Tabla I. Etiología de la epilepsia. |
|||
n |
% |
||
Estructural |
22 |
62,9 |
|
Displasia cortical focal (frontal, fondo de surco insular) |
5 |
||
Displasia hipocámpica |
1 |
||
Polimicrogiria |
1 |
||
Heterotopía en banda |
3 |
||
Tumor neuroectodérmico primitivo (extenso) |
1 |
||
Ganglioma temporal |
1 |
||
Túberes y nódulos subependimarios |
2 |
||
Secuelas de lesión isquémica/infecciosa |
6 |
||
Esclerosis mesial temporal |
2 |
||
Infecciosa |
4 |
11,4 |
|
Genética (CDKL5, duplicación 15q11-13, DCX) |
3 |
8,5 |
|
Vascular |
2 |
5,7 |
|
Mitocondrial |
1 |
2,4 |
|
Criptogénica |
10 |
28,6 |
Figura. La respuesta al estimulador del nervio vago fue significativamente mayor (p = 0,03) en los pacientes que tuvieron un inicio de la epilepsia más tardío.
Tabla II. Tipo de crisis y respuesta al estimulador del nervio vago. |
||||
n (%) |
Reducción |
Reducción |
||
Focales |
Sí |
16 (51,4%) |
6 (37,5%) |
10 (62,5%) |
No |
12 (70,6%) |
5 (29,4%) |
||
Generalizadas |
Sí |
8 (22,9%) |
3 (42,9%) |
4 (51,1%) |
No |
15 (57,7%) |
11 (42,3%) |
||
Espasmos |
Sí |
16 (45,7%) |
11 (68,8%) |
5 (31,3%) |
No |
7 (41,2%) |
10 (58,8%) |
||
Tónicas |
Sí |
20 (57,1%) |
12 (60%) |
8 (40%) |
No |
6 (46,2%) |
7 (53,8%) |
||
Atónicas |
Sí |
9 (25,7%) |
3 (33,3%) |
6 (66,7%) |
No |
15 (62,5%) |
9 (37,5%) |
||
Mioclónicas |
Sí |
8 (22,9%) |
4 (50%) |
4 (50%) |
No |
14 (56%) |
11 (44%) |
||
Ausencias |
Sí |
12 (34,3%) |
6 (50%) |
6 (50%) |
No |
12 (57,6%) |
9 (42,9%) |
Ten years’ experience with vagus nerve stimulation in a paediatric population Introduction. Fifty million people are affected by epilepsy. Up to 30% are not controlled with the aid of antiepileptic drugs. The vagus nerve stimulator (VNS) is a therapeutic alternative that must be taken into account. Aim. To determine the effect of the VNS in a cohort of paediatric patients with refractory epilepsy. Patients and methods. A retrospective study of children with a VNS implanted between 2008 and 2017 in a tertiary hospital. Epidemiological, aetiological, clinical and electrophysiological data, along with VNS parameters were analysed. Results. The study included 35 patients, with a mean age when the VNS was implanted of 12.84 years (range: 3.1-18.7 years) and a mean time between onset of epilepsy and implantation of 7.2 years (range: 1.3-17.7 years). The causation was structural in 62.9% of cases. The most frequent epileptic conditions were: Lennox-Gastaut syndrome and focal epilepsy, with a predominance of tonic seizures (57.1%). The video electroencephalogram showed multifocal anomalies (54%) and a pattern of epileptic encephalopathies (34.3%). Intellectual disability was associated in 94% of the cases. The mean of previous antiepileptic drugs was 9.6 ± 3 (range: 4-16). 43% responded to treatment (≥ 50% reduction in number of seizures), with a mean reduction of 67.3%, which improved with higher ages of onset of epilepsy. Three patients were seizure-free (8.5%). The number of seizures decreased by 33% at six months and by 47.4% at 24 months. There was also a notable degree of cognitive (57%) and behavioural improvement (53%). In 28% of cases there were some side effects, but in general they were mild. Conclusions. The VNS is a valid option in refractory epilepsy, with improvements not only in terms of seizures but also regarding cognitive-behavioural aspects, this being very important for the paediatric population. Key words. Efficacy. Paediatrics. Refractory epilepsy. Safety. Treatment. Vagus nerve stimulator. |