyglucose-positron emission tomography (FDG-PET) and amygdala volume were investigated. The amygdala volume were compared between ipsilateral and contralateral sides, TLE patients and 35 healthy controls, and patients at first and follow-up visit by 3.0 T MRI.Average seizure onset age was 42.0 years (SD 14.3). All patients had complex partial seizures, fourteen had occasional generalized tonic-clonic seizures which often happened during sleep. Ninety percent patients suffered from anxiety or depression. Thirty percent patients had memory decline. Interictal epileptiform discharges appeared predominantly in the anterior or inferior temporal area ipsilateral to AE. Interictal FDG-PET showed regional glucose hypometabolism in the ipsilateral temporal lobe. No hippocampal sclerosis (HS) was suspected in all patients. 22 patients demonstrated good seizure control and significantly reduced volume of the enlarged amygdala after treatment (P < 0.01). The other 11 patients showed initial response to treatment, followed by a gradual increase in seizure frequency over time, and no volume change of the enlarged amygdala after treatment.TLE with AE probably represents a distinct nosological and probably less homogeneous syndrome which is most likely a subtype of TLE without ipsilateral HS. The chronic and long lasting inflammatory processes or focal cortical dysplasia could lead to amygdala enlargement possibly.
Purpose: The superior frontal sulcus (SFS), located in the prefrontal and premotor cortex, is considered as one of the common locations of focal cortical dysplasia (FCD). However, the characteristics of seizures arising from this area are incompletely known. The primary purpose of this study was to investigate the clinical features and the epileptic networks of seizures originating from the SFS. Methods: We included seventeen patients with type II FCD within the SFS. SFS was identified both visually and automatically. Semiological features were evaluated and grouped. Interictal 18FDG-PET imaging in all patients was compared to controls using statistical parametric mapping (SPM-PET). In those subjects with stereoelectroencephalography (SEEG), two different quantitative intracranial electroencephalography analyses were applied. Finally, the locations of the SFS-related hypometabolic regions and epileptogenic zones (EZs) were transformed into standard space for group analysis. Results: We identified two semiological groups. Group 1 (9/17) showed elementary motor signs (head version and tonic posturing), while group 2 (8/17) exhibited complex motor behavior (fear, hypermotor, and ictal pouting). Based on SPM-PET, an SFS-supplementary motor area (SMA) epileptic propagation network was found in group 1, and an SFS-middle cingulate cortex (MCC)-pregenual anterior cingulate cortex (pACC) propagation network was discovered in group 2. Intracranial EEG analysis suggested similar affected structures with high epileptogenicity. The SFS-related hypometabolic regions and EZs in these groups showed a posterior-anterior spatial relationship. Conclusions: Even though originating from the spatially restricted cortex, SFS seizures can be divided into two groups based on semiological features. The SFS-SMA and SFS-MCC-pACC epileptic propagation networks may play pivotal roles in the generation of different semiologies. The posterior-anterior spatial relationship of both hypometabolic regions and EZs provides potentially useful information for distinguishing different types of SFS seizures and surgical evaluation.
Objective
To evaluate the efficacy and safety of domestic vagus nerve stimulator for the treatment of pharmaco-resistant epilepsy (PRE) through a prospective, multicenter, randomized, double-blind, parallel controlled trial.
Methods
A total of 72 patients with PRE in 5 hospitals were enrolled from August 2014 to December 2014. A domestic vagus nerve stimulator was used to conduct vagus nerve stimulation (VNS). All patients with PRE were divided into either a test group (n=35) or a control group (n=37) according to the principle of central randomization. Two weeks after procedure, the vagus nerve stimulator of the test group was turned on really. The parameters (electric current, pulse width, frequency, duration of stimulation, and time interval) of the stimulus set were optimized; whereas that of the control group was turned on simulatedly. At 4 months after operation, the stimulator was turned on and unblinded. According to the Mchugh classification and the modified Engel classification standards, the effectiveness and safety of using the stimulator to treat PRE were evaluated at 4 and 8 months after procedure in both groups.
Results
At 4 months after procedure, there were 16, 8, 8, 0, and 3 patients, respectively in the McHugh classification grade Ⅰ, Ⅱ, Ⅲ , Ⅳ and Ⅴ test groups, and 9, 3, 16, 0, and 9 patients in the control group, respectively. There were 8, 4, 12, and 11 patients, respectively in the modified Engel classification grade Ⅰ, Ⅱ, Ⅲ , Ⅳ and Ⅴ test groups, and there were 4, 5, 3, and 25 in the control group, respectively. At 4 months after procedure, the seizures in the test groups were improved obviously compared with before procedure. The improvement of the test groups were significantly better than the control group (the improvement rates of seizures were -63.0% and -34.0%, respectively; P=0.006). The symptoms were improved gradually after turning on the stimulator in the control group. At 8 months after procedure, there were 15, 10, 7, 2, and 1 patient, respectively in the Mchugh classification grade Ⅰ, Ⅱ, Ⅲ , Ⅳ, and Ⅴ test groups, and there were 9, 9, 19, 0, and 0 patients in control group, respectively. There were 7, 2, 19, and 9 patients respectively in the modified Engel classification grade Ⅰ, Ⅱ, Ⅲ and Ⅳ test groups, respectively, and there were 4, 2, 12, and 19 patients in the control group, respectively. The efficacy of the control group was gradually similar to the test groups. Compared with the baseline, the efficacy was improved significantly (P<0.001). At 8 months after procedure, the seizure frequency of 33.3% of patients reduced more than 80%, and that of 59.7% of patients reduced more than 50%.
Conclusions
Using domestic vagus nerve stimulators can significantly reduce the seizure frequency in patients with PRE. It has higher effectiveness and safety. It is suitable for the treatment of patients with PRE.
Key words:
Vagus nerve stimulation; Multicenter study; Randomized controlled trial; Clinical trial; Pharmaco-resistant epilepsy
Abstract Seizures are a well‐recognized and often prominent manifestation of autoimmune encephalitic syndromes. Progress in detection of pathogenic neural autoantibodies has led to increased awareness of autoimmune causes of seizures. Clinical studies of patients with these autoantibodies have improved our understanding of the seizure characteristics, treatments, and seizure prognosis in these disorders. The International League Against Epilepsy (ILAE) Autoimmunity and Inflammation Taskforce proposes conceptual definitions for two main diagnostic entities: (a) acute symptomatic seizures secondary to autoimmune encephalitis, and (b) autoimmune‐associated epilepsy, the latter of which suggests an enduring predisposition to seizures. Such a distinction is relevant when discussing the pathophysiology, treatment, prognosis, and social consequences of these disorders. We discuss the role of biomarkers in the application of these conceptual definitions and illustrate their use in patients cared for by members of the task force.
Brain tumors are common in epilepsy surgery and frequently occur in the temporal lobe, but the optimal surgical strategies to remove the tumor and epileptogenic zone remain controversial. We aim at illustrating the positron emission tomography (PET) metabolism and the stereoelectroencephalography (SEEG) epileptogenicity of temporal lobe long-term epilepsy-associated tumors (LEAT). In this study, 70 patients and 25 healthy controls were included. Our analysis leveraged group-level analysis to reveal the whole-brain metabolic pattern of temporal lobe LEATs. The SEEG-based epileptogenicity mapping was performed to verify the PET findings in the epileptic network. Compared to controls, patients with a temporal lobe LEAT showed a more widespread epileptic network based on 18FDG-PET in patients with a mesial temporal lobe LEAT than in those with a lateral temporal lobe LEAT. The significant brain clusters mainly involved the paracentral lobule (ANOVA F = 9.731, p < 0.001), caudate nucleus (ANOVA F = 20.749, p < 0.001), putamen (Kruskal−Wallis H = 19.258, p < 0.001), and thalamus (ANOVA F = 4.754, p = 0.011). Subgroup analysis and SEEG-based epileptogenicity mapping are similar to the metabolic pattern. Our findings demonstrate the metabolic and electrophysiological organization of the temporal lobe LEAT epileptic network, which may assist in a patient-specific surgical strategy.
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