Background and Purpose-Lacunar stroke is associated with endothelial dysfunction and histologically with intrinsic cerebral microvascular disease of unknown cause. Endothelial dysfunction could impair blood-brain barrier integrity.We assessed background blood-brain barrier leakage in patients with lacunar ischemic stroke compared with cortical stroke controls. Methods-We recruited patients with lacunar or mild cortical ischemic stroke and assessed generalized cerebral blood-brain barrier leak with MRI and intravenous gadolinium at least 1 month after stroke. We used detailed image processing to compare signal change before and for 30 minutes postcontrast throughout gray matter, white matter, and cerebrospinal fluid with summary analyses and general linear modeling. Results-Among 48 patients (29 lacunar, 19 cortical), postcontrast enhancement was significantly higher in cerebrospinal fluid (Pϭ0.04, Mann-Whitney U), and nonsignificantly higher in white matter, in lacunar than in cortical strokes, with no difference in gray matter. General linear modeling confirmed significantly greater postcontrast enhancement in cerebrospinal fluid in lacunar patients than in cortical controls (tϭ3.37, PϽ0.0008). Conclusion-These preliminary data suggest that the blood-brain barrier may be dysfunctional throughout subcortical white matter (white matter drains via interstitial spaces to cerebrospinal fluid) in patients with lacunar stroke. Further studies are required to confirm these findings and determine whether abnormal blood-brain barrier might predate development of lacunar disease. Blood-brain barrier dysfunction may be an important mechanism for brain damage in cerebral microvascular disease.

Objective EMPOwER, a double-blind, randomised, phase 3 study, evaluated the efficacy and safety of erenumab in adults with episodic migraine from Asia, the Middle East, and Latin America. Methods Randomised patients (N = 900) received monthly subcutaneous injections of placebo, erenumab 70 mg, or 140 mg (3:3:2) for 3 months. Primary endpoint was change from baseline in monthly migraine days at Month 3. Other endpoints included achievement of ≥50%, ≥75%, and 100% reduction in monthly migraine days, change in monthly acute migraine-specific medication treatment days, patient-reported outcomes, and safety assessment. Results At baseline, mean (standard deviation) age was 37.5 (9.9) years, 81.9% were women, and monthly migraine days was 8.2 (2.8). At Month 3, change from baseline in monthly migraine days (primary endpoint) was −3.1, −4.2, and −4.8 days for placebo, erenumab 70 mg, and erenumab 140 mg, respectively, with a statistically significant difference for erenumab versus placebo (P = 0.002 [70 mg], P < 0.001 [140 mg]). Both erenumab doses were also significantly superior to placebo on all secondary endpoints, including the proportion of patients achieving ≥50% reduction from baseline in monthly migraine days, change from baseline in monthly acute migraine-specific medication treatment days and change from baseline in the Headache Impact Test-6™ scores. The safety profile of erenumab was comparable with placebo; no new safety signals were observed. Conclusions This study of erenumab in patients with episodic migraine from Asia, the Middle East, and Latin America met all primary and secondary endpoints. A consistent numerical benefit was observed with erenumab 140 mg versus erenumab 70 mg across all efficacy endpoints. These findings extend evidence of erenumab’s efficacy and safety to patients under-represented in previous trials. ClinicalTrials.gov identifier: NCT03333109

Axonal Guillain-Barré Syndrome (GBS) was first described by Feasby et al. in 1986, challenging the existent notion of GBS being a primarily demyelinating disease. The severe course and slow recovery commonly seen in these patients was ascribed to axonal degeneration. Other authors challenged this claim on several grounds. Amidst these controversies, epidemics of a similar illness were reported from China, which were given the acronym AMAN, having exclusive motor involvement in contrast to the cases already described in which both motor and sensory involvement were present (AMSAN). Pathologically, Wallerian degeneration, minimal lymphocytic response, absent demyelination or inflammation and periaxonal macrophages are prominent features. Ultrastructural studies have revealed node of Ranvier to be the prime target of immune attack. A frequent occurrence of antecedent Campylobacter jejuni infection and a strong association between elevated titres of IgG GM1 and axonal GBS on a background of preceding C. jejunii infection has been observed and molecular mimicry between lipopolysaccharides of C. jejuni and neural epitopes has been proposed as a mechanism of injury. Clinically axonal variant is similar to AIDP, but a more severe course, with frequent respiratory involvement, ventilator dependence and significant residue may be seen. Diagnosis is essentially electrophysiological. Treatment is similar to AIDP, preferential benefit of either IVIG or plasmapheresis needs to be further evaluated. A critical review of existing literature in axonal GBS is presented.

Objective: To seek evidence of potential embolic sources or other stroke mechanisms in patients who, on chance observation, had several apparently recent small subcortical infarcts on diffusion weighted magnetic resonance imaging (DWI). Methods: Patients presenting with stroke and multiple hyperintense subcortical infarcts visible on DWI were identified prospectively. Detailed clinical and radiological assessments were done independently and blinded to each other. Results: Of 10 patients with multiple hyperintense subcortical infarcts on DWI, a definite embolic source was identified in only one. Most patients were hypertensive and smoked. The DWI appearance suggested that the subcortical lesions had occurred within several weeks rather than at exactly the same time. Most patients also had significant white matter hyperintensities and four had microhaemorrhages. Conclusions: Embolic sources were not identified in most patients but they did have systemic vascular risk factors and brain imaging features of ''small vessel disease.'' A more generalised intrinsic process affecting many small cerebral vessels contemporaneously could explain multiple acute small subcortical infarcts. White matter hyperintensities, microhaemorrhages, and multiple small subcortical infarcts may share a common pathophysiological mechanism such as a diffuse cerebral microvascular abnormality which requires further exploration.A bout 25% of first ever in a lifetime ischaemic strokes are caused by lacunar or small subcortical infarction.

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Tension type headaches are common in clinical practice. Earlier known by various names, the diagnosis has had psychological connotations. Recent evidence has helped clarify the neurobiological basis and the disorder is increasingly considered more in the preview of neurologists. The classification, clinical features, differential diagnosis and treatment of tension type headache are discussed in this paper.

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