Cerebral Small Vessel Disease: Comparison
Please note this is a comparison between Version 1 by Jakub Litak and Version 2 by Vivi Li.

Cerebral small vessel disease (CSVD) represents a cluster of various vascular disorders with different pathological backgrounds. The advanced vasculature net of cerebral vessels, including small arteries, capillaries, arterioles and venules, is usually affected. Processes of oxidation underlie the pathology of CSVD, promoting the degenerative status of the epithelial layer. There are several classifications of cerebral small vessel diseases; some of them include diseases such as Binswanger’s disease, leukoaraiosis, cerebral microbleeds (CMBs) and lacunar strokes.

  • CSVD
  • CMB
  • cerebral microbleeds
  • cerebral small vessel disease
  • CSVD,CMB,cerebral microbleeds,cerebral small vessel disease

1. Introduction

Cerebral small vessel disease (CSVD) represents a cluster of pathologies with a heterogeneous etiology and a pathomechanism affecting elements of the brain vascular system such as small arteries, capillaries, arterioles and venules. Histopathologic studies demonstrate reduced lumens in affected vessels and also demonstrate the thickening of walls, which impedes perfusion and transmural gas transfer [1]. The disease accounts for 20–30% of cases of ischemic stroke [2][3] and cerebral hemorrhage [4][5]. Moreover, CSVD has been shown to worsen functional outcomes after supra [6] and infratentorial [7] ischemic stroke because it disrupts the reorganization of brain networks that is essential for post-stroke recovery. Certain fluid biomarkers have been identified to correlate with CSVD. Some studies present elevated levels of Low Molecular Weight Neurofilament Protein (NF-L), tissue inhibitor of metalloproteinase-1, metalloproteinase-9 and metalloproteinase-2 in CSVD patients [8]. Imaging examination has revealed a direct relationship between Alzheimer’s Disease occurrence and certain identified cerebral vascular diseases, principally CSVD.

Cerebral small vessel disease (CSVD) represents a cluster of pathologies with a heterogeneous etiology and a pathomechanism affecting elements of the brain vascular system such as small arteries, capillaries, arterioles and venules. Histopathologic studies demonstrate reduced lumens in affected vessels and also demonstrate the thickening of walls, which impedes perfusion and transmural gas transfer [1]. The disease accounts for 20–30% of cases of ischemic stroke [2,3] and cerebral hemorrhage [4,5]. Moreover, CSVD has been shown to worsen functional outcomes after supra [6] and infratentorial [7] ischemic stroke because it disrupts the reorganization of brain networks that is essential for post-stroke recovery. Certain fluid biomarkers have been identified to correlate with CSVD. Some studies present elevated levels of Low Molecular Weight Neurofilament Protein (NF-L), tissue inhibitor of metalloproteinase-1, metalloproteinase-9 and metalloproteinase-2 in CSVD patients [8]. Imaging examination has revealed a direct relationship between Alzheimer’s Disease occurrence and certain identified cerebral vascular diseases, principally CSVD.

CSVD can be classified according to varied pathological, radiologic and clinical criteria. Most commonly, two types are identified: amyloid and non-amyloid related. CSVD has been recognized as a dynamic condition of the whole brain and as having a diffuse nature, and systems for the visual scoring of MRI images have been introduced to assess the total load of the disease [9][10]. The neuroimaging features are white matter hyperintensities (WMH), enlarged perivascular spaces (EPVS), lacunae, subcortical infarcts, microbleeds and brain atrophy. Some researchers include individual disease entities in this group, such as Binswanger’s disease, leukoaraiosis, cerebral microbleeds (CMBs) and lacunar strokes.

CSVD can be classified according to varied pathological, radiologic and clinical criteria. Most commonly, two types are identified: amyloid and non-amyloid related. CSVD has been recognized as a dynamic condition of the whole brain and as having a diffuse nature, and systems for the visual scoring of MRI images have been introduced to assess the total load of the disease [9,10]. The neuroimaging features are white matter hyperintensities (WMH), enlarged perivascular spaces (EPVS), lacunae, subcortical infarcts, microbleeds and brain atrophy. Some researchers include individual disease entities in this group, such as Binswanger’s disease, leukoaraiosis, cerebral microbleeds (CMBs) and lacunar strokes.