Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

78 children with acute lymphoblastic leukemia or non-Hodgkin-lymphoma were treated at the Children's Hospital of the University of Heidelberg from December 1971 to April 1979. Following cytostatic treatment and irradiation of the skull 11 children developed CNS-symptoms (mainly seizures and paresis) which were caused by intracerebral hemorrhage, infectious or degenerative CNS-diseases. Cranial axial tomography (CAT) was helpful in finding the cause of the CNS-complication. We recommend routine CAT in the beginning and during the course of treatment of leukemia to document CNS-changes as early as possible and to prevent further damage by alterations of therapy.
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PMID:[ZNS complications in children with acute lymphatic leukemia. Computer tomographic studies]. 29 67

Four patients with chronic lymphatic leukaemia, M. Hodgkin and metastatic breast carcinoma developed particularly severe generalised herpes zoster, with complications of herpes zoster pneumonia, signs of encephalitis and phrenic nerve paresis. Virus specific complement-fixing antibodies increased regularly or delayed, without strict correlation to the clinical course. However, in all these cases there was a relative or absolute deficiency of T-lymphocytes in the peripheral blood, as a result of the underlying illness and of treatment with cytostatic agents. Because of the vital role of cell-mediated immunity in the control of the varicella-zoster virus (VZV), the observed T-cell deficiency seems to be an important pre-condition for the development of severe generalised herpes zoster.
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PMID:[Severe generalized courses of zoster due to cellular immunologic defects. Importance of an absolute or relative T-cell deficiency]. 30 13

Fifteen cases of herpes zoster with lower motor neurone paresis involving the upper and lower limbs are reviewed. Five patients had an underlying disease--three had rheumatoid arthritis, two of whom were on prednisolone; one had chronic lymphatic leukaemia and one lymphosarcoma. Details are given of the time relationship between onset of pain, the appearance of the skin eruption and the later muscle weakness. Electromyographic evidence was available in 12 patients. The difficulty of assessing the muscle power in the presence of severe pain is discussed. Prognosis was generally very good; 11 patients recovered fully, three improved and one was unchanged after 5 months, when he died of lymphosarcoma. One patient was lost to follow-up at 5 months but was improving at the time.
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PMID:Herpes zoster and lower motor neurone paresis. 58 57

A 60-year-old man born in Miyazaki prefecture was admitted to our hospital complaining of skin rash in December 1989. On hematological examinations, leukocyte count was 14,200/microliters with 49% of abnormal lymphocytes showing lobulated nuclei. The surface marker study revealed their phenotype as CD4+8-. Anti human T cell leukemia virus type I (HTLV-I) antibody and monoclonal integration of proviral DNA were positive. From the above results, he was diagnosed as adult T-cell leukemia (ATL). Abnormal lymphocytes gradually decreased without treatment after the first admission. In January, 1990, he began to complain of neck pain. Two months later he was readmitted because of paresis of extremities and disturbance of urination. Vertebral bone mass and a compressed spinal cord in the 4th cervic level were confirmed by MR imaging. He received a resection of tumor and an anterior fusion of vertebrae. The bone tumor was histologically diagnosed as malignant lymphoma, diffuse medium-size cell type and the infiltrating cells had their phenotype as CD4+8+. He was postoperatively treated with combination chemotherapies, but neurological abnormalities did not improve. He died of pneumonia on 35 days after the operation. A postmortem examination revealed extradural tumor formation with ATL cells. This case is considered to be rare in respect of both the disappearance of most peripheral abnormal lymphocytes without any treatments and the cervical bone tumor showing immunophenotypic change.
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PMID:[Adult T-cell leukemia with cervical bone tumor showing immunophenotypic change]. 154 18

Leukemic involvement of the temporal bone is not uncommon and may present in a variety of ways including auricular or external canal skin lesions, red or thick tympanic membrane, middle ear effusions, otitis media, hearing loss or mastoiditis. Symptomatic facial nerve involvement, on the other hand, is extremely unusual. We discuss a pediatric patient whose sudden onset facial nerve paresis was the presenting symptom that led to her diagnosis of leukemia. At the time of mastoidectomy, a granulocytic sarcoma or chloroma was noted to be overlying the VIIth nerve.
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PMID:Facial nerve paresis as the presenting symptom of leukemia. 221 Sep 52

A 15 year-old girl who had c-ALL diagnosed in 1982 was presented in our clinic suffering from an ascended flaccid paresis and dysaesthesia of both legs. These are typical symptoms of polyradiculitis of the nerve roots L2-S2. A lumbal puncture revealed a pleocytosis with lymphoblasts which were up to 40% CD10 (cluster of differentiation) up to 70% CD19 and TdT (terminal transferase) positive. The diagnosis of late isolated CNS relapse was made. It is assumed that local residual infiltrations of leukemic cells into the nerve roots L2-S2 got into cell cycle and caused these rare CNS leukemia symptoms. Therefore the value of a craniospinal irradiation to prevent a CNS and systemic relapse is discussed.
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PMID:Syndrome of the posterior and anterior root in a late isolated CNS relapse of c-ALL. Case report. 232 Feb 72

To better understand the molecular mechanism involved in retrovirus ts1-induced paralytic disease in mice, we constructed a panel of recombinant viruses between ts1 and the wild-type viruses Moloney murine leukemia virus (MoMuLV) and MoMuLV-TB, a strain of MoMuLV. These recombinant viruses were constructed in an attempt to identify the sequence(s) in the genome of ts1 which contains the critical mutation(s) responsible for the neurovirulence of ts1. Two functionally distinct sequences in the genome of ts1 were found to be responsible for its paralytogenic ability. One of these sequences, the 0.77-kilobase-pair XbaI-BamHI (nucleotides 5765 to 6537) fragment which encodes the 5' half of gp70 and 11 base pairs upstream of the env gene coding sequence, determines the inability of ts1 to process Pr80env. The other sequence, the 2.30-kilobase-pair BamHI-PstI (nucleotides 538 to 8264 and 1 to 567) fragment, which comprises nearly two-thirds of the env gene, the long terminal repeat, and the 5' noncoding sequence, determines the enhanced neurotropism of ts1. Replacement of any one of these two regions with the homologous region from either one of the two wild-type viruses resulted in recombinant viruses which either totally failed to induce paralysis or induced a greatly attenuated form of paresis in some of the infected mice.
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PMID:The neurovirulent determinants of ts1, a paralytogenic mutant of Moloney murine leukemia virus TB, are localized in at least two functionally distinct regions of the genome. 371 56

Newborn inbred CFW/D mice were inoculated intraperitoneally with ts1, a neurotropic temperature-sensitive mutant of Moloney murine leukemia virus TB (MoMuLV-TB), with the parental wild type (wt) MoMuLV-TB, or with culture medium. A progressive symmetric hindlimb paresis that progressed to paralysis was observed in ts1-infected mice. Wt-infected mice and control mice had no neurologic signs. The severity and progression of neurologic signs correlated with the location, development, and progression of lesions. Lesions consisted of neuronal and glial cell vacuolization in the brain and the anterior horn of the spinal cord, spongiform change in the associated neuropil, spongiform change in lateral and ventral funiculi, and late fibrillary gliosis in the brainstem. There was no inflammation. Lesions were symmetric, increased in severity with time, and consistently arose at specific times in specific nuclei and areas of the brain and spinal cord. Similar, but less severe, histologic lesions were observed in corresponding areas of the central nervous system from wt-infected mice. Ultrastructurally, neuronal and glial cell vacuolization in ts1-infected mice at 31 days after inoculation was caused by dilatation of the endoplasmic reticulum and Golgi complex. Virions were observed in extremely low numbers predominantly in extracellular space and budding from membranes of neurons and glial cells. Virions were not observed in the endoplasmic reticulum or Golgi complex of neurons, nor were there cytoplasmic vacuoles that contained abnormal virions.
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PMID:Noninflammatory spongiform polioencephalomyelopathy caused by a neurotropic temperature-sensitive mutant of Moloney murine leukemia virus TB. 376 4

From 1972-1974, 228 children began treatment for acute lymphocytic leukemia and were prospectively assessed for neurologic complications. After CNS irradiation (2,400 rad) and intrathecal methotrexate (MTX), they received weekly intravenous maintenance therapy with MTX alone (40-60 mg/m2; 20 patients) or MTX (10-30 mg/m2) with other drugs (208 patients). Signs of leukoencephalopathy appeared in 11 children (nine without CNS leukemia) after 4-15 months of IV MTX alone, and included lethargy, seizures, spasticity, paresis, drooling, and dementia. Before or during the clinical onset, EEG frequencies slowed (all ten patients tested). Radionuclide scans showed periventricular accumulation of 99mTc (9/11 patients) and remained abnormal for greater than or equal to six months in eight patients. Cranial computed tomograms or neuropathology findings (five patients each) demonstrated leukoencephalopathy (nine patients) and radiation-related microangiopathy (ten patients). Severe neurologic and neuropsychologic dysfunctions were present in four long-term survivors.
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PMID:Progression of methotrexate-induced leukoencephalopathy in children with leukemia. 693 56

In a population based register of stroke (n = 536) compiled in Perth, Western Australia during an 18 month period in 1989-90, 60 cases (11%) of primary intracerebral haemorrhage were identified among 56 persons (52% men). The mean age of these patients was 68 (range 23-93) and 46 (77%) events were first ever strokes. The crude annual incidence was 35 per 100,000, with a peak in the eighth decade, and a male predominance. Deep and lobar haemorrhages each accounted for almost one third of all cases. The clinical presentations included sudden coma (12%), headache (8%), seizures (8%), and pure sensory-motor stroke (3%). Primary intracerebral haemorrhage was the first presentation of leukaemia in two cases (both fatal) and it followed an alcoholic binge in four cases. 55% had a history of hypertension. 16 (27%) patients, half of whom had a history of hypertension, were taking antiplatelet agents, and one patient was taking warfarin. There were only two confirmed cases of amyloid angiopathy. The overall 28 day case fatality was 35%, but this varied from 100% for haemorrhages in the brainstem to 22% for those in the basal ganglionic or thalamic region. Other predictors of early death were intraventricular extension of blood, volume of haematoma, mass effect, and coma and severe paresis at onset. Although based on small numbers, these data confirm the heterogeneous nature of primary intracerebral haemorrhage, but they also suggest a different clinical spectrum of this type of stroke in the community compared with the experience of specialist neurological units.
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PMID:Spectrum of primary intracerebral haemorrhage in Perth, Western Australia, 1989-90: incidence and outcome. 805 17


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