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Biomedical subjects

J Poirier

Publications and source records attributed to J Poirier.

At least 199 records · Page 11Linked to original sources
PubMed1986

Monstrocellular heavily lipidized malignant glioma.

A man of 32 years was admitted with a 3-month history of temporal lobe epilepsy. CT-Scan showed a well-circumscribed area of heterogenous contrast enhancement in the right temporal lobe. Gross total resection was performed but the tumor recurred: the patient died 6 months after the onset of symptoms. There was no autopsy. Histology revealed a highly pleomorphic neoplasm with extensive zones of necrosis. Monster cells, up to several hundred micrometers in diameter, with multiple and/or multi-lobed nuclei were numerous and showed emperipolesis for polymorphonuclear, mononuclear, and small tumor cells. Abundant mitoses were observed. Tumor cells of all sizes had ground-glass or vacuolated cytoplasm which obscured their glial nature. GFAP was demonstrated in some neoplastic cells. Reticulin fibers were confined to perivascular areas where mononuclear inflammatory cells were sometimes noted. Vascular proliferation was mild. Electromicroscopic study revealed that the cytoplasms of the tumor cells contained abundant lipid droplets, numerous mitochondria, and glio-filaments. Such a tumor has been reported recently as "malignant glioma with heavily lipidized tumor cells". This rare entity, previously reported as xanthosarcoma of the brain, represents a subgroup of primitive monstrocellular cerebral tumors.

Adult↗
PubMed1986

Thrombosis of a saccular microaneurysm causing cerebral (pontine) lacunae.

The authors present the case of a hypertensive patient with a thrombosis of a saccular microaneurysm (SMA) and underlying cerebral (pontine) lacunae. This SMA lay at the junction between the main vessel and two small feeding arteries penetrating into the necrotic territory. Microhemorrhages were observed in and outside the aneurysmal wall. Very sinuous narrow channels of recanalization crossed the thrombosis between the upstream and downstream vessels. The anatomical relationship between the SMA and the lacunae has been histologically demonstrated.

Aged↗
PubMed1986

Orthostatic hypotension from a cerebellar gangliocytoma (Lhermitte-Duclos disease). Case report.

A 49-year-old woman presented with orthostatic hypotension. Vertebral angiography and ventriculography revealed a tumor of the left cerebellar hemisphere. Ventriculoperitoneal shunting was followed by complete disappearance of the orthostatic hypotension. The tumor was subsequently removed and microscopic study showed Lhermitte-Duclos disease. Orthostatic hypotension has been rarely reported in association with tumors of the posterior fossa except for those tumors destroying the medullary centers and interrupting the baroreceptor reflex arc. This case is of interest because the tumor was restricted to the cerebellum. The authors have found no previous case in which orthostatic hypotension was a presenting symptom of Lhermitte-Duclos disease.

Cerebellar Neoplasms↗
PubMed1986

[Infections of the central nervous system in malignant hemopathies].

Central nervous system (CNS) infections in immunocompromised hosts are often accompanied by subtle disorders because immunosuppression usually decreases the inflammatory response. CNS infections in immunocompromised patients are usually caused by organisms different from those found in the general population. The organism causing CNS infection in an immunocompromised host can often be predicted if the type of immune abnormality of the patient is known. The common causes of CNS infection in immunocompromised hosts are reviewed here. Meningitis in patients with neutropenia is usually due to enteric Gram negative bacilli that live in the patient's own digestive tract. Pseudomonas aeruginosa is most common and is followed by E. Coli, Klebsiella, Enterobacter and Proteus. A major risk in patients with abnormal immunoglobulins or splenectomy is infection with encapsulated bacteria, particularly Streptococcus pneumoniae, Haemophilus influenzae and Neisseria meningitidis. Meningitis caused by any of the encapsulated bacteria can be fulminant. Listeria monocytogenes is the most common cause of bacterial meningitis in patients with impaired cellular immunity. Nocardia asteroides is a leading cause of brain abscess in patients with hematologic malignancy. Most patients have evidence of concomitant pulmonary lesions. Fungi are among the most common organisms involving the CNS in immunocompromised hosts. Susceptible patients include those with lymphoma or leukemia and those who receive therapies aimed at suppressing delayed hypersensitivity. Cryptococcus neoformans is a common fungal cause of CNS infection in immunocompromised hosts. The primary site of infection is the lung. Spread to the CNS is via the blood stream. The clinical course is highly variable: meningitis, meningoencephalitis and focal mass lesions. Candida causes meningitis or meningoencephalitis characterized by multiple small abscesses in neutropenic hosts. Organisms reach the CNS via the blood stream usually from the digestive tract or infected intravenous catheters. Aspergillus causes brain abscess, cerebral infarction and focal meningitis in patients with neutropenia. The primary infection is in the lung. The parasites that infest the CNS of immunocompromised patients are usually those that exploit a T-lymphocyte, mononuclear phagocyte host defect. The most common are Toxoplasma gondii and Strongyloides stercoralis. There have been a few cases of amebiasis with dissemination to the brain in patients with hematologic malignancies. Toxoplasma gondii causes major CNS disease in immunocompromised hosts: meningoencephalitis or mass lesions.(ABSTRACT TRUNCATED AT 400 WORDS)

Bacterial Infections↗
PubMed1986

[Non-dominant hemisphere syndrome as a result of a right thalamic infarct: an anatomoclinical case].

A 71 year old man had a massive left sensory deficit and hemiplegia, with left heminanopia, visual neglect and constructional apraxia. Moreover he experienced an extra-left arm and illusions of movements. 3 weeks later he suffered "thalamic" pain on left side; he died suddenly 6 weeks after the stroke. Post-mortem examination revealed: a) a right inner temporal and occipital infarction; b) a right thalamic infarction in the thalamogeniculate and paramedian territories; c) an infarction in the adjacent right internal capsule. Considering this case and pertinent literature on clinicopathological studies of right thalamic infarction, the authors suggest that a simultaneous ischaemia of thalamogeniculate and paramedian territories should be necessary to induce somatognosic and visuospatial disturbances.

Aged↗
PubMed1985

Ecogenetics of Parkinson's disease: 4-hydroxylation of debrisoquine.

It is postulated that Parkinson's disease is the result of environmental factors acting on genetically susceptible individuals against a background of normal ageing. Many potentially neurotoxic xenobiotics are detoxified by hepatic cytochrome P450. The function of one such system was studied in forty patients with Parkinson's disease and forty normal control subjects. Significantly more parkinsonian than control subjects had partially or totally defective 4-hydroxylation of debrisoquine. Poor metabolisers of debrisoquine tended to have had earlier onset of disease.

Adult↗
PubMed1985

1-Methyl-4-phenyl-pyridinium-induced inhibition of nicotinamide adenosine dinucleotide cytochrome c reductase.

The effect of 1-methyl-4-phenyl-pyridinium (MPP+), the main toxic metabolite of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a parkinsonism-causing neurotoxin, upon the activity of nicotinamide adenine dinucleotide (NADH) cytochrome c reductase (EC 1.6.99.3) and upon that of glutathione reductase (EC 1.6.4.2) was monitored spectrophotometrically. For the cytochrome c reductase, the increase in absorbance of reduced cytochrome c was measured at 550 nm; for evaluating glutathione reductase, the absorbance of nicotinamide adenine dinucleotide phosphate (NADPH) was followed at 340 nm. MPP+ but not MPTP reversibly inhibited NADH cytochrome c reductase, but not glutathione reductase. This may be a direct mechanism of cell toxicity by this neurotoxin.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1985

Comparative behavioral, biochemical and pigmentary effects of MPTP, MPP+ and paraquat in Rana pipiens.

We demonstrate that injections of 1-methyl-4-phenyl-1,2,3,6-tetra-hydropyridine (MPTP), 1-methyl-4-phenyl-pyridinium ion (MPP+) and Paraquat (PQ+) produce in Rana Pipiens different behavioral, biochemical and skin pigmentation changes. MPTP causes in frogs the main symptoms of Parkinsonism (rigidity, akinesia and tremor) and it darkens the skin of animals. It also decreases brain and, less so, adrenal medulla dopamine. These effects are blocked by Pargyline. MPP+ causes the same symptoms but more rapidly. In contrast, skin pigmentation is clearly lightened. Brain and particularly adrenal dopamine reserves are nearly abolished. Pargyline increases these effects. Paraquat, in a cumulative fashion, eventually causes the same behavioral changes and a slight increase in pigmentation. It initially produces an increase in brain and adrenal dopamine concentrations, but later a significant dopamine concentration decrease. Pargyline potentiates these long term effects, blocks the dopamine increase, but reverses the PQ+ effect upon melanin, producing the same depigmentation as MPP+ alone.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1985

A catalyst function for MPTP in superoxide formation.

We demonstrate that 1-methyl-4-phenyl-1,2-dihydropyridine (MPDP) can be generated, in an alternate pathway, from the catalyst action of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) upon the iron redox equilibrium reaction. Superoxide and ferric iron are instantaneously produced after addition of MPTP to a solution of ferrous iron. This reaction is oxygen and pH dependent. Superoxide, through a iron dependent Haber-Weiss reaction with peroxide, can generate the cytotoxic hydroxyl radical. A small portion of the superoxide reacts with MPTP to produce the reactive species X. which, in the presence of Fe+3 can also generate MPDP.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1985

The specific vulnerability of the substantia nigra to MPTP is related to the presence of transition metals.

We demonstrate that the high concentration of transition metals in the substantia nigra could be a major factor responsible for the specificity of cell damage by the Parkinsonism-causing neurotoxin MPTP. It will be shown that these metals in vitro, and MPTP, each potentiate the autoxidation of dopamine and the production of aminochrome through the generation of superoxide, hydroxyl radicals, hydrogen peroxide and reactive semiquinones. Moreover, the same metals contribute to the oxidation of MPTP itself, further enhancing dopamine autoxidation.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1985

Parkinsonian syndrome and central nervous system lymphoma involving the substantia nigra. A case report.

The clinical history and postmortem neuropathologic findings of a case of cerebral lymphoma revealed by a typical parkinsonian syndrome are reported. The clinical symptoms initially improved with dopa therapy. The tumor was classified as a diffuse, non-cleaved, large-cell lymphoma of B-cell origin producing monoclonal lambda light chains. The substantia nigra was infiltrated by the tumor and showed neuronal loss and extraneuronal pigment. The most striking histological feature was the presence of neuronophagic-like nodules composed of lymphomatous cells both in the locus niger and in the left thalamus. No tumoral mass effect and no histological stigmata of other etiologies of parkinsonian syndromes were observed. A hypothesis is that the neuronophagic-like nodules may reflect a neuronotoxic activity of the lymphoma and may be considered at the origin of parkinsonism.

B-Lymphocytes↗
PubMed1985

A retromedullary arteriovenous fistula associated with the Klippel-Trenaunay-Weber syndrome. A clinicopathologic study.

An intraspinal vascular malformation associated with the Klippel-Trenaunay-Weber (KTW) syndrome initially was thought to be intramedullary on angiographic findings. Postmortem examination revealed an entirely posterior extramedullary arteriovenous fistula (AVF) fed by the anterior spinal artery. The association of the KTW syndrome with a so-called intramedullary AVF has been described in the literature without any pathologic confirmation (11 cases). Our case emphasizes the difficulty of determining the exact morphology and location of spinal AVF on arteriography. The association of the KTW syndrome with a retromedullary AVF can be explained on a developmental basis.

Angiomatosis↗