On “Polysomnography reveals unexpectedly high rates of organic sleep disorders in patients with prediagnosed primary insomnia” (Sleep Breath 2011 doi 10.1007/s11325-011-0608-8)

Abstract

Dear Editor, We read with interest the study by Tatjana Cronlein and co-workers [1] and congratulate the authors on the work. Their study adds nicely to the existing evidence that comorbidity is important in insomnia and should be taken into account while evaluating these patients [2–4]. In a recent study, which the authors unfortunately fail to acknowledge in their list of references, our group has investigated with polysomnography 20 patients with otherwise unexplained insomnia [5] who were compared to healthy controls and patients with idiopathic restless legs syndrome (RLS). These 20 CNS-active drug-free insomniac patients in our study had been attentively selected from 153 consecutive insomnia patients who fulfilled general criteria for insomnia according to ICSD 2 (similar to DSM 4 criteria for insomnia), after exclusion of RLS and other sleep, neurological, or psychiatric comorbidity, by both thorough history taking and polysomnographic evaluation. Interestingly, in that study, 60% of patients had periodic leg movements during sleep (PLMS) ≥10/h and fulfilled periodicity and time distribution through the night criteria similar or identical to patients with RLS [6]. It must be recognized that the exact contribution of PLMS in patients without RLS to insomnia is incompletely understood or controversially discussed [7, 8], and that the contribution of PLMS to cardiovascular risk is still hypothetical [9]. In addition, the diagnostic concept of periodic limb movement disorder, which has been developed to describe patients with insomnia and PLMS (among other criteria), is still strongly debated, as well as the question if PLMS should be treated in the absence of RLS (e.g., [10]). However, since PLMS can be found with a certain frequency also in normal controls aged above 40 years [11], the lack of a control group precludes Cronlein et al. [1] from proving a causative role of PLMS in their insomniac patients. Moreover, several of the patients with PLMS alone in their group were under antidepressant therapy with substances known to be able to induce PLMS [12]. Correctly, the authors reduced the dosage of these drugs in these patients. However, it is well known that insomnia and depression constitute a tight association. This casts additional doubts on the real role of PLMS in insomnia in these patients in whom they might have appeared only as a consequence of their therapy. Nevertheless, we agree with the authors that polysomnography is useful in patients with otherwise unexplained insomnia. Thus the authors are in line not only with our own study [5], but also with many others [2–4].