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R A Prayson

Publications and source records attributed to R A Prayson.

At least 91 records · Page 5Linked to original sources
PubMed1997

Autopsy findings of fatal complication of posterior cerebral circulation angioplasty.

Percutaneous transluminal angioplasty is a technique widely used to treat stenotic atherosclerotic lesions of the coronary arteries. This technique is currently gaining acceptance for the treatment of cerebral atherosclerotic disease. Autopsy findings of fatal complications of percutaneous transluminal angioplasty of the posterior cerebral circulation have, to our knowledge, not yet been published. We report the case of a patient with severe diffuse atherosclerosis of vertebral and basilar arteries, whose symptoms were not ameliorated with standard medical therapy. Transfemoral percutaneous transluminal angioplasty was performed in an attempt to reestablish blood flow in the posterior cerebral circulation by angioplasty of a severely stenotic basilar artery. The patient suffered a fatal complication during the procedure due to rupture of the basilar artery by the percutaneous transluminal angioplasty guidewire apparatus, leading to massive subarachnoid hemorrhage. We report the clinical and autopsy findings of this case.

Aged↗
PubMed1997

Adult-onset nemaline myopathy: a case report and review of the literature.

Nemaline (rod) myopathy is a congenital muscle disease with a wide spectrum of phenotypes, ranging from forms with neonatal onset and fatal outcome to asymptomatic forms. An adult-onset variant is characterized by large numbers of rod-containing myofibers, numerous rods per affected myofiber, and the absence of specific structural abnormalities typical of other muscle diseases. Few cases fulfilling these criteria have been described in the literature. Rare cases have had an associated inflammatory component, and the majority of these have occurred in patients with an underlying immunologic disorder. We present an unusual case of an immunologically competent 65-year-old man with late-onset nemaline myopathy, who was previously diagnosed with an inflammatory myopathy based on a muscle biopsy that contained chronic inflammation. His symptoms consisted of a 2-year history of progressive proximal muscle weakness; his family history was unremarkable. A neurologic examination confirmed the presence of bilateral proximal muscle weakness, normal sensation, and decreased upper and lower extremity reflexes. Creatine kinase levels were normal, and electromyographic findings indicated a myopathic process. A modified trichrome stain of the right biceps muscle revealed granular, basophilic, centrally located rods in the atrophic myofibers. Ultrastructurally, these myofibers contained osmiophilic rectangular structures with a latticelike appearance typical of nemaline myopathy. This case illustrates that adult-onset nemaline myopathy, although rare, should be considered in the differential diagnosis of an inflammatory myopathy.

Age Factors↗
PubMed1996

Gliofibroma: a distinct entity or a subtype of desmoplastic astrocytoma?

Gliofibromas are rarely encountered astrocytic neoplasms characterized by an admixture of astrocytic and fibroblastic cell components. The exact nature of these rare tumors are still a matter of considerable debate. This article reports a case of gliofibroma occurring in a 3-month-old boy. The astrocytic component of the tumor stained diffusely positive for glial fibrillary acidic protein (GFAP) and S-100 protein. Prominent reticulin staining was observed within the fibroblastic component of the tumor. The MIB1 labeling index (positive number of tumor cells divided by total tumor cells counted X 100) was low (0.9), supporting the general slow growth of these tumors. Immunohistochemical staining with antibody against p53 protein was negative. Gliofibromas seem to be a low-grade variant of an astrocytoma that shares many features with other desmoplastic astrocytic neoplasms (desmoplastic infantile astrocytoma, desmoplastic infantile ganglioglioma) including a generally favorable prognosis.

Astrocytoma↗
PubMed1996

Leukocyte adhesion molecules and x-ray energy dispersive spectroscopy in Sturge-Weber disease.

We examined the light microscopic and ultrastructural features associated with Sturge-Weber disease, including x-ray energy dispersive spectroscopy to evaluate the chemical composition of the mineralized deposits and immunofluorescence microscopy with leukocyte adhesion molecules to examine the blood vessel proliferation further. Two patients (a 17-year-old girl and a 9-month-old boy) with Sturge-Weber disease comprise this series. Mineralized deposits stained strongly positive with von Kossa and negative with Prussian blue. Transmission electron microscopy of tissue removed during a functional hemispherectomy procedure in both cases indicated that most concretions were adjacent to or in the basal lamina of parenchymal vessels; no deposits were observed in leptomeningeal vessels. Energy dispersive spectroscopy of the deposits showed emission peaks corresponding predominantly to calcium, with lesser amounts of phosphorus. Fluorescent monoclonal antibodies to leukocyte adhesion molecules (endothelial cell, vascular cell, and intercellular: ELAM-1, VCAM-1, and ICAM-1) demonstrated strong positive staining of the meningeal vessels with all three antibodies. Cortical vessels were positive only for ICAM-1. Findings based on routine staining and energy dispersive spectroscopy indicate that the mineralized deposits detected in Sturge-Weber disease are composed primarily of calcium phosphate and are located primarily in and adjacent to the vascular basal lamina. There is an aberrant expression of ELAM-1 and VCAM-1 in the meningeal vascular proliferation similar to what is observed with other vascular malformations and tumors. Parenchymal vessel changes may be secondary to the meningeal vascular proliferation.

Adolescent↗
PubMed1996

Angiotropic large cell lymphoma: simultaneous peripheral nerve and skeletal muscle involvement.

Angiotropic large cell lymphoma is a rarely encountered disorder characterized by a proliferation of malignant lymphoid cells within vascular lumina. Sites usually affected include the skin and central nervous system, although involvement of multiple other organ symptoms have been described including peripheral nerve and skeletal muscle. Simultaneous involvement of both skeletal muscle and peripheral nerve has rarely been reported. In most of those cases the diagnosis was made only at the time of autopsy. A case of an elderly male with angiotropic large cell lymphoma and in whom the diagnosis was made antemortem on a peripheral nerve and skeletal muscle biopsy is reported.

Aged↗
PubMed1996

Malignant meningioma: a clinicopathologic study of 23 patients including MIB1 and p53 immunohistochemistry.

Malignant meningiomas are rarely encountered neoplasms. Few studies have examined MIB1 (marker of cell proliferation) or p53 (tumor suppressor gene) immunoreactivity in these tumors. This study retrospectively examines 23 malignant meningiomas (defined by the presence of either unequivocal brain invasion or metastasis) including MIB1 and p53 immunohistochemistry. The patients included 13 women and 10 men who ranged in age from 22 to 82 years (mean 63 years). Initial clinical presentation included weakness or numbness in 10 patients, visual signs or symptoms in 7 patients, and headaches in 6 patients. Histologically, nuclear pleomorphism was present in 23 of 23 tumors, disorganized architecture in 22 of 22, necrosis in 20 of 23, prominent nucleoli in 17 of 23, and hypervascularity in 4 of 23. One to 18 mitotic figures per 10 high power fields (HPF) (mean 6.1) were observed. Metastases were present in six patients (bone: 3 patients; lung: 2 patients; skin: 2 patients; kidney: 1 patient; and liver: 1 patient). MIB1 indices (positive tumor cells per 1,000 tumor cells evaluated x 100) in 20 tumors ranged from 1.3 to 24.2 (mean 11.7). p53 nuclear staining was observed in only 2 of 20 tumors. Follow-up information was available in 21 patients: 6 died of tumor (mean 27 months); 9 are alive with residual tumor (mean 35 months); 5 are alive with no evidence of tumor (mean 12 months); and 1 died 13 days postoperatively. There was no obvious correlation of the MIB1 index and tumor behavior. The majority of malignant meningiomas are characterized by nuclear pleomorphism, architectural disorganization, necrosis, prominent nucleoli, and increased mitoses. MIB1 labeling in most malignant meningiomas was high, consistent with the generally rapid growth of these tumors. Only a rare malignant meningioma demonstrated p53 alteration by immunostaining.

Adult↗
PubMed1996

Histopathologic findings in 107 uterine leiomyomas treated with leuprolide acetate compared with 126 controls.

The reported histopathologic findings in leiomyomas treated with leuprolide acetate (LA) differ. We examined 233 myomectomy specimens, including 107 myomas from 30 patients (mean age, 34.7 +/- 4.6 years) treated with LA. Their histopathologic findings were compared with those from a control group of 126 myomas from 30 untreated patients (mean age 32.7 +/- 5.3 years). The LA-treated leiomyomas had myxoid change (n = 2; 1.9%), total necrosis (n=4; 3.7%), focal necrosis (n = 5; 4.7%), calcifications (n = 5; 4.7%), hemorrhage (n = 8, 7.5%), vascular changes (n = 12; 11.2%), hydropic degeneration (n = 22; 20.5%), and hyalinization (n = 61; 57.0%). None of these changes differed significantly from the untreated controls. None of the LA-treated leiomyomas had nuclear atypia, whereas nuclear atypia occurred in four (3.2%) of the untreated leiomyomas; this difference was also not significant. Mitotic figures were present in 8.4% of the LA-treated myomas and 8.5% of untreated controls. The number of mitotic figures per 10 high-power fields was slightly higher in the untreated myomas, but the difference was not statistically significant (range, 0-3 for treated, 0-5 for controls). The degree of cellularity did not differ between the two groups. In conclusion, (a) LA-treated myomas do not significantly differ from untreated myomas with respect to nuclear atypia, calcification, total coagulative necrosis, focal coagulative necrosis, hemorrhage, vascular changes, myxoid change, hydropic degeneration, hyalinization, mitotic activity, or cellularity; and (b) the mechanism leading to a reduction in the size of myomas treated with LA is not apparent from routine histologic examination.

Adult↗
PubMed1996

Evaluation of nerve recovery from minimal-duration crush injury.

The recovery of damaged peripheral nerves has been the subject of multiple studies. The effects of an inadvertent clamping of a nerve has not been well examined. An experiment was performed to evaluate the effects of a minimal-duration crush injury on the rat sciatic nerve and to determine if walking track analysis was useful in evaluating the short-term functional deficit. Ten Sprague-Dawley rats underwent high-pressure, short-duration crush injuries. Walking track analysis was done regularly for 3 weeks. Histological specimens for light and electron microscopy were taken at postoperative days 3, 7, 14, 21, and 42 from similar animals. There was significant decrease in function by the second week, which then improved to control levels after week 3. Toluidine blue and electron microscopic findings confirmed the clinical course, while routine histological findings tended to lag behind the return of function. Walking track analysis appears to be an effective method of evaluating the short-duration nerve crush injury.

Animals↗
PubMed1996

Lewy body disease.

Lewy bodies have historically been considered a histopathologic hallmark of idiopathic Parkinson's disease. Recently, it has become clear that Lewy bodies play a role in neurodegenerative processes other than idiopathic Parkinson's disease, including diffuse Lewy body disease and diffuse Lewy bodies with concomitant Alzheimer's disease changes. It is likely that these processes represent a spectrum of neurodegenerative change in which Lewy bodies play a pivotal role. Although much is known and has been written regarding the histopathology and pathophysiology of Lewy body diseases, specific criteria for their diagnosis remain problematic. Within the spectrum of Lewy body disease, overlap in clinical presentation and histopathologic findings has caused some to dismiss attempts at subcategorizing Lewy body disease as artificial. We present, in brief, current information and theories concerning the pathology and pathogenesis of Lewy body disease.

Alzheimer Disease↗
PubMed1996

MIB1 and p53 immunoreactivity in protoplasmic astrocytomas.

Pure protoplasmic astrocytomas are a group of rarely encountered low grade astrocytic neoplasms. Relatively few studies have specifically examined this subset of tumors. A series of 18 protoplasmic astrocytomas in 14 males and four females (age range 2.5-52, mean 22 years) were studied in order to examine MIB1 (a marker of cell proliferation) and p53 (a tumor suppressor gene) immunoreactivity. All patients presented with seizures (mean duration 94 months) and three with headaches also. Eight tumors were located in the temporal lobe and six in the frontal lobe. All tumors were characterized by a proliferation of astrocytes with round nuclear contours arranged against a microcystic background. Only rare foci of mild vascular proliferation (3 tumors), rare mitotic figures (1 tumor), and mild nuclear atypia (3 tumors) were observed. Most tumors were primarily cortical in location. Necrosis was not seen in any of the tumors. MIB1 indices (number of MIB1 positive tumor cells/1000 tumor cells evaluated x 100) ranged from 0 to 4.3 (mean 0.7); in five tumors, no MIB1 staining was observed. p53 immunoreactivity was noted in 5 of 18 tumors (28%). Five patients received adjuvant radiation therapy and one adjuvant chemotherapy. At last known follow-up, 11 patients are alive with no evidence of residual tumor (mean 70 months), six patients are alive with evidence of residual tumor (mean 58 months), and one patient died of complications unrelated to the tumor (36 months) postoperatively. Based on these findings, the conclusions presented are as follows: (i) MIB1 indices are generally low in these tumors, corroborating the clinical impression of a slow growing neoplasm; and (ii) p53 immunoreactivity is observed in a minority of protoplasmic astrocytomas.

Adolescent↗
PubMed1996

Mesial temporal sclerosis. A clinicopathologic study of 27 patients, including 5 with coexistent cortical dysplasia.

OBJECTIVE: Mesial temporal sclerosis (MTS) is a fairly well-recognized cause of intractable epilepsy. Its coexistence with cortical dysplasia is less commonly described. Herein, we describe the clinical and pathologic features of MTS, including cases in which cortical dysplasia was also identified. DESIGN: Retrospective surgical series of 27 patients. SETTING: Tertiary referral center with a high volume of epilepsy surgery. PATIENTS: Patients with medically intractable epilepsy who underwent hippocampal resections and in whom an unequivocal histologic diagnosis of MTS could be made. RESULTS: The patients studied included 18 males and 9 females ranging in age from 15 to 48 years (mean 32 years). Mesial temporal sclerosis was characterized by severe neuronal loss accompanied by gliosis occurring in the CA1/prosubiculum (27 patients, 100%), focally in the dentate gyrus (12 patients, 44%), and in the CA4 region (11 patients, 41%). Five patients (24%) had coexistent cortical dysplasia with increased molecular layer neurons (five patients), gyral fusion (two patients), diffuse architectural disorganization of the cortex (one patient), and clusters of atypical neurons and glial cells within the cortex (one patient). Twenty-five (93%) of the 27 patients had white matter neuronal heterotopia. Follow-up data were available for each patient (mean 23 months). Twenty-two of the patients are free of seizures postoperatively, including all five with coexistent cortical dysplasia; the five remaining patients have fewer seizures. There appeared to be no difference clinically between patients with MTS and no dysplasia and those with coexistent cortical dysplasia. CONCLUSION: We conclude that (1) MTS most severely involves the CA1/prosubiculum and CA4 regions of the hippocampus (the dentate gyrus may also be focally severely involved); (2) MTS and cortical dysplasia do occasionally exist; and (3) surgical outcome for MTS appears to be independent of coexistent cortical dysplasia.

Adolescent↗
PubMed1995

Cortical dysplasia: a histopathologic study of 52 cases of partial lobectomy in patients with epilepsy.

In utero migrational abnormalities account for most cases of cortical dysplasia. The histopathologic appearance of cortical dysplasia is often varied, making recognition and classification difficult. We studied 52 patients with cortical dysplasia who underwent partial lobectomy for medically intractable seizures in order to devise a simple histopathologic classification schema. The incidence of observed dysplasia in lobectomy specimens over an 11-year period (n = 360) was 14%. Patients ranged in age from 3 months to 47 years at the time of surgery (mean, 19 years; 29 male and 23 female patients). The temporal lobe was involved in 34 patients, frontal lobe in 18, parietal lobe in four, and occipital lobe in three. In three patients multiple lobes showed dysplasia. Dysplasia was right-sided in 29 patients and left-sided in 23 patients. Dysplasia was focal in 23 patients, multifocal in four patients, and diffuse in 25 patients. Three main histologic patterns of cortical dysplasia were observed: (1) a cortical laminar architectural disorganization and/or malalignment of neurons (26 patients), (2) clusters of atypical neurons and glia within the cortex (28 patients), and (3) a hypercellular molecular layer with increased numbers of neurons and glia (31 patients). In 23 patients more than one pattern of dysplasia was identified. Coexistent tumors were present in 13 patients, including ganglioglioma (eight patients), dysembryoplastic neuroepithelial tumor (three patients), and low-grade astrocytoma (two patients). Tuberous sclerosis was present in four patients. We conclude that most types of cortical dysplasia can be divided into three main histologic patterns, facilitating the recognition of dysplasia. In addition to the known association with tuberous sclerosis, tumors may coexist with cortical dysplasia.

Adolescent↗
PubMed1995

Protoplasmic astrocytoma. A clinicopathologic study of 16 tumors.

UNLABELLED: Protoplasmic astrocytomas, composed of process-poor astrocytic cells and a microcystic background, are rare variants of low grade astrocytoma. Three hundred eight low grade astrocytomas over a 23-year period were reviewed. Sixteen (5.2%) were classified as pure protoplasmic astrocytoma. Patients (12 males, 4 females) ranged in age from 2.5 to 41 years (mean, 20.7 years). All patients presented with seizures and three had headaches. Duration of symptoms ranged from 7 months to 28 years (mean, 6.6 years). Nine tumors (56%) were left-sided and seven right-sided (44%). Seven (44%) occurred in the temporal lobe, six (37%) in the frontal lobe, two (13%) in the parietal lobe, and one (6%) in the thalamus. Surgery consisted of partial lobectomy with total tumor resection in nine and biopsy alone in seven. Five patients received adjuvant therapy with no apparent effect on survival. At frozen section, protoplasmic astrocytoma was most confused with fibrillary low grade astrocytoma (n = 6). Follow-up revealed 10 patients with no evidence of disease 2 to 108 months postoperatively (mean, 41 months), 5 patients were alive with disease 10 to 84 months postoperatively (mean, 56 months) and 1 patient died with disease at 36 months. Of patients with total tumor resection, eight had no evidence of disease and one died with disease. IN CONCLUSION: (1) protoplasmic astrocytomas in this study were more frequently observed in males at a younger mean age than fibrillary low grade astrocytomas as reported in literature; (2) temporal and frontal lobes were the most likely site of origin; and (3) complete excision may be beneficial, whereas adjuvant therapy appeared to have no effect on outcome.

Adolescent↗
PubMed1995

Vulvar vestibulitis. A histopathologic study of 36 cases, including human papillomavirus in situ hybridization analysis.

Vulvar vestibulitis is a recently described clinical condition of unknown etiology. Human papillomavirus (HPV) infection has been implicated as a causal pathogen by some investigators. Because reports on this entity are few, we studied the pathologic features of vestibulectomy specimens from 36 women with a clinical diagnosis of vulvar vestibulitis. The patients' ages ranged from 19 to 53 years (mean, 31 years). Bilateral excisions were performed in 34 patients and a unilateral excision in two. Minor vestibular glands or ducts were identified in 28 patients (78%). Chronic inflammation was present in all specimens. The inflammatory infiltrate consisted predominantly of T lymphocytes and plasma cells with smaller numbers of B lymphocytes. Lymphoid follicles were present in four patients, ulcers in two. The predominant site of inflammation was the squamous mucosa, especially the lamina propria, where the degree of inflammation was graded as mild in 11 patients, moderate in 21 patients, and severe in four patients. To a lesser degree, the inflammation also typically involved the periglandular/periductal connective tissue of the minor vestibular glands, where it was graded as mild in 25 patients and moderate in three patients. Foci of squamous metaplasia were observed in 27 of 28 patients with demonstrable vestibular ducts or glands. Nodular hyperplasia of a vestibular gland (so-called "adenoma") occurred in one patient. In six selected cases, fungi were not identified on silver stains. Morphologic findings of HPV infection, such as koilocytotic atypia or squamous dysplasia, were absent. In-situ hybridization studies for HPV types 6, 11, 16, 18, 31 and 35 were negative in all 36 cases. We conclude that (a) vestibulectomy specimens from patients with a clinical diagnosis of vulvar vestibulitis typically show a chronic inflammatory cell infiltrate that predominantly involves the mucosal lamina propria and periglandular/periductal connective tissue and (b) a pathogenetic role for HPV types 6, 11, 16, 18, 31 and 35 is not substantiated.

Adult↗
PubMed1995

Cortical architectural abnormalities and MIB1 immunoreactivity in gangliogliomas: a study of 60 patients with intracranial tumors.

Gangliogliomas are generally low grade neoplasms composed of mixtures of neoplastic glial and neuronal elements whose origin and exact nature are still controversial. We studied a series of 60 intracranial gangliogliomas looking for coexistent cortical architectural abnormalities (cortical dysplasia, microdysgenesis) and to determine if tumor behavior correlates with MIB1 (marker of cellular proliferation) labeling. The patients included 34 males and 26 females who ranged in age from 6 months to 55 years (mean 20 years). Thirty-eight tumors (63%) were located in the temporal lobe and 6 (10%) in the frontal lobe. Fifty-four patients (90%) presented with seizures (most with intractable epilepsy) and the duration of seizures ranged from 1 to 38 years (mean 14 years). In all cases, the predominant glioma component resembled a low grade fibrillary astrocytoma. In 14 tumors (23%), an oligodendroglial component was present. In one case, the glial component resembled an anaplastic astrocytoma. The tumors were characterized variously by perivascular chronic inflammation (N = 45, 75%), vascular proliferation (N = 36, 60%), granular bodies (N = 54, 90%), binucleated neurons (N = 36, 60%), calcification (N = 28, 47%), and cystic degeneration (N = 26, 43%). Meningeal involvement by tumor was observed in five (8%) cases. In 38 patients, sufficient tissue was resected to evaluate for the presence of concomitant cortical architectural abnormalities. Cortical architectural abnormalities were identified near to but clearly separate from the tumor in 19 (50%) patients. Only four patients including the anaplastic tumor died with tumor progression. MIB1 indices (positive tumor cells/1,000 tumor cells counted) in 54 cases ranged from 0 to 10.2 (mean 1.1 +/- 1.0).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Childhood ganglioglioma and medically intractable epilepsy. A clinicopathological study of 15 patients and a review of the literature.

Gangliogliomas are an increasingly recognized cause of epilepsy in children. Several studies have shown that early surgical treatment is beneficial, but controversy exists regarding the type of surgical treatment required for optimal seizure control and to prevent tumor recurrence. To address this issue, we performed a retrospective review of 15 children operated on at the Cleveland Clinic during a 7-year period with medically intractable epilepsy who were found to harbor a ganglioglioma during the course of their work-up. Nine patients with mostly nondominant hemisphere tumors underwent tumor resection without the use of electrocorticography to guide additional resection of epileptogenic foci, while 6 other patients with dominant hemisphere tumors had subdural electrode grids placed to extraoperatively map zones of ictal onset and eloquent areas. The extent of tumor resection was then correlated to seizure outcome and tumor recurrence. Of the 11 patients who received a gross total resection, 9 are seizure-free while 2 have a greater than 90% reduction in their seizure frequency (100% 'good' outcome). There was no tumor recurrence in this group. Of the 4 patients who underwent a subtotal tumor resection, 1 is seizure-free while 3 have persistent seizures (25% 'good' outcome). All patients in this group have stable disease on follow-up magnetic resonance imaging. In those patients who received subdural electrode grids, the extent of resection of the zones of ictal onset did not correlate with seizure outcome. The mean follow-up was 42 months. We conclude that complete tumor resection is the most important factor for optimal seizure control and to prevent tumor recurrence.

Adolescent↗
PubMed1995

Meningioangiomatosis. A clinicopathologic study including MIB1 immunoreactivity.

OBJECTIVE: To examine the etiology of and clinicopathologic findings associated with meningioangiomatosis and to evaluate MIB1 immunoreactivity (marker of cell proliferation) in this lesion. DESIGN: Retrospective surgical pathology series of three patients. SETTING: Tertiary referral center with a high volume of epilepsy surgery. PATIENTS: Individuals with meningioangiomatosis who underwent surgical resection of the lesion. RESULTS: Three patients aged 11, 14, and 32 years (two females, one male) comprise the study. All patients presented with a history of intractable seizures (2, 3, and 30 years duration). None of the patients had von Recklinghausen's disease. All three patients underwent gross total resection of the lesion, and postoperative seizure-free intervals range from 7 to 15 months. Histologically, the lesion is characterized by a proliferation of blood vessels and meningothelial cells arranged around vessels in the meninges, cortex, and underlying white matter. Psammoma body formation or dystrophic mineralization and gliosis of the intervening parenchyma was observed in all three cases. Bodian stains failed to demonstrate neurofibrillary tangles within intervening parenchymal neurons. Focal epithelial membrane antigen positivity was observed in two lesions and was absent in one. MIB1 staining was observed in two lesions (MIB1 index = 0.8 and 0.6) within the meningothelial cell nuclei and was absent in one case. CONCLUSIONS: Meningioangiomatosis is a rare malformative or hamartomatous lesion of the central nervous system characterized by a proliferation of vessels and perivascular cuffs of meningothelial cells. Absent MIB1 immunoreactivity or low MIB1 indices in the lesion support the clinical impression of a slow-growing lesion and further support a malformative or hamartomatous etiology.

Adolescent↗