Significance of Haemodynamic and Haemostatic Factors in the Course of Different Manifestations of Cerebral Small Vessel Disease: The SHEF-CSVD Study—Study Rationale and Protocol
Rationale. This paper describes the rationale and design of the SHEF-CSVD Study, which aims to determine the long-term clinical and radiological course of cerebral small vessel disease (CSVD) and to evaluate haemostatic and haemodynamic prognostic factors of the condition. Design. This single-centre, prospective, non-interventional cohort study will follow 150 consecutive patients with different clinical manifestations of CSVD (lacunar ischaemic stroke, vascular dementia, vascular parkinsonism or spontaneous deep, intracerebral haemorrhage) and 50 age- and sex-matched controls over a period of 24 months. The clinical and radiological course will be evaluated basing on a detailed neurological, neuropsychological and MRI examinations. Haemodynamic (cerebral vasoreactivity, 24？h blood pressure control) and haemostatic factors (markers of endothelial and platelet dysfunction, brachial artery flow-mediated dilatation test) will be determined. Discussion. The scheduled study will specifically address the issue of haemodynamic and haemostatic prognostic factors and their course over time in various clinical manifestations of CSVD. The findings may aid the development of prophylactic strategies and individualised treatment plans, which are critical during the early stages of the disease. 1. Background Effective therapeutic and preventive strategies in neurological diseases of the elderly are lacking. Cerebral small vessel disease (CSVD) is one of the most important and common vascular diseases of the brain. High morbidity rates are associated with CSVD; this disease leads to recurrent ischaemic and haemorrhagic strokes, gait disturbances, vascular dementia, and vascular parkinsonism [1, 2]. The course and prognosis of the disorder are not well known. Although patients with CSVD may exhibit white-matter lesion burdens on conventional MRIs that are almost identical, they may present clinically with a range of motor and cognitive deficits that is greatly varied. CSVD is related to vascular risk factors like hypertension, advanced age, and smoking; however, the direct pathophysiological mechanisms of the disease remain unclear [3]. Potential mechanisms include cerebrovascular risk factor-induced ischaemic cerebral changes and other nonspecific cerebral processes, such as generalised vascular disease or normal ageing [4]. The pathological components of CSVD probably include increased permeability of the blood-brain-barrier (BBB), enlargement of perivascular spaces, lacunar infarcts, white-matter lesions (WMLs), and microbleeds [5]. CSVD encompasses degenerative
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