Penetrating Vessels Research Articles

Direct 3D Analyses Reveal Barrel-Specific Vascular Distribution and Cross-Barrel Branching in the Mouse Barrel Cortex.

Whether vascular distribution is spatially specific among cortical columns is a fundamental yet controversial question. Here, we have obtained 1-μm resolution 3D datasets that cover the whole mouse barrel cortex by combining Nissl staining with micro-optical sectioning tomography to simultaneously visualize individual cells and blood vessels, including capillaries. Pinpointing layer IV of the posteromedial barrel subfield, direct 3D reconstruction and quantitative analysis showed that (1) penetrating vessels preferentially locate in the interbarrel septa/barrel wall (75.1%) rather than the barrel hollows, (2) the branches of 70% penetrating vessels only reach the neighboring but not always all the neighboring barrels and the other 30% extend beyond the neighboring barrels and may provide cross-barrel blood supply or drainage, (3) the branches of 59.6% penetrating vessels reach all the neighboring barrels, while the rest only reach part of them, and (4) the length density of microvessels in the interbarrel septa/barrel wall is lower than that in the barrel hollows with a ratio of 0.92. These results reveal that the penetrating vessels and microvessels exhibit a barrel-specific organization, whereas the branches of penetrating vessels do not, which suggests a much more complex vascular distribution pattern among cortical columns than previously thought.

Determination of vessel cross-sectional area by thresholding in Radon space.

The cross-sectional area of a blood vessel determines its resistance, and thus is a regulator of local blood flow. However, the cross-sections of penetrating vessels in the cortex can be non-circular, and dilation and constriction can change the shape of the vessels. We show that observed vessel shape changes can introduce large errors in flux calculations when using a single diameter measurement. Because of these shape changes, typical diameter measurement approaches, such as the full-width at half-maximum (FWHM) that depend on a single diameter axis will generate erroneous results, especially when calculating flux. Here, we present an automated method--thresholding in Radon space (TiRS)--for determining the cross-sectional area of a convex object, such as a penetrating vessel observed with two-photon laser scanning microscopy (2PLSM). The thresholded image is transformed back to image space and contiguous pixels are segmented. The TiRS method is analogous to taking the FWHM across multiple axes and is more robust to noise and shape changes than FWHM and thresholding methods. We demonstrate the superior precision of the TiRS method with in vivo 2PLSM measurements of vessel diameter.

Comparative Anatomy of the Carotid-Basilar Arterial Trunk and Hindbrain Penetrating Arteries in Vertebrates

Despite a long history of anatomical studies, the vascular organization of the brainstem is poorly known in most vertebrates. This review examines results from the past 150 years and compares them with a series of new vascular microdissections to provide an overall assessment of vertebrate hindbrain vasculature. The gross anatomy and embryology of cyclostomes, elasmobranchs, actinopterygians and tetrapods reveal a conserved suite of hindbrain vascular features including the: 1) origin and branching of cerebral carotids; 2) ontogenetic origins of the basilar artery from paired precursors, often followed by midline fusion to form an unpaired basilar; and 3) presence of a quasi-segmental series of transverse basilar artery branches that extend circumferentially around the brainstem giving off penetrating vessels. Phylogenetic analysis suggests that paired basilars are primitive for jawed vertebrates, with unpaired basilars arising independently in chondrichthyes, teleosts and tetrapods. Teleosts present a major exception to the general pattern, as penetrating arteries are restricted to a series of midline segmental basilar arterial stems that branch only within the neuroepithelium. This is clearly derived relative to all other vertebrates. Given the dissimilar body plans/lifestyles of groups served by the general brainstem vascular design, the conservation of adult hindbrain macrovasculature likely results from the similarity of embryonic cerebral blood supply across groups, rather than from convergence towards similar neurovascular functional designs. With the high degree of conservation in vertebrate brainstem neuronal anatomy, vascular patterning cues provided by the neuroepithelium practically assure that homologous brain regions are supplied by roughly similar arteries across taxa.

MR imaging of malignant primary breast lymphoma: including diffusion-weighted imaging, histologic features, and a literature review

To investigate the magnetic resonance (MR) imaging characteristics of malignant primary breast lymphoma (PBL), including features on diffusion-weighted imaging (DWI). The MR findings of three patients were reviewed retrospectively at our institutions. The signal intensity, shape, enhancement pattern, and DWI findings were examined and correlated with the histologic features. We also reviewed the MR findings of cases of PBL reported in the literature. The tumors in our cases showed early enhancement with penetrating vessels on early-phase dynamic MR images and a strong high signal intensity on DWI. The tumors had a cerebroid appearance and septal enhancement on delayed contrast-enhanced MR images, and we speculate that the fibrous tissue seen in the tumors may correspond to septal enhancement. After chemotherapy, all lesions decreased in size, while the ADCs were increased. All of the cases reported in the literature showed early or avid enhancement; this finding was similar to that observed in our cases. Although based on a small number of cases, we suggest that strong enhancement with penetrating vessels in masses on early images of dynamic MR, strong high intensity on DWI, a cerebroid appearance, and septal enhancement are useful diagnostic clues for a diagnosis of PBL.

OP0121 The Frequency of Bone Erosion and Oedema in Inflammatory and Degenerative Arthropathies Proximal to the Peri-Entheseal Cruciate Ligament Vascular Channels

BackgroundWe noted in mouse models of inflammatory arthritis (IA) that an early point of entry of inflammation into the marrow space occurs at sites where penetrating vessels entered the bone....

Comparative anatomy and development of the carotid‐basilar arterial trunk in vertebrates

In order to assess general patterns of vertebrate hindbrain vasculature, we dissected a wide taxonomic range of latex‐injected specimens. Examinations of distantly‐related taxa including cyclostomes, elasmobranchs, actinopterygians and sarcopterygian tetrapods demonstrated a conserved suite of hindbrain vascular features including: 1) the origin and branching of cerebral (internal) carotids; 2) the ontogenetic origins of the basilar artery from paired precursors; and 3) the presence of a quasi‐segmental series of transverse basilar artery branches that extend circumferentially around the brainstem, giving off penetrating vessels. The major exception to this general pattern is found in teleosts, in which a series of midline segmental central arterial stems arise from the basilar artery and branch into intramural vascular trees within the sub‐ependymal zone of the hindbrain. The restriction of penetrating arteries to a series of dominant medial segmental stems in teleosts is derived relative to other vertebrates and may be part of a set of key innovations in this group. Phylogenetic analysis suggests that paired basilar arteries are primitive for jawed vertebrates, with unpaired basilars arising independently in chondrichthyes, teleosts and tetrapods. The hypothesized independent development of unpaired basilar arteries may represent convergence towards similar neurovascular functional designs. Given the highly dissimilar body plans and lifestyles of these groups, the overall conservation of hindbrain macrovasculature likely results from the primitive, shared similarity of embryonic brain development.Grant Funding Source: None

The smallest stroke: occlusion of one penetrating vessel leads to infarction and a cognitive deficit

Microinfarctions are present in the aged and injured human brain. Their clinical relevance is controversial, with postulated sequelae ranging from cognitive sparing to vascular dementia. To address the consequences of microinfarcts, we used controlled optical methods to create occlusions of individual penetrating arterioles or venules in rat cortex. Single microinfarcts, targeted to encompass all or part of a cortical column, impaired performance in a macrovibrissa-based behavioral task. Furthermore, the targeting of multiple vessels resulted in tissue damage that coalesced across cortex, even though the intervening penetrating vessels were acutely patent. Post-occlusion administration of memantine, a glutamate receptor antagonist that reduces cognitive decline in Alzheimer's disease, ameliorated tissue damage and perceptual deficits. Collectively, these data imply that microinfarcts likely contribute to cognitive decline. Strategies that have received limited success in the treatment of ischemic injury, which include therapeutics against excitotoxicity, may be successful against the progressive nature of vascular dementia.

Atypical hemifacial spasm (Report of 36 Cases)

Objective To study the pathogenesis and surgical treatment of atypical hemifacial spasm.Methods The clinical data of 36 patients who underwent microvascular decompressions (MVD) for atypical hemifacial spasm(HFS)from July 2005 to July 2010 were retrospectively analyzed.Results The HFS disappeared immediately after MVD in 32 patients.The postoperative spasm was weaker in 4 patients and the residual spasm was disappeared within 5 months.There was no reoccurrence of spasm during follow -up period.The postoperative complications included:transient moderate facial paralysis accompanied with hearing dysfunction in 3 cases,and transient hearing dysfunction accompanied with tinnitus in 3.Conclusions Atypical hemifacial spasm is caused by vessels on the posterior rostral side of facial nerve.The effectiveness could be predicted after MVD.But the rates of facial paralysis and/or hearing loss are relatively higher.The rates of complications could be reduced significantly by correct identification of offending vessels,fewer disturbance to cranial nerves,avoiding the injury to the penetrating vessels,and intraoperative brain stem auditory evoked potential monitoring during. Key words: Microsurgical decompression; Atypical hemifacial spasm; Facial nerve ; Brain stem auditory evoked potential

Bidirectional encroachment of collagen into the tunica media in cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy

Arteries in cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) are susceptible to smooth muscle loss and fibrosis, but the molecular components underlying these dramatic vascular changes are not well characterized. The purpose of this study was to investigate the distribution of collagen isoforms in the cerebral vessels of North American CADASIL patients with classical NOTCH3 mutations. Expression of types I–VI collagen in brains obtained at autopsy from six CADASIL patients with cysteine-altering mutations in NOTCH3 was compared to control brain expression. We identified a consistent increase of types I, III, IV, and VI collagen in CADASIL brains. Strong accumulation of types I, III, IV and VI collagen was noted in all calibers of vessels, including small and medium-sized leptomeningeal arteries, small penetrating white matter arteries, and capillaries. Within leptomeningeal arteries, where we could define the three tunicae of each vessel, we found distinct collagen subtype distribution patterns in CADASIL. Types I and III collagen were largely found in either adventitial/medial or transmural locations. Type IV collagen was strictly intimal/medial. Type VI collagen was adventitial or adventitial/medial. Within the thickened penetrating arteries of CADASIL patients, all four collagens extended through most of the arterial wall. We observed increased staining of capillaries in CADASIL for types I, IV, and VI collagen. In conclusion, brain vascular collagen subtypes are increased in CADASIL in multiple layers of all sizes of arteries, with disease-specific changes most prominent in the tunica media and thickened small penetrating vessels. In diseased arteries, types I, III, and VI collagen spreads from an external location (adventitia) into the vascular media, while type IV collagen accumulates in an internal pattern (intima and media). These observations are consistent with a pathological role for collagen accumulation in the vascular media in CADASIL.

Enhancement Patterns and Parameters of Breast Cancers at Contrast-enhanced US: Correlation with Prognostic Factors

To investigate the correlation between enhancement patterns and parameters of contrast material-enhanced ultrasonography (US) with prognostic factors in breast cancers. The study was approved by the institutional ethics committee, and written informed consent was obtained. Surgical resection specimens of 74 malignant breast lesions in 74 women (mean age, 55 years; age range, 32-78 years) who had undergone contrast-enhanced US were included. Different contrast enhancement patterns (enhancement degree, order, and margin; internal homogeneity; perfusion defect; and radial or penetrating vessels) and parameters (wash-in time, peak intensity, time to peak, area under the time-intensity curve, ascending slope, and descending slope) were evaluated. Pathologic prognostic factors, including histologic grade, lymph node status, tumor diameter, microvessel density (MVD), estrogen and progesterone receptor status, and c-erb-B2, p53, and Ki-67 expression were determined. Correlation of enhancement patterns and parameters with prognostic factors was analyzed with the Pearson χ2 test, Spearman rank correlation test, and logistic regression analysis. Some enhancement features were associated, albeit not significantly, with prognostic factors. Perfusion defect was the most accurate enhancement criterion for higher histologic grade (grade III) (P=.016), negative estrogen receptor expression (P=.006), positive c-erb-B2 expression (P=.013), larger tumor diameter (≥2 cm) (P=.016), and increased MVD (P=.019). Radial or penetrating vessels were associated with lymph node status (P=.010). Hyperenhancement may be useful in reflecting increased MVD (P=.008) and positive p53 expression (P=.037). For contrast enhancement parameters, ascending slope was the best discrimination criterion for proliferative activity (P=.003). Enhancement patterns and parameters of contrast-enhanced US may be useful in the noninvasive prediction of prognostic factors of breast cancers.

Abstract 3685: Collagen Isoform Distribution Patterns In Cerebral Vessels In CADASIL

Objective: Arteries in CADASIL are susceptible to fibrosis and smooth muscle cell loss. The molecular components underlying vascular remodeling are not well characterized. The purpose of this study was to test the hypothesis that distinct collagen isoforms accumulation in the media of the cerebral vessels in CADASIL. Methods: Brain sections from six CADASIL patients with mutations in NOTCH3 were compared to age matched controls. Expression of Type I, II, III, IV, V, VI, and IX collagen were studied by immunohistochemistry. Results: We identified a consistent increase of Type I, III, IV, and VI collagen content in the large and small vessels of CADASIL brains relative to controls. We did not find Type II, V, IX collagen in the brain. Within leptomeningeal arteries where we could definitively visualize the three layers of each vessel, we found that Type I, III, IV and VI collagens were found in heterogeneous locations. Types I and III collagen was mostly transmural or adventitial/medial. Type IV was strictly intimal/medial. Type VI was largely adventitial/medial. The most significant difference between CADASIL and controls was the appearance of all four collagen types in the vascular media. Within the thickened penetrating arteries of CADASIL patients, all four collagens extended through most of the arterial wall. Finally, we observed increased staining of capillaries in CADASIL for Type I, IV, and VI. Conclusion: In CADASIL, brain vascular collagen subtypes are increased in multiple layers of both large and small vessels, with the most dramatic changes in the tunica media and thickened small penetrating vessels. These studies suggest that collagen accumulation in the vascular media may play a pathogenic role in small vessel disease.

Hemodynamic changes in the posterior cerebral circulation triggered by insufficient sympathetic innervation – Cause of primary intracerebral hemorrhage?

Primary intracerebral hemorrhage (ICH) is caused by hypertensive disease of small penetrating blood vessels in the basal ganglia, brain stem and cerebellum. Those regions are supplied by arteries of the so-called posterior brain circulation with insufficient sympathetic innervation. We propose the following hypothesis: due to insufficient sympathetic innervation hemodynamic changes occur in the vascular bed of the posterior brain circulation serving as a key factor for arterial rupture. If autoregulation is insufficient to maintain normal cerebral blood flow, in abrupt rise in the blood pressure, the amount of blood is rising causing higher static pressure, and according to Laplace’s law higher pressure and larger radius leads to higher wall tension and subsequent rupture of arterial wall previously weakened by prolonged hypertension.

Small vessel stroke and white matter lesions

Damage to small penetrating vessels is an important unifying cause of ischemic and hemorrhagic strokes. Both types of stroke involve tiny arterioles and are often pathologic twins, arteriolosclerosis and lipohyalinosis being the predominant underlying causes.1 Another entity increasingly linked to small vessel damage is extensive leukoaraiosis: white matter lesions frequently seen on T2-weighted magnetic resonance scans of older people. In this issue of Neurology ®, Rost et al.2 report hospital-based findings from 3 stroke registries showing a greater burden of leukoaraiosis in participants with small vessel stroke (including both ischemic and hemorrhagic forms) compared to other ischemic stroke subtypes, supporting a link among these 3 entities. Thought of together, as peas in a pod, ischemic and hemorrhagic small vessel damage accounts for about one-third of all strokes and represents an important cause of morbidity and mortality. Ischemic small vessel stroke, often referred to as “lacunar,” is usually manifested as infarctions less than 1.5 cm in diameter on CT or MRI, and attributed to thrombosis of a penetrating vessel in the basal ganglia, thalamus, deep white matter, or brainstem. Studies suggest that lacunar strokes are associated with lower short-term disability and mortality than other ischemic stroke subtypes, and reported 1-year case-fatality rates are low, near 3%. …

Clinical relevance of normal and enlarged Virchow-Robin spaces

Virchow-Robin spaces ensheathe the penetrating vessels of the brain. They communicate with the subpial space, are filled with interstitial fluid and contain a specific population of macrophages.Virchow-Robin spaces are a common finding in both CT and MR imaging. Recent radiologic studies have led to a concise definition of Virchow-Robin spaces.Virchow-Robin spaces appear isointense to cerebrospinal fluid on all imaging sequences. They are typically localised in the basal ganglia, subcortically or in the midbrain and pons. Enlarged Virchow-Robin spaces may appear as a single or multiple lesion(s). They may cause hydrocephalus in rare cases. Some studies indicate that enlarged Virchow-Robin spaces occur more frequently in elderly patients, in patients with arterial hypertension or CADASIL.In this review we illustrate the diagnostic criteria of normal and enlarged Virchow-Robin spaces and discuss their clinical relevance. Furthermore, we present an overview of the current knowledge on the anatomy, physiology and pathology of Virchow-Robin spaces.

Noradrenergic innervation of the rat spinal cord caudal to a complete spinal cord transection: Effects of olfactory ensheathing glia

Transplantation of olfactory bulb-derived olfactory ensheathing glia (OEG) combined with step training improves hindlimb locomotion in adult rats with a complete spinal cord transection. Spinal cord injury studies use the presence of noradrenergic (NA) axons caudal to the injury site as evidence of axonal regeneration and we previously found more NA axons just caudal to the transection in OEG- than media-injected spinal rats. We therefore hypothesized that OEG transplantation promotes descending coeruleospinal regeneration that contributes to the recovery of hindlimb locomotion. Now we report that NA axons are present throughout the caudal stump of both media- and OEG-injected spinal rats and they enter the spinal cord from the periphery via dorsal and ventral roots and along large penetrating blood vessels. These results indicate that the presence of NA fibers in the caudal spinal cord is not a reliable indicator of coeruleospinal regeneration. We then asked if NA axons appose cholinergic neurons associated with motor functions, i.e., central canal cluster and partition cells (active during fictive locomotion) and somatic motor neurons (SMNs). We found more NA varicosities adjacent to central canal cluster cells, partition cells, and SMNs in the lumbar enlargement of OEG- than media-injected rats. As non-synaptic release of NA is common in the spinal cord, more associations between NA varicosities and motor-associated cholinergic neurons in the lumbar spinal cord may contribute to the improved treadmill stepping observed in OEG-injected spinal rats. This effect could be mediated through direct association with SMNs and/or indirectly via cholinergic interneurons.

10 Gy total body irradiation increases risk of coronary sclerosis, degeneration of heart structure and function in a rat model

Purpose: To determine the impact of 10 Gy total body irradiation (TBI) or local thorax irradiation, a dose relevant to a radiological terrorist threat, on lipid and liver profile, coronary microvasculature and ventricular function.Materials and methods: WAG/RijCmcr rats received 10 Gy TBI followed by bone marrow transplantation, or 10 Gy local thorax irradiation. Age-matched, non-irradiated rats served as controls. The lipid profile and liver enzymes, coronary vessel morphology, nitric oxide synthase (NOS) isoforms, protease activated receptor (PAR)-1 expression and fibrinogen levels were compared. Two-dimensional strain echocardiography assessed global radial and circumferential strain on the heart.Results: TBI resulted in a sustained increase in total and low density lipoprotein (LDL) cholesterol (190 ± 8 vs. 58 ± 6; 82 ± 8 vs. 13 ± 3 mg/dl, respectively). The density of small coronary arterioles was decreased by 32%. Histology revealed complete blockage of some vessels while cardiomyocytes remained normal. TBI resulted in cellular peri-arterial fibrosis whereas control hearts had symmetrical penetrating vessels with less collagen and fibroblasts. TBI resulted in a 32 ± 4% and 28 ± 3% decrease in endothelial NOS and inducible NOS protein, respectively, and a 21 ± 4% and 35 ± 5% increase in fibrinogen and PAR-1 protein respectively, after 120 days. TBI reduced radial strain (19 ± 8 vs. 46 ± 7%) and circumferential strain (−8 ± 3 vs. −15 ± 3%) compared to controls. Thorax-only irradiation produced no changes over the same time frame.Conclusions: TBI with 10 Gy, a dose relevant to radiological terrorist threats, worsened lipid profile, injured coronary microvasculature, altered endothelial physiology and myocardial mechanics. These changes were not manifest with local thorax irradiation. Non-thoracic circulating factors may be promoting radiation-induced injury to the heart.

Effects of epinephrine and vasopressin on cerebral microcirculatory flows during and after cardiopulmonary resuscitation*

Both epinephrine and vasopressin increase aortic and carotid arterial pressure when administered during cardiopulmonary resuscitation. However, we recently demonstrated that epinephrine reduces cerebral cortical microcirculatory blood flow. Accordingly, we compared the effects of nonadrenergic vasopressin with those of epinephrine on cerebral cortical microvascular flow together with cortical tissue Po2 and Pco2 as indicators of cortical tissue ischemia. Randomized, prospective animal study. University-affiliated research laboratory. Domestic pigs. The tracheae of ten domestic male pigs, weighing 40 +/- 2 kg, were noninvasively intubated, and the animals were mechanically ventilated. A frontoparietal bilateral craniotomy was created. Microcirculatory blood flow was quantitated with orthogonal polarization spectral imaging. Blood flow velocity in pial and cortical penetrating vessels measuring <20 microm was graded from 0 (no flow) to 3 (normal). Cerebral cortical tissue carbon dioxide and oxygen tensions (Pbco2 and Pbo2) were measured concurrently using miniature optical sensors. Ventricular fibrillation, induced with an alternating current delivered to the right ventricular endocardium, was untreated for 3 mins. Animals were then randomized to receive central venous injections of equipressor doses of epinephrine (30 microg/kg) or vasopressin (0.4 units/kg) at 1 min after the start of cardiopulmonary resuscitation. After 4 mins of cardiopulmonary resuscitation, defibrillation was attempted. Spontaneous circulation was restored in each animal. However, postresuscitation microvascular flows and Pbo2 were greater and Pbco2 less after vasopressin when compared with epinephrine. We observed that a significantly greater number of cortical microvessels were perfused after vasopressin. Cortical microcirculatory blood flow was markedly reduced after epinephrine, resulting in a greater severity of brain ischemia after the restoration of spontaneous circulation in contrast to the more benign effects of vasopressin.

MANAGEMENT TO PREVENT BLEEDING DURING ENDOSCOPIC SUBMUCOSAL DISSECTION USING THE FLUSH KNIFE FOR GASTRIC TUMORS

The gastric vasculature responsible for intraoperative bleeding in endosocpic submucosal dissection (ESD) is the ramified vascular network occupying the middle of the submucosal layer and large vessels penetrating the muscle layer. Appropriate management for these vessels must be addressed. The trimming of the ramified vascular network can be safely performed with coagulation mode following shallow mucosal cutting. A large penetrating vessel usually requires precoagulation prior to dissection. These procedures are effectively performed with the water jet short needle knife (Flush knife).

Vascular Remodeling in Transplant Vasculopathy

As therapeutic strategies to prevent acute rejection progressively improve, transplant vasculopathy (TV) constitutes the single most important limitation for long-term functioning of solid organ allografts. In TV, allograft arteries characteristically develop severe, diffuse intimal hyperplastic lesions that eventually compromise luminal flow and cause ischemic graft failure. Traditional immunosuppressive strategies that check acute allograft rejection do not prevent TV; indeed 50% of transplant recipients will have significant disease within five years of organ transplantation, and 90% will have significant TV a decade after their surgery. TV can involve the entire length of the transplanted arterial bed, including penetrating intraorgan arterioles. Indeed, the luminal narrowing of such penetrating vessels may be the most functionally significant because arterioles represent the major contributors to tissue vascular resistance. Because of the diffuseness of TV involvement in the allograft vascular bed, the only currently definitive therapy requires re-transplantation. Nevertheless, as we better understand the pathogenesis and critical mediators of these lesions, pharmacological advances can be anticipated. Other articles in this thematic review series focus on the specifics of the inciting injury, the cytokines and chemokines that drive TV development, and the nature of the recruited cells in TV lesions, as well as the pathogenic similarities between TV and other vascular lesions such as atherosclerosis. This review focuses on the mechanisms of vascular wall remodeling in TV, including the intimal accumulation of smooth muscle-like cells and associated extracellular matrix, medial smooth muscle cell degeneration, and adventitial fibrosis. A brief overview highlights the aneurysmal changes that can accrue when vessel wall inflammation has a cytokine profile distinct from the typical proinflammatory interferon-gamma-dominated milieu.

Perivascular Spaces: Normal and Giant

The purpose of this paper is to discuss both normal perivascular spaces (PVSs) and pathological giant perivascular spaces (GPVSs). The anatomy and physiology of normal PVSs, including important immunological and lymphatic roles, are described. Special attention is given to the Magnetic Resonance Imaging (MRI) findings of both normal and GPVSs. Furthermore, the clinical features and pathogenesis of GPVSs are explored, with special emphasis on the pathological implications of these lesions, and their relevance. It is important that symptomatic GPVSs not be mistaken for more devastating disease processes. When the lesions in question occur in a characteristic location along the path of a penetrating vessel, are isointense with cerebrospinal fluid on all MRI sequences, do not enhance with contrast material, are not calcified, and have normal adjacent brain parenchyma, their appearance is pathognomonic of GPVSs. The clinician should realize that an extensive differential diagnosis is superfluous and that biopsy is unnecessary in these patients. Instead, the clinical focus should be aimed at neurosurgical intervention, as dictated by the symptoms of mass effect.