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M Poisson

Publications and source records attributed to M Poisson.

At least 55 records · Page 3Linked to original sources
PubMed1994

[Radiation-induced neuropathies. Experimental and clinical data].

In contrast with the central nervous system, the peripheral nerves are usually considered radioresistant. However, experimental and clinical data show evidence of peripheral nerve injury after radiation therapy. The physiopathology remains unclear. Vascular alterations appear to play an important role. Direct damage to axon or Schwann cell and nervous compression in areas of radiation fibrosis could also be involved. Clinically, brachial plexopathy is a well-recognized complication but all the structures of the peripheral nervous system can be involved: cranial nerves, roots, plexus and nerve trunks. A syndrome of early and reversible plexopathy differs from the classical progressive form with pejorative outcome. Radiation-induced peripheral nerve tumors are infrequent.

Animals↗
PubMed1994

[Paraneoplastic cerebellar degeneration].

Paraneoplastic cerebellar degeneration (PCD) is a rare complication of systemic cancer. PCD may present as a "pure", severe pan-cerebellar syndrome of subacute progression or be only one clinical feature in the setting of extensive CNS disease. The most characteristic form of "pure" PCD is associated with the presence of an anti-Purkinje cell antibody (AB), called anti-Yo, in patients with breast or ovarian cancer. The primary tumor is very often unknown when the cerebellar signs occur, and extensive investigations, including laparotomy or prolonged follow-up may be required to demonstrate its presence. More rarely, others AB than anti-Yo are discovered during PCD. Almost 50% of patients with "pure" PCD do not have circulating anti-neuronal AB. In the cases, the primary cancer is more often known and the clinical course of the cerebellar syndrome may be slower. Cerebellar degeneration may also occur during paraneoplastic encephalomyelitis. In this setting, the cerebellar signs which may be isolated at the onset, become associated with other signs of neuraxis involvement (limbic encephalitis, brainstem encephalitis, myelitis and particularly, subacute sensory neuronopathy) during the course of the disease. When a paraneoplastic encephalomyelitis is associated with a small cell lung cancer, an antineuronal AB called anti-Hu is frequently found. Finally PCD may be associated with the opsoclonus-myoclonus syndrome with the Lambert-Eaton syndrome.

Adult↗
PubMed1994

[Cerebral lymphoma in AIDS: clinical study and clinicopathological correlations].

We report the natural history of 17 brain lymphomas (11 primary, 6 disseminated) from a post-mortem series of 130 patients with AIDS. Primary lymphomas appeared lately in the course of AIDS. They were often associated with a severe T-cell immunodepression and with more frequent opportunistic disorders than disseminated lymphomas. Associated Kaposi's sarcomas were surprisingly frequent. All patients presented with neurological manifestations. Heterogeneous features were seen at CT examination. The CSF was abnormal in 12/13 cases, with an increase of protein contents and secretion of immunoglobulins; it contained activated lymphocytes in 5/6 cases of disseminated lymphomas, and malignant cells in only one case. Cellular density never exceeded 8/mm3 for primary lymphomas, and the lymphocytes were considered normal. The pre-mortem diagnosis of cerebral lymphomas was made in five patients, with a time lapse of 1 to 7 months between the first neurological symptoms and death, and of 5 to 30 days between the diagnosis and death. Cerebral biopsy was diagnostic in 4 cases of primary cerebral lymphomas. In only 1/6 patients with disseminated lymphomas, the diagnosis had been made when the patient was still alive, based on CSF and bone marrow lymphomatous infiltrations. The diagnosis of cerebral lymphoma (7 primary, 5 disseminated) was post-mortem in 12 cases. It was made only at microscopic examination in 2/12 cases of primary lymphomas. The histopathological study frequently showed a multicentric involvement, and always an immunoblastic cell type with plasmablastic differentiation and frequent medium size cells. Marked gliosis and significant necrosis were often observed. Neuropathological lesions associated with HIV-1 infection (toxoplasmosis, CMV and HIV-1 encephalitis) were seen in 8 cases with primary lymphomas.

Adult↗
PubMed1994

[Primary meningeal gliomatosis].

A 44 year old woman presented with chronic meningitis. Magnetic resonance imagery showed a diffuse contrast enhancement of the leptomeninges. Cerebrospinal fluid studies showed a high hyperproteinorachia and light pleiocytosis. A left temporal tumor appeared four months later. Histological studies revealed an anaplastic oligosatrocytoma leading to the diagnosis of primary leptomeningeal gliomatosis.

Adult↗
PubMed1994

Oncogene amplification in human gliomas: a molecular cytogenetic analysis.

Nine cases of malignant gliomas were selected for the presence of double minutes (dmin) or homogeneously staining regions (hsr) detected by conventional cytogenetics. Analyses were performed on fresh (2 cases) or xenografted (5 cases) tumors or both (2 cases). A modified comparative genomic hybridization technique (mCGH) was applied exhibiting a single amplified locus in 8 tumors and 4 amplified loci in one tumor. Recurrent sites of amplification were detected in 7p11-p12 (5 cases) and 1q32.1 (2 cases). Signals were also observed in 4q11-q12, 5p15.1, 7q31, 8q24.1 and 9p2 in one tumor each. Southern blotting demonstrated that the genes for EGFR (epidermal growth factor receptor), PDGFRA (platelet derived growth factor receptor alpha), MET and MYC oncogenes were involved in 7p11-p12, 4q11-q12, 7q31 and 8q24.1 amplifications, respectively. These amplifications were found by in situ hybridization on tumor spreads, in dmin or episomes for EGFR, dmin for PDGFRA and MET, and hsr and dmin for MYC genes. Other mCGH signals, for which no target genes could be proposed, were confirmed by chromosome paintings on tumor metaphases. In one of the tumors, the coamplification of DNA from 5p15.1 and 9p2 bands in the same dmin was demonstrated.

Adult↗
PubMed1993

Experimental carcinomatous plexopathy.

To understand the pathophysiology of carcinomatous plexopathy better, we studied nerve lesions induced by an experimental thyroid carcinoma implanted over the brachial plexus in 30 Fisher rats. We performed a morphological study including light and electron microscopic examination and teased fibre preparations of brachial plexuses from implanted and control animals. The control side was normal in all. A large tumour always grew within 2 months in all implanted animals and a third of the rats eventually developed weakness of the corresponding anterior limb extremity. On gross examination the tumour always surrounded the brachial plexus, which showed a variety of microscopic abnormalities, ranging from isolated endoneurial oedema to total degeneration of nerve fibres in 41% of the implanted rats. The most frequent lesions consisted of segmental demyelination associated with endoneurial oedema at the site of compression. Some axons degenerated distally and regeneration by sprouting of the proximal stump was noted 80 days after implantation. All subpopulations of nerve fibres were equally affected. Invasion of the intrafascicular area by the tumour was an uncommon finding, in comparison with the constant entrapment of the branches of the plexus by the tumour. This invasion by the tumour induced demyelination of nerve fibres at the site of compression, and sometimes at a distance from the tumour. Regeneration did not occur when the tumour had invaded the intrafascicular area.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Diffuse primary leptomeningeal gliomatosis.

A 38 year old patient developed multiple cranial nerve palsy, seizures and progressive alteration in consciousness. CSF examination revealed tumor cells and a tentative diagnosis of leptomeningeal carcinomatosis from an unknown primary tumor was made. Treatment with intrathecal methotrexate and cranial radiation therapy was started without effect. At autopsy widespread leptomeningeal gliomatosis originating from a previously unknown astrocytoma of the hippocampus was found.

Adult↗
PubMed1993

Treatment of recurrent malignant supratentorial gliomas with the association of procarbazine, thiotepa and vincristine: a phase II study.

Twenty patients previously treated with surgery, radiation therapy and chemotherapy with a nitrosourea for malignant supratentorial gliomas received a combination of procarbazine, thiotepa and vincristine (P.T.V.) at tumor recurrence. Procarbazine was given at a dose of 100 mg/m2 per os from day 1 (D1) to day 15 (D15), thiotepa was administered i.v. at a dose of 35-45 mg/m2 at D1, and vincristine at a dose of 1.4 mg/m2 at D1 and D8. Courses of therapy were repeated every four weeks. Tolerance was evaluated in 20 patients. Three patients developed peripheral neuropathy after 2 or 3 courses of vincristine which was then discontinued. Blood toxicity over grade I occurred in 8 patients (40%). One patient developed a grade i.v. pancytopenia. All 20 patients could be evaluated for therapeutic response. A partial response was noted in 3 patients (15%): 1 glioblastoma multiforme, 1 anaplastic oligodendroglioma and 1 anaplastic astrocytoma. In these three patients time to tumor progression was 10, 11+ and 5 months, respectively. Stabilization lasting 4 months was observed in one patient (anaplastic astrocytoma). Estimated median duration of survival for the entire group was 4.5 months following the onset of PTV (13 months following the date of histology).

Adult↗
PubMed1992

Treatment of malignant gliomas with surgery, intraarterial chemotherapy with ACNU and radiation therapy.

Forty patients with malignant supratentorial gliomas received iterative intraarterial (IA) infusions of ACNU, 1-(4-amino-2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl)-3-nitrosourea at a dose of 150 mg repeated every 6 weeks. Group A consisted of eighteen patients previously treated with surgery, radiation therapy (RT) and sometimes chemotherapy, who received IA ACNU at tumor recurrence. Group B consisted of twenty two patients who received IA ACNU in the postoperative pre-RT period. In group A, 8/18 patients (44%) had an objective response, including 6/12 anaplastic astrocytomas (AA) and 2/6 glioblastoma multiforme (GBM), while 10/18 patients (56%) did not respond. Median survival time was 6 months for GBM and 12 months for AA. In group B, 6/22 patients (27%) had an objective response (4/18 GBM and 2/4 AA) and 16/22 patients (73%) did not respond. Nine patients had such an extensive tumor after one or two courses of IA ACNU that RT was cancelled. Median survival time was 8 months for GBM and 8 months for AA. Three patients (8%) had ophthalmologic toxicity on the infused side. There was no case of leukoencephalopathy.

Adult↗
PubMed1992

[Primary non-Hodgkin's malignant lymphoma of the central nervous system].

The incidence of primary central nervous system lymphoma (PCNSL) is increasing, not only in immunodeficiency states, but also in apparently normal individuals. The most common presentation of PCNSL is that of an intracranial mass lesion. Ocular involvement is associated in 20% of patients. CT/MR scan typically shows one or several periventricular tumors with indistinct margins that diffusely and densely enhance following contrast infusion. The diagnosis relies on lumbar puncture, vitreous biopsy, or stereotactic biopsy of a brain lesion demonstrating lymphomatous cells. If possible, corticosteroids should be used only after definite diagnosis. Corticosteroids have a cytotoxic effect responsible for transient remission in 40% of patients. Whole brain radiation therapy induces a complete or partial response in 80% of patients but recurrence always occurs and the median survival does not exceed 14-18 months. The addition of systemic and intrathecal chemotherapy seems to substantially improve the prognosis with median survival exceeding 3 years in some studies. PCNSL associated with AIDS generally occurs at a late stage of the disease and is the fourth cause of death in AIDS patients. Radiation therapy is useful but the median survival does not exceed 5.5 months because patients most often die of opportunistic infections.

Acquired Immunodeficiency Syndrome↗
PubMed1992

[Orbital myositis, recurrence of Whipple's disease].

Whipple's disease, a chronic systemic and multi-organ disease can be associated with ophthalmological manifestations with or without CNS involvement. Myositis rarely occurs during Whipple's disease. Antibiotic treatment prevents CNS recurrence. We report here the association of an orbital pseudotumor with Whipple's disease. This myositis was discovered on a follow-up CT examination. It appeared only one year after the end of a long course of antibiotic treatment, but it resolved within a few weeks when treatment was reintroduced. Relations between these two diseases are discussed.

Eye Diseases↗
PubMed1992

[Chorea disclosing polycythemia and renal adenocarcinoma].

A 79-year-old woman had chorea complicating polycythaemia. The polycythaemia and the chorea disappeared after surgical removal of a renal carcinoma. The literature on polycythaemic chorea is reviewed and its pathophysiology discussed.

Adenocarcinoma↗
PubMed1992

[Chromosome abnormalities and adenine metabolism in human glial tumors].

Most chromosome aberrations in gliomas are numerical, resulting in either gains or deficiencies of whole chromosomes. In tumors of low malignancy, the karyotype is frequently normal or exhibits a loss of sex chromosome and a gain of chromosome 7. These two anomalies may not be directly related to malignancy. In the highly malignant cases, the two most frequent aberrations are the gain of chromosome 7 and the loss of chromosome 10, other anomalies such as losses or deletions of chromosomes, 9, 22, 6, 13 and 14 being detected at various frequencies. Several of these chromosomes carry important genes of adenine metabolism: AK1 and AK3 (adenylate kinase) and MTAP (methylthioadenosine phosphorylase) for chromosome 9; ADK (adenosine kinase) and mitochondrial ATPase for chromosome 10; ADSL (adenylosuccinate lyase) for chromosome 22, NP (nucleoside phosphorylase) for chromosome 14. We performed the corresponding assays of enzyme activity on both fresh tumors and tumors grafted on nude mice, which showed that these enzymes had a relatively low activity although the tumors were proliferating. However, chromosome losses do not seem to directly cause the metabolic alterations by gene dosage effect. Interestingly, chromosome 10, frequently deficient, also carries genes of importance for glycolysis (hexokinase) and glutamate metabolism (glutamate dehydrogenase and glutamate oxaloacetate transaminase). The deficiency for these genes could be taken into account for a better type of chemotherapy by antimetabolics.

Adenine↗