Migraine is a destabilizing neuroinflammatory disorder characterized by recurrent headache attacks. Evidences show tumor necrosis factor (TNF)-α play a role in neuroimmunity pathogenesis of migraine. TNF-α increase prostanoid production, hyperexcitability of neurons, and nociceptor activation resulted in neuroinflammation and neurogenic pain. ω-3 fatty acids and curcumin exert neuroprotective and anti-inflammatory effects via several mechanisms including suppression of TNF-α gene expression and its serum levels. The aim of this study is an evaluation of synergistic effects of ω-3 fatty acids and nano-curcumin on TNF-α gene expression and serum levels in migraine patients. The present study performed as a clinical trial over a 2 month period included 74 episodic migraine patients in 4 groups and received ω-3 fatty acids, nano-curcumin, and combination of them or placebo. At the start and the end of the study, the gene expression of TNF-α and TNF-α serum levels was measured by real-time PCR and ELISA method, respectively. Our results showed that the combination of ω-3 fatty acids and nano-curcumin downregulated TNF-α messenger RNA (mRNA) significantly in a synergistic manner (P < 0.05). As relative to gene expression, a significant greater reduction in serum levels of TNF-α were observed in the combination group, but no significant differences in other groups. Supplementation with ω-3 fatty acids or nano-curcumin alone did not show significant reduction either in mRNA or serum levels of TNF-α. In addition, a much greater reduction in attack frequency was found in the combination group (P < 0.001). These findings indicated that ω-3 fatty acids and curcumin supplementation can be considered as a new promising approach in migraine management.

This study showed that the DASH diet is associated with lower headache severity and duration in migraine patients.

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The independent inverse association of AQI with 25(OH)D explains the high prevalence of vitamin D deficiency in children in Isfahan. Dietary intake of vitamin D was not sufficiently low to explain the very low level of serum 25(OH)D. In regions with plenty of sunlight, air pollution should be considered to be a factor in the causation of hypovitaminosis D.

Ependymomas are glial tumors derived from ependymal cells lining the ventricles and the central canal of the spinal cord. Two thirds of ependymomas arise in the infratentorial or intraventricles, whereas one-third are located in supratentorial space. But supratentorial “cortical” ependymomas are very rare. We report a case of a cortical ependymoma in a 17-year-old boy. The patient presented with transient recurrent right weakness and diplopia. This tumor was located in the left parieto-occipital region and he had gross total excision. Microscopy and immunohistochemistry showed grade III differentiation ependymoma.

Background: Guillain-Barre syndrome (GBS) is an autoimmune acute inflammatory demyelinating polyneuropathy usually elicited by an upper respiratory tract infection. Several studies reported GBS associated with coronavirus-2019 (COVID-19) infection. In this study, we describe nine GBS patients following the COVID-19 vaccine. Methods: In this study, nine patients introduce from six referral centers of neuromuscular disorder in Iran between April 8 and June 20, 2021. Four patients received the Sputnik V, three patients administrated the Sinopharm, and two patients received the AstraZeneca vaccine. All patients were diagnosed with GBS, including nerve conduction studies and/or cerebrospinal fluid analysis. Results: The median age of the patients was 54.22 years (range, 26-87 years), and seven patients were male. The patients were treated with intravenous immunoglobulin (IVIg) or plasma exchange (PLEX). All patients were discharged with some improvement. Conclusion: The link between the COVID-19 vaccine and GBS is not well understood. Given the prevalence of GBS in the general population, this association may be coincidental. Therefore, more studies are needed to investigate a causal relationship.

The autoimmune disease myasthenia gravis (MG), can mimic a variety of neurological disorders leading to a delay in diagnosis and treatment. On occasions, misdiagnosis of MG could lead to unnecessary therapeutic interventions. We report the case of a 50 year-old man, in whom MG was mistaken for motor neuron disease (MND). Subsequently, correct diagnosis and optimal management resulted in saving his life and significant improvement in his functional status. We discuss the importance of considering MG as one of the potential differential diagnoses among cases of new onset or recurrent unexplained bulbar symptoms, despite exaggerated deep tendon reflexes. Also, a literature review on the misdiagnosis of MG and the potential pitfalls in MG diagnosis are discussed.

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