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At least 19 recordsLinked to original sources

PubMed2026

A comparative evaluation of multiple enlarged perivascular space segmentation tools.

BACKGROUND: Enlarged perivascular spaces (ePVS) are a marker of cerebral small vessel disease, potentially reflecting reduced waste clearance. Because manual quantification is unfeasible in large datasets, we developed and evaluated an automated tool. METHODS: Detection Of Regions of Enlarged perivascular Spaces (DORES), a 3D nnU-Net-based deep learning algorithm was developed for ePVS segmentation using T1-weighted and fluid-attenuated inversion recovery magnetic resonance imaging (MRI). DORES was developed in two stages: an initial model trained on 35 manually segmented scans and a final model on 1460 pseudo-labeled sessions from the Vanderbilt Memory and Aging Project (VMAP). A subset of VMAP participants with 3 T brain MRI underwent whole-brain manual ePVS tracing (n = 35, 73 ± 9 years, 51% male) and visual rating (n = 388, 71 ± 8 years, 54% male) by a neuroradiologist. DORES was evaluated and compared against three other segmentation tools using Dice and F1 scores, absolute volume and element differences, correlation, and agreement. External validation used an Alzheimer's Disease Neuroimaging Initiative 3 subset with manual tracings (ADNI3, n = 18, 73 ± 9 years, 67% female). RESULTS: DORES achieved Dice scores of 0.61 ± 0.16 (white matter) and 0.72 ± 0.08 (basal ganglia) in VMAP, with strong correlations and agreement for ePVS count and volume. Performances modestly declined in ADNI3 across algorithms. Scanner-stratified analyses showed stronger correlations for Philips versus Siemens images in the basal ganglia, indicating scanner-dependent differences in measurement consistency. CONCLUSIONS: DORES provides a multimodal nnU-Net-based pipeline for ePVS segmentation in older adults. The model demonstrates robust within-cohort performance and reasonable external validity, though scanner-related effects limit application across sites.

Humans↗

PubMed2004

Enlarged perivascular spaces are associated with cognitive function in healthy elderly men.

OBJECTIVES: Increased white matter (WM) lesions on magnetic resonance imaging (MRI) are associated with worse cognitive function in older people. Enlarged perivascular spaces (EPVS) commonly coexist with and share some risk factors for WM lesions but are not quantified in published scales. It is not known whether the extent of EPVS is also associated with cognitive function. We tested the hypothesis that more EPVS would be associated with worse cognitive function. METHODS: Ninety seven healthy men (65-70 years), not on medications, underwent MRI scanning and comprehensive cognitive testing. EPVS were quantified in both the basal ganglia/centrum semiovale and the hippocampus, and WM lesions were measured. RESULTS: Scores on published WM lesion rating scales intercorrelated highly significantly and positively (rho = 0.61 to 0.91, p<0.0001). A summary (WML) factor derived from principal components analysis of the WM scales correlated with EPVS in the basal ganglia/centrum semiovale (rho = 0.48, p<0.0001) but not in the hippocampus. EPVS scores in the basal ganglia/centrum semiovale correlated significantly and negatively with non-verbal reasoning (rho = -0.21, p = 0.038) and general visuospatial ability (rho = -0.22, p = 0.032), adjusted for prior intelligence. The WML factor correlated significantly and negatively with visuospatial ability, as previously reported, and showed an unexpected positive correlation with one test of verbal memory (list-learning). CONCLUSIONS: These findings suggest that increased EPVS are correlated with worse cognitive function. Future studies examining changes in WM with ageing should consider incorporating measures of EPVS and examine the sequence of EPVS and WM lesion development over time. More work is needed to develop valid and reliable measures of EPVS.

Aged↗

PubMed1991

Focal high signal on MR scans of the midbrain caused by enlarged perivascular spaces: MR-pathologic correlation.

Punctate and linear foci of abnormal signal were observed near the substantia nigra in the midbrains of 32 (20%) of 157 patients undergoing high-resolution MR imaging of the brainstem. The lesions were most easily seen on long TR/long TE images, where they were of high signal intensity. Their location was consistently in the lower mesencephalon near the junction of the substantia nigra and cerebral peduncle. Unilateral lesions were observed in 18 cases, while bilateral lesions were noted in 14. A review of anatomic specimens revealed the constant presence of penetrating branches of the collicular or accessory collicular arteries in this location. Enlarged perivascular spaces around these vessels were frequently seen in the specimens and probably account for punctate and linear foci observed on high-resolution MR images of the midbrain.

Adult↗

PubMed2005

Enlarged perivascular spaces mimicking multicystic brain tumors. Report of two cases and review of the literature.

The authors present two cases in which enlarged Virchow-Robin spaces were located in the basal ganglia and the thalamomesencephalic region. The incidence of such huge cystic lesions is extremely rare. The expanding nature of these lesions, demonstrated by the patients' progressive symptoms due to compression of the adjacent brain parenchyma and obstructive hydrocephalus, mimicked that of brain tumors. The two patients were successfully treated by neuroendoscopic cystocisternostomy or ventriculocystostomy. To the authors' knowledge there have been only two published reports on expanding Virchow-Robin spaces that produced a compressive effect or consequent hydrocephalus and were directly fenestrated using neuroendoscopic techniques. Neuroendoscopy appears to offer an effective surgical option in the treatment of symptomatic Virchow-Robin spaces.

Basal Ganglia↗

PubMed1986

[Ultrastructure of capillary permeability in human brain tumors. 3: Mechanisms of contrast enhancement in non-glial tumors].

In order to elucidate mechanisms of contrast enhancement on computed tomography observed in non-glial tumors, tumors vessels were studied with conventional ultrathin section and freeze-fracture replica techniques. The materials were obtained from surgically removed specimens in 19 cases of tumors (6 of meningioma, 6 of hemangioblastoma, 5 of pituitary adenoma, and 2 of acoustic neurinoma). The following results were obtained. The common findings of these non-glial tumor vessels in ultrathin preparations were surface infoldings, increased pinocytotic vesticles and many fenestrations of endothelial cells, irregularity of basal laminae, and enlarged perivascular spaces. In freeze-fracture replicas of vascular endothelium, pinocytotic vesicles and fenestrations were 22 and 26 per micron2 on the average respectively. Tight junctions between endothelial cells were composed of one or two strands which appeared to be a discontinuous array of particles. As for the each non-glial tumor, menigiomas showed endothelial thickness and finger-like projections, variable lengths of tight junctions and marked enlargement of perivascular space which contained many collagen fibrils. Thinning of endothelium and many fenestrations were observed in hemangioblastomas, pituitary adenomas, and acoustic neurinomas. Fenestrations were most frequently observed in pituitary adenomas. The results indicate that extravasation of contrast material through fenestrations has an important role in marked contrast enhancement of non-glial tumors, in addition to the osmotic opening of tight junctions by contrast material. The irregular basal lamina and large perivascular space may also contribute to an increased extravasation of contrast material.

Adenoma↗

PubMed2000

MR imaging and histologic features of subinsular bright spots on T2-weighted MR images: Virchow-Robin spaces of the extreme capsule and insular cortex.

PURPOSE: To determine the cause and frequency of high-signal-intensity foci detected in the insular cortex and extreme capsule on thin-section, high-spatial-resolution, coronal, T2-weighted magnetic resonance (MR) images. MATERIALS AND METHODS: The authors assessed high-signal-intensity areas in the insular cortex and extreme capsule on coronal MR images obtained in 56 patients with seizure and five control subjects. Images were obtained with thin-section, high-spatial-resolution, T2-weighted, fast spin-echo; three-dimensional, spoiled gradient-recalled-echo; and fluid-attenuated inversion-recovery sequences. In two formalin-fixed brain specimens, MR imaging findings were correlated with gross anatomic and histologic findings. RESULTS: Subinsular bright spots were found in 53 of the 56 (95%) patients (96 of 112 [86%] hemispheres) and all five control subjects. The spots were elliptical in 30 patients, round in 14 patients, linear in 22 patients, and dotlike in seven patients and often had a featherlike configuration. The spots were isointense to cerebrospinal fluid on T2-weighted, fast SE images and were located in the anterior extreme capsule white matter and insular cortex. MR imaging of brain specimens revealed bilateral elliptical areas of high signal intensity that corresponded to small multiple cavities at gross anatomic inspection. At microscopic examination, these cavities were perivascular spaces of mostly arteriolar origin. CONCLUSION: High-signal-intensity subinsular foci at MR imaging are due to enlarged perivascular spaces. In most cases, these foci can be visualized on thin-section, high-spatial-resolution, coronal T2-weighted images; they should not be mistaken for pathologic conditions when they occur unilaterally.

Adolescent↗

PubMed2002

White matter lesions and dementia: MRI-pathological correlation.

An MRI-pathological correlation study was performed to determine the pathological background of white matter lesions depicted on MR images. The pathological findings were various combinations of myelin loss, axonal loss, scattered microinfarcts, astrogliosis, dilatation of perivascular space, and relative preservation of subcortical U-fibers. Concerning the dilated perivascular space, we proposed a new classification according to the present study: (1) état criblé in the basal ganglia and the thalamus, (2) état criblé in the cerebral white matter, (3) enlarged perivascular space of the lenticulostriate arteries, and (4) état criblé in other sites. In conclusion, when effects of white matter lesions on cognitive function are to be evaluated, it is necessary to clarify tissues in at least three sequences: T2-weighted, T1-weighted, and FLAIR method.

Alzheimer Disease↗

PubMedDate not supplied

Antibody-mediated CNS demyelination: focal spinal cord lesions induced by implantation of an IgM anti-galactocerebroside-secreting hybridoma.

O1 hybridoma cells, which secrete an IgM antigalactocerebroside, were implanted into the spinal cord of cyclosporine-treated juvenile or adult rats, and the animals were sacrificed approximately 2-3 wk later. About half the recipient animals developed myelin lesions. In some, sharply circumscribed foci of demyelination formed within the dorsal columns. Cellular reaction consisted of macrophages containing refractile globules in the parenchyma and within enlarged perivascular spaces as well as thickened endothelial cells. "Shadow plaques" also developed, i.e. regions in which axons were surrounded by thin myelin sheaths, compatible with remyelination. In addition, we found damaged axons, some of which were swollen with organelles, comparable to the enlarged axon profiles seen at sites of constriction or interruption. Compromise of the blood-brain barrier at sites of hybridoma growth was demonstrated by extravasation of Evans blue dye. Discontinuation of cyclosporine was followed by an anti-hybridoma, complement-fixing antibody response within 2-3 d. This model of focal CNS demyelination and remyelination, with evidence of some axon damage, is mediated by a defined IgM antiglycolipid monoclonal antibody secreted within the spinal cord parenchyma. The lesions, which are similar to those of multiple sclerosis, probably result from the interaction between the intrathecally secreted IgM antibody and complement entering from the circulation at foci of compromised blood-brain barrier plus activation of endogenous or hematogenous macrophages via their complement receptors.

Age Factors↗

PubMed1989

Ultrastructure of capillary walls in human brain tumors.

Changes in capillary walls between human glial, non-glial and metastatic brain tumors were studied with conventional ultrathin section and freeze-fracture replica techniques. The following results were obtained. (1) In glial tumors, ultrathin section studies showed cell junctions of the capillaries were either short or elongate. Moreover, endothelial hyperplasia, surface infolding of endothelial cells, irregularity of the basal lamina and a large extravascular space were observed. Freeze-fracture replicas of capillary endothelium showed tight junctions as two to seven strands. In addition, pinocytotic vesicles had increased markedly and were an average of 25 per microns 2. Both ultrathin and freeze fracture studies showed that, in contrast to malignant gliomas, there were only slight changes in benign astrocytomas. (2) In non-glial tumors, ultrathin sections showed surface infoldings, increased vesicles, many fenestrations of endothelial cells, irregularity of basal lamina and enlarged perivascular space. Freeze-fracture replicas of vascular endothelium, showed that the average number of pinocytotic vesicles and fenestrations were 25 and 22 per microns 2, respectively. Moreover, the tight junction was composed of one or two strands which appeared to be a discontinuous array of particles. (3) In metastatic brain tumors, ultrathin studies showed capillary endothelia were proliferated, had marked infolding, and showed an increased number of pinocytotic vesicles and many fenestrations. Moreover, short and elongate intercellular junctions were presented but no open junction was detected. Finally the basal lamina lost its three-layered appearance and was irregular in width. Freeze-fracture replicas showed pinocytotic vesicles had increased and were 24 per microns 2 on average in four cases, but fenestrations and tight junctions could not be detected. The most fundamental feature of vessels in these three different kinds of tumors was whether they were fenestrated or not. Glial tumors were non-fenestrated, whereas non-glial and metastatic tumors were fenestrated.

Brain Neoplasms↗

PubMed1990

An electron microscopic and electron probe study of the microcirculation in cold-induced oedema.

An ultrastructural study of adult mongrel dogs and cats was made to evaluate the changes in the microcirculation during cerebral oedema formation. Two to five cold injuries were made in one hemisphere in dogs and one lesion was made in cats. In several dogs arterial hypertension was induced with a balloon in the aorta. Intracranial pressure (ICP) and water content were measured. The specimens from the oedematous region were studied with transmission electron microscopy (TEM) and electron probe x-ray micro-analysis (EPMA). The TEM data showed swelling of the endothelium and astrocytic foot processes, enlarged perivascular spaces and increased number of endothelial vesicles. The EPMA findings indicated increases in Fe and Ca content in the perivascular spaces. In some cases, the amount of chloride in red cells was increased. The altered distributions of these metals suggested tissue injury and impairment of red cell and vessel wall functions.

Animals↗

PubMed1994

Focal microvascular occlusion after acute subdural haematoma in the rat: a mechanism for ischaemic damage and brain swelling?

Using a rat model of subdural haematoma (SDH) which is associated with ischaemic damage in the ipsilateral hemisphere, we have studied the microcirculation and the time course of development of ischaemia beneath the subdural haematoma. The latter was investigated by measuring cerebral blood flow (CBF) using the hydrogen clearance technique, the former by electron microscopy (EM) and carbon black angiography. CBF fell below 5 ml/100g/min within five minutes of SDH and remained low (< or = 7 ml/100g/min) for over two hours. Contralateral CBF fell to 54% of control but normalized by 1 hour. Carbon black angiography showed absent perfusion beneath the SDH. EM demonstrated: 1) normal cortical vessel traversing the haematoma; 2) occlusion of cortical vessels under SDH by clotted red cells and platelets; 3) massively enlarged perivascular spaces due to swelling of astrocytes. No vasospasm was seen. The "ischaemic core" may develop where microvascular occlusion occurs, and this microcirculatory disturbance initiates ischaemic cell damage with release of glutamate, which spreads outward from the core. This causes further damage of neurons and swelling of astrocytes, resulting in severe ischaemic necrosis, and progressive brain edema. The cause of microvessel occlusion remains unknown.

Animals↗

PubMed1993

Pathogenesis of primary central nervous system lymphoma: invasion of malignant lymphoid cells into and within the brain parenchyme.

The pattern of invasion of lymphoid cells to the central nervous system (CNS) was analyzed for malignant lymphocytes in 19 primary CNS lymphomas (PCNSL) and six intracerebral metastatic lymphomas, and for reactive lymphocytes in four encephalitides and three astrocytomas. The identical spreading pattern in both primary and metastatic lymphomas suggests that even in the so-called primary CNSL the malignant transformation has occurred outside the CNS. The compact perivascular cuffs of both malignant and reactive lymphocytes were never seen around the smallest capillaries, and they were most common around vessels larger than 15 microns in diameter. Perivascular lymphocytes resided within the reticulin network, which was immunopositive for collagen type III and IV, laminin and fibronectin. These findings imply that lymphocytes extravasate at the level of arterioles and venules and spread along the enlarged perivascular space. When the outer boundary of the perivascular network was broken, malignant lymphocytes spread diffusely into the CNS parenchyme; a pattern which is different from that of other CNS metastases. The widespread immunopositivity for the homing cell adhesion molecule CD44 in the CNS vessels and parenchyme, especially in the white matter which is the predilection site of PCNSL, suggest that this adhesion molecule and its ligands participate in spreading of malignant lymphocytes within the CNS parenchyme.

Adult↗

PubMed1998

Atypical juvenile neuronal ceroid lipofuscinosis with granular osmiophilic deposit-like inclusions in the autonomic nerve cells of the gut wall.

In this 8-year-old boy, who had been exposed to alcohol and oxazepam during pregnancy, visual failure was the first symptom of a neuronal ceroid lipofuscinosis (NCL) disorder, noticed at the age of 5 years. Ophthalmological examinations revealed a cystic type of macular degeneration, which would be more likely to be found in variant late infantile NCL. However, vacuolated lymphocytes were found in peripheral blood films and a diagnosis of the juvenile form of NCL (JNCL) was made. Molecular genetic studies showed the patient to be homozygous for the major mutation of JNCL, a 1.02-kb deletion. In whole-night polysomnography, there was significantly more epileptiform activity than in other JNCL patients under 10 years of age. Using magnetic resonance imaging, the signal intensity of the white matter was increased, especially in the periventricular area. In addition, there were enlarged perivascular spaces in the watershead areas. The corpus callosum was thin. Finally, in the autonomic ganglion cells of the submucosal nerve plexus there were membrane-enclosed homogeneous and granular cytosomes resembling the granular osmiophilic deposits of infantile NCL. However, extraneural cells, including blood capillaries and smooth muscle, showed inclusions with fingerprint and curvilinear profiles. The features of the present case indicated a phenotypic variant of JNCL.

Child↗

PubMed2004

Effects of umbilical cord occlusion in late gestation on the ovine fetal brain and retina.

OBJECTIVE: Previous studies on the effects of umbilical cord occlusion (UCO) on the fetal brain have focused on short-term alterations, and in most cases have used only subjective techniques to evaluate brain injury. Our aim was to assess quantitatively the persistent consequences of UCO on the developing brain; we also examined the retina. METHODS: We subjected fetal sheep to a single episode of UCO at 126 days of gestation (term approximately 147 days) to induce at least 10 minutes of isoelectric fetal electrocorticogram (ECoG). RESULTS: UCO resulted in fetal asphyxia and transient mild alterations in fetal mean arterial pressure (MAP). UCO did not result in significant injury to the developing brain or retina when assessed 15 days after the insult. There was no change in the endogenous expression of brain-derived neurotrophic factor (BDNF) protein in the hippocampus, nor was there a significant loss of CA1 hippocampal pyramidal cells. However, this insult did result in subtle neuropathologic alterations in the brain, including a reduction in the weight of the cerebral hemispheres, an increase in the areal density of cerebellar Purkinje cells, and enlarged perivascular spaces around blood vessels and inflammatory cells in the cerebral white matter. UCO did not affect the thickness of the central or peripheral retina or the numbers of retinal dopaminergic, cholinergic, and nitrergic amacrine cells. CONCLUSIONS: Thus, while 10 minutes of UCO did not result in overt injury to the fetal brain or retina, the observed changes in the fetal brain suggest altered growth of neural processes, which may contribute to neurologic deficits postnatally or to increased vulnerability of the brain to later insults during either the remainder of gestation or after birth.

Animals↗

PubMed2002

Venous collagenosis and arteriolar tortuosity in leukoaraiosis.

Leukoaraiosis (LA), an age-related white matter degeneration, is thought to be caused by chronic ischemia. To understand the pathogenesis of LA, we studied the pathology, particularly of the blood vessels, in 186 brains [84 of them with magnetic resonance imaging (MRI)] over the past 10 years. With normal aging, there is gradual thickening of the walls of periventricular veins and venules with collagen subtypes I and III. This venous collagenosis (VC) was increased in brains with LA. Occasionally, LA lesions are not periventricular, but nearer the cortex. In such cases, the most severe VC occurs in the LA lesion rather than near the ventricle. Therefore, LA and VC are not independent degenerative processes coincidentally found near the ventricles, and although damage to the ependyma could be a cause of VC, it cannot be the only cause. Whether VC precedes LA is unknown, but our experience suggests that severe VC is usually accompanied by LA. Arteriolar tortuosity, another age-related vascular pathology, is common in LA. Our thick celloidin sections show three-dimensional views of tortuous arterioles. The tortuosity is much more severe in the white matter and there is considerable loss of parenchyma around them. Staining for collagen IV in the basal lamina reveals tortuous vessels in an "empty bag" that represents the limits of the surrounding parenchyma. These enlarged perivascular spaces correspond to état criblé. The demyelination in LA lesions is accompanied by loss of cells, mostly oligodendrocytes. In studies of apoptosis in LA, we found increased apoptosis within the lesion compared to the surrounding white matter. In conclusion, our studies support the concept that LA results from chronic ischemia due to age-related vascular pathology.

Aged↗

PubMed1997

Experimental syringomyelia: late ultrastructural changes of spinal cord tissue and magnetic resonance imaging evaluation.

BACKGROUND: In human hydrosyringomyelia and in the late stage of experimental syringomyelia, the spinal cord tissue adjacent to the syrinx is exposed to a similar pathophysiologic condition. We investigated the ultrastructural changes in the late stages of kaolin-induced syringomyelia, and in addition, we presented magnetic resonance imaging (MRI) findings of the cervicomedullary junction and syrinx, and the nature of edema in the spinal cord of this experimental model. METHODS: Syringomyelia was induced in rabbits by intracisternal injection of kaolin. MRI was performed at 6 weeks, and 6 and 12 months following injection, and the animals were killed by transcardial perfusion of formaldehyde solution and examined by transmission electron microscopy. Evans blue was injected intravenously in six rabbits, 6 weeks and 12 months following kaolin injection and was examined by confocal laser scanning microscopy. RESULTS: MRI showed that the syrinx communicated with the fourth ventricle in most animals. Demyelination of varying degrees and slight edematous change were seen in the perisyrinx white matter. No extravasation of Evans blue was seen by confocal microscopy. Abundant astrocytic proliferation with a large number of glial filaments was seen at the margin of the syrinx and between the axons in the perisyringeal region. The perivascular space enlargement occurred in both the gray and white matter. The endothelial junctions appeared intact. Regenerating axons and remyelination by oligodendrocytes were seen occasionally. CONCLUSIONS: The MRI confirmed the communication between the fourth ventricle and the syrinx. The ultrastructural changes were almost identical to those of the early stage syrinx, but the astrocytic proliferation was more severe, and the edema was less in the late stage. The perisyrinx edema appeared to be of the interstitial type, as in hydrocephalus. Axonal degeneration and demyelination continued with abortive attempt at regeneration and remyelination in the less edematous late stage, which might be the cellular basis for the persistence or worsening of clinical symptoms and signs in the chronic stage of syringomyelia even after surgical treatment.

Animals↗

PubMed1995

Neuropathology of lightning-strike injuries.

When a person is struck by lightning a spectrum of neurologic damage can result. Approximately one third of the strikes prove to be fatal. The possibility of damage to the CNS relates to the type of lightning injury (direct strike, stride potential, or side flash), the intensity and duration of the current, the pathway of the current within the body, and secondary injuries to brain either from cardiac arrest and hypoxia or from physical trauma. Direct strikes to the head have a high degree of fatality and often result in petechiae or larger brain hemorrhages. Although there may be some predilection for the petechiae to occur in the brainstem, the larger hemorrhages may be particularly located near the pathway of the electrical current and result from direct damage to brain vasculature. Enlarged perivascular spaces seen histologically are relatively subtle; they have been attributed to the effects of gas bubbles from electrolysis, heat formation, or both. Small vessel thrombi and neuronal changes may be present nearby. Some brain tissue softening and edema may be direct effects of passage of current. Often, however, hypoxic encephalopathy and cerebral edema occur following cardiopulmonary arrest when the passage of the current through the body presumably generates cardiac arrhythmias. Considerably less is known about the spinal cord injuries in lightning strike, although one detailed recent study suggests that demyelination may be an underlying mechanism. Similarly, myelin damage appears to be a feature of electrical and possibly lightning injury to the peripheral nervous system.

Brain Injuries↗

PubMed2006

48 year old male with sudden onset of right sided weakness.

This 48 year-old male presented with sudden right sided weakness and hypertension, and on CT was found to have a deep left hemispheric intracerebral hematoma. There were accompanying bilateral hypointensities in the occipital lobes, unchanged 1 day later, when expansion of the hematoma and uncal herniation resulted in death. The past medical history included liver transplantation followed by long term cyclosporin, features of thrombotic thrombocytopenic purpura (TTP) attributed to cyclosporin, type 1 diabetes mellitus and acute renal failure attributed to diabetic nephropathy. There was a 2-month history of hypertension poorly responsive to therapy. The occipital lobes at autopsy showed focal cortical hemorrhages with bilateral discoloration of white matter sparing subcortical zones. Microscopy showed white matter pallor with parenchymal cysts, enlarged perivascular spaces and focal acute hemorrhages consistent with edema secondary to acute hypertension. Cortical hemorrhages were associated with intravascular thrombi and fibrin exudates, as well as an accompanying microinfarct, attributed to TTP. The occipital pathology reflects the posterior leukoencephalopathy syndrome (PLS) combined with cortical lesions of TTP. PLS is usually diagnosed radiologically by occipital hypointensities, and is reversible, so that autopsy pathology is rarely examined. TTP may predispose to the development of the PLS in certain cases.

Brain Edema↗