BackgroundAntibodies against gastrointestinal antigens may indicate altered microbiota and immune responses in the gut. Recent experimental data suggest a connection between gastrointestinal immune responses and CNS autoimmunity.MethodsAntibodies against gliadin, tissue transglutaminase (tTG), intrinsic factor (IF), parietal cells (PC) and Saccharomyces cerevisiae (ASCA) were screened in the sera of 45 patients with AQP4‐seropositive neuromyelitis optica (NMO) and NMO spectrum diseases (NMO/NMO‐SD), 17 patients with AQP4‐seronegative NMO, 85 patients with clinically definite multiple sclerosis (MS), and 48 healthy controls (HC).ResultsThirty‐seven percentages of patients with AQP4‐seropositive NMO/NMO‐SD and 28% of patients with MS had at least one particular antibody in contrast to 8% of HC (P < 0.01, respectively). Antibodies were most common (46%) in AQP4‐seropositive myelitis (P = 0.01 versus HS, P = 0.05 versus MS). Anti‐gliadin and ASCA were more frequent in the AQP4‐seropositive NMO‐spectrum compared to controls (P = 0.01 and P < 0.05, respectively).ConclusionAntibody responses against gastrointestinal antigens are common in MS and AQP4‐seropositive NMO/NMO‐SD, especially in longitudinally extensive myelitis.

BACKGROUND:The long-term effect of neuromyelitis optica (NMO) on the brain is not well established.METHODS:After 22 years of NMO, a patient's brain was examined by quantitative T1- and T2-weighted mono- and biexponential diffusion and proton spectroscopy. It was compared to 3 cases with short-term NMO and 20 healthy subjects.RESULTS:Although routine T1- and T2-weighted images appeared to be normal, quantitative T1-, T2- and diffusion-weighted magnetic resonance imaging identified areas with high diffusivity and altered relaxation time in 'normal appearing white matter' (NAWM). In such abnormal NAWM regions, biexponential diffusion analysis and quantitative spectroscopy indicated extracellular edema and axonal loss, respectively. Repeated analysis 6 months later identified the same alterations. Such patchy alterations were not detectable in the NAWM of the 3 cases with short-term NMO, and they were also not quantitatively different from the controls.CONCLUSION:After NMO of 22-year duration, metabolic changes, altered diffusivity and magnetic resonance relaxation features of patchy brain areas may suggest tissue damage in NAWM that persist for at least 6 months.

The authors report long-lasting airplane headache in a patient with non-allergic, chronic rhinosinusitis. Association of mucosal inflammation with compromised sinonasal ventilation and sinus barotrauma created a base for not only the pain but also for the prolongation of symptoms. Effective therapy with antihistamine and nasal decongestant supports the theory that sinonasal barotrauma plays a triggering role in the pathophysiology of airplane headache.

Short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT) is characterized by severe and frequent daily pain attacks causing transient physical disability for the patients during the headache period. Currently there is no option for abortive treatment of the attacks, mainly due to the short-lived nature and frequency of the repeated headaches, while highly efficacious therapy is also unavailable for short-term prevention. We report rapidly suppressed headache attacks with orally administered methylprednisolone in eight headache periods of three patients with idiopathic, episodic SUNCT syndrome. The remission was maintained until the period was over in all cases. Although the mechanism of methylprednisolone action is unclear, it is probably based on the anti-inflammatory effects of the drug.

Objective.—To determine whether migraineurs may have a systemic deficiency of magnesium.Background.—Magnesium deficiency has been shown to play a potential role in the pathogenesis of migraine, but there are no data on total body magnesium status in migraineurs.Methods.—An oral magnesium load test was performed by giving 3000 mg of magnesium lactate during a 24‐hour interictal period to 20 patients with migraine (15 women and 5 men; mean age, 37.9 years) and 20 healthy volunteers (16 women and 4 men; mean age, 39.6 years). Baseline and postload magnesium concentrations were determined from serum and 24‐hour urine specimens.Results.—There was no significant difference between the groups in the baseline serum and urine magnesium concentrations, although the latter tended to be lower (P = .064) in the migraine group. The postload magnesium concentrations were significantly higher within both the migraine (P < .0001 and P < .0001) and the control (P = .0009 and P < .0001) groups compared to the baseline values. After loading, the 24‐hour urinary magnesium excretions were significantly lower (P = .0007) in the patients with migraine than in the controls, but serum values did not differ.Conclusions.—Magnesium retention occurs in patients with migraine after oral loading, suggesting a systemic magnesium deficiency.