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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The case of a twelve year old child with intracerebral hypertension and cerebellar syndrome in whom the neuroradiological and neurological examinations were suggestive of posterior cranial fossa tumor is reported. The brain scan depicted the scintigraphic pattern of midline neoplasms, most likely medulloblastoma or astrocytoma. At surgery a Cysticercus cellulosae was removed from the fourth ventricle. The authors suggest that in geographical areas with high prevalence of neurocysticercosis in the infantile population the hypothesis of the pseudotumoral form of the disease be remembered when one attempts to characterize the type of neoplasms of the posterior fossa as detected by brain scan.
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PMID:[Cysticercosis of the fourth ventricle simulating a posterior fossa neoplasm in cerebral scintillography. Report of a case]. 75 15

Autonomic dysfunction in a child may present confusing clinical phenomena which mimic other diseases. Various clinical manifestations were seen during the 6-year course of a child with an astrocytoma of the hypothalamus. These ranged from the initial features of the diencephalic syndrome of infancy to autonomic seizures with striking paroxysms of hypertension, tachycardia, and sweating. Disturbances in hormonal regulation and gastrointestinal abnormalities were possibly related to the autonomic disturbance. The mechanisms for these findings were poorly understood. We conclude that a diencephalic lesion should be suspected in any child exhibiting such findings.
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PMID:Hypothalamic symptomatology and its relationship to diencephalic tumor in childhood. 84 44

The ability of angiotensin peptides to stimulate prostaglandin release and raise intracellular calcium levels by activating a phosphoinositide-specific phospholipase C was assessed in three human astrocytoma cell lines (CRTG3, STTG1, and WITG2). The addition of angiotensin II to CRTG3 cells resulted in a dose-dependent release of prostaglandin E2 and prostacyclin, the production of inositol 1,4,5-trisphosphate, and the mobilization of intracellular calcium. Angiotensin-(1-7), previously considered to be an inactive metabolite of angiotensin II, was as potent as angiotensin II for prostaglandin release but did not activate phospholipase C or mobilize intracellular calcium. In contrast, angiotensin-(2-8) caused only a slight increase in prostaglandin release, even though it was as effective as angiotensin II in augmenting inositol 1,4,5-trisphosphate production and calcium mobilization. Moreover, neither the release of prostaglandins in response to angiotensin II or angiotensin-(1-7) nor the mobilization of intracellular calcium in response to angiotensin II required extracellular calcium. Angiotensin II and angiotensin-(1-7) caused the release of prostaglandins from all three human astrocytoma cell lines, but changes in the level of intracellular calcium in response to angiotensin II only occurred in CRTG3 cells. Although previous studies have provided evidence for angiotensin receptor subtypes on the basis of selectivity of antagonists or signal transduction mechanisms, these data suggest that human astrocytes contain multiple angiotensin receptor subtypes on the basis of their response to different angiotensin heptapeptides--angiotensin-(1-7) and angiotensin-(2-8).(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1991 Jul
PMID:Human astrocytes contain two distinct angiotensin receptor subtypes. 186 Jul 9

Between March, 1983, and February, 1989, 19 infants or children with chiasmal/hypothalamic gliomas were treated with chemotherapy after either surgical or radiological diagnosis. The patients ranged in age from 15 weeks to 15.6 years (median 3.2 years) at the start of therapy. Twelve patients were treated immediately after diagnosis because of progressive symptoms, and seven received chemotherapy after either radiographic progression or clinical deterioration, including progressive visual loss or intracranial hypertension. Based on biopsy results, seven of these tumors were classified as juvenile pilocytic astrocytomas, two as astrocytomas, two as highly anaplastic astrocytomas, and one as a subependymal giant-cell astrocytoma. There was associated neurofibromatosis in four patients. The two initial patients were treated with either actinomycin D and vincristine or 5-fluorouracil, hydroxyurea, and 6-thioguanine. The remaining patients received nitrosourea-based therapy; 15 evaluable patients were treated with a five-drug regimen that included 6-thioguanine, procarbazine, dibromodulcitol, 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea (CCNU), and vincristine and one received 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) and 5-fluorouracil. Fifteen of the 18 evaluable patients initially managed with chemotherapy either responded to therapy or their condition stabilized. Median time to tumor progression has not been reached at a median follow-up period of 79 weeks (range 6.6 to 303 weeks), and no tumor-related death has occurred with a median follow-up period of 79 weeks (range 18 to 322 weeks) from the initiation of therapy. The four patients who failed therapy or whose disease progressed after chemotherapy were treated satisfactorily with radiation therapy. Initial improvement or stabilization of visual function was obtained in 16 patients. Endocrine function remained stable in all patients during treatment, although three patients required pharmacological treatment for endocrinopathy that was present at diagnosis. These preliminary results suggest that nitrosourea-based cytotoxic regimens are useful for the initial treatment of children with chiasmal/hypothalamic gliomas, and allow potentially harmful radiation therapy to be deferred until progression of disease.
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PMID:Management of chiasmal and hypothalamic gliomas of infancy and childhood with chemotherapy. 190 97

The case of a male child with Russel's syndrome due to a pilocytic astrocytoma located in the diencephalic region is presented. The diagnosis was made in the 16th month of age, but symptoms began in the 4th months of life, when he started losing weight. By the time he was admitted weight was 6150g and he was 74cm tall, with an emaciated aspect, no panniculus adiposus, irritated, and with symptoms of intracranial hypertension. There was convergent strabismus, vertical nystagmus of the left eye and bilateral papilledema. Tendinous reflexes were exacerbated and he had spastic tetraparesis. The endocrine evaluation showed a basal raise of GH (23ng/ml), TSH (6.2mUI/1) and prolactin (26ng/ml). The first two hormones did not respond to the acute test with TRH, while prolactin had a poor response. He was submitted to radiotherapy with linear acceleration (total dose of 4000 rads) and surgery, during which the tumor could not be completely removed due to its large size. After 9 months, the child is doing well, with a considerable weight gain (2500g).
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PMID:[Russel's syndrome: diencephalic tumor in a child]. 211 20

The short- and long-term outcome and special problems of 24 children with infantile spasms and tuberous sclerosis (TS) was studied. The diagnosis of TS is frequently missed: white spots on the skin have to be carefully looked for. In the present study, these spots were always found, and calcifications or hypodense areas of the brain were revealed by CT scans before one year of age. In addition to epilepsy, manifestations of TS included: giant cell astrocytoma, iridic heterotopia, cardiac rhabdomyoma, brain cysts, polycystic kidneys with severe arterial hypertension, retinal phakomas, angiofibroma and white spots on the skin. Long-term outcome was poor. None of the children had normal intelligence and all but one had epilepsy, which was often intractable. Behavioural problems were common. The prognosis, in terms of later intelligence, epilepsy and behavioural problems, was worse than in those with 'idiopathic' infantile spasms or in those with simultaneous neurological disorders. An early diagnosis of TS in patients with infantile spasms clarifies the prognosis and avoids some of the hazards of ACTH therapy. TS children have a high relapse rate after ACTH therapy, so prolonged courses may be indicated.
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PMID:Tuberous sclerosis and infantile spasms. 215 40

Hydrocephalus with spinal tumor is rare, and its cause is obscure. We report one patient with a thoracic astrocytoma who developed ventricular dilatation and intracranial hypertension. The pathophysiology is reviewed.
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PMID:Hydrocephalus and intraspinal tumor in childhood. 234 May 27

A 6 year-old girl was admitted with symptoms of increased intracranial pressure. These manifestations spontaneously disappeared, then recurred a few days later, leading to the discovery of hydrocephalus with increased protein concentration in the cerebrospinal fluid. A cervical spine tumor was diagnosed by magnetic nuclear resonance examination. The patient was successfully operated on for a benign astrocytoma. In the absence of a cerebral tumor, cervical spinal tumors should be looked for when recurring symptoms of intracranial hypertension occur in a child.
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PMID:[Intermittent intracranial hypertension revealing a tumor of the cervical spine]. 260 27

Four boys and four girls with brain tumors who were admitted to our department in the last 8 years are herein described. They presented with epileptic fits, which began before the age of 14 years, with neither intracranial hypertension nor localizing signs during the first 6 months of the illness. The length of time between the first fit and the diagnosis of a tumor ranged from 2 months to 11 years (median of 3 years), during which period all patients but one received anticonvulsant therapy. The nontreated patient was under psychiatric treatment for 1 year. The electroencephalographic evolution was disconcerting, showing asymmetry of the recording with association of slow polymorphic waves and acute irregular waves, suggesting encephalitis. The neuroradiological diagnosis was made by cerebral arteriography in one patient and in the others by angiography and CT scans (which revealed hypodense cerebral areas in five cases and hyperdense areas in the other two). The histology of the tumor was that of a grade I astrocytoma in six cases; a grade III oligondendroglioma in one case, and a meningioma in the other. All patients underwent surgical treatment. Four also received radiation therapy, two for a partially excised astrocytoma and one each for an oligodendroglioma and a meningioma. Postoperatively, all patients were put on anticonvulsant drug therapy. There were no mortalities. To date, only one astrocytoma has recurred. The sequellae observed were hemiparesis in one case and marked psychomotor deficit in another. These two patients also still have epileptic fits. The others are all psychologically and neurologically normal, and two are now off antiepileptic drugs.
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PMID:Epilepsy and brain tumors in infancy and adolescence. 377 77

In 3 patients with low-grade astrocytomas clinical pharmacology of interferon-beta (10(7) U/mg protein) was investigated. Interferon-beta with escalating dosage (2.3, 6.9, 23, 69 X 10(6) U/patient) was given to each patient in 4 infusions at weekly time intervals. In these patients dose-dependent plasma-levels of interferon-beta of up to 5800 IU/ml were achieved. Plasma concentrations showed a biphasic decline (T1 1/2:0.095-0.49 hrs and T2 1/2: 5-14.5 hrs). Side effects were: mild fatigue, myalgia, tachycardia, hypertension, and fever; the latter was well controlled by pretreatment application of paracetamol. Hematological changes included lymphopenia (2-6 hrs after infusion) and granulocytosis (3-6 hrs after infusion). Natural Killer cell activity was also monitored: 6 hours after infusion a drop of activity - not clearly dose dependent - was observed to a minimum of 1% pretreatment activity; 24 hrs after infusion activity increased up to a maximum of 400%. In this phase I study high biological activity of interferon-beta could be detected in plasma of astrocytoma patients - clinical tolerance was good and only mild toxicity was observed.
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PMID:Interferon-beta in patients with low-grade astrocytomas--a phase I study. 403 71


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