Virchow Robin Research Articles

Five-Year Serial Brain MRI Analysis of Military Members Exposed to Chronic Sub-Concussive Overpressures.

The Canadian Special Operations Forces Command conducts explosives operations and training which exposes members to explosive charges at close proximity. This 5-year longitudinal trial was conducted in follow-up to our initial trial which examined military breachers with MRI and EEG pre and post blast exposure. To examine brain MRI findings in military personnel exposed to multiple repeated blast exposures. Five-year longitudinal prospective trial. Ninety-two males aged 23-42 with an average of 9.4 years of blast exposure. 3 T brain MRI/T1-weighted 3D with reconstruction in three planes, T2-weighted, T2-weighted fluid attenuated inversion recovery (FLAIR) 3D with reconstruction in three planes, T2-weighted gradient spin echo (GRE), saturation weighted images, DWI and ADC maps, diffusion tensor imaging. All MRI scans were interpreted by the two neuroradiologists and one neuroradiology Fellow in a blinded fashion using a customized neuroradiology reporting form. Matching parametric statistics represented the number of participants whose brain parameters improved or deteriorated over time. Odds ratio (OR) and 95% confidence intervals (CI) were computed using log regression modeling to determine volume loss, white matter lesions, hemosiderosis, gliosis, cystic changes and enlarged Virchow Robin (VR) spaces. A Kappa (κ) statistic with a 95% CI was calculated to determine rater variability between readers. A significant deterioration was observed in volume loss (OR = 1.083, 95% CI 0.678-1.731, permutation test), white matter changes (OR: 0.754, 95% CI 0.442-1.284, permutation test), and enlargement of VR spaces (OR: 0.775, 95% CI 0.513-1.171). Interrater reliability was low: κ = 0.283, 0.156, and 0.557 for volume loss, white matter changes, and enlargement of VR spaces, respectively. There were significant changes in brain volume, white matter lesions, and enlargement of VR spaces. 2 TECHNICAL EFFICACY: Stage 2.

Dilated Virchow Robin spaces in multiple sclerosis - a generalised marker of disease?

Dilated Virchow Robin spaces in multiple sclerosis - a generalised marker of disease?

White-Matter Lesions and Cortical Cerebral Blood Flow Evaluation by 3D Arterial Spin-Labeled Perfusion MRI in Asymptomatic Divers: Correlation with Patent Foramen Ovale Ocurrence.

Cerebral white-matter lesions (cWML) can be caused by dilation of Virchow-Robin spaces or may correspond to true lacunar ischemic lesions. The aim of our study was to evaluate in asymptomatic divers the relationship between the presence of patent foramen ovale (PFO) and cWML, as well as their possible effects on cortical cerebral blood flow (CBF) by magnetic resonance (MRI) through the arterial spin labeling (ASL) sequence. Transthoracic echocardiography was performed for the identification of PFO, and cerebral magnetic resonance including the 3D-ASL sequence for CBF quantification. Thirty-eight divers, with a mean age 45.8 ± 8.6 years, were included. Nineteen healthy volunteers, mean age 41 ± 15.2 years, served as the control group. A total of 28.9% of divers had completed more than 1000 dives. It was found that 26.3% of divers presented with PFO in the echocardiographic study. cWML was evidenced in 10.5% of diver MRI studies. There was no statistically significant relationship between the presence of PFO and cWML (p = 0.95). We observed a lower blood flow in all brain areas assessed by the 3D-ASL sequence in the group of divers, compared with the control group. We did not find statistical differences in CBF as a function of the presence or absence of PFO, number of dives, or cWML evidence.

Infiltration of meningeal macrophages into the Virchow-Robin space after ischemic stroke in rats: Correlation with activated PDGFR-β-positive adventitial fibroblasts.

Macrophages play a crucial role in wound healing and fibrosis progression after brain injury. However, a detailed analysis of their initial infiltration and interaction with fibroblasts is yet to be conducted. This study aimed to investigate the possible route for migration of meningeal macrophages into the ischemic brain and whether these macrophages closely interact with neighboring platelet-derived growth factor beta receptor (PDGFR-β)-positive adventitial fibroblasts during this process. A rat model of ischemic stroke induced by middle cerebral artery occlusion (MCAO) was developed. In sham-operated rats, CD206-positive meningeal macrophages were confined to the leptomeninges and the perivascular spaces, and they were not found in the cortical parenchyma. In MCAO rats, the number of CD206-positive meningeal macrophages increased both at the leptomeninges and along the vessels penetrating the cortex 1 day after reperfusion and increased progressively in the extravascular area of the cortical parenchyma by 3 days. Immunoelectron microscopy and correlative light and electron microscopy showed that in the ischemic brain, macrophages were frequently located in the Virchow-Robin space around the penetrating arterioles and ascending venules at the pial surface. This was identified by cells expressing PDGFR-β, a novel biomarker of leptomeningeal cells. Macrophages within penetrating vessels were localized in the perivascular space between smooth muscle cells and PDGFR-β-positive adventitial fibroblasts. In addition, these PDGFR-β-positive fibroblasts showed morphological and molecular characteristics similar to those of leptomeningeal cells: they had large euchromatic nuclei with prominent nucleoli and well-developed rough endoplasmic reticulum; expressed nestin, vimentin, and type I collagen; and were frequently surrounded by collagen fibrils, indicating active collagen synthesis. In conclusion, the perivascular Virchow-Robin space surrounding the penetrating vessels could be an entry route of meningeal macrophages from the subarachnoid space into the ischemic cortical parenchyma, implying that activated PDGFR-β-positive adventitial fibroblasts could be involved in this process.

Variances of quantifying of Virchow–Robin spaces detecting the different functional status of glymphatic system in simple febrile seizures affected by seizures duration

The Virchow-Robin spaces (VRs) in the cerebral glymphatic system play a vital role in waste clearance from the brain. Simple febrile seizures (SFS) are a common type of seizures marked by an inappropriate fluid exchange. The mechanism of evident differences in glymphatic function among SFS with varying seizure duration is unknown. Therefore, the goal of this study was to see whether there were any variations in glymphatic function among SFS based on seizures duration. We retrospectively studied 30 children with SFS lasting more than 5 minutes (SFS > 5M), 40 children with SFS lasting 5 minutes or less (SFS ≤ 5M), and 35 healthy controls aged 6 to 60 months who underwent magnetic resonance imaging (MRI). A custom-designed automated method that used T2-weighted imaging (T2WI) to segment the visible VRs. The VRs metrics were measured and compared studied groups. The VRs metrics, seizure duration the time gap between seizure onset and MRI scan were studied as well. VRs counts were lower (P < .001) in the SFS ≤ 5M (445.80 ± 66.10) and the control (430.77 ± 182.55) groups in comparison to SFS > 5M (642.70 ± 100.62). Similar results were found for VRs volume (VRsvol_SFS > 5M, 8514.63 ± 835.33mm3, VRsvol_SFS ≤ 5M, 6390.43 ± 692.74 mm3, VRsvol_control, 6048.37 ± 111.50 mm3; P < .001). However, in the SFS ≤ 5M, VRs measurements were lower than in the SFS > 5M (P < .001). VRs measurements were positively connected with seizure duration and inversely correlated with the course following seizure onset and MRI scan time in both SFS groups. SFS are positively correlated to glymphatic dysfunction since they cause enlarged VRs; additionally, VRs can be used as a biomarker in SFS > 5M and contribute to the mechanism.

Mixed Cerebrovascular And Alzheimer’s Type Pathology Mimicking Lewy Body Disease And Its Possible Contribution To the Increased Risk of Developing Cognitive Impairment In Elderly Patients with Bipolar Disorder/Schizophrenia

BackgroundIt has been recently reported that bipolar disorder (BD), as compared to other major adult psychiatric disorders, was associated with an increased risk of developing Parkinson’s disease (PD), cerebrovascular disease (CVD), and dementia in a later life (PMID: 33075191). The similar to BD increased risk of developing dementia was also observed for schizophrenia (SCZ) (PMID: 33075191). Surprisingly, the most common cause of dementia, Alzheimer’s disease (AD) (PMID: 31564456), was absent in elderly BD patients with cognitive impairment when AD was probed by its signature biomarkers in the cerebrospinal fluid (PMID: 26876913). Altogether, these data question AD contribution to the increased risk for dementia development in elderly patients with BD. Therefore, the main objective of this study was to address the above issue by probing postmortem AD related pathology in two brains of 83‐year‐old individuals. The first subject (D1) was diagnosed with BD, SCZ, and PD, whereas the second (D2) had Lewy Body Dementia (LBD). PD, PD dementia, and LBD constitute Lewy Body Disease (PMID: 30665447).ResultsParaffin embedded tissue sections from specific regions of each brain underwent H&amp;E staining, as well as immunohistochemical staining for β‐amyloid and phospho‐tau. Upon examination, Lewy bodies were not observed in D1 and D2 brains and the substantia nigra was well preserved in both brains, thereby not confirming the respective PD and LBD diagnoses. However, D1 brain displayed Alzheimer’s type pathology in the frontal, temporal, and occipital cortices as well as in the hippocampus. The respective pathological features included senile plaques and neurofibrillary tangles (NFTs) in the cortices and hippocampus as well as granulovacuolar degeneration (GVD) in pyramidal neurons of the hippocampus. Interestingly, in the same brain, a strong diffused β‐amyloid staining of potential significance was observed within the cerebellar neurons. Overall, the severity of the respective Alzheimer’s type pathology in D1 brain could be characterized by its clinical stage as mild to moderate. Importantly, there were also vascular changes in D1 brain consistent with hypertensive CVD including hyaline atherosclerosis, microbleeds, and dilated Virchow Robin spaces. Some blood vessels showed β‐amyloid deposits within the vessel wall and lumen which is indicative of amyloid angiopathy. In D2 brain, the AD pathology was also present in the form of NFTs and GVD in the hippocampus and was accompanied by mild neuronal loss in the hippocampus and cortex. Striking vascular pathology including thick‐walled blood vessels with microbleeds was also observed.Conclusionsi) AD could be present in elderly BD/SCZ patients and advance to clinical stage associated with cognitive impairment. ii) CVD in conjunction with AD could mimic Lewy Body Disease and contribute to the increased risk of dementia development in older BD/SCZ patients. iii) A proper diagnosis of dementia associated with mixed CVD/AD pathology in elderly patients with BD/SCZ would be important for their adequate treatment and care.

Mixed Cerebrovascular and Alzheimer’s Type Pathology Mimicking Lewy Body Disease and Its Possible Contribution to Cognitive Impairment in Elderly Patients with Bipolar Disorder/Schizophrenia

The fast aging human population requires new approaches to reliable diagnosis and proper treatment of dementia in elderly patients with psychiatric disorders such as bipolar disorder (BD) and schizophrenia (SCZ). As compared to other psychiatric disorders, BD and SCZ are characterized by increased and similar risk for dementia as well as cerebrovascular (CVD) and Parkinson’s (PD) diseases independent of the patient’s age. There are reports in the literature suggesting BD and SCZ in older patients could cause dementia without contribution from the neurodegenerative diseases, including Alzheimer’s disease (AD), due to the absence of the known neuropathology associated with cognitive decline in such individuals. This view contradicts a plethora of data highlighting AD as a major cause of dementia in the elderly. This issue was addressed by examining postmortem cerebral pathology in an 83-year-old female diagnosed with BD, SCZ, and PD (D1) and comparing it to that of a second donor (D2), an age-matched male diagnosed with Lewy Body Dementia (LBD). Upon thorough histochemical and immunohistochemical examinations of both brains, the PD and LBD diagnoses in D1 and D2 were not confirmed. Instead, AD-related pathology was observed in both subjects with AD advancing to its clinical stage (mild to moderate) only in D1. Diffuse β-amyloid peptide 1-42 (Aβ1-42) staining, most likely reflecting a presence of the Aβ1-42 soluble form, was also detected in cerebellar neurons and cerebellar extracellular space in D1 and D2. Cerebrovascular pathology was pronounced and distinct in both brains and included amyloid angiopathy, hyaline atherosclerosis, microbleeds, and dilated Virchow Robin spaces in D1 as well as thick-walled blood vessels with microbleeds in D2. It was concluded that a mixed AD and cerebrovascular pathology could mimic Lewy Body Disease and potentially contribute to dementia development in elderly BD and SCZ patients.

Multifocal Primary Central Nervous System (CNS) Diffuse Large B-Cell Lymphoma (DLBCL) in a Patient with Aquired Immunodeficiency Syndrome (AIDS)

Abstract Introduction/Objective Primary CNS DLBCL is a rare entity, with an incidence of less than 0.47 per 100,000, however, in immunocompromised patients, especially those with Human Immunodeficiency Virus (HIV-1) infection, the incidence increases dramatically to 2-6 percent. Here we present a case of multifocal DLBCL in a young 28-year-old homeless male with untreated AIDS and polysubstance abuse. Methods/Case Report He presented to the hospital with altered state of consciousness; a Computerized Tomography (CT) scan showed three ring-enhancing masses; one in the left fronto-temporal region, the largest in the left basal ganglia and the third in the cerebellum. The main lesion was biopsied and diagnosed as DLBCL. The patient developed aspiration pneumonia and demised from respiratory failure Results (if a Case Study enter NA) NA Conclusion Coronal sections of the brain revealed a large grey-tan, soft lesion of poorly defined, irregular borders located in the left basal ganglia that measured 5 x 4 x 4 cm, extended dorsally and laterally. A similar lesion was observed in the deep left cerebral hemisphere, affecting the temporal lobe and extending rostrally into the frontal lobe, but completely separate from the tumor in the basal ganglia. A third, much smaller lesion was found in the right cerebellar hemisphere. Histologically, the tumor was composed of sheets of atypical lymphoid cells with increased nuclear to cytoplasmic ratio, increased mitotic activity, and showed scattered areas of necrosis. In the peripheral areas, tumor cells were located in the Virchow Robin space, and in more central areas they have broken into the brain parenchyma. Tumor cells were positive for CD20 and CD79a, indicating their B-cell origin. Other markers positive by immunohistochemistry were PAX5, MUM1 and BCL6 and the Epstein-Barr Virus (EBV) latent membrane protein (LMP). Fluorescence In situ hybridization (FISH) corroborated the presence of Eptein-Barr encoded RNAs.

Tumefactive Virchow Robin Spaces and its Mimics in Paediatric Patients: A Pictorial Review

Tumefactive Virchow Robin Spaces and its Mimics in Paediatric Patients: A Pictorial Review

Cribriform Appearance of White Matter in Canavan Disease Associated with Novel Mutations of ASPA Gene

Cribriform appearance of the brain in Canavan disease is a rare finding. The two presented cases broaden the magnetic resonance imaging (MRI) phenotype wherein numerous oval, cystic structures, a few resembling dilated Virchow-Robin (VR) spaces, were noted in the centrum semiovale, periventricular, and lobar white matter producing a cribriform pattern. Besides, discrete round to oval cysts were present at the gray-white matter junctions in the second case, which were larger and appeared morphologically distinct from the VR spaces. These cysts did not elongate in any plane on imaging and were more representative of giant intramyelinic vacuoles. Genetic analysis revealed novel mutations in the aspartoacylase or ASPA gene that possibly accounts for the severe form of Canavan disease, which probably explains the imaging findings. The multicystic appearance of the white matter in Canavan disease is unusual and possibly represents two different histopathological substrates.

Delleman–Oorthuys syndrome: A case report of an atypical variant

A 4-year-old male child, born to nonconsanguineous parents, was brought with a history of a fleshy red mass in both eyes and abnormally shaped eyelids since birth. Evaluation revealed delayed developmental milestones and temporoparietal alopecia over the right side along with focal areas of hyperpigmented skin over the face, chest, back, and both upper limbs. Ocular evaluation revealed skin tags over the upper eyelids, epibulbar dermoid along with upper lid coloboma, and microcornea in both eyes. He had deformed temporoparietal bones on both sides. Magnetic resonance imaging brain revealed generalized cerebral atrophy with prominent Virchow–Robin spaces and enlarged ventricular system but atypically normal corpus callosum. He was diagnosed as an atypical variant of Delleman syndrome (a rare congenital disorder involving eyes, skin, and brain and comprising orbital cyst, eyelid colobomas, skin appendages, polymicrogyria as well as characteristic mid-hindbrain abnormalities). Multidisciplinary treatment approach and long-term neurological follow-up are recommended in these patients.

Satellitosis, a Crosstalk between Neurons, Vascular Structures and Neoplastic Cells in Brain Tumours; Early Manifestation of Invasive Behaviour.

Simple SummaryThis article reviews the concept of cellular satellitosis as originally described histologically by Santiago Ramón y Cajal in 1899 and Hans Joachim Scherer, more specifically in the context of glioblastoma invasiveness, during the early part of the 20th century. With the advent of new and emerging molecular technologies in the 21st century, the significance of both vascular and neuronal satellitosis by neoplastic cells offers intriguing possibilities into further clarifying the development, pathobiology and therapy of malignant glioma through closer investigation into the nature of these histological hallmarks.The secondary structures of Scherer commonly known as perineuronal and perivascular satellitosis have been identified as a histopathological hallmark of diffuse, invasive, high-grade gliomas. They are recognised as perineuronal satellitosis when clusters of neoplastic glial cells surround neurons cell bodies and perivascular satellitosis when such tumour cells surround blood vessels infiltrating Virchow–Robin spaces. In this review, we provide an overview of emerging knowledge regarding how interactions between neurons and glioma cells can modulate tumour evolution and how neurons play a key role in glioma growth and progression, as well as the role of perivascular satellitosis into mechanisms of glioma cells spread. At the same time, we review the current knowledge about the role of perineuronal satellitosis and perivascular satellitosis within the tumour microenvironment (TME), in order to highlight critical knowledge gaps in research space.

Intrathecal Inflammation in Progressive Multiple Sclerosis

Progressive forms of multiple sclerosis (MS) are associated with chronic demyelination, axonal loss, neurodegeneration, cortical and deep gray matter damage, and atrophy. These changes are strictly associated with compartmentalized sustained inflammation within the brain parenchyma, the leptomeninges, and the cerebrospinal fluid. In progressive MS, molecular mechanisms underlying active demyelination differ from processes that drive neurodegeneration at cortical and subcortical locations. The widespread pattern of neurodegeneration is consistent with mechanisms associated with the inflammatory molecular load of the cerebrospinal fluid. This is at variance with gray matter demyelination that typically occurs at focal subpial sites, in the proximity of ectopic meningeal lymphoid follicles. Accordingly, it is possible that variations in the extent and location of neurodegeneration may be accounted for by individual differences in CSF flow, and by the composition of soluble inflammatory factors and their clearance. In addition, “double hit” damage may occur at sites allowing a bidirectional exchange between interstitial fluid and CSF, such as the Virchow–Robin spaces and the periventricular ependymal barrier. An important aspect of CSF inflammation and deep gray matter damage in MS involves dysfunction of the blood–cerebrospinal fluid barrier and inflammation in the choroid plexus. Here, we provide a comprehensive review on the role of intrathecal inflammation compartmentalized to CNS and non-neural tissues in progressive MS.

Dilated Virchow Robin spaces in brainstem

Virchow Robin spaces are normally found pial-lined perivascular spaces traversing from subarachnoid space to the brain parenchyma. Giant dilated Virchow robin spaces (dVRS) are rare. They do not require any surgical intervention unless they are causing symptoms. Here we report a young boy with an incidentally detected giant dVRS in brainstem which was referred for surgery with an initial impression of glioma. Knowledge about such an entity is important to prevent mismanagement.

Morphofunctional Changes and Compensatory Mechanisms in the Human Brain with Aging and in Alzheimer's Disease

The article focuses on age-related morphofunctional changes in the human brain and the issue of compensatory-adaptive mechanisms developed in normal aging. According to the scientific literature, the volume of white matter is reduced to a greater extent with aging, the fact associating with myelin fibers degeneration, the appearance of Virchow–Robin spaces and a decrease in the effectiveness of the blood-brain barrier. Atrophic processes in gray matter are currently associated not only with the death of neurons, but with degenerative changes in synapses, a decrease in their number, and reduction of dendritic branches and spines. A decrease in the size of pericarions resulting in a decrease in the number of large neurocytes and an increase in the proportion of small neurons is noted in certain brain structures. However, age-related neuronal hypertrophy is observed in the nuclei of the hypothalamus, Meinert’s basal nucleus. This is mostly manifested in the female group, and is undoubtedly associated with a decrease in estrogen levels and the period of menopause. An increase in the metabolic activity of neurons manifested by related changes in the size of the pericarions and nuclei of neurons and their Golgi complex can be attributed to compensatory-adaptive mechanisms that can delay or prevent the development of neurodegenerative disorders, such as Alzheimer's disease. Neurons with a higher metabolic activity have better ability to self-repair. Due to this, neuron reactivation techniques are being developed with aging based on the selection of the correct stimulus. The growth of the glial cell population is also considered to be compensatory, since these cells are crucial for neuron adaptation and able to affect the level of neuronal RNA synthesis. Furthermore, the article highlights literature data on possible triggers of the compensatory capabilities of the brain with aging and under pathological processes.

Quantification of visible Virchow–Robin spaces for detecting the functional status of the glymphatic system in children with newly diagnosed idiopathic generalized epilepsy

PurposeThe cerebral glymphatic system, particularly the Virchow–Robin Spaces (VRS), plays an important role in waste clearance from the brain. Idiopathic generalized epilepsy (IGE) is a common epilepsy type associated with blood-brain-barrier dysfunction, abnormal exchange of cerebrospinal fluid and interstitial fluid. These disorders may be reflected in the glymphatic system. Therefore, this study investigated the relationships between visible VRS on MRI and seizures, to detect changes in glymphatic function. MethodsWe retrospectively included 32 children with newly diagnosed IGE and 30 controls aged 3–13 years. Visible VRS were identified using a custom-designed automated method. VRS counts and volume were quantified and compared between children with IGE and controls. Meanwhile, Correlations of VRS counts and volume with seizure duration and course after seizure onset were respectively explored via Spearman’s coefficient (r). ResultsIn this study, visible VRS counts were higher in IGE than control group (VRS_epilepsy, 234.34 ± 113.88 vs. VRS_control, 111.83 ± 52.46; P < 0.001), as similar results were found in VRS volume (VRS_epilepsy, 1377.47 ± 778.79 mm3 vs. VRS_control, 795.153 ± 452.49 mm3; P = 0.001). Visible VRS counts and volume positively correlated with seizure duration (r_counts = 0.638, r_volume = 0.639; P < 0.001) and gradually decreased with time after seizure onset (r_counts = −0.559, r_volume = −0.558; P < 0.001). ConclusionEpileptic seizures can induce changes in VRS counts and volume, which were associated with seizure duration and post-onset course. Quantitative metrics of VRS visible on MRI might be potential biomarkers for monitoring glymphatic function.

Central nervous system variations and abnormalities in anhidrotic ectodermal dysplasia (AED): neuroimaging findings.

Anhidrotic ectodermal dysplasia (AED) is a rare, mostly X-linked recessive genodermatosis, characterized by congenital defects of ectodermal derivative structures as the central nervous system (CNS) is primarily ectodermal in origin. To evaluate CNS variations and abnormalities in AED. A retrospective analysis was made of the neurological and neuroimaging findings of 17 children (12 boys, 5 girls; median age = 8 years; age range = 2-14 years) diagnosed with AED in our pediatric clinics during 2008-2016. The pattern of CNS variation and abnormalities were evaluated by comparing of these findings with an age- and gender-matched healthy control group with no family history. Of the 17 AED cases identified on the basis of neuroimaging findings, 6 (35.3%) were seen to be normal. Associated CNS variation and abnormalities including cavum septum pellucidum (35.3%), callosal dysgenesis (11.8%), prominent Virchow-Robin spaces (64.7%), cortical sulcal dilation (41.1%), mega cisterna magna (35.3%), focal cortical dysplasia (11.8%), and delayed myelination (58.8%) were observed in 11 (64.7%) children with AED. AED suggests a spectrum of CNS variation and abnormalities, presenting with neurological and neuroimaging findings, demonstrated in the embryonic surface- and neuro-ectoderm derived structures. The results of this study suggest that CNS variation and abnormalities might be associated with AED.

Swiss Cheese Pattern a Harbinger of Dementia or an Incidental Finding in an Unusual Case?

Virchow Robin (VR) spaces are pial-lined, fluid filled, structures which surround the walls of small penetrating arterioles and venules as they course from subarachnoid penetrating arterioles and venules as they course from subarachnoid

Large anterior temporal Virchow–Robin spaces: Evaluating MRI features over the years—Our experience and literature review

Dilated Virchow–Robin spaces (VRSs) are expansions of the normal perivascular spaces with a short axis greater than 2 mm or, according to some authors, greater than 3 mm. They are usually documented at the basal ganglia, at the convexity white matter (WM) and centrum semiovale, and at the mesencephalon. The anterior temporal WM is a recently described preferential location for large (≥5 mm) VRSs. The aim of our study was to evaluate the magnetic resonance imaging (MRI) features and their modifications during a long-term follow-up period (≥24 months) of the anterior temporal VRSs with a retrospective analysis among all brain MRI studies performed at our institution between January 2010 and January 2017. In our study, the presence and the stability of characteristic MRI features certainly increased our diagnostic confidence allowing us to continue conservative approach while the surrounding signal change, as reported in the literature, should not in itself prompt alternative diagnoses to be entertained.

Cerebral Small Vessel Disease Associated with Subclinical Vascular Damage Indicators in Asymptomatic Hypertensive Patients.

Background: Cerebral small vessel disease (CSVD) is frequent in patients with cardiovascular risk factors including arterial hypertension, and it is associated with vascular damage in other organs and the risk of stroke, cognitive impairment, and dementia. Early diagnosis of CSVD could prevent deleterious consequences. Objective: To characterize CSVD associated with indicators of subclinical vascular damage in asymptomatic hypertensive patients. Materials and Methods: Participants were hypertensive (HT) and non-hypertensive (non-HT) individuals; without signs of cerebrovascular disease, dementia, and chronic renal failure. For CSVD, white matter hyperintensities (WMH), enlarged Virchow–Robin perivascular spaces (EVRPS), lacunar infarcts, and microbleeds were investigated. Subclinical vascular damage was evaluated (hypertensive retinopathy, microalbuminuria, and extracranial carotid morphology: intima media thickness (IMT) and atheroma plaque). Results: CSVD MRI findings were more frequent in HT; as well as greater intimal thickening. The IMT and/or plaque was significantly associated with all MRI variables; but retinopathy was correlated with EVRPS and lacunar infarcts. Only microalbuminuria was related to the greater severity of WMH in HT. Multivariate analysis evidenced that CSVD was independently associated with the combination of indicators of vascular damage and systolic blood pressure. Conclusions: Combining indicators of subclinical vascular damage, such as carotid morphological variables, microalbuminuria, and hypertensive retinopathy for early detection of CSVD in asymptomatic hypertensive patients could prove to be useful to take actions for the prevention of irreversible brain damage, which could lead to cognitive impairment, dementia and stroke.