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Biomedical subjects

G Said

Publications and source records attributed to G Said.

140 records · Page 8Linked to original sources

A clinicopathologic study of acrodystrophic neuropathies.

Sixteen patients presenting with trophic changes associated with a peripheral neuropathy were investigated. Muscle power was normal in all patients, but neurogenic muscle atrophy was demonstrated in 4 of the 7 patients who had a muscle biopsy. Alcoholism was responsible for the neuropathy in 11 patients. In the other patients, one had primary hemochromatosis without diabetes and another a dominantly inherited primary hypertrophic neuropathy. Qualitative and quantitative light and electron microscopic studies, including teased nerve fiber preparations, showed axonal loss as the most salient feature. In the alcoholic patients, the large myelinated fibers were primarily involved, followed by small myelinated and unmyelinated fibers. The lesions were predominant distally as shown in patients who had a sural nerve biopsy at both calf and ankle levels. A mechanism of dying-back degeneration of the longest sensory fibers is the most plausible explanation for neurological and pathological abnormalities. In alcoholic neuropathy with trophic changes, loss of sensory fibers is more important than in alcoholic neuropathy without trophic changes. In familial and sporadic cases, axonal loss is more severe and unmyelinated fibers are more severely affected than in alcoholic acrodystrophic neuropathy. Patients with peripheral neuropathies who present with loss of pain sensation but have preserved muscle power are especially exposed to the development of trophic changes induced by usual trauma in insensitive tissues.

Adult↗

Tellurium-induced myelinopathy in adult rats.

Tellurium is known to induce a neuropathy in young rats but not in adult rats. In the present study adult rats were fed a diet containing 1.25% tellurium every day for 30 days. By the end of this period, the rats moved with difficulty but did not show paralysis. Study of teased nerve fiber preparations in conjunction with light and electron microscopy revealed myelin abnormalities consisting of myelin bubbling, segmental demyelination, and remyelination. In some animals, these abnormalities had a patchy distribution, affecting several adjoining nerve fibers in sciatic nerves, brachial plexus, and spinal roots. The intramyelinic edema sometimes was associated with splitting of the axons.

Animals↗

Nerve lesions induced by macrophage activation.

The neuropathies associated with infectious processes, including leprosy, retroviral infections and Chagas' disease, represent the largest group of neuropathies in the world. Segmental demyelination and axonal degeneration of nerve fibres are associated with inflammatory infiltrates which contain a large number of mononuclear phagocytes. In order to learn more about the role played by macrophage activation in the nerve lesions observed in inflammatory neuropathies, we have performed a morphological study of nerves injected with products of activation of macrophages including proteolytic enzymes and cytokines (tumour necrosis factor and alpha beta-interferon). We have also studied the effects on nerve fibres of macrophages activated by ingestion of proteose-peptone, a foreign protein, and in the course of a delayed-type hypersensitivity (DTH) reaction. We have found that proteases and urokinase were potent demyelinating agents and that activated macrophages were also able to induce significant demyelination of neighbouring fibres. In contrast, injection of TNF alpha induced more severe nerve lesions consisting of axonal degeneration of the majority of nerve fibres. We thus conclude that infected macrophages which penetrate the endoneurium and macrophages activated in a DTH reaction can both cause neuropathy.

Animals↗

[Inflammatory neuropathies].

Inflammatory neuropathy is the term used for all neuropathies associated with an inflammatory infiltrate of the nerves and/or nerve roots. Broadly speaking, there are two types of inflammatory neuropathies: those caused by an identified infectious agent, and those of uncertain origin for which an autoimmune process is usually blamed. Among the neuropathies of infective origin, leprosy is the most important owing to its frequency and to the physiopathological and therapeutic problems it still poses to clinicians and researchers, since the form and severity of nerve lesions depend on cellular immunity to the bacillus' antigen rather than on the bacillus itself. Retroviral infections, caused by the virus of AIDS more than by the virus of tropical spastic paraplegia, are responsible for numerous neuropathies the mechanisms of which are discussed here. The principal inflammatory neuropathies of uncertain origin are polyradiculitis and its different forms, and the heterogeneous group of neuropathies associated with Sjögren's syndrome.

Chronic Disease↗

[Neuropathy in long term treatment with metronidazole (author's transl)].

Two patients developed a sensory neuropathy while under treatment with Metronidazole for Crohn's disease. Recovery took place within a few months after drug withdrawal but was still incomplete in one patient one year after cessation of Metronidazole intake. The incidence of neuropathy appears to be high in long term use of this drug. The morphological study of a sural nerve biopsy showed a severe loss of myelinated fibers (1 800 par mm2). Quantitative teased fibers preparation showed that 56 per cent of the fibers were undergoing wallerian degenerations ; segmental demyelination with subsequent remyelination was found in 4 per cent of the fibers and seem to be secondary to axonal involvement.

Adult↗

[Forced downward and convergent deviation of the eyes and periodic ocular movements in aneurysmal hemorrhage of the mesencephalic tegmentum].

The authors report a case of forced convergent and downward deviation of the eyes with paralysis of upward gaze and, at times, with lateral periodic alternating movements. Pathological examination disclosed a subarachnoid aneurysm behind the midbrain with a fresh hematoma within the mesencephalic tegmentum at the level of the superior colliculi. The clinical and pathological data are discussed.

Eye Movements↗