Objective: Sleep-related hypermotor epilepsy (SHE) is a focal epilepsy characterized by seizures occurring mostly during sleep, ranging from brief seizures with paroxysmal arousals (SPAs) to hyperkinetic seizures and ambulatory behaviors. SPAs are brief and stereotypic seizures representing the beginning of a major seizure. Distinguishing SPAs from disorders of arousal (DOAs) and their briefest episodes called simple arousal movements (SAMs) is difficult. We performed a characterization of SPAs and SAMs to identify video-polysomnographic (VPSG) features that can contribute to the diagnosis of SHE or DOA. Methods: Fifteen SHE, 30 DOA adult patients, and 15 healthy subjects underwent full-night VPSG. Two neurologist experts in sleep disorders and epilepsy classified all the sleep-related movements and episodes recorded. For each SPAs and SAMs, sleep stage at onset, duration, limb involvement, progression, and semiology have been identified. Results: A total of 121 SPAs were recorded, emerging mostly during stage 1-2 nonrapid eye movement (NREM) sleep (median duration: 5 seconds). At the beginning, the SPAs motor pattern was hyperkinetic in 78 cases (64%), involving more than three non-contiguous or all body parts. The standard was a constant progression of movements during SPAs without any motor arrests. In DOA patients a total of 140 SAMs were recorded (median duration: 12 seconds) mostly emerging during stage 3 NREM sleep. In SAMs, we did not observe any tonic/dystonic or hypermotor patterns or stereotypy; motor arrest was present over the course of about half of the episodes. In comparison with both DOA and healthy subjects, SHE patients showed a higher number of sleep-related movements per night and a reduction of sleep efficiency. Significance: SPAs and SAMs present different semiological and clinical features. Their recognition could be useful to drive the diagnosis when major episodes are not recorded during VPSG in patients with a clear clinical history of SHE or DOA.
The role of childhood trauma in the development of borderline personality disorder (BPD) in young age has long been studied. The most accurate theoretical models are multifactorial, taking into account a range of factors, including early trauma, to explain evolutionary pathways of BPD. We reviewed studies published on PubMed in the last 20 years to evaluate whether different types of childhood trauma, like sexual and physical abuse and neglect, increase the risk and shape the clinical picture of BPD. BPD as a sequela of childhood traumas often occurs with multiple comorbidities (e.g. mood, anxiety, obsessive-compulsive, eating, dissociative, addictive, psychotic, and somatoform disorders). In such cases it tends to have a prolonged course, to be severe, and treatment-refractory. In comparison with subjects who suffer from other personality disorders, patients with BPD experience childhood abuse more frequently. Adverse childhood experiences affect different biological systems (HPA axis, neurotransmission mechanisms, endogenous opioid systems, gray matter volume, white matter connectivity), with changes persisting into adulthood. A growing body of evidence is emerging about interaction between genes (e.g. FKBP5 polymorphisms and CRHR2 variants) and environment (physical and sexual abuse, emotional neglect).
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