Paediatria Croatica, Vol. 53 No. 3, 2009.
Sažetak sa skupa
IMPLANTING A VAGUS NERVE STIMULATOR IN A TEN-YEAR OLD BOY WITH PHARMACORESISTANT SYMPTOMATIC EPILEPSY
D. Čokolić Petrović
; KB Osijek
K. Hafner
Sažetak
We present a patient, a ten-year old boy who has brain damage in the irrigation region of the middle cerebral artery and suffers from pharmacoresistant epilepsy, and at the age of just under 11 years he had a vagus nerve stimulator implanted.
The family history is negative for epilepsy, non-epileptic and other cerebral seizures. He was born from the second, regularly controlled pregnancy on term. Due to threatened asphyxia and slow heart beat the birth was concluded by vacuum extraction, and after the birth he was primarily reanimated, and his APGAR score was low. At three months of age, due to suspected hemiparetic form of the right extremities he was hospitalized for diagnostic examination and an MR of the brain was performed. Organic brain damage was confirmed in the left hemisphere in the irrigation area of the ACM as a result of perinatal damage in the form of thrombosis or haemorrhage. He had his first generalized convulsion at 4 months, but no continuous AET was introduced at that time. He received physical therapy both as an in and out patient. At six years of age, after an attack of vertigo lasting five minutes with unstable gait and acutely altered EEG with a spike wave complex, AET was introduced using carbamazepine. From this time on partially complex seizures followed which made him briefly disturbed and disoriented, sometimes with perioral cyanosis with piloerection and derealisation. After the first epileptic convulsion (grand mal) status, valproates were also introduced. Grand mal seizures continued from that time, on average 2-3 times a year, with frequent epileptic status and he was hospitalized on several occasions with intensive treatment and endotracheal intubation in order to calm the seizure. After two years of treatment, valproates were replaced by topiramat and carbamazepine with oxcarbazepine. Due to the further frequent seizures he also received lamotrigine, and topiramate was discontinued and later replaced with levetiracetamon. So despite three anti-epileptics (levetiracetam, lamotrigine, oxcarbazepine) he was still having seizures. In the last year (but also previous years) before the installation of the vagus nerve stimulator, he had on average 5-6 complex partial seizures a week, 2-3 times a month a simple partial motor seizure, an atonic seizure up to 3 times a year (then frequently in series or status). In his neurological status there was slight right-hand hemiparesis together with cerebral palsy. The EEG finding was diffusely paroxysmally dysrhythmically altered with elements of spike wave complexes of a slower variety by the focal left F-T-P. During several days of video EEG monitoring two partial complexes of epileptic seizures were confirmed, with temporal pseudo-absence and the accompanying changes to the EEG finding.
A neurosurgeon was consulted, who, in view of the pharmacoresistant seizures, suggested surgical treatment of the epilepsy, that is one of three options: hipocampectomy, resection of the apical part of the temporal lobe, or implantation of a vagus nerve stimulator.
In view of the clinical picture of epileptic seizures and the findings of the electrophysiological examinations and the pharmacoresistant form of the disease, the neurosurgeon indicated the implantation of a vagus nerve stimulator, having previously informed the parents about the procedure, the effectiveness of the treatment and possible side effects. After the pre-operative work up, at the age of 10 years and 11 months the boy had a vagus nerve stimulator implanted. The previous AET was continued and after the implantation of the vagus nerve stimulator the number of seizures decreased significantly.
We would conclude that earlier consideration should be given to the possibilities of surgical treatment of epilepsy if it demonstrates the criteria of refractoriness since these methods, alongside the suitable antiepileptic therapy, contribute to improving the quality of life of the patient with symptomatic epilepsy.
Ključne riječi
Hrčak ID:
43626
URI
Datum izdavanja:
20.11.2009.
Posjeta: 1.518 *