This is a cross-sectional study of 50 patients recruited either inpatient or outpatient clinic departments at Ain Shams University Specialized Hospital from July 2018 to November 2018. All patients provided informed written consent to participate in the study. We recruited both sexes and age above 40 years. The included patients had the diagnosis of cerebrovascular stroke CVS (lacunar infarcts) verified by brain MRI. We excluded patients with bilaterally absent transtemporal window, patients with any other cause of non-ischemic leukoencephalopathy, or patients diagnosed clinically and radiologically as normal pressure hydrocephalus. We also excluded border zone infarcts, large artery atherosclerosis infarcts which defined as cortical or cerebellar lesions and brainstem or subcortical hemispheric lesions greater than 2 cm in diameter on MRI brain, and various types of intracerebral hemorrhage on CT brain. Cardiac source of emboli, e.g., atrial fibrillation (AF), paroxysmal AF, prosthetic valve, valvular heart disease, or hematological diseases and coagulopathies, all are excluded. The included patients were submitted to detailed medical history, thorough general and neurological examination, full metabolic profile, electrocardiogram and transthoracic echocardiogram using Doppler echocardiography unit (GE Vingmed Ultrasound AS, Horten, Norway), carotid and vertebral duplex, and CT brain using (General electric, Boston, MA, USA). All recruited patients were submitted to MRI brain including T1- and T2-weighted images, diffusion-weighted images (DWI), fluid attenuated inversion recovery (FLAIR), magnetic resonance angiography (MRA), and gradient recalled echo (GRE) T2*-weighted images, using a machine 1.5 T General Electric machine manufactured at United States. Four MRI features were considered: (1) periventricular hyperintensities (PVH) and deep white matter hyperintensities (DWMH) will be rated on the Fazekas scale  using FLAIR and T2-weighted sequences. PVH were graded as; 0 = absence, 1 = caps or pencil thin lining, 2 = smooth “halo” and 3 = irregular periventricular hyperintensities extending to deep white matter. Separated DWMH were graded as; 0 = absence, 1 = punctate foci, 2 = beginning confluence of foci, and 3 = large confluent areas. (2) Lacunae that are defined as small (< 20 mm), subcortical lesions of increased signal on T2-weighted and FLAIR, decreased signal T1-weighted images. (3) Microbleeds that are defined as small (< 10 mm), homogeneous, round foci of low signal intensity on GRE image in 7 anatomical locations; gray/white matter, subcortical white matter, basal ganglia, thalamus, brainstem, cerebellum, internal and external capsule . (4) Enlarged perivascular spaces (EPVS) that defined as small sharply delineated structures of cerebrospinal fluid (CSF) intensity measuring < 3 mm following the course of perforating vessels, are visualized clearly on T2-weighted image as hyperintensities. They can be rounded or oval. It may be linear if running longitudinally in the centrum semiovale or short linear at the insular or temporal white matter. They will be rated on the potter scale which includes 3 major anatomical regions; centrum semiovale, basal ganglia including; caudate nucleus, internal capsule, thalamus, lentiform nucleus, extreme/external capsule and insular cortex, and midbrain. Basal ganglia and centrum semiovale regions are rated from 0 to 4, in which 0 means no EPVS, 1 means 1–10 EPVS (mild), 2 means 11–20 EPVS (moderate), 3 means 21–40 EPVS (frequent), and 4 means > 40 EPVS (severe), while midbrain region is rated 0 if no EVPS visible or 1 if EPVS visible . We followed Staals and his colleagues to scale cerebral SVD from 0 to 4 in which one point was awarded when DWMH (Fazekas score 2 or 3) and/or PVH (Fazekas score 2 or 3) are present, one point was awarded when 1 or more lacunae are present, one point was awarded when 1 or more microbleeds are present, one point was awarded when moderate to severe (Potter scale grade 2–4) enlarged perivascular spaces are present . All recruited patients were submitted to TCD examination using (EZ-Dop, the DWL Doppler Company, Singen, Germany), where intracranial vessels were examined by the transtemporal, transformational, transorbital and submandibular approach using a 2-MHz probe, intracranial hemodynamic parameters such as the end-diastolic velocity (EDV), the peak systolic velocity (PSV), mean cerebral blood flow velocities (MFV), the resistivity index (RI), and the pulsatility index (PI) are recorded automatically. Breath holding test was done to evaluate vasomotor reactivity (VMR) and asymptomatic carotid stenosis greater than or equal to 70%. 2 MHz probe was fixed above the temporal bone for MCA monitoring and patients were asked to take a normal breath and hold it for 30 s. The breath holding index (BHI) was calculated as follows; ((mean MCA velocity test – mean MCA velocity baseline) ÷ mean MCA velocity baseline) × (100 ÷ seconds of breath holding). A normal breath holding index is greater than or equal to 0.69. Monitoring MCA with 2 MHz probe for 30 min to detect microemboli signals was done .
Statistical analysis of data
Recorded data were analyzed using the Statistical Package for Social Sciences, version 20.0 (SPSS Inc., Chicago, IL, USA). Quantitative data were expressed as mean ± standard deviation (SD). Qualitative data were expressed as frequency and percentage. Probability (p value): p value < 0.05 was considered significant, p value < 0.001 was considered as highly significant, p value > 0.05 was considered insignificant.