In addition to the nonepileptic conditions previously discussed, two sleep related conditions can occasionally be confused with convulsive epileptic seizures. These are periodic limb movements of sleep (PLMS) and REM sleep behavior disorder (RBD) (see also Chapter 16).
PLMS is characterized by recurrent muscle contractions, primarily of the lower extremities, during sleep (50-53). Simultaneous movements of the upper extremities may occur. The movements tend to occur in clusters, each movement occurring approximately 20 to 30 seconds after the preceding movement, and each cluster lasting from minutes to hours. The movements tend to be more prominent in stage I and stage II sleep and tend to occur early in the night. The movements are characterized by extension of the great toe and flexion at the ankle, knee, and hip. Patients may complain of frequent awakenings, insomnia, or daytime sleepiness, all symptoms that are commonly associated with disrupted sleep. As one might expect, spouses often complain of disrupted sleep.
PLMS is present in 80 to 90% of patients with restless legs syndrome (RLS) and in a lower percentage of patients with other types of sleep disorders (52). PLMS may be present as a distinct disorder called periodic limb movement disorder (PLMD). In addition, PLMS may occur in patients without symptoms. Asymptomatic patients are usually discovered because of complaints by the spouse or when the patient is undergoing evaluation for other reasons. The prevalence of PLMS increases with age, being present in approximately 5% of the 30- to 50-year age group, 30% of 50- to 65-year-olds, and 30 to 45% of patients over 65 years of age.
The mechanism and etiology of PLMS are not known. Using functional MRI in patients with RLS and sensory discomfort in the legs, Bucher et al. showed that during PLMS, activation occurred in the red nuclei and brainstem near the reticular formation (54). Activation was not associated with sensory discomfort alone. Voluntary imitation of PLMS produced activation in the motor cortex and globus pallidus, but not in the brain-stem areas activated by PLMS. Based on these and other data, these investigators hypothesized that PLMS may result from activation of the reticular formation that in turn produces disinhibition of spinal pathways.
The observable phenomena associated with PLMS are usually not difficult to differentiate from convulsive epileptic seizures. If primarily unilateral, PLMS could possibly mimic simple partial seizures, including epilepsia partialis continua (EPC). However, PLMS occurs at a much slower frequency—every 20 to 30 sec—than EPC. The absence of cortical discharges differentiates PLMS from myoclonic seizures. Bilateral PLMS does not mimic the normal progression of a generalized tonic-clonic or clonic-tonic-clonic seizure.
When associated with RLS, PLMS is easily diagnosed and does not require further diagnostic work up. If PLMS is not associated with RLS, the diagnosis can be made with polysomnography or with video-EEG monitoring that includes electrodes for recording muscle activity.
Treatment of PLMS depends on the severity of the sleep disturbance. Treatment is not necessary in asymptomatic individuals. The three primary classes of medications used for the treatment of PLMS are dopaminergic agents (52,55), benzodiazepines (52,56), and opiates (52). Data from one controlled, doubleblind study suggests that carbidopa/levodopa may be more effective than propoxyphene in controlling the movements and symptoms of PLMS (57).
Was this article helpful?