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Restless legs syndrome (RLS) is a sleep-related disorder defined by an urgency to move the legs, usually combined with uncomfortable or unpleasant sensations, which occurs or worsens during rest, usually in the evening or at night, and disappears with the movement of the legs. RLS can be classified as idiopathic or primary, and secondary to comorbid conditions (eg, renal disease, polyneuropathy). The pathophysiology of RLS is still unclear. This article provides an updated practical guide for the treatment of primary RLS in adults., Competing Interests: Disclosure The authors declare that they have no conflict of interest. This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Objective: Sometimes during surgery for meralgia paresthetica, it can be difficult to find the lateral femoral cutaneous nerve (LFCN). The aims of this study were to study the prevalence of different anatomical variations in patients, compare preoperative ultrasound (US) data with intraoperative findings, and investigate the effect of type of anatomical variation on duration of surgery and success rate of localizing the LFCN., Methods: Fifty-four consecutive patients with idiopathic meralgia paresthetica who underwent either a neurolysis or neurectomy procedure were included. All patients preoperatively underwent US of the LFCN. Anatomical variations were categorized into type A, B, C, D, and E using the classification of Aszmann and Dellon. The cross-sectional area of the LFCN at the inguinal ligament and the distance of the LFCN to the anterior superior iliac spine were noted. Correlations with intraoperative findings were investigated, as well as the effect on duration of surgery and success rate of finding the LFCN. Clinical outcome was assessed using the Likert scale., Results: The most frequent anatomical variant was type B (79%), followed by type C (9%), D (5%), and E (7%). No type A was encountered. Correlation between preoperative US and intraoperative findings was 100%. During surgery, the LFCN could be identified in all cases. Duration of surgery did not significantly vary for the different anatomical variants., Conclusions: Preoperative US is reliable in detecting anatomical variations of LFCN. This information can be very helpful in identifying the LFCN more frequently and easily during surgery, especially in more medial variants., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Background: There is still debate in the literature on the existence of the arcade of Struthers and moreover the potential role of this structure to cause compression of the ulnar nerve., Case Description: In this article we present a patient with ulnar neuropathy caused by a muscular arcade of Struthers, which was detected preoperatively using ultrasound. Symptoms completely recovered following decompression of the nerve by transection of this muscular arcade., Conclusions: This case demonstrates that a muscular arcade of Struthers can cause symptoms of ulnar neuropathy. Ultrasound in this case proved to be helpful in the preoperative workup, clearly demonstrating this unusual site of compression., (Copyright © 2020 Elsevier Inc. All rights reserved.)

This article provides an updated practical guide for the treatment of primary restless legs syndrome (RLS). Articles that appeared after the American Academy of Neurology guideline search were reviewed according to the same evidence rating schedule. We found limited evidence for nonpharmacologic treatment options. In moderate to severe primary RLS, pharmacologic options may be considered, including iron suppletion, an α2δ ligand, a dopamine agonist, a combination of an α2δ ligand and a dopamine agonist, or oxycodone/naloxone. This article includes treatment options in case of augmentation., (Copyright © 2020 Elsevier Inc. All rights reserved.)

This article provides an updated practical guide for the treatment of primary restless legs syndrome (RLS). Articles that appeared after the American Academy of Neurology guideline search were reviewed according to the same evidence rating schedule. We found limited evidence for nonpharmacologic treatment options. In moderate to severe primary RLS, pharmacologic options may be considered, including iron suppletion, an α2δ ligand, a dopamine agonist, a combination of an α2δ ligand and a dopamine agonist, or oxycodone/naloxone. This article includes treatment options in case of augmentation., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Objectives: Migraine is a suggested risk factor for aneurysmal subarachnoid hemorrhage (aSAH). An increased risk of aSAH in migraineurs may be explained by an increased prevalence of unruptured intracranial aneurysms (UIA). We performed a case-control study to compare lifetime migraine prevalence in patients with UIA, patients with a history of transient ischemic attact (TIA) or ischemic stroke and controls without a history of aSAH, TIA or ischemic stroke., Materials and Methods: Patients with UIA were recruited from two university hospitals. Data on patients with TIA/stroke were retrieved from a previous study. Partners of patients with UIA or TIA/stroke were included as controls. Migraine history was assessed via a telephone interview based on the International Classification of Headache Disorders, second edition criteria. We calculated odds ratios (OR) for migraine with univariable and multivariable logistic regression analyses, adjusted for age, sex, hypertension and smoking., Results: We included 172 patients with UIA, 221 patients with TIA or stroke, and 164 controls. In UIA patients, migraine prevalence was 24.4% compared with 14.6% in controls (UIA vs. controls; OR 1.9; 95% confidence interval [CI] 1.1-3.5) and 22.2% in TIA/stroke patients (UIA vs. TIA/stroke; OR 1.1; 95% CI 0.7-1.8). After adjustments, the OR for migraine in UIA patients versus controls were 1.7 (95% CI 1.0-3.1) and 0.9 (95% CI 0.5-1.0) versus TIA/stroke. Results were comparable for migraine with and without aura., Conclusions: Migraine prevalence is possibly increased in patients with UIA compared with controls and comparable with the prevalence in patients with TIA or stroke. Further studies are needed to confirm our findings and to investigate the underlying pathophysiology.

Objective: To determine the sensitivity, specificity and the positive and negative predictive value of taking a detailed sleep history for making the diagnosis of psychophysiological insomnia., Design: Retrospective case file study., Method: We examined 767 patients referred to the Amsterdam Centre for Sleep and Wake Disorders, and who underwent polysomnography for the first time between 1 January and 31 December 2010. We compared the probable diagnosis made following history-taking with the final diagnosis made after polysomnography. In this we differentiated between organic and non-organic insomnia. The sensitivity, specificity, positive and negative predictive values of the sleep history were calculated., Results: In 24.8% of the 303 patients whose histories did not indicate organic insomnia, polysomnography showed there to be an organic cause. Primary causes were obstructive sleep apnoea (13.2%), upper airway resistance syndrome (5.4%), and periodic limb movement disorder (4.0%) or a combination of these. In the histories of 464 patients there were indications that the insomnia had an organic cause and in 325 of them this was confirmed by polysomnography. The sensitivity of detailed history taking to psychophysiological insomnia was 62.1%, the specificity 81.3%, the positive predictive value was 75.2% and the negative predictive value was 70.0%. In patients under the age of 40 with a score on the Epworth sleepiness scale < 10 (i.e. no hypersomnolence), a BMI < 25 kg/m2 and indications of psychophysiological insomnia, organic insomnia could not be demonstrated, with the exception of one parasomnia., Conclusion: History-taking only meant that the organic cause was missed in a substantial percentage of patients with insomnia, in particular in older patients with hypersomnolence and a high BMI.

We report on a family with an autosomal dominant cerebellar ataxia in which we identified a novel mutation in exon 5 of the PRKCG/SCA14 gene that results in a Val138Glu substitution in the encoded protein PKCgamma. While most affected subjects displayed a late-onset uncomplicated form of spinocerebellar ataxia with occasional mild extrapyramidal features (such as postural tremor), one patient presented with a very mild nonprogressive ataxia since the age of 3 years and predominant multifocal myoclonus., ((c) 2006 Movement Disorder Society.)