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J Neurol Neurosurg Psychiatry 63:808 doi:10.1136/jnnp.63.6.808
  • Letters to the editor

Exacerbation of epilepsy by obstructive sleep apnoea

  1. T C BRITTON,
  2. M O’DONOGHUE,
  3. J S DUNCAN
  1. National Hospital for Neurology and Neurosurgery, National Society for Epilepsy
  2. Chalfont St Peter, Buckinghamshire SL9 0LR, UK
  3. The National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK
  1. Dr T C Britton, The Neuroscience Unit, Mapother House, King’s College Hospital, Denmark Hill, London SE5 9RS, UK.
  1. N P HIRSCH
  1. National Hospital for Neurology and Neurosurgery, National Society for Epilepsy
  2. Chalfont St Peter, Buckinghamshire SL9 0LR, UK
  3. The National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK
  1. Dr T C Britton, The Neuroscience Unit, Mapother House, King’s College Hospital, Denmark Hill, London SE5 9RS, UK.

    Identification and avoidance of factors that trigger or exacerbate seizures is important in patients with epilepsy. The most common factors are sleep disturbance, alcohol ingestion, drugs, stress, and photosensitivity. The present case is the first report of seizures exacerbated by obstructive sleep apnoea. Treatment with continuous positive airway pressure (CPAP) given through a nasal mask abolished nocturnal seizures and greatly reduced the frequency of daytime attacks.

    The patient, now aged 30 years, was born three weeks prematurely. Moderate mental retardation was noted at the age of five years and subsequent chromosomal analysis disclosed trisomy 4p. Dysmorphic features associated with trisomy 4p1 included dysplasia of the nasal bones, hypertelorism, and a short neck. Radiology of the cervical spine showed incomplete fusion of the neural arch of C5 with a small spinous process of C6. He was not obese. Epilepsy began at 12 years of age with atypical absence and tonic-clonic seizures. Treatment with valproate, ethosuximide, nitrazepam, carbamazepine, clobazam, and vigabatrin in various combinations had failed to control his attacks. He was referred to the National Hospital for Neurology and Neurology-National Society for Epilepsy at Chalfont with the following pattern of seizures: tonic seizures causing a sudden fall to the ground between three times a day to three times a week; tonic seizures characterised by elevation and stiffening of both arms occurring four to five times a day; and episodes three to four times a night in which he would have serial tonic seizures over one hour periods, interspersed with rocking movements and rolling from side to side. His medication on admission comprised slow release carbamazepine (400 mg twice daily), vigabatrin (1.5 g twice daily), and temazepam (10 mg at night). The vigabatrin was replaced with lamotrigine (150 mg twice daily) and temazepam was stopped, with only a modest improvement in seizure frequency.

    Because of a history of loud nocturnal snoring and daytime hypersomnolence, the patient underwent a sleep study. Overnight observation and continuous monitoring of oxygen saturation (SpO2) disclosed a baseline SpO2 of 95%, with frequent cyclical dips to 80%. During the study, which lasted seven hours 47 minutes, there were 106 episodes of desaturation to below 90%, each episode lasting 20 seconds. The cyclical dips were associated with upper airway obstruction, consistent with the syndrome of obstructive sleep apnoea. Rhinolaryngological assessment disclosed a deviated nasal septum, but it was considered that the level of obstruction was at the level of the palate and secondary to his dysmorphic features. It was decided to try nasal CPAP before proceeding to sleep nasendoscopy and uvulopalatopharyugoplasty.

    The patient tolerated the CPAP mask well and his snoring was abolished. A repeat sleep study showed that nocturnal oxygen saturation averaged 97% with no significant dips. An immediate improvement in daytime alertness was noted. On follow up three months later, all the nocturnal attacks had been abolished and his daytime tonic seizures were reduced to two per week, without falling. His daytime alertness remained much improved and he no longer had morning headaches. The improvement has now been maintained for more than two years.

    Obstructive sleep apnoea typically presents with daytime sleepiness and unrefreshing and restless nocturnal sleep.2 3 It is usually associated with obesity but may also occur in patients with nasopharangeal abnormalities and in patients taking sedatives or alcohol. The diagnosis depends on awareness of the condition and can be confirmed by sleep studies. Treatment with nasal CPAP is often successful but surgery to correct significant narrowing of the nose or pharynx is sometimes required.3 In the present patient, the obstruction was related to his dysmorphism, but the sedative effect of his antiepileptic medication may also have contributed.

    Obstructive sleep apnoea may have exacerbated this patient’s epilepsy simply by producing interrupted and unrefreshing sleep. Sleep deprivation is a potent trigger for seizures.4Alternatively, the hypoxaemia associated with the obstructive sleep apnoea may have triggered the seizures. Hypoxaemia is known to precipitate seizures in patients with epilepsy.5

    Obstructive sleep apnoea should be considered as a cause of poor seizure control in any patient with disturbed sleep, as the correct diagnosis can lead to highly effective non-pharmacological treatment. Failure to make the correct diagnosis may result in the patient being treated with more antiepileptic medication that could exacerbate obstructive sleep apnoea and thereby worsen seizure control.

    Since submitting this communication, Tirosh and colleagues6 reported four boys with neurodevelopmental deficits and obstructive sleep apnoea. Treatment with CPAP produced several clinical benefits including a significant decrease in seizure frequency in one boy.

    Acknowledgments

    We thank Dr CI Roberts who referred the patient.

    References

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