The association between stroke and dementia is frequent. The prevalence of poststroke dementia (PSD) ranges from 6 to 32%, depending on the population studied, the criteria used for the diagnosis of dementia, and the time interval between the stroke and the neuropsychological assessment. The risk of PSD is high immediately after stroke and remains higher than in controls in stroke patients nondemented 3 months after stroke. Not all cases of PSD are vascular in origin, with about one third of demented patients diagnosed as having Alzheimer’s disease plus stroke. The pathophysiology of PSD is probably multifactorial, with an influence of vascular lesions, associated Alzheimer’s lesions and white matter changes. The risk of dementia is higher in older patients and in patients with preexisting cognitive decline – no dementia, severe stroke, a history of stroke, white matter changes and cerebral atrophy. The influence of stroke location, vascular risk factors and silent infarcts remains to be determined. PSD adversely influences the outcome in stroke patients.

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is characterized by a cerebral non-atherosclerotic, nonamyloid angiopathy mainly affecting the small arteries penetrating the white matter. In the brain vessels of two patients with CADASIL, abnormal patches of granular osmiophilic material have recently been described. Here we report the observation of similar granular osmiophilic material within the vessel walls of muscle and skin biopsies from a 54-year-old woman belonging to a CADASIL family, who suffered from subcortical dementia with leukoencephalopathy demonstrated on neuroimaging. Postmortem examination disclosed changes of the vessel walls in all the organs chiefly leading to cerebral lesions. Ultrastructural study showed destruction of the vascular smooth muscle cells (VSMC) and the granular osmiophilic material already found in muscle and skin biopsies in this patient. Both changes were found all along the arterial tree. The findings of this study indicate that CADASIL is a systemic vascular disease involving arterial VSMC and that the lesions are different in each organ and vessel wall, depending on their fine structure. Moreover, it emphasizes that skin and muscle biopsies might be useful for diagnosis of and research into CADASIL.

; for the ESO-KSU session participants* Abstract About the meeting: The purpose of the European Stroke Organisation (ESO)-Karolinska Stroke Update Conference is to provide updates on recent stroke therapy research and to give an opportunity for the participants to discuss how these results may be implemented into clinical routine. Several scientific sessions discussed in the meeting and each session produced consensus statements. The meeting started 20 years ago as Karolinska Stroke Update, but since 2014, it is a joint conference with ESO. Importantly, it provides a platform for discussion on the ESO guidelines process and on recommendations to the ESO guidelines committee on specific topics. By this, it adds a direct influence from stroke professionals otherwise not involved in committees and work groups on the guidelines procedure. The discussions at the conference may also inspire new guidelines when motivated. The topics raised at the meeting are selected by the scientific programme committee mainly based on recent important scientific publications. The ESO-Karolinska Stroke Update consensus statement and recommendations will be published every 2 years and it will work as implementation of ESO-guidelines Background: This year's ESO-Karolinska Stroke Update Meeting was held in Stockholm on 13-15 November 2016. There were 10 scientific sessions discussed in the meeting and each session produced a consensus statement (Full version with background, issues, conclusions and references are published as web-material and at http://www.eso-karolinska.org/2016 and http://eso-stroke.org) and recommendations which were prepared by a writing committee consisting of session chair(s), secretary and speakers and presented to the 312 participants of the meeting. In the open meeting, general participants commented on the consensus statement and recommendations and the final document were adjusted based on the discussion from the general participants. Recommendations (grade of evidence) were graded according to the 1998 Karolinska Stroke Update meeting with regard to the strength of evidence. Grade A Evidence: Strong support from randomised controlled trials and statistical reviews (at least one randomised controlled trial plus one statistical review). Grade B Evidence: Support from randomised controlled trials and statistical reviews (one randomised controlled trial or one statistical review). Grade C Evidence: No reasonable support from randomised controlled trials, recommendations based on small randomised and/or non-randomised controlled trials evidence.

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Background: Accumulating evidence from randomized-controlled clinical trials (RCTs) suggest that tenecteplase may represent an effective treatment alternative to alteplase for acute ischemic stroke (AIS). In the present systematic review and meta-analysis we sought to compare the efficacy and safety outcomes of intravenous tenecteplase to intravenous alteplase administration for AIS patients with large vessel occlusions (LVO). Methods: We searched MEDLINE and Scopus for published RCTs providing outcomes of AIS with confirmed LVO receiving intravenous thrombolysis with either tenecteplase at different doses or alteplase at standard dose 0.9mg/kg. The primary outcome was the odds of modified Rankin Scale (mRS) score of 0-2 at 3 months. Results: We included 4 RCTs including a total of 433 patients. Patients with confirmed LVO receiving tenecteplase had higher odds of successful recanalization (OR=3.05, 95%CI: 1.73-5.40; Figure A), mRS scores of 0-2 [odds ratio (OR)=2.06, 95%CI: 1.15-3.69; Figure B], and functional improvement defined as 1-point decrease across all mRS grades (common OR=1.84, 95%CI: 1.18-2.87; Figure C) at 3 months compared to patients with confirmed LVO receiving alteplase. There was little or no heterogeneity between the results provided from included studies regarding the aforementioned outcomes (I 2 ≤20%). No difference in the outcomes of early neurological improvement, symptomatic intracranial hemorrhage (ICH), any ICH and the rates of mRS 0-1 or all-cause mortality at 3 months were detected between patients with LVO receiving intravenous thrombolysis with either tenecteplase or alteplase. Conclusion: AIS patients with LVO receiving intravenous thrombolysis with tenecteplase have significantly better recanalization and clinical outcomes compared to patients receiving intravenous alteplase.

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The patient reported had had a continuous headache involving the whole skull for 7 years. Many drugs had failed to relieve the pain, but with indomethacin the headache completely disappeared within 3 days. Nine months later the treatment was discontinued without any relapse. This variety of headache, not previously reported, was quite similar to the "hemicrania continua" except for its localization.

Stroke patients have an elevated risk of developing long-term cognitive disorders or dementia. The latter is often associated with atrophy of the medial temporal lobe. However, it is not clear whether hippocampal and entorhinal cortex atrophy is the sole predictor of long-term post-stroke dementia. We hypothesized that hippocampal deformation (rather than atrophy) is a predictive marker of long-term post-stroke dementia on a rat model and tested this hypothesis in a prospective cohort of stroke patients.Male Wistar rats were subjected to transient middle cerebral artery occlusion and assessed 6 months later. Ninety initially dementia-free patients having suffered a first-ever ischemic stroke were prospectively included in a clinical study. In the rat model, significant impairments in hippocampus-dependent memories were observed. MRI studies did not reveal significant atrophy of the hippocampus volume, but significant deformations were indeed observed-particularly on the ipsilateral side. There, the neuronal surface area was significantly lower in ischemic rats and was associated with a lower tissue density and a markedly thinner entorhinal cortex. At 6 months post-stroke, 49 of the 90 patients displayed cognitive impairment (males 55.10%). Shape analysis revealed marked deformations of their left hippocampus, a significantly lower entorhinal cortex surface area, and a wider rhinal sulcus but no hippocampal atrophy. Hence, hippocampal deformations and entorhinal cortex atrophy were associated with long-term impaired cognitive abilities in a stroke rat model and in stroke patients. When combined with existing biomarkers, these markers might constitute sensitive new tools for the early prediction of post-stroke dementia.