Several medications do appear to possess the potential

Several medications do appear to possess the potential to induce or intensify RLS, including antiemetics, antipsychotics and antidepressants (tricyclic, serotonin reuptake inhibitors, selective noradrenergic–serotonergics) [9]. Amytriptiline chloride is a potent antidepressant with sedative and anticholinergic properties, acting by inhibiting the membrane pump mechanism responsible for the rock inhibitor and serotonin uptake by adrenergic and serotonergic neurons. It also shows, in less proportion, activity upon the blockage of dopamine reuptake, with possible psychomotor activation [12], this action being possibly related to the development of RLS. It is considered one of the drugs of first choice for the treatment of chronic pain, acting upon different nociceptive mechanisms. Some of its side effects include excessive sleepiness, insomnia, nightmares, paresthesias and extrapiramidal symptoms [3]. These effects might result in sleep disturbances. Establishing a relationship cause/effect between a clinical event and the use of a medication presents intrinsic difficulties, bearing in mind inespecificity and the superimposition of several factors. One way of establishing a causal relationship with higher security is the use of algorithms with diagnostic criteria for DAR, such as the probability scale of DAR according to Naranjo et al. [11]. In this system, a punctuation between 5 and 8 indicates a probable causality, establishing that the reaction follows a reasonable chronological sequence from the initial administration of the drug, with a previously know response and which cannot be totally explained by the clinical course of the patient [10,11].
Conclusion
Acknowledgements
Introduction In sleep related rhythmic movement disorder (RMD), the International Classification of Sleep Disorders Version 3 (ICSD3) [1] describes three typical subtypes (body rocking, head banging, and head rolling), and less common forms of body rolling, leg banging, and leg rolling. Vetrugno and Montagna [2] described in their review on RMD that the whole body or parts of it, such as the hands, arms, or legs, may also be rolled and rocked repetitively. However, involvement of the arms or hands in RMD has not been described by the ICSD3 [1]. In addition, to our knowledge, no precise description on RMD of arm banging type has been found. We here describe a 2-year-old male patient who performed arm banging on his face during sleep every night since 7 months of age.
Patient׳s medical reports Our patient was an otherwise healthy first boy from healthy non-consanguineous parents. Except for his mother, family history is not remarkable. His mother has been of recurrent episodes of involuntary eating and drinking during arousals from sleep, associated with diminished levels of consciousness and subsequent recall since her twenties. She is not diagnosed as having sleep related eating disorder [1], because she has no problematic consequences of these episodes. The boy was born at 40 gestational weeks, and weighed 3725g after an uneventful pregnancy. Since 7 months of age, he has exhibited arm banging on his face every night. An electroencephalogram (EEG) performed at a university hospital showed no abnormal findings. The banging usually involves each side of his arm, but sometimes occurs bilaterally simultaneously. He hit his face with the fist or the palm of his each arm. Because this banging resulted in hitting his face or even his eyes, his parents watched him, and prevented him from hitting himself by putting their arm in front of his face. This has caused sleep deprivation in the parents. When he was 23 months of age, EEG recording with video recording was performed from 19:40 to 2:01 at another university hospital. We succeeded in obtaining video recordings of three episodes at 21:53 (80s), 23:14 (110s), and 0:05 (110s). Each episode composed of banging of 1–2Hz without accompanying epileptic discharges. The first episode appeared to begin from sleep stage 1 (N1) and the sleep stage appeared to return to N1 after the episode. The sleep stage just before the second episode was N3 (Fig. 1) and the sleep stage after the episode appeared to be N1 (Fig. 2). The EEG recording before and after the third episode was insufficient to determine the sleep stage. No abnormal findings were obtained on this EEG recording. No snoring was observed. Laboratory examinations and magnetic resonance imaging of his brain showed no obvious abnormalities.