The episodes can be suppressed by the administration of clonazepam in doses of 0.5 to 1.0 mg at bedtime and by melatonin, 3 to 12 mg. The advantage of the latter is that sleep apnea is not affected as it is with benzodiazepines. Discontinuation of medication, even after years of effective control, has resulted in relapse. Antidepressants are said to exacerbate the disorder with the possible exception of bupropion.
Nocturnal Epilepsy (See Also Chap. 15)
It has long been known that seizures, both convulsive and nonconvulsive, often occur during sleep, especially in children. This is such a frequent occurrence that the practice of inducing sleep has been adopted as an activating EEG procedure to obtain confirmation of epilepsy. Seizures may occur soon after the onset of sleep or at any time during the night, but mainly in stages 1 and 2 of NREM sleep or, rarely, in REM sleep. They are also common during the first hour after awakening. On the other hand, deprivation of sleep may also be conducive to a seizure.
Sleeping epileptic patients may attract attention to their seizures by a cry, violent motor activity, unusual but stereotyped actions, such as sitting up and crossing the arms over the chest, the adoption of a “fencing” posture, or labored breathing. After the tonic-clonic phase, patients become quiet and fall into a state resembling deep sleep, but they cannot be aroused from it for some minutes or longer. If the nocturnal seizure is unobserved, the only indication of it may be disheveled bedclothes, a few drops of blood on the pillow from a bitten tongue, wet bed linen from urinary incontinence, or sore muscles. Or the occurrence of a seizure may be disclosed only by confusion, muscle soreness, or headache, the common aftermaths of a major generalized seizure. Rarely, a patient may die in an epileptic seizure during sleep, sometimes from smothering in the bed clothes or aspirating vomitus or for some obscure reason (possibly respiratory or cardiac dysrhythmia). The question sometimes arises whether night terrors or sleep walking represent epileptic automatisms. Usually no such relationship is established. Measurement of serum creatine kinase concentration in the hours following an event may distinguish seizure from night terrors, and the other described sleep-related motor behaviors.
One type of nocturnal frontal lobe seizure disorder is characterized by paroxysmal bursts of generalized choreoathetotic, ballistic, and dystonic movements occurring during NREM sleep (Lugaresi et al, 1986). Sometimes the patient appears awake and has a fearful or astonished expression, or there are repetitive utterances and an appearance of distress, similar to what is seen in night terrors, the main differential diagnosis discussed further on. The attacks may begin at any age, affect both sexes, and are usually nonfamilial. A fencing posture, in which one arm is thrust forward and the other is flexed occurs in some instances. The main form of this disorder is characterized by attacks lasting 60 s or less; they may be diurnal as well as nocturnal; some patients in addition have epileptic seizures of the more usual type; and all respond to treatment with carbamazepine. The studies of Tinuper and coworkers, using prolonged video-EEG monitoring, indicate that these brief attacks of nocturnal paroxysmal dystonia may actually be epileptic seizures of frontal lobe origin. In a rarer disorder that simulates these seizures, the attacks are longer (2 to 40 min), ictal and interictal EEGs are normal, and the events are not suppressed by antiepileptic drugs. Except for the lack of familial incidence and occurrence only during sleep, the disorder is very much the same as the “familial paroxysmal dystonic choreoathetosis” (see “Paroxysmal Choreoathetosis and Dystonia” in Chap. 4).