Status Epilepticus in a Heavy Snorer

Cure Sleep Apnea Without Cpap

Sleep Apnea Homeopathic Cure

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Peter Hollinger, Christian W Hess and Claudio Bassetti


A 50-year-old railwayman suffered from idiopathic absence seizures until the age of 16 years and had been seizure-free without antiepileptic treatment since then. Hypothyroidism and arterial hypertension were adequately treated. He was a heavy, habitual snorer. His wife witnessed nocturnal apneas and he reported excessive daytime sleepiness (e.g. falling asleep when watching television or when traveling in the train, or in the car as a passenger). One day after lunch he was tired and nervous and shortly thereafter had three generalized tonic—clonic seizures in succession, corresponding to tonic—clonic status epilepticus. The patient was treated with intravenous benzodi-azepines, phenytoin, and muscle relaxation, followed by intubation. He was transferred to our department.


On admission the patient was intubated and unconscious as a result of the sedatives and relaxants. His body mass index was 42.5, indicating that he was massively overweight. There were no focal neurological deficits, and a computed tomography scan of the brain was normal.

The patient became seizure-free after intubation and muscle relaxation and he was able to be extubated the next day. An EEG performed 1 day after the status epilepticus showed a mild slowing of the background activity (around 8 Hz) but was otherwise normal. An EEG performed 2 days after the status epilepticus was completely normal. A magnetic resonance imaging scan of the brain and a lumbar puncture also revealed normal results.

The Epworth Sleepiness Score estimated for the 3 months before the status epilepticus was abnormal, with 19 points (a normal score being less than 10); this was consistent with the history of excessive daytime sleepiness.

Polysomnography performed 9 days after admission showed severe obstructive sleep apnea with an apnea—hypopnea index of 74 (a normal index being less than 10) and 53 oxygen desaturations per hour (normal being less than 3) (Figure 62.1).

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FIGURE 62.1 Tests performed 9 days after admission. The patient's hypnogram (top) (MT, movement time; AWK, awake). Oxygen saturation (middle). The occurrence of apneas and hypopneas (bottom).

FIGURE 62.1 Tests performed 9 days after admission. The patient's hypnogram (top) (MT, movement time; AWK, awake). Oxygen saturation (middle). The occurrence of apneas and hypopneas (bottom).

The mean oxygen level during desaturations was 83, and the minimal oxygen desaturation level was 68%. Sleep latency was 21 min, total sleep time was 357 min, rapid eye movement (REM) latency was 123 min, stage transitions numbered 144 and sleep efficiency was 74%. Stage 1 sleep accounted for 18% of the sleep period, stage 2 for 24%, REM sleep for 8%, and slow wave sleep for 18%.


Generalized idiopathic epilepsy with status epilepticus and obstructive sleep apnea.


Treatment with nocturnal continuous positive airway pressure (CPAP) was initiated, with good compliance. Owing to the history of absence seizures in childhood, the phenytoin was replaced with valproate, which, however, had to be discontinued because of severe generalized exanthema. Carbamazepine was not tolerated either (again because of generalized exanthema). Finally, phenylbarbital (phenobarbital) was tried and found to be well tolerated.






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FIGURE 62.2 Tests performed 1 year after the initiation of CPAP treatment. The hypnogram (top) is much less fragmented than the earlier test and there is more REM sleep. There are no episodes of oxygen desaturation (middle). There are no episodes of apnea or hypopnea.

In the absence of clinical seizures, EEGs 4 and 9 months later showed frequent generalized epileptiform activity in the form of spike—wave bursts without clinical correlates, occurring approximately every 6 min.

A control polysomnography performed 1 year after the initiation of CPAP treatment showed normal findings with an apnea—hypopnea index of less than 1, and 0.3 oxygen desaturations an hour (Figure 62.2). Sleep latency was 6 min, total sleep time was 384 min, REM latency was 155 min, stage transitions numbered 78, and sleep efficiency was 85%. Stage 1 sleep accounted for 20% of the sleep period, stage 2 for 52%, REM sleep for 14%, and slow wave sleep for 2%.

The Epworth Sleepiness Score had normalized to five points and the multiple sleep latency test was also normal, with a mean sleep latency of 12.5 min (normal being less than 10 min).

Two years after the status epilepticus, the patient remains seizure-free on 300 mg phenylbarbital (phenobarbital), works to full capacity, and is highly satisfied with his CPAP treatment.


Why did we choose this case?


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This patient's history highlights one possible pathogenic interaction between obstructive sleep apnea and epilepsy. We hypothesize that this patient's childhood epilepsy remained asymptomatic for many years until the detrimental effect of obstructive sleep apnea triggered an episode of status epilepticus. Although the exact time of onset of signs and symptoms of obstructive sleep apnea cannot be determined precisely from the patient's history, he clearly exhibited symptoms of obstructive sleep apnea (snoring, apneas, and sleepiness) for a few months before the episode of status epilepticus. In addition he was massively overweight, which is a well-known risk factor for obstructive sleep apnea.

Furthermore, the patient remained clinically seizure-free after treatment with anti-epileptic drugs and CPAP, despite the persistence on EEG of generalized spike—wave activity. Control polysomnography demonstrated a complete normalization of the initial sleep disordered breathing, thus excluding persistent obstructive sleep apnea as a cause of persisting EEG abnormalities. The patient was sleepy before the inititation of CPAP treatment and showed marked lessening of excessive daytime sleepiness with CPAP (with normalization of the Epworth Sleepiness Score from 19 to 5 points), which explained his compliance with the treatment device.

Since additional investigations excluded factors known to cause status epilepti-cus, including for example fever or inflammatory or structural brain pathology, we postulate that status epilepticus arose from an idiopathic predisposition for generalized epilepsy (as manifested by childhood absence seizures) and severe obstructive sleep apnea.

What did we learn from this case?

In patients with a hitherto well-controlled seizure disorder and recently increasing seizure frequency, new onset of epileptic seizures, or status epilepticus, it is obviously important to exclude such causes as degenerative, structural or inflammatory brain disease, or poor compliance to drug treatment. In the absence of such factors, one should also ask about symptoms of obstructive sleep apnea such as snoring, observed apneas, and excessive daytime sleepiness. Fatigue or sleepiness in patients under anti-epileptic drug treatment should not automatically be attributed to the drug, since a treatable sleep disorder, including obstructive sleep apnea, might underlie this specific complaint.1 In the presence of obstructive sleep apnea, CPAP treatment should be considered, although at best 80% of patients in larger series may be compliant with this treatment.2 Poor compliance is especially likely in patients who do not report excessive subjective daytime sleepiness.

Our group has shown that the frequency of epilepsy and obstructive sleep apnea is higher than what could be estimated by pure coincidence, suggesting a specific pathogenic link. Obstructive sleep apnea induces sleep fragmentation caused by recurrent arousals and thus leads to sleep deprivation, which is well known to precipitate epileptic seizures.

Obviously, obstructive sleep apnea represents only one of several potential pathogenic mechanisms in the etiology of seizures. Hence, despite optimal treatment with CPAP, seizures may persist. The effect of CPAP treatment on seizure frequency in a single patient may be difficult to estimate considering the fact that most patients already receive antiepileptic drug treatment and that CPAP is prescribed only as an adjunctive treatment. Prospective studies with larger samples of patients with obstructive sleep apnea and epilepsy are needed.


1. Malow BA, Fromes GA, Aldrich MS. Usefulness of polysomnography in epilepsy patients . Neurology 1997;48:1389-94 .

2. Strollo PJ, Rogers RM . Obstructive sleep apnea . N Engl J Med 1996;334:99-104 .


Hollinger P, Bassetti C, Gugger M , Hess CW. Epilepsy and obstructive sleep apnea . Neurology 2000;54(suppl 3):A27 .

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