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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case is reported in which a diffuse subarachnoid dissemination occurred after successful removal of a posterior fossa hemangioblastoma. The patient was a 51-year-old man who suffered from headache and gait disturbance, and who was admitted to our hospital on September 25, 1985. Neurological examination revealed trunkal ataxia and increased intracranial pressure. A CT scan with contrast media revealed a high-density lesion with surrounding low-density area in the posterior fossa. Right vertebral angiography demonstrated a round tumor stain behind the medulla oblongata, which was fed by the right posterior inferior cerebellar artery. The complete resection of the tumor was carried out. A biopsy specimen from the tumor showed a picture characteristic of hemangioblastoma. Fourteen months later the patient was readmitted due to the sudden onset of disturbance of consciousness. A CT scan revealed a large intracerebral hematoma in the right putaminal region. Right carotid angiography demonstrated two small tumor stains in the right temporal lobe. An emergency operation to extirpate the hematoma was performed. But the disturbance of consciousness did not improve, and the patient died. At necropsy a lot of small round tumors were recognized at the surface of the bilateral cerebral and cerebellar cortex. They were present in the subarachnoid space and partially invaded the cerebral and cerebellar parenchyma, extending through Virchow-Robin's space. There was no recurrence of the tumor at the site of the original operation. No doubt, a subarachnoid dissemination had occurred. However the histological findings of tumors were similar to the findings recorded in the first biopsy.
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PMID:[A case of hemangioblastoma with subarachnoid dissemination]. 230 11

Five children with subacute or acute onset of cerebellar ataxia and opsoclonus are described. Two had cerebrospinal fluid pleocytosis at the onset of ataxia and were initially thought to have acute parainfectious cerebellar ataxia of childhood. All were found to have tumors of neural crest origin (two neuroblastomas, three ganglioneuroblastomas). Tumors were small and only found by computed tomographic techniques. Urinary catecholamine metabolites were elevated in only two of the patients. Four of the five failed to improve neurologically with resection of the tumor. All four have had a steroid-sensitive chronic ataxic syndrome that worsens with acute nonspecific illnesses and has resulted in long-term deficits, particularly in speech and gross motor function. This is a metabolic encephalopathy associated with permanent residual neurologic deficits but without visible lesions on neuroimaging studies. We stress the frequency of cerebrospinal fluid pleocytosis in patients with tumor-associated opsoclonus and the clinical difficulty in separating tumor-associated cases from those due to other causes [corrected].
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PMID:Opsoclonus-ataxia due to childhood neural crest tumors: a chronic neurologic syndrome. 234 82

Although cerebral venous malformations have been reported to cause epilepsy, progressive neurological deficits, and hemorrhage, their clinical significance remains controversial. In an attempt to clarify the natural history of the lesion and suggest an appropriate management strategy, the authors review their experience with 30 patients. In four patients with cerebellar venous angioma, an acute episode of ataxia was documented. The coexistence of a cavernous malformation was pathologically confirmed in the two patients who underwent surgery for bleeding presumed caused by the venous angioma. Infarction was shown in two patients and a tumor in two others. Follow-up periods ranged between 18 and 104 months, with only five patients symptomatic at the time of this report. Rebleeding had not occurred, nor had acute episodes of neurological dysfunction been documented. This clinical experience suggests that a venous malformation is frequently associated with other, more symptomatic conditions and is often erroneously identified as the source of the symptoms. Because the nature of the relationship between the venous malformation and the allied conditions remains ambiguous, it is recommended that patients harboring a "symptomatic" venous malformation undergo high-field magnetic resonance imaging to rule out underlying pathology, and that any such pathology be treated independently of the venous malformation.
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PMID:Cerebral venous malformations. 239 88

The nitrosourea-induced rat glioma clone RG2 was tested for its capacity to form multicellular tumor spheroids (MTS's). Resulting spheroids were investigated by light and electron microscopy with regard to their proliferation patterns and morphological features. Using microsurgical techniques and avoiding mechanical injury of the brain tissue, the authors successfully transplanted avascular MTS's under the dura of the cerebellum, above the vermis, in 43 adult syngeneic Fischer CD rats. The rate of tumor establishment was 93%, and the tumors that were solid and spheroid in shape grew exponentially. Neovascularization could be observed at 3 days after implantation, and invasion of the cerebellum occurred by 3 to 5 days. Neurological deterioration, including ataxia, impairment of walking, and apathy, could be observed after 10 days. The mean survival time was approximately 16 days. The subdural cerebellar tumors were studied by histological techniques, and two morphometric methods were applied to check the growth of implanted spheroids. All tumors were deeply stained with the Evans blue dye-albumin complex, demonstrating disturbance of the blood-brain barrier. The easy accessibility of the cerebellar vermis in rats, the microsurgical implantation of glioma spheroids under the dura avoiding nerve tissue disruption, and the high percentage of reproducible establishment of tumors favor this experimental brain-tumor model. This should be an excellent model for study of experimental therapies.
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PMID:RG2 glioma growth in rat cerebellum after subdural implantation. 242 62

We have studied an unusual, spontaneous, intradural extramedullary spinal cord tumor in 12 dogs. Animals presented with paraparesis and ataxia early in life (11/12 ranged from 6 to 38 months of age) suggesting that these tumors may be congenital. Various breeds of dogs were represented with four cases in German Shepherds and three in retrievers; there was no sex predisposition. Post-mortem examinations revealed a single intradural mass consistently located between T10 and L2, which produced extensive compression of the spinal cord. Metastasis was never observed and significant pathological changes in other organs were lacking. Microscopic examination revealed solid sheets of ovoid to fusiform cells interspersed with areas of acinar and tubular differentiation. Some areas were rarified and focal squamous metaplasia was observed. Ultrastructural features included the presence of a continuous basal lamina, junctional complexes, microvilli and occasional cilia at the apices of acinar complexes. Immunocytochemical studies did not support a neurectodermal origin. At least 13 case reports of this entity have been previously published and have been designated ependymomas, medulloepitheliomas and neuroepitheliomas. A recent case was diagnosed as a nephroblastoma and we feel that this is an interesting and provocative diagnosis. These tumors could result from remnants of renal primordium which becomes trapped between the dura and the developing spinal cord. However, firm evidence of such a histogenesis is not yet at hand.
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PMID:A novel intradural extramedullary spinal cord tumor in young dogs. 245 49

A 58-year-old female had a 1-year history of headache, ataxia, and taste disturbance and then developed speech disturbance. She was found to have a meningioma of the fourth ventricle, a very rare site for this type of tumor. It did not adhere to the cerebellar tentorium or dura mater and was totally removed without difficulty. Magnetic resonance imaging, but not computed tomography or angiography, provided adequate information for correct diagnosis. The literature concerning fourth ventricle meningiomas is reviewed and the diagnostic advantages and limitations of computed tomography, angiography, and magnetic resonance imaging are discussed.
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PMID:Meningioma of the fourth ventricle--case report. 247 68

The association of opsoclonus and malignant neoplasia is infrequent. The clinical and neuropathological data of two patients in whom opsoclonus and ataxia developed 7 and 11 months before the detection of a bronchial carcinoma are reported. Loss of Purkinje cells, edema of dentate nucleus and peridental demyelination were the most important neuropathological findings; neither carcinomatous metastases nor inflammatory signs were found in the brain. From the review of the pathological reports of paraneoplastic opsoclonus, the following conclusions can be drawn: the changes in the cerebellum are produced by the paraneoplastic cerebellar degeneration and are unrelated to the origin of opsoclonus, which has other anatomic substrates; paraneoplastic opsoclonus is a "remote effect" of cancer with an inflammatory basis, for which neurotoxic and immunological mechanisms have been hypothesized.
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PMID:Paraneoplastic opsoclonus: a neuropathologic study of two cases. 255 25

A 73-year-old man presented a progressive neurologic syndrome with impairment of multiple cranial nerves, ataxia and limb weakness. Neuroradiological evaluation showed multiple supra and infratentorial lesions, which completely disappeared after steroid treatment on two occasions. These neuroradiological modifications were closely correlated with clinical picture and CSF findings. Post-mortem examination showed multifocal primary CNS immunoblastic large cell lymphoma. Immunohistochemistry showed that the tumor was of B-cell origin.
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PMID:Steroid-induced disappearance of primary central nervous system lymphoma. Clinical, neuroradiological and pathological findings. 261 26

Brainstem tumors arise in portions of the rhombencephalon and mesencephalon. Some authorities include diencephalic tumors in this group. We have reviewed our clinical experience of 69 children (less than 21 years of age) with brainstem tumors evaluated and treated at Duke University Medical Center (DUMC) from 1960 to 1986. There were 19 patients with group 1 tumors (thalamus, third ventricle region, or midbrain) and 50 with group II tumors (pons, medulla oblongata). The common presenting signs and symptoms were ataxia, headache, motor loss, and cranial nerve palsies. The most commonly employed diagnostic imaging studies were air examinations and CT. Preradiotherapy confirmation of malignancy was obtained in five group I patients (astrocytoma, 4; germinoma, 1) and 8 group II patients (astrocytoma, 3; anaplastic astrocytoma, 2; glioblastoma multiforme, 3). All patients received radiotherapy. The 5-year survival rate for the entire population was 40%. The survival rate for group I patients was significantly better than that observed for group II patients. In the 50 group II patients neither patient sex nor age nor presence of cranial nerve palsies nor pretreatment CT scan findings nor field size influenced survival. A long duration of symptoms positively influenced survival. The vast majority of tumor recurrences were within the radiation field. Half of the patients had either stable or improved Karnofsky status 6 months following completion of irradiation. The management strategy for childhood brainstem tumors is discussed.
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PMID:Selection of a management strategy for pediatric brainstem tumors. 270 33

Acute cerebellar encephalopathy (ACE)--ataxia often associated with opsoclonus, polymyoclonus, and irritability--may be associated with neuroblastoma and should be suspected in a child who presents with ACE. The survival in ten children with ACE associated with neuroblastoma was 100%. Most of the tumors were ganglioneuroblastomas. The abdomen was the most common location for the tumor in this study although it also can be found in the mediastinum. All patients with this syndrome had a localized tumor. With ACTH therapy, ACE may resolve early postoperatively, but it tends to recur in most patients, continuing for as long as 3 years after the initial operation. Treatment with ACTH or prednisone modifies and rapidly clears the symptoms during the acute episode of recurrent ACE as well as helps to resolve subsequent neurologic sequelae. Significant neurologic sequelae persisted in seven of ten patients and included deficits in cognition or intellect, hyperactivity, impulsivity, emotional lability, and mild motor deficits. Seizures were seen in one patient.
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PMID:Clinical outcome in children with acute cerebellar encephalopathy and neuroblastoma. 272 81


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