Objectives: The objectives of this study were to compare the results of pharmacologic management options and vestibular rehabilitation (VR) programs in the context of dizziness, balance problems, and headache in patients with vestibular migraine. Materials and Methods: Sixty patients with migraine with vestibular symptoms were evaluated in three groups in the neurology, physical medicine, and rehabilitation and otorhinolaryngology clinics of a medical school hospital. The groups were defined as routine pharmacologic therapy (PT), VR, or both. Patients were evaluated with static posturography, the Dizziness Handicap Inventory (DHI), and the Activities-Specific Balance Confidence (ABC) Scale as primary outcome measures and symptom frequency and severity (headaches and vertigo attacks) as secondary outcome measures. In-group and between-group comparisons were made using relevant statistical methods. Results: DHI scores were significantly reduced (P < 0.001) in all treatment groups. ABC scores increased significantly (P < 0.001) in patients taking PT and those on VR + PT. Posturographic examinations revealed that sway velocity values recorded on foam with eyes closed, which targets vestibular assessment, were significantly reduced (P < 0.001) in groups taking VR either alone or with PT. VR benefited patients with migraine in terms of headaches, vertigo attack frequency, intensity, and duration. Conclusion: Patients with predominant vestibular disorders can benefit from VR alone, and patients with combined symptoms (headache and vertigo) can benefit from pharmacologic and rehabilitation therapies.

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Cutaneous silent period (CSP) is the temporary suppression of voluntary muscle contraction by sensory stimulation. Here, we aimed to summarize the effect of physiological and pathological conditions on CSP and to reappraise its clinical utility in daily practice. We performed a literature search using the term “cutaneous silent period.” The search included all articles published in English in the PubMed, Cochrane Library, Google Scholar, and MEDLINE databases until October 2018. We have analyzed all articles covering CSP to collect the work on physiological conditions such as temperature, recording site, stimulus intensity, nonpharmacological interventions, and different medications or pathological conditions. Temperature, gender, recording site, stimulus duration, and stimulus intensity affect the parameters related to CSP. CSP onset latency is mainly affected by interventions affecting A-delta fibers. CSP shows changes in entrapment neuropathies and polyneuropathies. CSP is mainly mediated by A-delta fibers with contribution of large-diameter fibers. It is a spinal inhibitory response. It should be recorded under optimum temperature. Its clinical use in the diagnosis or assessment of neuropathic pain is limited. It is sometimes used to show functions of A-delta fibers.

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Objective: This study aimed to evaluate primary headache disorders and other causative comorbidities (e.g., epilepsy, atopic disorders, recurrent abdominal pain, motion sickness, and headache) in children with tic disorders (TDs) and their mothers. Materials and Methods: In a multi-center, cross-sectional, familial association study using case–control design, youth (between 7 and 17 years) with TDs (TD, as per Diagnostic and Statistical Manual of Mental Disorders-5 criteria) and age- and sex-matched healthy controls and their mothers were evaluated in the aspect of functional syndromes spectrum including migraine, epilepsy, atopic disorders, motion sickness, and recurrent abdominal pain. Results: Seventy-nine youth with TD and 101 controls were included. Causative comorbidities, other than epilepsy and motion sickness were more common in children with TD with an odds ratio (OR) of 2.1 (atopy) and 3.9 (food allergy). Specifically, recurrent abdominal pain and migraine were found in 36.7% and 31.7% of children (vs. 18.8% and 16.8% of controls, ORs 2.5 and 2.3, respectively). Mothers of youth with TDs also have higher rates of atopy, drug allergy and allergic dermatitis (ORs; 3.8, 3.2 and 2.1; respectively). Conclusion: Results of recent studies suggest a possible link between atopic disorders, migraine, recurrent abdominal pain and TDs. Our results contribute to those studies and suggest that this relationship may extend to the mothers of children as well.

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Context: This was an investigation of inflammation markers on the prediction and prognosis of patients with sleep apnea. Aims: Clinical detection of inflammatory markers is useful to assess systemic inflammation in patients with obstructive sleep apnea syndrome (OSAS). The aim of the study was to evaluate whether the lymphocyte-to-C-reactive protein (CRP) ratio (LCR) was a predictive marker in diagnosing and determining the severity of OSAS. Settings and Design: This was a retrospective clinical study. Subjects and Methods: One hundred and forty-one patients who had undergone polysomnography were included in the study. The sex, age, Apnea–Hypopnea Index (AHI), body mass index, and complete blood count parameters of the patients were recorded. AHI scores were used to classify the severity of OSAS. Statistical Analysis Used: Differences among the groups for each parameter were analyzed using Student's t-test and one-way analysis of variance with Tukey correction for normally distributed parameters and the Mann–Whitney U test and Kruskal–Wallis test for nonnormally distributed parameters. The correlation between LCR, neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio, CRP, and AHI scores was assessed using Pearson's correlation coefficient. Results: First, the patients were divided into four groups according to their AHI results, as control group, mild, moderate, and severe OSAS groups. The median LCR levels were 2.57 (1.59, 3.51) in the control group, 1.28 (0.74, 3.27) in Group 2, 1.63 (0.86, 2.6) in Group 3, and 1.05 (0.62, 2.31) in Group 4. In the comparison of all patients with OSAS and the control group, the median LCR level was 1.27 (0.7, 2.74) in patients with OSAS and 2.57 (1.59, 3.51) in the control group (P = 0.002). Conclusions: This study demonstrated that LCR is an important marker for systemic inflammation in patients with OSAS. LCR may be a new predictive marker in the diagnosis and prognosis of patients with OSAS.

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Trigeminal neuropathy is an infrequent condition, usually limited to the sensorial component of the nerve, and it is one of the most common neurologic manifestations of mixed connective tissue disease (MCTD). However, to the best of our knowledge, no cases have been reported with MCTD presenting as trigeminal sensory and motor neuropathy. Herein, we report a 28-year-old female with unilateral trigeminal sensory–motor neuropathy who presented with numbness over the distribution of the right trigeminal region and right masseter atrophy. We also reviewed the literature for trigeminal neuropathy associated with MCTD.

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Objectives: Several large-scale genome association studies have shown that variants in the “Clusterin”' (CLU) gene are important risk factors for Alzheimer's disease (AD). It has also been shown that plasma CLU levels were elevated in patients with AD and associated with disease severity and progression. In this study, we aimed to investigate whether the CLU rs11136000 polymorphism was associated with AD in our cohort of Turkish patients. We also evaluated the association of serum CLU levels and rs11136000 genotypes between patients and controls. Materials and Methods: Genotyping was performed in 327 patients who were diagnosed as having AD (mean age: 67.2 ± 10.8 years) and 344 controls (mean age: 57.7 ± 13.1 years). The rs11136000 genotypes were determined using quantitative real-time polymerase chain reaction with hydrolysis probes. Serum CLU levels were assessed in 25 patients with AD and 10 controls using enzyme-linked immunosorbent assay. Results: Our results showed no significant difference in genotype and allele frequencies of CLU rs11136000 polymorphisms between patients with AD and controls. Serum CLU levels in patients with AD did not differ from those of the controls. Furthermore, serum CLU levels showed no major difference between carriers of CC and TT + CT genotypes in the controls and patients with AD. Conclusion: Our results suggest that the CLU rs11136000 polymorphism is not associated with AD in our Turkish patients, and rs11136000 genotypes may not have an effect on serum CLU levels.

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Objectives: In this study, we aimed to compare the neutrophil/lymphocyte ratio (NLR) levels of migraine patients with and without gliotic lesions on brain magnetic resonance imaging (MRI). Materials and Methods: The records of the patients who were followed up in the neurology outpatient clinic of Ufuk University, Faculty of Medicine, between 2016 and 2019 with the diagnosis of migraine between the ages of 18 and 50 were reviewed retrospectively. Eighty-six patients without systemic, neurological, and infectious diseases between 18 and 50 years of age were included in the study. Patients were divided into two groups: Group 1 – subclinical ischemic/gliotic lesions on MRI and Group 2 – normal MRI. Subparameters and calculated NLRs in whole blood results were compared between the two groups. Results: When the two groups were compared in terms of leukocyte and neutrophil counts, a statistically significant difference was found. The leukocyte and neutrophil counts of the patients in Group 1 were significantly higher than those of Group 2 (P = 0.038/P = 0.004). NLR was higher in patients with gliotic lesions on MRI than in patients with normal MRI and was statistically significant (P = 0.016). Conclusion: This study aimed to evaluate the relationship between NLR and white matter lesions in patients with migraine. We have conducted this study to see if we can confirm this with a parameter in migraine patients with white matter lesions. Despite the small number of patients, leukocyte count, neutrophil count, and NLR were significantly higher in migraine patients with white matter lesions which support our hypothesis.

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Objective: Anti-neuronal antibodies are found in sera of neuro-Behçet's disease (NBD) patients. In this study, our aim was to analyze the potential mechanisms by which NBD immunoglobulin (Ig) Gs affect neuronal dysfunction. Materials and Methods: Purified IgGs obtained from pooled sera of six each NBD patients and healthy controls (HCs) were administered to Sprague Dawley rats through intraventricular injection. Control rats received phosphate-buffered saline (PBS) only. Locomotor activity was assessed by open field test on days 0, 10, and 25. Cerebral expression levels of intracellular pathway factors associated with cell survival and viability were measured by real-time polymerase chain reaction. Results: Rats treated with NBD IgG exhibited reduced motor activity. On day 25, the mean number of crossings was 44 ± 7, 90 ± 12, and 93 ± 5 and the mean number of rearings was 18 ± 7, 34 ± 5, and 35 ± 6 for NBD IgG, HC IgG, and PBS groups, respectively (P < 0.001). Relative expression levels of Akt-1 (0.4 ± 0.2, 1.0 ± 0.3, and 0.9 ± 0.6; P = 0.004), DJ-1 (0.6 ± 0.2, 1.0 ± 0.6, and 0.9 ± 0.5; P = 0.047), mouse double mininute-2 (0.5 ± 0.3, 0.9 ± 0.2, and 1.0 ± 0.2; P = 0.002), and mechanistic target of rapamycin (0.4 ± 0.2, 0.8 ± 0.4, and 0.9 ± 0.6; P = 0.006) were significantly lower in NBD-IgG group than HC IgG and PBS groups. By contrast, the expression levels of factors associated with apoptosis (caspase 3, mitochondrial carrier homolog 1, and B-cell lymphoma-2) were comparable among different treatment arms. Conclusion: Our results suggest that at least a fraction of NBD IgG interacts with neuronal surface antigens and subsequently decreases neuronal viability through Akt pathway inhibition. By contrast, NBD IgG does not appear to activate neuronal apoptosis. Further identification of the binding sites of serum IgG ıs required.

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