Vascular cognitive impairment (VCI) is the second most common type of dementia after Alzheimer's disease (AD). Stroke and cardiovascular risk factors have been linked to both AD and VCI and potentially can affect cognitive function in mid and later life. Various pharmacological agents, including donepezil, galantamine, and memantine, approved for the treatment of AD have shown modest cognitive benefits in patients with vascular dementia (VaD). However, their functional and global benefits have been inconsistent. Donepezil has shown some cognitive benefit in patients with VaD only, and galantamine has shown some benefit in mixed dementia (AD/VaD). The benefits of other drugs such as rivastigmine, memantine, nimodipine, and piracetam are not clear. Some other supplements and herbal therapies, such as citicoline, actovegin, huperzine A, and vinpocetine, have also been studied in patients with VaD, but their beneficial effects are not well established. Non-drug therapies and lifestyle modifications such as diet, exercise, and vascular risk factor control are important in the management of VCI and should not be ignored. However, there is a need for more robust clinical trials focusing on executive function and other cognitive measures and incorporation of newer imaging modalities to provide additional evidence about the utility of these strategies in patients with VCI.

Background:In-hospital stroke (IHS) represents 5–15% of all hospitalized acute stroke cases, and is associated with poor outcomes. IHS represents an important area for prevention since many cases occur in high-risk patients undergoing cardiovascular procedures. Our objectives were to compare the quality of care, treatments, and outcomes of IHS with out-of-hospital stroke (OHS) cases. Methods: A 6-month prospective cohort of IHS and OHS stroke cases from a statewide acute stroke registry of 15 representative hospitals was assembled. Data were abstracted on demographic, clinical characteristics, in-hospital care (including tPA treatment), discharge instructions, and in-hospital outcomes (mortality and modified Rankin Scale [mRS] at discharge). Results:177 (6.5%) of the 2,743 cases in the registry were IHS cases. 40% of IHS cases were admitted with a cardiovascular or neurologically related problem, and 68% underwent an invasive diagnostic or surgical procedure prior to their stroke. IHS cases were less likely to have the cerebral vasculature examined or to have a lipid panel drawn. Compared to OHS, IHS had higher case fatality (14.6 vs. 6.9%; p = 0.04), greater functional impairment (mRS ≧4) (61 vs. 36%; p < 0.001), and were less likely to be discharged home (23 vs. 52%, p < 0.01). Conclusions:In this prospective registry, 1 in 15 acute stroke cases occurred in the hospital, and almost 70% had an invasive procedure undertaken prior to their stroke event. In-hospital cases received similar quality of care as OHS cases, but had significantly worse outcomes.

Cerebral hyperperfusion is a relatively rare syndrome with significant and potentially preventable clinical consequences. The pathophysiology of cerebral hyperperfusion syndrome (CHS) may involve dysregulation of the cerebral vascular system and hypertension, in the setting of increase in cerebral blood flow. The early recognition of CHS is important to prevent complications such as intracerebral hemorrhage. This review will focus on CHS following carotid endarterectomy and carotid artery stenting. We will discuss the typical clinical features of CHS, risk factors, pathophysiology, diagnostic modalities for detection, identification of patients at risk, and prevention and treatment. Although currently there are no specific guidelines for the management of CHS, identification of patients at risk for CHS and aggressive treatment of hypertension are recommended.

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Background and Purpose An urgent need exists to develop therapies for stroke which have high efficacy, long therapeutic time windows and acceptable toxicity. We undertook preclinical investigations of a novel therapeutic approach involving supplementation with carnosine, an endogenous pleiotropic dipeptide. Methods Efficacy and safety of carnosine treatment was evaluated in rat models of permanent or transient middle cerebral artery occlusion. Mechanistic studies used primary neuronal/astrocytic cultures and ex vivo brain homogenates. Results Intravenous treatment with carnosine exhibited robust cerebroprotection in a dose-dependent manner, with long clinically-relevant therapeutic time windows of 6 h and 9 h in transient and permanent models, respectively. Histological outcomes and functional improvements including motor and sensory deficits were sustained at 14 d post-stroke onset. In safety and tolerability assessments, carnosine did not exhibit any evidence of adverse effects or toxicity. Moreover, histological evaluation of organs, complete blood count, coagulation tests and the serum chemistry did not reveal any abnormalities. In primary neuronal cell cultures and ex vivo brain homogenates, carnosine exhibited robust anti-excitotoxic, antioxidant, and mitochondria protecting activity. Conclusion In both permanent and transient ischemic models, carnosine treatment exhibited significant cerebroprotection against histological and functional damage, with wide therapeutic and clinically relevant time windows. Carnosine was well tolerated and exhibited no toxicity. Mechanistic data show that it influences multiple deleterious processes. Taken together, our data suggest that this endogenous pleiotropic dipeptide is a strong candidate for further development as a stroke treatment.