Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A computer model of a neocortical pyramidal cell has been constructed using ideas similar to those used for hippocampal pyramidal cells. This model has been applied to the study of (a) repetitive firing, and (b) the paroxysmal depolarizing shift (PDS), an important intracellular event during seizures. Although calcium spikes have not been demonstrated directly in neocortical cells, we have postulated (by analogy with hippocampal pyramidal cells) a dendritic calcium conductance and a 'slow potassium' conductance modulated by intracellular calcium ion. With these dendritic ionic conductances, the model is able to reproduce the following experimental features of neocortical pyramidal cells: the afterdepolarization and succeeding afterhyperpolarization after an antidromic spike, and the f-I (firing rate-injected current) curve. Some of the differences between 'fast' and 'slow' pyramidal tract neurons (PTNs) -- narrower spikes and a steeper f-I curve in the fast PTNs -- may be explained by differences in Hodgkin-Huxley potassium kinetics between the two kinds of cell. The same model which faithfully reproduces repetitive firing behavior also reproduces (given appropriate synaptic inputs) the following intracellular events recording during epileptic seizures: (a) a burst of action potentials superimposed on and followed by a PDS, and (b) rapid repetitive firing succeeded by an IPSP. Thus, a single set of parameters can reporduce both normal physiological behavior and 'epileptic' behavior: the particular behavior seen depending on how the cell is stimulated. This overall result is the same as for our model of the CA1 hippocampal cell. It suggests that certain acutely acting epileptogenic agents, e.g. penicillin, may act by increasing synaptic input (perhaps both excitatory and inhibitory) to pyramidal cells, rather than by altering their membrane properties. As in our CA1 hippocampal cell model, bursting seems to be a phenomenon generated by the apical dendrite.
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PMID:Neocortical pyramidal cells: a model with dendritic calcium conductance reproduces repetitive firing and epileptic behavior. 22 13

Focal and generalized seizures occurred in 4 patients with acute lymphoblastic leukemia and non-Hodgkin-lymphoma. The etiology of the neurological complications could be established by cranial computerized tomography (CT): i.e., 1. localized metastasis with calcification and 2. acute intracerebral hemorrhage during induction therapy in two patients with malignant lymphomas; 3. diffuse cerebral infiltration with blast cells and 4. cerebral atrophy in two children with acute lymphoblastic leukemia who were in relapse. Accurate diagnosis of cerebral complications in hemoblastoses is essential for appropriate therapy and CT may lead to more effective treatment in patients with lymphoid malignancy and seizures.
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PMID:Cranial computerized tomography in children with lymphoid malignancy and seizures. 27 69

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

We describe the clinical course of a 20-year-old man who suffered generalized convulsive seizures with postictal aphasia and hemiparesis of the right side. Computed tomography (CT) displayed a left postcentral lesion with prominent perifocal edema and only a little contrast medium enhancement. The completely removed tumor proved to be a primary cerebral non-Hodgkin lymphoma consisting of T-cells. Only ten days after the operation the patient once more presented a clinical deterioration. A nuclear magnetic resonance imaging (MRI) displayed an annular structure in the area previously operated upon, suspected to be an abscess. The second operation disclosed a large recurrence of the primary T-cell lymphoma extending diffusely into the white matter. On account of the rapid recurrence, a whole brain irradiation was started twelve days after the second operation. Four cycles of chemotherapy followed. Immunohistochemical studies of the anaplastic large lymphoma cells showed staining with the pan T-cell markers (UCHL1, CD3) and with the CD30 (Ki-1) antibody. The B-cell markers (L26, LN1) were negative. The EMA (epithelial membrane antigen) was only partially expressed. Further investigation excluded the presence of systemic lymphoma manifestation. 24 months after the last operation the patient remained free of symptoms. The last MRI displayed no evidence for the recurrence of a lymphoma. In reference to this unusual clinical course the few previously reported cases of the extremely rare primary cerebral T-cell lymphoma are reviewed.
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PMID:Primary cerebral anaplastic T-cell-lymphoma (type Ki-1): review and case report. 131 14

4.5 months after successful kidney transplantation a Non-Hodgkin-lymphoma with polymorph centroblastic appearance of the tonsillar gland developed in a 21 years old male patient during immunosuppressive therapy with cyclosporine A and prednisone parallel to infection with Epstein Barr virus. Focal epileptic seizures occurred and were due to cerebral posttransplantation lymphomas as proven by brain biopsy. Reduction of immunosuppressive therapy led to complete remission as shown by CCT and MRI.
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PMID:[Regression of cerebral post-transplantation lymphoma under cyclosporin A reduction]. 228 May 83

T-cell lymphoma may involve the CNS as either a primary or secondary neoplasm. This report describes 8 patients with either primary or secondary T-cell malignancies in the CNS. Five patients presented with symptoms and signs of CNS disease that included seizures, visual impairment, cranial nerve palsies, sensory and motor deficits, gait ataxia, and paraparesis. Three of them had primary parenchymal CNS lymphoma, and 2 had epidural lymphoma that originated in adjacent bone marrow. Three patients were neurologically asymptomatic, but had leptomeningeal tumor and focal parenchymal infiltration at postmortem examination. Histologically, 4 lymphomas were large cell, 3 were mixed large and small cell, and 1 could not be classified by the working formulation for non-Hodgkin's lymphomas. The clinical and pathologic manifestations of T-cell lymphoma in the CNS may be diverse. This report demonstrates that neurologic abnormalities may be the presenting signs of either primary CNS or systemic T-cell lymphoma.
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PMID:T-cell lymphoma in the CNS: clinical and pathologic features. 278 32

Four men and four women, aged 16 to 43, developed dural sinus thrombosis, five patients with acute lymphoblastic leukemia (L.A.L.) and three with non Hodgkin malignant lymphoma (N.H.M.L.). All the cases of L.A.L. were F.A.B.-2 subtype without any unusual hematological features. In 6 cases, the disorders occurred during the phase of therapeutical induction (E.O.R.T.C.-A.L.L.-H.R. protocol) at D5, D10, D15, D26, D30, D38, and in 2 cases during maintenance after a period of remission. All patients had received Vincristine and Prednisone, intrathecal Methotrexate in 5 cases, encephalic irradiation in 3 cases and L-Asparaginase in one case. Three women were taking contraceptive drugs. The neurological symptoms and signs were headache due to intracranial hypertension in 6 cases, Grand Mal seizures in 5 cases, focal seizures in 2 cases, a regressive hemiparesis in 4 cases, stupor in 3 cases. CT scan was abnormal in 4 cases, displaying oedema in 3 cases and an hemorrhagic infarction in 1 case. Angiography showed in all cases occlusion of the superior sagittal sinus in 7 cases and of the transverse sinus on 1 case. Six patients received anticoagulant therapy. Outcome was fatal in 3 cases: in 2 cases of L.A.L., the condition worsened rapidly after the onset and death was related to a tentorial herniation; in 1 case of N.H.M.L. death resulted from an intercurrent infection.
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PMID:[Dural venous sinus occlusions in hemopathies]. 385 30

A case of acute central nervous system toxicity following the intravenous injection of vincristine was observed in a patient treated with a chemotherapy regimen including cyclophosphamide, doxorubicin and prednisone for non-Hodgkin lymphoma. The neurological symptoms consisted of right-sided epileptiform jacksonian seizures limited to the face, that lasted about 10 min, followed by spontaneous recovery. A cerebrospinal fluid study and computed tomographic scan of the brain failed to reveal any central nervous system lymphomatous involvement.
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PMID:Unilateral seizures following vincristine intravenous injection. 642 13

Mycobacterium avium complex infections rarely involve the central nervous system, even in patients with widely disseminated disease. We report a case of disseminated M. avium complex infection presenting with central nervous system symptoms in a patient with Hodgkin's disease. Neurologic findings included disorientation, nuchal rigidity, seizures, an extensor plantar response, cerebrospinal fluid studies consistent with meningitis, and eventually, coma and death. Organisms of the M. avium complex were cultured from several sites. Histopathologically, the central nervous system lesions consisted of small aggregates of lymphocytes and macrophages containing acid-fast organisms present in a predominantly perivascular location. In view of the life-threatening nature and potential treatability of this uncommon presentation of M. avium complex infection, we suggest that these organisms be sought in immunocompromised patients presenting with unexplained central nervous system symptoms.
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PMID:Symptomatic Mycobacterium avium complex infection of the central nervous system. A case report and review of the literature. 875 61

We analyzed 168 consecutive patients with Hodgkin's disease who were treated at the University of Nebraska Medical Center between 1985 and 1990 with high-dose chemotherapy followed by autologous bone marrow transplantation (BMT) or peripheral stem-cell transplantation (PSCT), and describe their neurologic complications. All these patients had relapsed or had failed to achieve a remission with initial chemotherapy. Early complications, defined as those occurring during the first 6 weeks following the transplantation, occurred in 65 patients (39%) and included encephalopathy, seizures, psychiatric symptoms, and cerebral hemorrhage; these were mild and reversible in 47 and fatal in 18 patients. The major cause of these early neurologic complications was pulmonary failure. Late neurologic complications, defined as those occurring 6 weeks after the BMT or PSCT was performed, occurred in 21% of patients and included encephalopathy, peripheral neuropathy, cerebral hemorrhage, and spinal cord compression. Serious nervous system complications following autologous BMT or PSCT for Hodgkin's disease are less frequent than those following allogeneic BMT and are usually a result of injury to other organ systems.
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PMID:Neurologic complications after high-dose chemotherapy and autologous bone marrow transplantation for Hodgkin's disease. 816 25


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