Abstracts

Rationale: REM sleep behavior disorder (RBD) is a parasomnia characterized by dream-enacting behaviors associated with nightmares and loss of muscle atonia during REM sleep. The origin of RBD is thought to be related to dysfunction of the brainstem structures that regulate muscle atonia and their anatomic connections with other brain structures involved in REM sleep regulation such as the limbic system (e.g., amygdala, hippocampus). It has been described that RBD may occur in the setting of limbic encephalitis linked to potassium channel antibodies, a disorder with prominent amygdala-hippocampal damage sparing the brainstem. The aim of our study was to evaluate if RBD is present in patients with epilepsy secondary to bilateral amygdalar-hippocampal damage due to bilateral mesial temporal sclerosis without brainstem impairment. Methods: Four patients with temporal lobe epilepsy secondary to bilateral amygdalar-hippocampal damage due to bilateral mesial temporal sclerosis (and no evidence of previous or current autoimmune encephalitis) were interviewed and asked about epilepsy and sleep disorder symptoms, and they underwent one full-night of polysomnography to rule out the presence of RBD. Electromyographic activity during REM sleep was quantified in the mentalis and upper and lower extremities. Three of them also had prolonged video EEG monitoring in the setting of presurgical evaluation. Results: All patients (3 men, one women) had temporal lobe epilepsy. In spite of bilateral mesial temporal sclerosis on MRI, seizures arose from one mesial temporal region only in the three patients who were monitored. Seizure semiology was consistent with temporal lobe epilepsy, including two patients with auras of fear and panic. Mean age was 37 years (26-54). Mean time of epilepsy evolution was 13 years. All patients were treated with two antiepileptic drugs; seizures were controlled in one patient and were refractory to medical treatment in the other three. MRI showed bilateral mesial temporal sclerosis and no brainstem lesions. None of the patients reported frequent nightmares or dream-enacting behaviors. Polysomnography excluded RBD demonstrating normal REM sleep atonia in all muscles evaluated and no abnormal behaviors. Conclusions: Our study demonstrates the absence of RBD in patients with bilateral mesial temporal sclerosis without brainstem damage not due to autoimmune encephalitis. This suggests that the limbic damage occurring in epileptic patients with bilateral mesial temporal sclerosis is not severe enough to damage REM sleep modulation.