Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To clarify clinical features and to elucidate prognostic factors and prognosis, the authors retrospectively analyzed 16 cases of gliomatosis cerebri treated at Seoul National University Hospital between January 1988 and December 1995. Age at diagnosis ranged from 19 to 62 (median 34) years and male to female ratio was 10:6. Most presented with headache or seizure, and the mean duration of symptoms was 12.8 months. A poorly defined diffuse high signal intensity lesion, extending in T2-weighted images for two lobes or more, was the characteristic magnetic resonance (MR) image finding. On postcontrast T1-weighted MR imaging, focal enhancement of the lesion was detected in five cases. All patients underwent histological confirmation by craniotomy (9 cases) or stereotactic biopsy (7 cases). Histologically, all patients had compatible findings of gliomatosis cerebri which are the widespread infiltration of neoplastic glial cells with minimal destruction of pre-existing structures. After histological diagnosis, external radiation therapy was begun except in one case, who declined this treatment. Fourteen patients completed the whole procedure and received the planned dose (mean 5780 cGy). Median survival time after diagnosis was 38.4 months. In univariate analysis, the Ki-67 labelling index (> 1) showed significant correlation with the length of survival (p = 0.006). It is suggested that 1) gliomatosis cerebri can be diagnosed by a combination of MR imaging findings and histological examination; 2) histological diagnosis and external radiation therapy might be a good treatment modality; 3) the Ki-67 labelling index correlates significantly with survival time.
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PMID:Gliomatosis cerebri: clinical features, treatment, and prognosis. 981 Apr 41

We describe a case of anaplastic astrocytoma in a 14-year-old boy arising at the site of a dysembryoplastic neuroepithelial tumor (DNT) 3 years after combined radiation and chemotherapy. The subtotally excised superficial right temporoparietal tumor was originally diagnosed as mixed oligoastrocytoma in 1974; the patient was treated with radiation therapy postoperatively. One year later he underwent a craniotomy to remove cyst fluid and no change was reported in the size of the residual tumor. Postoperatively, he received a 6-week course of chemotherapy (lovustine, CCNU). He remained clinically and radiographically stable until 3 years later, when seizure activity returned and imaging studies were consistent with tumor recurrence. He was lost to follow-up until 1986, when records showed that he had died. Review of the initial biopsy showed cortical fragments containing abundant calcifications and multinodular structures typical of the complex form of DNT, in addition to specific glioneuronal elements. The Ki-67 labeling index ranged from 0.1% to 3% focally. The specimen from the third surgery showed an anaplastic astrocytoma (Ki-67 up to 12%) and morphologic features characteristic of radiation effect. This is the first documented case of malignant transformation of DNT following radiation and adjuvant chemotherapy. The implications of malignant transformation in subtotally excised complex DNTs and the intriguing issue of the contribution of radiation/chemotherapy are discussed.
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PMID:Malignant transformation of a dysembryoplastic neuroepithelial tumor after radiation and chemotherapy. 1291 47

We here show that the early postmitotic stage of granule cell development during adult hippocampal neurogenesis is characterized by the transient expression of calretinin (CR). CR expression was detected as early as 1 day after labeling dividing cells with bromodeoxyuridine (BrdU), but not before. Staining for Ki-67 confirmed that no CR-expressing cells were in cell cycle. Early after BrdU, CR colocalized with immature neuronal marker doublecortin; and later with persisting neuronal marker NeuN. BrdU/CR-labeled cells were negative for GABA and GABAA1 receptor, but early on expressed granule cell marker Prox-1. After 6 weeks, no new neurons expressed CR, but all contained calbindin. Stimuli inducing adult neurogenesis have limited (enriched environment), strong (voluntary wheel running), and very strong effects on cell proliferation (kainate-induced seizures). In these models the induction of cell proliferation was paralleled by an increase of CR-positive cells, indicating the stimulus-dependent progression from cell division to a postmitotic stage.
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PMID:Transient calretinin expression defines early postmitotic step of neuronal differentiation in adult hippocampal neurogenesis of mice. 1466 11

Meningiomas are variously benign, atypical or anaplastic neoplasms and can be treated by surgical removal. However, recurrence can be seen even after complete surgical resection in benign meningiomas and some are histologically aggressive. As predictors of recurrence or malignant proliferation some immunohistochemical markers have been used. In this study, we postoperatively identified TfR (transferrin receptor) staining and Ki-67 proliferative index in patients with intracranial meningiomas and evaluated the correlation between these parameters and the recurrence or malignant proliferation. Immunohistochemical techniques (streptavidin-biotin complex) were used to assess the TfR expression and Ki-67 labelling index in 50 surgically removed intracranial meningiomas. Significantly high TfR expression was observed in all types of meningiomas, eight of which recurred. Four cases died because of primary intracranial pathology and one died from uncontrollable epileptic seizures. Ki-67 levels were high in the cases which showed recurrence and showed atypical features. Based on our observations and the results presented above, meningioma patients with TfR score of 3 or higher and high Ki-67 labelling index must be carefully followed up for recurrence, as well as for malignant transformation. Thus, we suggest that TfR and Ki-67 immunostains should be applied routinely in patients with meningiomas.
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PMID:Prognostic importance of transferrin receptor expression and correlation with K1-67 labelling indices in intracranial meningiomas. 1475 79

Granule cell dispersion (GCD) is observed in approximately 40% of cases of hippocampal sclerosis (HS) in patients with epilepsy. Studies in animal models suggest that GCD may be a consequence of enhanced proliferation of granule cell precursors as a result of seizures. We quantified the number of cells in cycle in subfields of the hippocampus with immunohistochemistry for Mcm2 in 14 HS cases with or without severe GCD compared to 6 epilepsy patients without classical HS or GCD as well as 5 postmortem controls. Higher numbers of Mcm2-positive cells were seen in the region of the granule cell layer in patients with severe GCD, and immunolabeling with Geminin and Ki-67 confirmed a proportion were progressing through cycle. Double labeling with Mcm2 and GFAP confirmed the majority of these cycling cells were GFAP-negative and occasional cells stained colocalized with stem cell marker nestin. These findings support the view that GCD may be a phenomenon related to increased progenitor cell proliferation in patients with hippocampal damage and chronic epilepsy.
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PMID:Cell proliferation and granule cell dispersion in human hippocampal sclerosis. 1580 50

We report five cases of sporadic meningioangiomatosis, three males and two females, ranging in age from 12 to 36 years at diagnosis. The lesion was found incidentally by MRI after a head trauma in one case; the other four subjects had a seizure disorders, which improved following surgical resection of the cortical lesions. Grossly, the lesionectomy specimens were of a whitish color and firm consistency. Histological examination revealed that the lesions were confined to the cortex with focal involvement of the overlying leptomeninges, and revealed unifying features of meningioangiomatosis, such as proliferating microvessels with perivascular cuffs of spindle-cell proliferation within the cortex. Two cases had numerous calcifications; one was associated with a prominent fibrocalcifying component. Immunostaining results were variable among the cases. Only vimentin was consistently positive. Some of the spindle cells were weak positive for EMA in two cases. Immunoreactions with anti-CD34 detected within the cytoplasm of the spindle cells were observed in three of the five cases. The Ki-67 proliferation index of all the cases was very low, less than 0.1%. Neurofibrillary tangles were identified in only one of the five cases using the Bodian and immunostaining methods. These findings indicate that meningioangiomatosis lesions show a wide range of clinicopathological features, making diagnosis difficult. A histopathological spectrum and differential diagnoses were discussed with a review of the literature. Since this lesion is a distinct clinicopathological entity and hamartomatous in nature, it is important to make a correct diagnosis in order to avoid further aggressive treatment.
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PMID:Histopathological study of five cases with sporadic meningioangiomatosis. 1677 Nov 83

Previous studies of Ammon's horn sclerosis (AHS) suggest that AHS is both the result of and the cause of seizures, and support the idea that seizures cause alterations in cell numbers and location. To test the hypothesis that epilepsy induces neurogenesis/gliogenesis, hippocampal cell proliferation was assessed in AHS. Twelve and four resected hippocampi in patients with AHS and with tumor-related epilepsy (TRE), respectively, and 11 autopsy controls were immunostained for Ki-67. Total number of Ki-67-positive cells (KiPC) in each hippocampal area was counted. Selected cases were further studied with double immunohistochemical labeling. KiPC were observed in all three groups. Total numbers of KiPC were significantly higher in AHS cases than in controls, but were not significantly different between TRE cases and controls. Significant differences were observed in the dentate gyrus, the cornu ammonis (CA)-4 region, and the fissura hippocampi between the AHS and control groups. In double immunolabeling, nestin was positive in some KiPC. The existence of neurogenesis/gliogenesis was shown in the hippocampi of pediatric patients with AHS. Increased numbers of progenitor cells in the hippocampi with AHS appear not to be due to seizures per se, but to be more associated with the specific cause of epilepsy.
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PMID:Evidence of increased cell proliferation in the hippocampus in children with Ammon's horn sclerosis. 1730 Jun 71

Malformations of cortical development (MCD) are a well-recognized cause of chronic epilepsy. Most MCD are defined by the neuronal component of the lesion and are considered to be relatively "static" lesions. Twenty-one cases of MCD type II (Taylor type cortical dysplasia) were retrospectively evaluated with Ki-67 antibody looking for evidence of cell proliferation and evaluating populations of cells that may be proliferating. Resections were from 13 males and 8 females who ranged in age at the time of surgery from 6 weeks to 57 years (mean 8.6 y) and who had a duration of seizures before surgery of 1.5 months to 34.4 years (mean 6.5 y). Dysmorphic neurons were observed in all cases and balloon cells in 18/21 (86%) cases. Ki-67 labeling indices ranged from 0.2% to 4.9% (mean 2.0%). Coimmunolabeling with Ki-67 and antibodies to glial fibrillary acidic protein, CD68, and CD45RB showed that the majority of the Ki-67-positive cells were astrocytic (glial fibrillary acidic protein positive). In 9/21 cases (43%), endothelial cell staining with Ki-67 was also observed. These results suggest that low rates of cell proliferation are observable in type II MCD. The proliferating cells appear to be primarily astrocytic and endothelial in nature and suggest that these lesions are not static. Dysmorphic neurons and balloon cells in MCD were not observed to stain with Ki-67.
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PMID:Ki-67 immunoreactivity in type II malformations of cortical development. 1852 81

Papillary glioneuronal tumors (PGNT) are a rare, recently described form of mixed neoplasm composed of glial and neuronal components. PGNT usually occur in children and young adults, and typically demonstrate low-grade pathology, with a low proliferative index of 1-3%. Here we describe a newly diagnosed case of PGNT with a more aggressive phenotype that required irradiation and chemotherapy. The patient was a 19-year-old female who developed progressive headaches and visual seizures. An MRI revealed a heterogeneously enhancing solid mass in the left temporo-occipital region, with significant surrounding edema and mass effect. The mass was resected under stealth guidance without complication. Postoperative MRI scans showed patchy enhancement and residual T2 and FLAIR abnormality. Pathology revealed a highly cellular neoplasm with papillary-like structures, containing cells with glial and neuronal differentiation. Regions of mitoses and focal necrosis were noted, along with a Ki-67 labeling index of 26%. The diagnosis was aggressive PGNT, and treatment consisted of conformal irradiation and concomitant temozolomide over 6 weeks. Postirradiation follow-up MRI scans demonstrated a reduction of residual enhancement and FLAIR abnormality. The patient continues standard-dose adjuvant temozolomide on a monthly basis, with further improvement on subsequent MRI scans and a stable neurologic exam. This patient demonstrates that PGNT may, in rare cases, display an aggressive clinicopathologic phenotype that requires a therapeutic approach more consistent with a high-grade glioma.
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PMID:Aggressive papillary glioneuronal tumor: case report and literature review. 1880 63

Since there is limited information in the literature, the purpose of this study was to investigate clinical signs, morphology, and temporal progression of lesions from Days 3 to 168 in a kainic acid (KA)-induced Fischer-344 (F-344) rat model of mesial temporal lobe epilepsy (MTLE). Following a single KA subcutaneous dose of 9 mg/kg to young adult male rats, 95% survived, 93% exhibited status epilepticus, and 80% eventually developed spontaneous motor seizures. Histopathology included hematoxylin and eosin (H&E), autofluorescence, Fluoro-Jade B, Timm's, ED-1/CD68, GFAP, doublecortin, and Ki-67. Neuronal degeneration occurred on Day 3 in the hippocampal CA1, CA3, and dentate hilar regions; amyg-daloid and thalamic nuclei; and frontoparietotemporal, entorhinal and piriform cortices. Degeneration severity peaked on Day 6 and decreased progressively until Day 168. Aberrant mossy fiber (MF) sprouting was present in the inner molecular layer of dentate gyrus on Days 6-168. Microliosis and astrogliosis peaked on Day 28 and generally colocalized with the distribution of neuronal degeneration. Important correlates to human MTLE included induction of spontaneous seizures, more severe neuronal damage of CA1 than CA3 (in contrast to other animal models but similar to humans), hilar neuronal loss, activated microgliosis and astrogliosis, aberrant MF sprouting, and dentate granule cell neurogenesis. Aberrant MF sprouting prior to spontaneous motor seizures and reduced seizure frequency with a decrease in aberrant MF sprouting support the hypothesis that MF sprouts are necessary for spontaneous seizure generation and maintenance.
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PMID:Temporal profile of clinical signs and histopathologic changes in an F-344 rat model of kainic acid-induced mesial temporal lobe epilepsy. 1912 89


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