Gülnihal Kutlu

Migraine is a primary headache disorder frequently accompanied by cranial autonomic symptoms, and recent reports have described cutaneous phenomena such as the “red forehead dot” and glabellar erythema, suggesting a link with localized autonomic dysfunction. We present two male patients with migraine who developed transient glabellar erythema during attacks. In the first case, unilateral erythema appeared during the peak of the migraine attack and resolved within 12–24 hours, whereas in the second case, symmetrical diffuse erythema involving both sides of the glabella were observed prior to headache onset and gradually regressed as the attack subsided. In both patients, neurological examination, laboratory tests, and cranial imaging were normal during the interictal period. These findings suggest that glabellar erythema may represent a rare manifestation of migraine-related autonomic dysfunction with variable distribution patterns. Recognition of this phenomenon may help prevent misdiagnosis and unnecessary diagnostic procedures.

Purpose Empirical evidence suggests that the duration of the Cutaneous Silent Period (CuSP) is significantly extended in pathological states such as Idiopathic Parkinson’s Disease (IPD), Restless Legs Syndrome (RLS), and dystonia, all of which are correlated with the degeneration of dopaminergic neurons. This neurodegenerative process is a critical factor in the etiology of Obstructive Sleep Apnea (OSA). In light of this active participation, the present study sought to assess the CuSP in patients with OSA. Methods A cohort comprising forty individuals diagnosed with OSA and forty healthy controls, all of whom underwent polysomnographic assessments, was incorporated into this investigation. The study meticulously analyzed the onset time, termination time, and duration of the CuSP in both median nerves utilizing electromyographic techniques. Results In the study examining the median nerve CuSP study, right and left CuSP was significantly prolonged in patients with OSA (p = 0.001, p < 0.001). Additionally, the onset time of the right and left CuSP was found to be shorter in the patient group (p = 0.017, p = 0.003). Conclusion The findings indicate that the duration of the CuSP is significantly prolonged in patients with OSA, similar to observations in IPD, RLS and dystonia. These results highlight the potential clinical relevance of CuSP duration as a biomarker for OSA-related neuronal alterations.

PurposeTo investigate corneal microstructural alterations in patients with trigeminal neuralgia using in vivo confocal microscopy and to compare these findings with healthy controls.MethodsIn this prospective, cross-sectional study, sixty patients with unilateral trigeminal neuralgia and sixty matched healthy controls underwent central corneal imaging using in vivo confocal microscopy. Images were obtained from all corneal layers. Quantitative analysis of the subbasal nerve plexus assessed corneal nerve fiber density (CNFD), corneal nerve fiber length (CNFL), and corneal nerve branch density (CNBD). Qualitative evaluation of epithelial morphology, dendritic cell density, stromal keratocyte activation, and endothelial features was performed. Associations between corneal findings and disease duration were analyzed.ResultsCompared with controls, trigeminal neuralgia patients demonstrated significant reductions in CNFD, CNFL, and CNBD (all p < 0.001), accompanied by increased nerve tortuosity, fragmentation, and focal nerve dropout. Dendritic cell density and anterior stromal keratocyte activation were increased, particularly in patients with longer disease duration, while posterior stromal layers and endothelial morphology remained preserved. Disease duration was independently associated with greater subbasal nerve loss and inflammatory changes.ConclusionsTrigeminal neuralgia is associated with significant neurodegenerative and inflammatory alterations of the cornea, primarily involving the subbasal nerve plexus. In vivo confocal microscopy provides a sensitive, non-invasive tool for detecting these changes and may aid in assessing disease severity and progression. To our knowledge, this is the first study to demonstrate disease duration-dependent multilayer corneal microstructural alterations in trigeminal neuralgia using in vivo confocal microscopy.

Epilepsy is a clinical condition characterized by increased excitability of cortical neurons in the brain. Electroencephalogram (EEG) detects the brain’s electrical activity and can reveal epileptogenic electrical foci. This study evaluated the relationship between interictal EEG (iiEEG) abnormalities and prognosis in newly diagnosed epilepsy patients with abnormal initial iiEEG. Patients were monitored with serial EEG recordings at 1, 3, 6, 9, and 12 months and classified into two groups based on seizure frequency. Group 1 (≥1 seizure/month) showed significant improvement in both seizure frequency and iiEEG findings over time. In Group 2 (

This study aimed to reduce alpha and beta brainwave power through external audio-visual stimulation (AVS) and to evaluate its clinical effect on anxiety levels, as measured by the State-Trait Anxiety Inventory (STAI), alongside electroencephalography (EEG) data. Thirty participants received AVS, while 12 received audio-visual white noise as a control. EEG recordings were obtained before, during, and after the stimulation. A digital FFT-based power spectrum analysis was performed, and raw sum values (sum of spectral line values) within defined frequency ranges were extracted. The STAI was administered to assess both trait and state anxiety. Statistical analysis was conducted using SPSS. In the AVS group, significant reductions in alpha and beta power were observed between the pre-, during-, and post-stimulation phases (p < 0.05). Comparison of pre- and post-STAI scores revealed a statistically significant decrease in anxiety levels within the AVS group (p < 0.001), with no similar effect observed in the control group. Audio-visual stimulation significantly reduced alpha and beta EEG power during exposure and led to a marked decrease in self-reported anxiety. These findings provide both neurophysiological and clinical support for the use of AVS as a nonpharmacological method to alleviate anxiety symptoms.