الفهرس 
CSVD PATHOPHYSIOLOGYOnly 14 pages are availabe for public view
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Abstract
C
SVD is among the neurological diseases known to reduce the quality of life in the elderly. It has a strong role in age-related disabilities such as cognitive impairment, gait apraxia, urinary incontinence, and depression as well as being a leading cause of vascular dementia.
Diagnosis of CSVD is based on brain imaging biomarkers, in the form of recent small subcortical infarcts, WMH, lacunes, CMBs, EPVS, and cerebral atrophy.
MRI visual rating scales have been used as a tool to diagnose CSVD, and to assess progression and prognosis. Studies have shown that the role of rating scales is better in differential diagnosis rather than lesion progression.
There is growing evidence that various subtypes of stroke have very diverse underlying pathophysiologies and respond to treatments in different ways. Significant advancements have been made in the prevention and treatment of atherosclerotic and cardioembolic stroke, but little has been made in the treatment of SVD.
The effectiveness of CSVD prevention and treatment is limited by our incomplete understanding of its pathophysiology. Currently, the method of treatment is tailored based on the profile of risk factors, the type and severity of biomarkers, and the severity of clinical consequences.
Antiplatelet monotherapy offers long-term secondary stroke protection in patients with lacunar stroke. Further research is necessary to determine whether phosphodiesterase inhibitors (cilostazol) offer further benefits to patients with cerebral small vessel disease.
In our study, we attempted to investigate the MRI characteristics and progression in patients suffering from incidental cerebral small vessel disease and compliant on a single antiplatelet (Either Aspirin 150 mg/d or Cilostazol 200 mg/d) in an Egyptian sample.
In this longitudinal observational study, 93 patients with Incidental CSVD were recruited and assessed using clinical scales and brain MR imaging.
All participants had a visit at baseline, then at 6 and 12 months for clinical assessment, and a phone call follow-up at 3 & 9 months to ensure compliance and ask about adverse or new events.
All participants were subjected to comprehensive neurological assessment including history taking (past medical history, vascular risk factors, detailed history of current illness and drug history) and neurological examination. Blood tests including Lipid panel (Total Cholesterol, LDL, HDL, Triglycerides), and glycated HBA1C were evaluated at baseline screening. Cognitive assessment was done using the Arabic version of MoCA. Gait assessment scores were compared between baseline and follow-up and included: 10MWT, self-selected velocity and fast velocity, TUG, and BBS. Arabic version of BDI was used to assess depression. Urinary problems were assessed using The Arabic ICIQ-SF Scale. MRI Brain was performed using a 3.0 Tesla MR Scanner at baseline and after 12 months. Visual analysis was done through rating scales and Lesion load was calculated using the VolBrain software analysis tool for a part of the sample.
Our primary outcome was a change in WMH volume and count on brain FLAIR & T1 imaging from baseline to follow-up compared between both the Aspirin and Cilostazol groups. Other secondary clinical outcomes were measured as changes in cognition, motor function, mood, urinary symptoms, and disability.
Clinical assessment showed almost stationary results in the follow-up interview. There was no significant difference between baseline and follow-up visual rating scales, or the lesion load after 12 months as regards lesion count and volume.
This indicates that there was no significant difference between Aspirin and Cilostazol in clinical and radiological progression in CSVD, but further research is needed on a bigger sample to be able to replicate these results.