Clinical Case 1

Patient 17 years of age who come referred by her neurologist to assess possible OSAS in connection with epileptic seizures (grand mal) not responsive to medication ant. 9 / 09

Background:

  • Seizures Generalized every 3 weeks in the last two years. (a dozen income UVI)
  • Diagnosis 2007 of epilepsy with tonic-clonic in tto with Depakine
  • 5 / 08 is changed medication for slowing and weight gain Kepros
  • 3 / 09 back with the Kepros Depakine
  • 5 / 09 is added to lamotrigine and Depakote Kepros.
  • 4 / 09 MR 4 / 09 asymmetry of temporal horns right hippocampal atrophy and incipient.
  • 7 / 09 Video 24 hours sleep EEG Ruber Clinic. Study shows abnormal slowing and epileptiform activity right. Decreased deep sleep periods are REM

15 months after

Results:

  • From 10/09 the patient has not had any seizures
  • Currently being treated with Kepros 1500 mg/12 h, Stada Lamotrigine 100 mg / 8 h and Magnesium
  • The patient has stopped snoring and apnea pauses
  • Currently a 3 family Epworth withdraws a new sleep study

Discussion:

  • Control of apnea decreases repeated awakenings and improved sleep architecture and thus the control of seizures
  • Other authors consider that the respiratory acidosis associated with OSAS protects the CNS from the crisis so give this disease a protective value of epilepsy
  • The prevalence of epilepsy in the population is between 0.5% and 1% being the great evil of 6% of these. Being the dare of 5% in the general population. The coexistence of both diseases is 1 case per 5 million
  • In this case the drastic elimination of seizures after surgery, and clinical resolution of their apnea show that OSAS may be a factor that hinders the control of this disease in patients who suffer