Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013362 (dysarthria)
 3,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Abnormally high uptake of technetium-99m hexakis-2-methoxyisobutylisonitrile (99mTc-SESTAMIBI) in the right ventricle and in the septum was observed in a 47-year-old woman initially presenting with dysarthria and left hemiparesis. Endomyocardial biopsy demonstrated a high-grade malignant non-Hodgkin's lymphoma. Complete remission was achieved by combined cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) chemotherapy and radiotherapy of the heart and mediastinum. The post-remission single photon emission tomography (SPET) 99mTc-SESTAMIBI study showed a homogeneous distribution pattern, in agreement with echocardiography computed tomography and magnetic resonance imaging. Increased uptake of 99mTc-SESTAMIBI, a myocardial perfusion agent, has been observed in some benign and malignant tumours. It may prove to be useful in the diagnosis and follow-up of malignancies.
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PMID:Abnormal uptake of technetium-99m hexakis-2-methoxyisobutylisonitrile in a primary cardiac lymphoma. 153 70

Three children with acute lymphocytic leukemia (ALL) developed delayed-onset transient hemiparesis and facial palsy after intrathecal (IT) administration of methotrexate (MTX) alone or as part of triple intrathecal chemotherapy for central nervous system (CNS) prophylaxis. The hemiparesis developed 10 to 14 days after IT therapy. Two of three children also experienced transient, profound expressive dysarthria. These episodes occurred during maintenance treatment after multiple IT administrations and without previous CNS toxicity. Two of three children received intermediate-dose MTX, 1 g/m2, not less than 5 weeks before events. These patients had not received cranial irradiation and had no evidence of CNS leukemia before or after these episodes. Ischemic changes on computerized tomographic scan or magnetic resonance imaging studies were documented in all three cases. Such changes are unusual manifestations of neurotoxicity in children after intrathecal therapy.
Cancer 1991 Apr 15
PMID:Hemiparesis and ischemic changes of the white matter after intrathecal therapy for children with acute lymphocytic leukemia. 200 23

An 81-year-old man who had suffered from hypertension for the preceding three years was admitted as an emergency to the department of neurology of our hospital with the chief complaint of dysarthria. He was diagnosed to have multiple lacunar cerebral infarcts by cranial CT, while the laboratory data showed liver dysfunction characteristic of cholestasis. Mild respiratory insufficiency and renal dysfunction were also found. Further radiological examinations on the liver and biliary tree (US, CT and ERC) were performed, and they revealed that the common bile duct was dilated due to two stone-like masses. He was referred to our department of surgery and underwent laparotomy. Intraoperative endoscopy disclosed intraductal papillomatous lesions. Because of the multiple complications of the patient, resection of the entire common bile duct including the gallbladder and the papilla of Vater without any resection of the pancreas was performed instead of pancreatoduodenectomy. The postoperative course was uneventful and he was discharged on the 31st POD. One year after operation, there is no sign of recurrence either clinically or radiologically. The potentially curative operation for cancer of the distal bile duct is pancreatoduodenectomy, but this is of so great a surgical stress that such a high risk case as described above might be unable to survive it. Even if he survived the perioperative period, he might have a poor quality of life due to postoperative complications. The macroscopic appearance of bile duct cancer is correlated to its invasive spread and prognosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Selective resection of the distal bile duct in a high risk patient with polypoid cancer of the intrapancreatic bile duct]. 213 Jul 95

Acute cerebellar toxicity with ataxia and dysarthria is a well-known side effect during high-dose cytarabine therapy. Dose, age, previous neurological disorders, hepatic dysfunction, and renal insufficiency have been inconsistently reported as risk factors. The present paper presents a patient with renal insufficiency who developed severe cerebellar toxicity following treatment with a dose of cytarabine (8 g/m2 over 5 days) not generally expected to be associated with neurotoxicity. Together with a review of the literature, the present case gives evidence of renal insufficiency as a major risk factor in the development of cerebellar toxicity during cytarabine therapy. Reduced doses of cytarabine should be considered in patients with renal impairment.
Cancer Chemother Pharmacol 1990
PMID:Cerebellar toxicity during cytarabine therapy associated with renal insufficiency. 224 95

Neurological disorders associated with a malignant neoplasm, which is not caused by a direct effect such as metastasis, infiltration or compression, is called carcinomatous neuromyopathy. Subacute cerebellar degeneration recognized in this category is characterized by acutely or subacutely progressive cerebellar ataxia and widespread loss of Purkinje cells. There have been several reports of subacute cerebellar degeneration in lung carcinoma, ovarian carcinoma and Hodgkin's disease, but rare in urogenital malignancies. We present a patient with neurological disorder considered subacute cerebellar degeneration associated with HCG-beta positive seminoma. A 29-year-old man noticed a left intrascrotal mass in the summer of 1984. The mass began to grow in April, 1985 and diplopia, gait disturbance and dysarthria appeared late in May. He consulted our hospital on July 20, 1985. Serum human chorionic gonadotropin (HCG)-beta was elevated to 200 ng/ml but alpha-fetoprotein and carcinoembryonic antigen were normal. Left high orchiectomy was performed and the tumor was diagnosed histologically as typical seminoma. Bulky metastatic tumor was recognized in retroperitoneum on abdominal CT but brain CT was normal. VAB VI chemotherapy was performed. The retroperitoneal metastatic tumor disappeared and HCG-beta was normalized and complete remission achieved, but cerebellar symptoms still remain 14 months after remission. This case is considered to be subacute cerebellar degeneration associated with seminoma and is the second case with testicular carcinoma reported.
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PMID:[Subacute cerebellar degeneration with HCG-beta positive seminoma of the testis]. 245 60

Eighteen patients with advanced solid cancer were treated with daily 5'-dFUrd infusions given over 1 h on days 1-5 of a 4-week cycle. Nine patients received 3 g/m2 5'-dFUrd daily and another nine patients 5 g/m2. One patient on 5 g/m2 5'-dFUrd was not fully evaluable for tolerability due to early death (progressive disease) 4 weeks after the first cycle. A total of 48 cycles was given. The gastrointestinal and hematological toxicity was generally mild (grade 1-2). Central neurotoxicity (ataxia, unsteadiness, diplopia, dysarthria, sometimes confusion) was observed in 7 of 8 patients on 5 g/m2 5'-dFUrd leading to premature discontinuation of treatment in 3 patients (after 2 cycles). Only 3 of the 9 patients in the 3 g/m2 group had slight signs of cerebellopathy. Typically, the reversible neurological side effects started at the end of the 2nd week of a cycle. The serum elimination kinetics of 5'-dFUrd and its metabolites 5-FU and 5'-dFUH2 have been investigated in the serum and showed very low intra- and interindividual variations. Peak concentrations of the 5'-dFUrd at the end of the infusion approximated 500 mumol/l and 1000 mumol/l for the 3 g/m2 and 5 g/m2 group, respectively. The peak of the serum 5-FU was reached at the same time, the ratio 5-FU/5'-dFUrd being around 10%. The elimination half-life time for 5-FU was protracted by a factor of 2-3 compared with the direct injection of 5-FU. Monthly infusion of 5'-dFUrd 5 mg/m2 per day on days 1-5 lead to an unacceptable frequency and degree of neurological toxicity. Similar infusions of 5'-dFUrd 3 g/m2 per day on days 1-5 were well tolerated.
Cancer Chemother Pharmacol 1986
PMID:Phase I/II tolerability/pharmacokinetic study with one-hour intravenous infusion of doxifluiridine (5'-dFUrd) 3 g/m2 VS 5 g/m2 QD x 5 per month. 294 31

Four different antineuronal autoantibodies have been identified in 23 of 47 patients with paraneoplastic cerebellar degeneration (PCD). The most common, an antibody against 34- to 38-kDa and 62- to 64-kDa protein antigens in the cytoplasm of Purkinje cells, was found in 18 patients. It is a highly specific marker for a severe stereotypical subacute pancerebellar syndrome of truncal and appendicular ataxia, dysarthria, and nystagmus in women with cancer (usually ovarian or breast carcinoma). Different anti-Purkinje cell antibodies (APCA) were found in 2 other patients with PCD. With two possible exceptions, an APCA was not found in patients with other neurological diseases, with cancer not associated with neurological symptoms, or in normal subjects. Antibodies reactive with neuronal nucleoproteins were identified in 3 other patients with PCD: an antibody that recognized 35- to 40-kDa neuronal antigens was found in 2 women with small-cell lung carcinoma, while an antibody in a woman with breast carcinoma identified 53- to 61-kDa and 79- to 84-kDa antigens. Detection of an antineuronal antibody in a patient without known cancer should prompt a careful search for a tumor at a site appropriate to the antibody type.
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PMID:Paraneoplastic cerebellar degeneration: clinical-immunological correlations. 323 56

The clinical and pathological findings in 4 adults with cancer and opsoclonus were compared with those of 15 other patients described elsewhere. The clinical syndrome of paraneoplastic opsoclonus is characterized by the acute onset of opsoclonus and truncal ataxia, often accompanied by encephalopathy, myoclonus and a cerebrospinal fluid pleocytosis. Unlike most other paraneoplastic syndromes, the course is often remitting and relapsing. Neuropathological examination in 3 of our patients showed lymphocytic cuffing of occasional blood vessels throughout the central nervous system, associated with a mild, diffuse proliferation of microglia in 1 patient. Apart from a mild, patchy loss of Purkinje cells in 1 patient, there was no loss of neurons from the cerebellum, brainstem, cerebral hemispheres, or spinal cord. These patients differ from those with the more common paraneoplastic cerebellar degeneration by the predominance of truncal over limb ataxia, the presence of myoclonus, the absence of severe dysarthria, a tendency for remission, and the preservation of Purkinje cells.
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PMID:Opsoclonus, myoclonus, ataxia, and encephalopathy in adults with cancer: a distinct paraneoplastic syndrome. 335 11

A case of multiple spontaneous intracerebral hematomas is presented. A 67-year-old man with 7 years history of hypertension had sudden clumsiness in his right hand and an hour later dysarthria appeared. A CT scan taken 3 hours after the onset revealed two well demarcated high density areas in the left putamen and in the parietal subcortex. A diagnosis of multiple intracerebral hematomas was made. On neurological examination he was midly stuporous (13 points of Glasgow Coma Scale). Dysarthria, right hemiparesis and right extensor plantar response were seen. CT scan of 6 hours later disclosed the same findings as the previous study. He recovered well and neurologically free in a few days. On the following CT scans both hematomas were isodense 2 weeks later, and ring-like enhancement effect was noted. CT scan showed normal appearance 7 weeks later. On MRI using 0.5 T unit t-1 and t-2 weighted spin echo images of these hematomas also showed the similar chronological changes. The history, these CT and MRI studies suggest that two hematomas of this case occurred almost simultaneously in one cerebral hemisphere. No causative factors such as blood dyscrasias, AVM, angioma, septicemia, malignancies or sinus thrombosis was identified. We consider that a hypertensive intracerebral hematoma of the putamen was followed by the parietal intracerebral hematoma within a few hours, although amyloid angiopathy was not completely excluded because no cerebral biopsy of the lesion was performed.
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PMID:[A case report of simultaneous multiple intracerebral hematomas]. 338 86

A 65 year old man developed progressive signs of pontine and medullary dysfunction with striking bilateral paralysis of lateral gaze, dysarthria, dysphagia, and ataxia. A respiratory death occurred seven months from the onset. Pathological examination revealed focal brain-stem changes of perivascular lymphocytic cuffing, microglial infiltration, glial nodules, and neuronophagia. No underlying malignancy or general disease impairing immunity mechanisms was discovered.
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PMID:Subacute brain-stem encephalitis. 485 9


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