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Neuropatie tossiche occupazionali: quadri morfologici in biopsie del nervo periferico
No full textMany peripheral neuropathies are caused by the (acute or chronic) toxic action of metals, solvents, pesticides, and other occupational and environmental contaminants. These agents often reproduce the anatomoclinical pictures of hereditary (e.g., Charcot-Marie-Tooth disease), autoimmune (Guillain-Barrè syndrome), or dysmetabolic (thiamine deficiency, diabetic neuropathy) forms. Toxic peripheral neuropathies can be classified on the basis of etiology, clinical features (sensitive, motor, sensitive-motor), or histopathology: neuronopathies (uncommon, mostly secondary to retrograde axonal degeneration; e.g., arsenic, thallium), axonopathies (acrylamide, esacarbons, carbon disulphide, organophosphate-induced delayed neuropathy), myelinopathies (trichloroethylene), mixed forms (axonal and demyelinating: lead). For many substances, experimental research has led to the identification of the molecular and cellular targets of neurotoxicity. Several compounds are active by biotransformation (e.g., the esacarbons n-hexane and MnBK are neurotoxic since they are metabolized to 2,5-hexanedione), Genetic, physiological and environmental factors determine the individual metabolic set-up, and they may give origin to differences in the workers' sensitivity. Cessation of exposure is often followed by (microscopically observable) regenerative phenomena and clinical improvement. The morphology of neuropathies can be studied through peripheral nerve biopsy. Samples of sural nerve (or other nervous trunks of the limbs), adequately fixed, sectioned, and stained, allow the observation of alterations in axonal fibres (e.g., giant-axonal neuropathy, dying back neuropathy), myelin (demyelination), Schwann cells, interstitium, and blood vessels; possible inflammatory infiltrates; fibre density; regenerative phenomena (growth cone, remyelination). In occupational medicine, biopsy is indicated when the anamnestic-clinical picture, laboratory tests, and instrumental exams leave doubts about the nature, type, and entity of the neurological damage. In such cases, current optical and electron microscopy techniques can be very useful for injury evaluation, prognosis, and follow-up
Muscle pathology in upper motor neuron paraplegia
Full text linkDuring the last 30 years acceptance of the muscle biopsy by paraplegic patients have accumulated a large body of knowledge on effects of spinal cord injury (SCI) on the skeletal muscle microstructure. Light and electron microscopy analyses combined with computerized methods provided a large body of knowledge on the progression of muscle atrophy and on the effects of rehabilitation strategies. Beside a summary of normal human muscle results, we will here discuss the time-course of muscle events related to SCI affecting the upper motor neuron. Furthermore the concomitant events on the microcirculation of skeletal muscle will be described in relation to the frequent complications of deep venous thrombosis, decubitus ulcers and paraosteoarthrosis
Flaccid paraplegia: improvement of the muscle capillary supply after early-started daily functional electric stimulation (FES) in human permanent lower motoneuron denervation
No full textMorphological alterations of microvasculature and neoangiogenesis in the pressure ulcers repair in paraplegics.
No full textFlaccid paraplegia: improvement of the muscle capillary supply after early-started dailt functional electric stimulation (FES) in human permanent lower motoneuron denervation
No full textPeripheral microcirculatory lesions in myotonic dystrophy. A light and an electron microscopic study on digital biopsies.
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