Leiomyoblastoma is uncommon and has been known as a neoplasm of smooth muscle origin. However, with recent pragress in immunohistochemical staining techniques, many clinicopathological discrepancies have been pointed out about the origin of leiomyoblastoma. We present here a case of gastric leiomyoblastoma did not expressed desmin and neuron specific enolase, and was thought to be of unknown derivation.
Desmin ; Leiomyoma, Epithelioid* ; Muscle, Smooth ; Phosphopyruvate Hydratase

Leiomyoblastoma is uncommon and has been known as a neoplasm of smooth muscle origin. However, with recent pragress in immunohistochemical staining techniques, many clinicopathological discrepancies have been pointed out about the origin of leiomyoblastoma. We present here a case of gastric leiomyoblastoma did not expressed desmin and neuron specific enolase, and was thought to be of unknown derivation.
Desmin ; Leiomyoma, Epithelioid* ; Muscle, Smooth ; Phosphopyruvate Hydratase

Since granular cell tumor was first described by Abrikossoff in 1926, it has been known as a rare disease. The histogenesis of this tumor is still controversial, but the origin is thought to be from a Schwann cell. About one third of the tumors occur in the tongue, and uncommonly in the perianal region. We report a case of granular cell tumor that developed in the perianal region. The tumor grew slowly for 5 years and was removed by a local excision. This tumor showed positive staining with neuron-specific enolase (NSE).
Granular Cell Tumor* ; Phosphopyruvate Hydratase ; Rare Diseases ; Tongue

A case of peripheral neuroblastoma of a 33-year-old male, which was located on the left buttock, is presented. Histologcally, this tumor demonstrated smaliound cell infiltrations which were arranged in a characteristic rosette pattern and the tumor cells were positively stained with neuron specific enolase. We review the clinical, histopathological ultrastructural and immunohisto chemical characteristics of this rare tumor, as well as the differential diagnosis with other small round cell tumors.
Adult ; Buttocks ; Diagnosis, Differential ; Humans ; Male ; Neuroblastoma* ; Phosphopyruvate Hydratase

PURPOSE: We studied the plasma neuron-specific enolase (NSE) and glutamic acid levels as a marker of the severity of acute ischemic stroke (AIS). METHODS: We enrolled 93 patients who visited to the emergency department from April to September, 2005. The AIS patients included those who visited the emergency department within 24 hours due to ischemic stroke symptoms. The AIS patients was subclassified according to large-vessel, small-vessel, cardioembolic, or unclassified infarction. RESULTS: The plasma NSE and glutamic acid level were 15.1+/-7.9 ng/ml and 204.5+/-86.5 nM/ml, respectively, in the AIS patients. Plasma NSE and Glutamic acid in the was higher than reference range (NSE 0-12 ng/ml, Glutamic acid 0-130 nM/ml). According to the type of infarction, no differences were observed in the plasma NSE and glutamic acid levels. CONCLUSION: In cases of AIS, NSE and glutamic acid have no statistical usefulness in classifying the type of infarction. However, the value of plasma NSE and glutamic acid levels have statistical usefulness in deciding on the existence or nonexistence of an AIS.
Cerebral Infarction ; Emergency Service, Hospital ; Glutamic Acid* ; Humans ; Infarction ; Phosphopyruvate Hydratase* ; Plasma* ; Reference Values ; Stroke*

The clinical and pathological features of five patients with intraventricular neurocytoma are reported. Distribution among men and women is equal. The patients' age at diagnosis ranged from 20 to 57 years. The lesions were located in the lateral and third ventricles. Raised intracranial pressure was the main cause of the clinical manifestations. An isodense mass with multiple intratumoral cysts and homogeneous contrast enhancement was the characteristic computerized tomographic finding. Cerebral angiography showed homogeneous vascular staining in four patients. Magnetic resonance images revealed a mass isointense with the cerebral cortex on both T1- and T2-weighted images. Gadolinium-diethylenetnaminepenta-acetic acid-enhanced images showed homogeneous enhancement. Total removal of the tumor was performed in five patients. Histologically, all tumors were composed of small uniform cells with perinuclear halo and regular round nuclei. Immunohistochemical studies demonstrated strong positivity for neuron-specif ic enolase in all five cases and for synaptophysin in two cases.
Cerebral Angiography ; Cerebral Cortex ; Diagnosis ; Female ; Humans ; Intracranial Pressure ; Male ; Neurocytoma* ; Phosphopyruvate Hydratase ; Synaptophysin ; Third Ventricle

The clinical and pathological features of five patients with intraventricular neurocytoma are reported. Distribution among men and women is equal. The patients' age at diagnosis ranged from 20 to 57 years. The lesions were located in the lateral and third ventricles. Raised intracranial pressure was the main cause of the clinical manifestations. An isodense mass with multiple intratumoral cysts and homogeneous contrast enhancement was the characteristic computerized tomographic finding. Cerebral angiography showed homogeneous vascular staining in four patients. Magnetic resonance images revealed a mass isointense with the cerebral cortex on both T1- and T2-weighted images. Gadolinium-diethylenetnaminepenta-acetic acid-enhanced images showed homogeneous enhancement. Total removal of the tumor was performed in five patients. Histologically, all tumors were composed of small uniform cells with perinuclear halo and regular round nuclei. Immunohistochemical studies demonstrated strong positivity for neuron-specif ic enolase in all five cases and for synaptophysin in two cases.
Cerebral Angiography ; Cerebral Cortex ; Diagnosis ; Female ; Humans ; Intracranial Pressure ; Male ; Neurocytoma* ; Phosphopyruvate Hydratase ; Synaptophysin ; Third Ventricle

PURPOSE: Neuron-specific enolase(NSE) has been established as a reliable marker of neuronal damage in various neurologic disorders. The aim of this study was to evaluate whether febrile seizure cause brain damage, based on the serum and cerebrospinal fluid (CSF) levels of NSE. METHODS: Twenty-one pateints were enrolled. The maximal seizure duration was 90 mins. Blood and CSF samples for the measurement of NSE were obtained immediately after the seizure. NSE was measured using an immunoradiometric assay(IRMA). RESULTS: The CSF NSE level of the febrile seizure group was 11.7+/-2.04 ng/mL and that of the control group was 11.3+/-5.7 ng/mL. The serum NSE level of the febrile seizure group was higher than the serum NSE level of the control group, but there was no significant correlation. The serum NSE level of the febrile seizure group was 19.0+/-7.5 ng/mL and that of the control group was 12.8+/-5.1 ng/mL. The serum NSE level of the febrile seizure group was significantly higher than the serum NSE level of the control group. The CSF/serum ratio of NSE in the febrile seizure group was 0.7+/-0.3 and that of the control group was 1.0+/-0.5. The CSF/serum ratio of NSE in the febrile seizure group was lower than the CSF/serum ratio of NSE in the control group and there was a significant correlation. There was no significant correlation between seizure duration, serum NSE, CSF NSE, and the ratio of the CSF to the serum level of NSE. CONCLUSION: Children with febrile seizure are at relatively low risk for neuronal damage following seizures.
Brain ; Cerebrospinal Fluid* ; Child* ; Humans ; Nervous System Diseases ; Neurons ; Phosphopyruvate Hydratase* ; Seizures ; Seizures, Febrile*

PURPOSE: Neuron-specific enolase(NSE) has been established as a reliable marker of neuronal damage in various neurologic disorders. The aim of this study was to evaluate whether febrile seizure cause brain damage, based on the serum and cerebrospinal fluid (CSF) levels of NSE. METHODS: Twenty-one pateints were enrolled. The maximal seizure duration was 90 mins. Blood and CSF samples for the measurement of NSE were obtained immediately after the seizure. NSE was measured using an immunoradiometric assay(IRMA). RESULTS: The CSF NSE level of the febrile seizure group was 11.7+/-2.04 ng/mL and that of the control group was 11.3+/-5.7 ng/mL. The serum NSE level of the febrile seizure group was higher than the serum NSE level of the control group, but there was no significant correlation. The serum NSE level of the febrile seizure group was 19.0+/-7.5 ng/mL and that of the control group was 12.8+/-5.1 ng/mL. The serum NSE level of the febrile seizure group was significantly higher than the serum NSE level of the control group. The CSF/serum ratio of NSE in the febrile seizure group was 0.7+/-0.3 and that of the control group was 1.0+/-0.5. The CSF/serum ratio of NSE in the febrile seizure group was lower than the CSF/serum ratio of NSE in the control group and there was a significant correlation. There was no significant correlation between seizure duration, serum NSE, CSF NSE, and the ratio of the CSF to the serum level of NSE. CONCLUSION: Children with febrile seizure are at relatively low risk for neuronal damage following seizures.
Brain ; Cerebrospinal Fluid* ; Child* ; Humans ; Nervous System Diseases ; Neurons ; Phosphopyruvate Hydratase* ; Seizures ; Seizures, Febrile*

BACKGROUND: Neuron-specific enolase (NSE) is a useful indicator of neuronal injury in acute cerebral infarction. We investigated the changes in serial serum NSE levels in patients with acute cerebral infarction. METHODS: We measured serial serum NSE levels at 24, 48, 72, and 96 hours, and 2 weeks after the onset of cerebral infarction in 30 patients (15 territorial and 15 lacunar infarctions). We also measured the NSE levels in age-matched controls (n=15) who had no evidence of acute stroke or other neurological disorders. The NSE level was measured using a radioimmunoassay. RESULTS: The initial serum NSE level was significantly higher in the cerebral infarction group than in the control group (6.6+/-2 vs 4.7+/-1.6 ng/mL [mean+/-SD], p=0.006). This difference was also observed between the territorial and lacunar infarction groups until 72 hours after the cerebral infarction. The serum NSE level peaked at 72 hours after the infarction in both lacunar and territorial infarction groups. The correlation between the NSE level and the score on the NIH Stroke Scale was strongest at 48 hours after the cerebral infarction (r=0.469). CONCLUSIONS: Serum NSE level can be a good indicator for distinguishing lacunar from territorial infarction during the acute stage of cerebral infarction.
Cerebral Infarction ; Humans ; Infarction ; Nervous System Diseases ; Neurons ; Phosphopyruvate Hydratase ; Stroke ; Stroke, Lacunar