BackgroundMigraine is a common headache disorder that may be associated with vascular disease and cerebral white matter hyperintensities (WMHs) on magnetic resonance imaging (MRI) scan. High sensitivity C-reactive protein (hs-CRP) is a marker of inflammation that may predict subclinical atherosclerosis. However, the relation between migraine, vascular risks, and WMHs is unknown. We evaluated hs-CRP levels and the relation between hs-CRP level and WMHs in adult migraine patients.MethodsThis case–control study included 432 subjects (216 migraine patients [without aura, 143 patients; with aura, 73 patients]; 216 healthy control subjects without migraine; age range 18–50 y). Migraine diagnosis was determined according to the International Classification of Headache Disorders II diagnostic criteria. The migraine patients and control subjects had no known vascular risk factors, inflammatory disease, or comorbid disease. The presence and number of WMHs on MRI scans were determined, and serum hs-CRP levels were measured by latex-enhanced immunoturbidimetry.ResultsMean hs-CRP level was significantly greater in migraine patients (1.94 ± 2.03 mg/L) than control subjects (0.82 ± 0.58 mg/L; P ≤ .0001). The mean number of WMHs per subject and the presence of WMHs was significantly greater in migraine patients (69 patients [31.9%]; 1.68 ± 3.12 mg/dL) than control subjects (21 subjects [9.7%]; 0.3 ± 1.3; P ≤ .001). However, there was no correlation between hs-CRP level and WMHs in migraine patients (r = 0.024; not significant). The presence of WMHs was increased 4.35-fold in migraine patients (odds ratio 4.35, P ≤ .001).ConclusionsHigh hs-CRP level may be a marker of the proinflammatory state in migraine patients. However, the absence of correlation between hs-CRP level and WMHs suggests that hs-CRP is not causally involved in the pathogenesis of WMHs in migraine patients. The WMHs were located mostly in the frontal lobe and subcortical area.

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These data suggest that increased hypoxia severity may mediate increased inflammation and activation of platelets and contribute to the pathogenesis of WMH in patients with OSA. In addition, patients with severe OSA may show significant variability in inflammation and vascular risk. Further prospective data are needed.

Guillain-Barré syndrome (GBS) is an acute inflammatory demyelinating peripheral nerve disorder. It is known that gadolinium enhancement on magnetic resonance imaging (MRI) reflects alteration of the blood-nerve barrier secondary to inflammation. Enhancement of the cauda equina roots with gadolinium on lumbosacral magnetic resonance imaging have been demonstrated in several reports. Although about 50% of GBS patients clinically exhibit facial nerve involvement, it has never been demonstrated on MRI. We aimed to observe facial nerve involvement in a GBS patient who has prominent facial diplegia. With the guidance of the literature, we predict that MRI in selected GBS patients may be an adjunct tool for the clinician in both diagnosis and monitoring the treatment response.

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Guillain-Barré syndrome (GBS) is an acute inflammatory polyneuropathy which follows a precipitating event in approximately two thirds of cases. Although its pathogenesis is unclear, it is likely to be a consequence of an immune-mediated process. In the literature there are three case reports of GBS following subarachnoid hemorrhage, subdural hematoma, and facial bone fracture after head trauma.The unique feature of our case with GBS after subdural hematoma is the presence of cerebellar symptoms. We believe that GBS results from an aberrant immune response following trauma that somehow mistakenly attacks the nerve tissue of its host, and we discuss the effects of the trauma of head injury on cellular and humoral immunities and the absence of antiganglioside antibody (anti-GD1b IgG, which is accused of ataxia and cerebellar symptoms) in this case report.

Amaç: Migren inflamasyon ve vasküler hastalıklar ile ilişkili olabilen yaygın bir baş ağrısı türüdür. Biz genç erişkin migren hastalarında C-reaktif protein ve periferik kandaki bağışıklık hücre sayısını değerlendirdik. Hastalar ve Yöntem: Bu olgu-kontrol çalışması, 260 migren hastası (aurasız, 169 olgu, auralı, 91 olgu) ve 260 sağlıklı kontrol katılımcı (yaş aralığı, 18-50 yıl) olmak üzere 520 kişiyi içermektedir. Katılımcıların hiçbirinde bilinen bir anemi, vasküler risk faktörü veya inflamatuar hastalık yoktu. Migren ve kontrol olgularında serum C-reaktif protein ve tam kan sayımı parametrelerini değerlendirdik. Bulgular: C-reaktif protein, lökosit, nötrofil, lenfosit, trombosit sayıları ve ortalama trombosit hacmi migren hastalarında kontrol grubuna (P <0.001) oranla anlamlı olarak farklıydı. Ancak bu parametreler, C-reaktif protein hariç, auralı ve aurasız migrenlerde benzerdi. Lojistik regresyon analizinde migren hastalığı C-reaktif protein seviyesi (OR, 2.36; 95% CI, 1.73 ile 3.23; P< 0.001), ortalama trombosit hacmi (odds ratio [OR], 2.32; 95% confidence interval [CI], 1.78-3.0; P<0.001), ve lökosit sayısı (OR, 1.61; 95% CI, 1.32-1.94; P< 0.001) ile anlamlı olarak ilişkiliydi. Sonuç: Periferik inflamasyonun artmış seviyeleri migren hastalarında ortaya çıkabilir ve migren patogenezinde rol oynayabilir.

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