Primary leptomeningeal oligodendroglioma: case report.
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Adult↗
Biomedical subjects
M L Estes
Publications and source records attributed to M L Estes.
Symptomatic Mycobacterium avium complex infection of the central nervous system. A case report and review of the literature.
Mycobacterium avium complex infections rarely involve the central nervous system, even in patients with widely disseminated disease. We report a case of disseminated M. avium complex infection presenting with central nervous system symptoms in a patient with Hodgkin's disease. Neurologic findings included disorientation, nuchal rigidity, seizures, an extensor plantar response, cerebrospinal fluid studies consistent with meningitis, and eventually, coma and death. Organisms of the M. avium complex were cultured from several sites. Histopathologically, the central nervous system lesions consisted of small aggregates of lymphocytes and macrophages containing acid-fast organisms present in a predominantly perivascular location. In view of the life-threatening nature and potential treatability of this uncommon presentation of M. avium complex infection, we suggest that these organisms be sought in immunocompromised patients presenting with unexplained central nervous system symptoms.
Adult↗
The neuropathology of cardiac allograft transplantation. An autopsy series of 18 patients.
OBJECTIVE: To examine the neuropathologic findings associated with cardiac transplantation and to assess the role, if any, that the neuropathology had in the patient's death. DESIGN: Retrospective autopsy series of 18 patients. SETTING: Tertiary referral center with a high volume of cardiac transplantation. PATIENTS: Cardiac transplant patients who died and in whom a complete autopsy was performed. RESULTS: Eighteen patients, including 11 men and seven women, comprised the study group. Patients ranged in age from 27 to 59 years (mean 48 years). Postoperative survival ranged from 1 to 1517 days (mean 334 days). Autopsies in 15 (83%) patients showed neuropathology; in only one patient, however, was cause of death attributed to these findings. The most common neuropathology was related to anoxia or infarction: ischemia or focal neuronal necrosis (n = 9), diffuse anoxic encephalopathy (n = 3), infarction (n = 6). Other findings included infection with Nocardia, Aspergillus, and Staphylococcus (n = 3) and hemorrhage (n = 3). Of the seven patients who received transplants for ischemic heart disease, five had evidence of cerebral ischemia or infarction. Systemic pathology encountered included infection in 13 patients, ischemia and/or infarction in 11 patients, and hemorrhage in six patients. Cause of death was attributed to infection in nine patients, cardiac rejection in five patients, disseminated intravascular coagulation/hemorrhage in three patients, and systemic amyloidosis in one patient. CONCLUSIONS: The most common neuropathologic findings are related to ischemia and infarction. Neuropathologic findings were only rarely the main cause of death, but they were a significant cause of morbidity in patients who have undergone cardiac allograft transplantation.
Adult↗
Regulation of monocyte chemoattractant protein-1 expression in adult human non-neoplastic astrocytes is sensitive to tumor necrosis factor (TNF) or antibody to the 55-kDa TNF receptor.
Infiltration of the central nervous system (CNS) by monocytes is a characteristic of many non-malignant disease processes, although the signals regulating such traffic are unclear. Tumor necrosis factor (TNF) and other inflammatory cytokines have been shown to elicit production of monocyte chemoattractant activity in glioma cells, but the regulation of such activity in non-neoplastic adult astrocytes has not been examined. We previously observed that TNF constituted a proliferative signal for non-neoplastic adult human astrocytes in vitro involving the 55-kDa TNF receptor. In the present study, we demonstrate that TNF exposure enhances the expression of monocyte chemoattractant protein-1 (MCP-1) mRNA and functional monocyte chemoattractant activity in non-neoplastic astrocytes. Results indicated that MCP-1 mRNA expression was maximal within 3 h, and was further augmented by the protein synthesis inhibitor cycloheximide (CY). Antibody (htr-9) directed against the 55-kDa TNF receptor also elicited MCP-1 mRNA expression while antibody to the 75-kDa TNF receptor (utr-1) was ineffective. Secretion of monocyte chemoattractant activity was significantly greater in TNF- or htr-9-treated astrocytes than in utr-1-treated or untreated controls; activity was abolished by treatment with antibody to MCP-1. These findings suggest that non-neoplastic adult human astrocytes may contribute to CNS inflammatory responses by mediating recruitment of peripheral blood monocytes.
Antibodies, Monoclonal↗
Diffuse bilateral cerebral astrocytomas with atypical neuroimaging studies.
The authors describe the clinical behavior of eight patients with cerebral astrocytomas, in whom computerized tomography (CT) or magnetic resonance (MR) imaging of the brain was characterized by diffuse bilateral cerebral hemisphere tissue density abnormalities and minimal focal mass effect. Five patients were newly diagnosed, and three others had been treated for focal low-grade astrocytoma. Histological diagnoses included anaplastic astrocytoma (three patients), low-grade astrocytoma (three patients), glioblastoma (one patient), and gliosis with later development of glioblastoma (one patient). In five patients, brain tumor was not suspected from the neuroimaging studies, the findings of which were mistaken for radiation leukoencephalopathy, vasogenic edema, or multiple sclerosis. Serial CT scans or MR images undertaken over intervals of 3 to 184 weeks showed progression of abnormal tissue densities in seven patients and multifocal contrast-enhancing masses developed on CT scan in two patients. An autopsy in each of four patients showed diffuse cerebral infiltration by astrocytoma. It is concluded that neuroimaging studies in some patients with diffusely infiltrating cerebral astrocytoma are atypical for neoplasm and can be mistaken for other diseases, especially those that predominantly affect cerebral hemisphere white matter.
Adolescent↗
Astrocyte expression of mRNA encoding cytokines IP-10 and JE/MCP-1 in experimental autoimmune encephalomyelitis.
Mononuclear leukocytes preferentially accumulate in the central nervous system (CNS) during the course of experimental autoimmune encephalomyelitis (EAE). To address factors that govern leukocyte trafficking in EAE, we monitored expression of mRNAs encoding IP-10 and JE/MCP-1, which are members of a family of chemoattractant cytokines. A transient burst of IP-10 and JE/MCP-1 mRNA accumulation in the CNS occurred, in close relation to the onset of histologic and clinical disease. In situ hybridizations showed, unexpectedly, that astrocytes were the major source of mRNAs encoding IP-10 and JE/MCP-1. These observations implicate astrocyte-derived cytokines as potential chemoattractants for inflammatory cells during EAE.
Animals↗
Anaplastic astrocytoma with granular cell differentiation: case report and review of the literature.
In contrast to the relatively common soft tissue form of granular cell tumor (GCT), intercerebral GCTs are rare neoplasms. The Schwann cell is the accepted cell of origin for soft tissue GCTs. However, the origin of intracerebral tumors is controversial. We report a case of a GCT intimately associated with an anaplastic astrocytoma. Immunohistochemical staining with glial fibrillary acidic protein demonstrated focal positive staining within the granular cells. Six GCTs from other body sites were stained with glial fibrillary acidic protein for comparison and all were negative. The granular cell component was diffusely positive for S-100 and negative for epithelial membrane antigen and cytokeratin. Ultrastructurally, filaments characteristic of astrocytic cells were demonstrated within some granular cells. Based on our light microscopic, electron microscopic, and immunohistochemical findings, the granular cell component of this anaplastic astrocytoma is likely astrocytic in origin. We propose that these tumors be designated astrocytic neoplasms with granular cell differentiation and their prognoses dictated by the grade of the glial component.
Astrocytoma↗
Divergent responses of human astrocytoma and non-neoplastic astrocytes to tumor necrosis factor alpha involve the 55 kDa tumor necrosis factor receptor.
The effects of tumor necrosis factor (TNF) on DNA synthesis, proliferation, and induction of gene/protein expression of TNF were compared in neoplastic and non-neoplastic adult human astrocytes. Previously, we demonstrated that TNF induced proliferative responses in non-neoplastic adult human astrocytes. In astrocytoma cells, however, TNF elicited both proliferative and cytostatic responses depending upon cell density and TNF concentration. This bimodal effect persisted even in a homogeneous, cloned astrocytoma cell line (STT-9C), and was inhibitable by neutralizing antibody to TNF. TNF treatment enhanced expression of TNF mRNA in astrocytoma cells but not in non-neoplastic astrocytes, and cell-associated or secreted TNF was detectable in any culture. The involvement of receptors in astrocyte responses to TNF was examined in serological studies using monoclonal antibodies Utr-1 to the 75 kDa, and Htr-9 to the 55 kDa TNF receptor. Antibody to the 55 kDa TNF receptor alone was able to mimic the effects of TNF in both neoplastic and non-neoplastic astrocyte cultures while antibody to the 75 kDa TNF receptor had no effect. These data indicate that the bimodal actions of TNF on human astrocytoma cells as well as the stimulatory effects on non-neoplastic adult astrocytes are regulated at least in part by the 55 kDa TNF receptor. Astrocyte TNF receptors, however, do not appear to constitute part of an autocrine growth pathway in either non-neoplastic or neoplastic human astrocytes.
Astrocytes↗
Meningeal myofibroblastoma.
Myofibroblastoma is a recently described benign mesenchymal tumor. Only one case has been reported previously in the CNS. We report a second case of myofibroblastoma arising in the meninges in a 70-year-old woman who presented with visual changes. The histologic appearance was characterized by alternating areas of spindled and rounded cells separated by collagen and amianthoid fibers. Immunostaining demonstrated strong vimentin and focal smooth-muscle actin positivity; staining for epithelial membrane antigen, cytokeratin, S-100, desmin, myosin, glial fibrillary acidic protein, and factor VIII-related antigen was negative. Ultrastructurally, the myofibroblasts had features of both smooth-muscle cells and fibroblasts. Differentiating the benign myofibroblastoma from more aggressive meningeal sarcomas and meningeal meningiomas is important. The tumor most likely arises from myofibroblasts that probably reside in the meninges.
Aged↗
Stereotactic brain biopsy for diagnosis of progressive multifocal leukoencephalopathy.
We describe three patients in whom the diagnosis of progressive multifocal leukoencephalopathy (PML) was made by stereotactic biopsy. All three patients had a rapidly progressive clinical course pathologically characterized by demyelination, Alzheimer I astrocytes, and basophilic intranuclear inclusions in oligodendrocytes. In each case, the diagnosis was confirmed with immunohistochemical staining of oligodendrocytes for the JC virus and in one case by electron microscopy. Determination of the adequacy of tissue received at the time of frozen section is critical and can direct the appropriate submission of tissue to maximize available diagnostic procedures.
Adult↗
Mixed vascular malformations of the brain: clinical and pathogenetic considerations.
The clinical relevance of any scheme for classification of vascular malformations of the brain remains controversial. Widely accepted pathologic classifications include discrete venous, arteriovenous, capillary, and cavernous malformations. Of 280 cases of possible vascular malformations evaluated by a single cerebrovascular service during a 5-year period, 14 were instances of mixed vascular malformations including definite features of more than one pathologically discrete type of malformation within the same lesion. There were six instances of mixed cavernous and venous malformations in the same lesion; in all instances, the cavernous malformation accounted for the clinical presentation. There were three cases of mixed venous and arteriovenous malformations (arterialized venous malformations), presenting with the typical histoarchitectural appearance of a venous malformation, but with arteriovenous shunting; all cases were symptomatic, two with hemorrhage and one with focal neurological symptoms. There were five cases of predominantly cavernous malformations with features of arteriovenous malformation or capillary telangiectasia in the same lesion. These five cases presented clinically as angiographically occult lesions indistinguishable from a cavernous malformation. Lesions including a venous malformation were recognizable preoperatively because of characteristic imaging features of the venous malformation. Other mixed vascular malformations were indistinguishable on diagnostic studies from pure cavernous malformations. Of the 14 mixed vascular malformations, 11 included a cavernous malformation that was usually responsible for the symptomatic presentation. In the other three cases, manifestations of clinical lesions were due to arteriovenous shunting within a venous malformation. We conclude that mixed vascular malformations of the brain are rare entities with distinct clinical, radiological, and pathological profiles. Their identification generates several hypotheses about common pathogenesis or causation-evolution among different types of lesions.
Adolescent↗
Modulation of proliferation and antigen expression of a cloned human glioblastoma by interleukin-4 alone and in combination with tumor necrosis factor-alpha and/or interferon-gamma.
As part of continuing studies to investigate the possible regulatory effects of cytokines on malignant astrocytes, we investigated the effects of interleukin-4 (IL-4) alone and in combination with tumor necrosis factor-alpha (TNF alpha) and/or interferon-gamma (IFN gamma) on the cell growth and major histocompatibility complex (MHC) antigen expression of a cloned human glioblastoma cell line (9C). The 9C cells were treated with IL-4 alone or in combination with TNF alpha and/or IFN gamma and were examined for proliferation by crystal violet assay and for Class II MHC antigen by flow cytometry. Results indicated that IL-4 alone did not affect 9C proliferation. In combination with TNF alpha or IFN gamma, however, IL-4 significantly and dose-dependently inhibited cell growth. As previous reports have shown, TNF alpha combined with IFN gamma exerted an additive growth suppressive effect on glioblastoma cells, probably by enhancing TNF receptor expression. This additive effect of TNF alpha and IFN gamma was further enhanced by IL-4. In contrast, IL-4 did not modulate expression of Class II MHC antigen on 9C cells, even in combination with IFN gamma, which predictably enhanced this antigen. These results suggest that IL-4 is capable of modulating glioblastoma growth only in the presence of other cytokines, such as TNF alpha and/or IFN gamma. Further, the effect of IL-4 on glioblastoma proliferation is selective and independent of the mechanisms involved in regulating MHC antigen expression.
Brain Neoplasms↗
Pathological heterogeneity of angiographically occult vascular malformations of the brain.
There is considerable confusion in the literature regarding the pathological substrates of angiographically occult vascular malformations (AOVMs) of the brain and their clinical significance. We retrospectively reviewed the cases of 34 consecutive patients with AOVMs undergoing surgical excision at a single institution during a 10-year period. Pathological specimens were reexamined, and the lesions were classified according to strict histopathological criteria. There were 21 cavernous malformations, 3 arteriovenous malformations, 3 venous malformations, 2 capillary malformations, and 5 mixed (pathologically heterogeneous) lesions. The initial pathological diagnostic report had been imprecise or had misidentified the lesion type in 18 of the 34 cases (53%), most commonly labeling a cavernous malformation as an arteriovenous malformation or not recognizing mixed features within the same lesion. Clinical presentation (including hemorrhage) and outcome were not significantly different among the various lesion types. Preoperative diagnostic imaging included a variety of modalities that were introduced or evolved during the period of the study and generally suggested a suspected vascular malformation but did not predict pathological subtypes. Acute hematomas in this surgical series made the identification of underlying vascular malformations highly speculative. We conclude that the majority of AOVMs requiring surgical intervention are cavernous malformations, although there was a notable pathological heterogeneity of the remaining lesions. Histopathological subtypes of AOVMs are not associated with unique clinical or radiographic features.
Adolescent↗
Effect of recombinant tumor necrosis factor-alpha on three-dimensional growth, morphology, and invasiveness of human glioblastoma cells in vitro.
In order to investigate the antiproliferative and anti-invasive effects of tumor necrosis factor (TNF)-alpha on human glioblastoma cells, an in vitro three-dimensional (anchorage-independent) assay was performed using Matrigel, a mixture of extracellular matrix proteins. Four glioblastoma-derived cell lines, including one cloned line, were cultured in Matrigel with or without TNF-alpha. In the Matrigel containing TNF-alpha, three of the four cell lines, including the cloned line, showed significant growth inhibition in a dose-dependent manner. Dramatic three-dimensional morphological differences were observed between TNF-treated and untreated glioblastoma cells cultured in Matrigel. Untreated cells formed large and highly branched colonies throughout the gel. In contrast, the majority of TNF-treated cells demonstrated truncated branching processes and, at a high TNF-alpha dose, an increasing number of cells remained in relatively small spherical aggregates, their cell processes being significantly reduced. Quantitative invasion assay using a micro-Boyden chamber system confirmed that TNF-treated cells lost invasiveness in a dose-dependent manner. These results suggest that TNF-alpha exerts not only antiproliferative but also anti-invasive effects on human glioblastoma cells in vitro. It is believed that this is the first report showing the anti-invasive effect of TNF-alpha on tumor cells.
Brain Neoplasms↗
Acute necrotising myopathy in association with carcinoma of the tongue.
Acute necrotising myopathy (ANM) is a rare complication of carcinoma. The myopathy is proximal, rapidly progressive, associated with rhabdomyolysis and usually fatal. We report an unusual case of acute necrotising myopathy in a woman with squamous cell carcinoma of the tongue who is alive, without tumour recurrence two years after diagnosis. This association of ANM with head and neck cancer is unique.
Biopsy↗
Interleukin-4 down-regulates adult human astrocyte DNA synthesis and proliferation.
The T lymphocyte-derived cytokine, interleukin-4 (IL-4), was found to inhibit dose dependently basal DNA synthesis of cultured non-neoplastic human astrocytes isolated from epilepsy white matter tissue. The mitogenic effect of tumor necrosis factor on astrocytes was also inhibited by IL-4, and the inhibitory effect was abrogated by anti-IL-4 antibody but not by irrelevant IgG. Immunofluorescent analysis indicated significantly reduced numbers of glial fibrillary acidic protein-positive astrocytes incorporating nuclear bromodeoxyuridine in IL-4-treated cultures compared to control. These findings indicate that human adult astrocyte proliferation, in contrast to that reported for endothelial cells or fibroblasts, is sensitive to down-regulation by IL-4.
Astrocytes↗
Further observations on the pathology of subcortical lesions identified on magnetic resonance imaging.
We performed postmortem magnetic resonance imaging and pathologic examinations on the brains of seven consecutive patients older than 50 years of age who died of non-neurologic causes. Multiple hyperintense subcortical lesions were identified in each patient, and a total of 29 lesions were examined histologically (eight rims, six caps, six punctate lesions, and nine patches). Rims were characterized by subependymal gliosis and loss of the ependymal lining; caps were associated with myelin pallor, gliosis, and arteriosclerosis; punctate lesions were characterized by dilated perivascular spaces and perivascular gliosis; and patches were associated with myelin pallor and dilated perivascular spaces. The pattern of myelin pallor defined the size and shape of caps and patches. Arteriosclerosis was identified in six of six caps, three of six punctate lesions, and in three of nine patches. These data indicate that (1) each type of hyperintense subcortical lesion has a distinct pathologic correlate; (2) arteriosclerosis is not invariably associated with all types of hyperintense subcortical lesions on magnetic resonance imaging; and (3) myelin pallor appears to contribute to the magnetic resonance imaging signal at 1.5 tesla.
Aged↗
Perineurial cell hypertrophic mononeuropathy manifesting as carpal tunnel syndrome.
A 42-year-old man showed signs and symptoms suggestive of carpal-tunnel syndrome, but EMG showed an isolated motor axon-loss lesion affecting the right median nerve distally. After the MRI revealed a mass in the median nerve, surgical exploration showed a diffusely swollen median motor branch. Biopsy showed a lesion with marked onion-bulb formation composed of perineurial cells as identified by immunohistochemical analyses and electron microscopic examination. Although we previously coined the term "perineurioma" for this condition, re-reviews of our cases do not support the idea that the onion-bulb lesion is a benign tumor; instead, it appears to be reactive hyperplasia. Although rare, electromyographers and neurologists need to be aware of this problem because it is self-limited and does not require surgical resection.
Adult↗