Background and purpose: To assess the anatomical distribution of the ischemic strokes of the brainstem, the effect of anatomical distribution on clinical features and prognosis, and the association between etiology and anatomical involvement. Methods: A retrospective search of the patient database of our institution was performed for a total of 227 patients who were admitted to the Department of Neurology, Medical Faculty of Bezmialem Vakif University between January 2012 and September 2014. Patients with adequate diagnostic data and 3-month follow-up visit were included in the study. Results: Twenty-one (9%), 136 (60%), and 65 (29%) patients had an infarction only at the mesencephalon, pons, and medulla, respectively. However, a single patient (0.5%) had an infarction both at the mesencephalon and pons, 3 (1.5%) at the pons and medulla, and 1 (0.5%) at the mesencephalon, pons, and medulla. While anterior involvement was more common in the mesencephalon and pons, posterior and lateral involvement occurred more frequently in the medulla. Large arterial atherothrombosis was the predominant cause of the strokes in all anatomical sites, particularly in infarcts involving the pons. Cardioembolic events were more common in patients with mesencephalic infarcts. Also, ischemia due to dissection was more common in infarctions involving the medulla, especially the lateral medulla. In subjects with simultaneous infarcts at other sites in addition to the brainstem, there was a significantly higher co-occurrence of medullary infarcts with cerebellar infarcts, mesencephalic infarcts with posterior cerebral artery infarcts, and pons infarcts with anterior circulation and multiple infarcts. Conclusion: Determination of risk factors and infarct localization as well as prediction of etiological parameters may assist in improving survival rates and therapeutic approaches.

Objective: Diabetic polyneuropathy is one of the most common complications of type 2 diabetes mellitus (DM) and represents a major cause of morbidity and impaired quality of life. This study aimed to investigate the associations between inflammation, oxidative stress, matrix metalloproteinases (MMPs), DNA damage, and the presence of distal symmetric diabetic polyneuropathy (DPNP) and diabetic neuropathic pain (DNP). Methods: A total of 108 patients with Type 2 DM and 42 healthy controls (HC) were enrolled prospectively. Diabetic patients were classified as having DPNP based on clinical and electrodiagnostic findings. DNP was evaluated using the Douleur Neuropathique 4 (DN4) questionnaire. Serum levels of interleukin-6 (IL-6), tumor necrosis factor- α (TNF- α ), interleukin-1β (IL-1β), MMP-2, MMP-9, MMP-10, Oxidative Stress Index (OSI), and DNA damage were measured. Results: Levels of IL-6, TNF-α, IL-1β, MMP-9, MMP-10, OSI, and DNA damage were significantly higher in diabetic patients compared with HC ( p < 0.001 for all). Among diabetic patients, all biomarkers except MMP-2 were significantly elevated in those with DPNP and DNP ( p < 0.001 for all). In diabetic patients, the levels of IL-6, TNF-α and IL-1β showed strong correlations with each other and with MMP-9 and OSI levels. Multivariable analysis demonstrated that the presence of DPNP was independently associated with increased levels of MMP-9, MMP-10, and OSI whereas the presence of DNP was independently associated with increased OSI levels. Conclusion: Inflammation, oxidative stress, and matrix metalloproteinase activation are strongly associated with DPNP and DNP in patients with Type 2 DM. Correlations among these parameters are consistent with the presence of an interconnected pathophysiological network. These findings provide additional insight into the complex pathophysiology of diabetic neuropathy.

Objective: Our objective was to describe morphologic features and longitudinal changes observed on high-resolution vessel wall imaging (HR-VWI) in a selected retrospective case series of patients evaluated for suspected inflammatory intracranial vasculopathy. Methods: This retrospective case series included patients who underwent 3T intracranial HR-VWI for suspected inflammatory intracranial vasculopathy. Clinical and imaging data were collected from medical records and imaging archives. Three radiologists reviewed baseline and follow-up examinations for vessel wall enhancement (VWE) pattern and grade, wall thickness, luminal narrowing, arterial distribution, diffusion-restricted lesions, and susceptibility-sensitive findings. Analyses were descriptive and patient-level. Each patient contributed one baseline and one final examination to longitudinal summaries; intermediate scans characterized individual trajectories only. Results: Nineteen patients were included, and 17 underwent serial HR-VWI. Median age was 46 years (IQR, 35.5–60.0 years), and 11 patients were female. Follow-up HR-VWI was available in 17 patients over a median of 391 days (IQR, 237–1819 days; range, 15–4034 days). VWE was present in all patients, with a purely concentric pattern in 15/19 (78.9%). The middle cerebral and internal carotid arteries were involved in 17/19 and 13/19 patients, respectively. Among the 17 patients with paired examinations, VWE grade decreased in 13 patients (76.5%) and remained stable in four patients (23.5%), with the median decreasing from 3.0 to 1.0. Maximum wall thickness decreased in 16 patients and remained stable in one, with the median changing from 2.0 mm to 1.4 mm. Conclusions: In this selected retrospective case series of patients evaluated for suspected inflammatory intracranial vasculopathy, 3T HR-VWI commonly demonstrated concentric VWE and provided descriptive longitudinal information regarding enhancement evolution. These findings should not be interpreted as evidence of diagnostic performance.

Introduction: Migraine is a highly disabling neurological condition with substantial variability in its clinical presentation. This study aimed to explore the influence of familial transmission of comorbid medical conditions on the phenotype of chronic and episodic migraine. Methods: A total of 500 patients who presented to a private tertiary headache clinic were categorized into episodic and chronic migraine groups based on the International Classification of Headache Disorders-3 criteria. Data on demographics, clinical symptoms, and familial medical history were collected. Statistical analysis included chi-square and independent sample t-tests to evaluate the impact of familial comorbidities on migraine phenotypes. Results: Of the participants, 63% were diagnosed with episodic migraine and 37% with chronic migraine. Significant findings included higher rates of medication overuse (63.31%) and allodynia (58.82%) in patients with chronic migraine. Notably, patients with a maternal history of hypercholesterolemia showed a higher prevalence of chronic migraine (78.6%), whereas those with both parents affected tended to have episodic migraine. Educational levels are inversely correlated with the prevalence of chronic migraine, suggesting a socioeconomic influence on migraine chronification. Discussion: This study highlights significant associations between familial health conditions and migraine phenotypes. The findings suggest that the maternal transmission of comorbidities, particularly hypercholesterolemia, may influence the development of chronic migraine. These results underscore the importance of considering familial medical history in the management and understanding of migraine.