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Objective: Osmotic demyelination syndrome has been reported in patients with end-stage renal disease, but the specific MRI findings in this patient group have not been documented in detail. Our aims were to present the brain MRI findings during an episode after hemodialysis and at follow-up, and to identify possible factors that may contribute to lesion development., Materials and Methods: Seventeen patients with osmotic demyelination syndrome who had undergone hemodialysis at least once and had brain MRI examinations were retrospectively reviewed. Neurologic and MRI examinations were performed during a clinical episode. Serum levels of sodium, creatinine, blood urea nitrogen, and glucose were assessed, and serum osmolality and the ratio of blood urea nitrogen to creatinine (BUN:Cr) were calculated. Follow-up MRI was performed in nine cases. Laboratory and imaging findings were evaluated., Results: An altered level of consciousness and convulsions were the most common neurologic symptoms. The pons was involved in 11 patients (65%) and extrapontine sites in 12 (71%). Four patients had dysequilibrium syndrome. Follow-up MRI showed complete resolution in six patients and lesion reduction in three within a short time. The most common biochemical changes at the time of MRI were hyponatremia and low BUN:Cr in the blood. Only one patient showed rapid correction of hyponatremia and a rapid change in osmolality during the acute stage., Conclusion: In patients who develop osmotic demyelination syndrome after hemodialysis, the lesions may involve the pons or the pons and extrapontine sites. Most lesions that were followed up resolved rapidly and almost completely, favoring transient edema rather than demyelination. Blood chemistries suggested underlying changes in osmolality, particularly as a result of urea shift from the extracellular fluid.

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To evaluate the effects of interferon beta-1a(INFβ-1a) on brain metabolites in patients with multiple sclerosis (MS), we performed Magnetic Resonance Spectroscopy Imaging (MRSI) on five patients treated with INFβ-1a (Rebif 44 μg), and on five untreated patients. Six healthy volunteers were used as controls. Patients were evaluated at the beginning, in the first, third, sixth, and twelfth month. There were no significant differences in normal appearing white matter (NAWM) metabolite peaks of the control group and patients with MS. However, in white matter lesions (WML) and NAWM there was significant differences between the basal and the other months' metabolic peaks (p < 0.05) in the treatment group although no differences emerged in the untreated group. These data suggest that INFβ-1a has a favorable effect on restoration of metabolites in MS lesions. [ABSTRACT FROM AUTHOR]

The article presents a case study of a 43-year-old woman admitted to gynecology with metrorrhagia. It mentions that cervical cancer was diagnosed and radical hysterectomy with lymph node dissection was performed. Topics discussed include usefulness of leucovorin and anti-inflammatory agents, treatment of overdose of intrathecal methotrexate by dilution and removal from the cerebrospinal fluid with specific antidotal therapy and discontinuation of intrathecal methotrexate treatment.

Aim To compare the relationship between white matter hyperintensities (WMH) on brain magnetic resonance imaging and retinal nerve fiber layer (RNFL), choroid, and ganglion cell layer (GCL) thicknesses in migraine patients and healthy subjects. We also assessed the role of cerebral hypoperfusion in the formation of these WMH lesions. Methods We enrolled 35 migraine patients without WMH, 37 migraine patients with WMH, and 37 healthy control subjects examined in the Neurology outpatient clinic of our tertiary center from May to December 2015. RFNL, choroid, and GCL thicknesses were measured by optic coherence tomography. Results There were no differences in the RFNL, choroid, or GCL thicknesses between migraine patients with and without WMH ( p > 0.05). Choroid layer thicknesses were significantly lower in migraine patients compared to control subjects ( p < 0.05), while there were no differences in RFNL and GCL thicknesses ( p > 0.05). Conclusions The 'only cerebral hypoperfusion' theory was insufficient to explain the pathophysiology of WMH lesions in migraine patients. In addition, the thinning of the choroid thicknesses in migraine patients suggests a potential causative role for cerebral hypoperfusion and decreased perfusion pressure of the choroid layer. [ABSTRACT FROM AUTHOR]

Objective: This study evaluated the association between hypoxia parameters with white matter hyperintensity (WMH) and silent cerebral infarcts (SCI) on brain magnetic resonance (MR) images of patients with obstructive sleep apnea (OSA). Methods: In this retrospective study, the study group was composed of 453 patients who were evaluated by overnight polysomnography (PSG). Data on hypoxia parameters, such as total sleep duration with oxygen saturation < 90% (ST90), percentage of cumulative time with oxygen saturation < 90% (CT90), and the lowest oxygen saturation (min SaO2), were obtained from PSG. The presence of WMH and SCI was evaluated in all participants using brain MR images. Results: Hypoxia parameters, such as ST90, CT90, and min SaO2, were significantly associated with WMH (P < 0.001). The multiple regression analysis showed that CT90 was independently associated with SCI (P = 0.038). In addition, when participants were divided into two groups according to CT90 < 10% and CT90 = 10%, age (P = 0.002), sex (P = 0.015), body mass index, Apnea-Hypopnea Index score, Epworth Sleepiness Scale score, and the presence of WMH, hypertension, and diabetes mellitus were significantly higher in the CT90 ≥ 10% group compared with the CT90 < 10% group (P < 0.001 for all parameters). CT90 ≥ 10% increased the risk of WMH 2.34-fold (95% confidence interval, 1.44-3.85; P = 0.006). Conclusion: The severity of nocturnal intermittent hypoxia may contribute to the pathogenesis of WMH and SCI in patients with OSA. Amaç: Çalışmanın amacı obstruktif uyku apne sendrom'lu (OSA) olgularda hipoksi parametreleri ile beyin manyetik rezonans görüntülemede saptanan beyaz cevherde hiperintens odaklar (WMH) ve sessiz serebral infarkt (SCI) ile ilişkisini değerlendirmek. Metod: Bu retrospektif çalışmada tüm gece polisomnografi yapılmış toplam 453 olgu alındı. Hipoksi parametreleri toplam uyku süresinde oksijen saturasyonun %90'nın altında kaldığı süre (ST90), ST90'nın toplam uyku süresine oranı (CT90) ve en düşük oksijen saturasyonu (minSaO2) polisomnografiden (PSG) elde edildi. Tüm olguların beyin manyetik rezonans görüntülemerinde WMH ve SCI varlığı değerlendirildi. Bulgular: Hipoksi parametreleri ST90, CT90 ve min SaO2 WMH varlığı ile anlamlı ilişkiliydi (P < .001). Multipl regresyon analizinde CT90 bağımsız olarak SCI ile birlikteydi (P = 0.038). İlave olarak, katılımcılar CT90 < %10 ve CT90 ≥ %10 olarak iki gruba ayrıldığında, CT90 ≥ %10 grubunda yaş (P = .002), cinsiyet (P= .015), vücut kitle indeksi, apne-hipopne indeksi, Epworth uykululuk ölçeği, WMH varlığı, hipertensiyon ve diabetes mellitus CT90 < %10 grubuna oranla anlamlı olarak daha yüksekti (P < .001, tüm parametrelerde). CT90 ≥ %10 olması WMH riskini 2.34 kat (95% CI 1.44 to 3.85, P= 0.006) arttırmaktadır. Sonuç: OSA'de nokturnal intermittent hipoksi şiddeti WMH ve SCI patogenezine katkı sağlıyor olabilir. [ABSTRACT FROM AUTHOR]