Photochemically induced experimental ischemic neuropathy: A clinical, electrophysiological and immunohistochemical study

Wiethölter, H.; Krüger, Jutta; Melville, Christian; Cornelius, Carl‐Peter

doi:10.1016/0022-510x(93)90156-s

Cited by 9 publications

(5 citation statements)

References 33 publications

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“…Thus, although there is not an immune attack on the nerve blood vessels per se, vessel coagulation with resultant ischemia-induced nerve damage does result. Earlier anatomic work had shown that this type of ischemic lesion produced axonal neurofilament disintegration within 4 h, followed by Wallerian degeneration-induced macrophage infiltration and phagocytosis of the necrotic debris (340). Although no studies have yet been done to examine potential immune mediators at either peripheral or central sites, what is known is that damage occurs to both myelinated and unmyelinated fibers and this ischemic nerve lesion indeed produces both mechanical allodynia and thermal hyperalgesia (93,156).…”

Section: Animal Modelsmentioning

confidence: 96%

Beyond Neurons: Evidence That Immune and Glial Cells Contribute to Pathological Pain States

Watkins

Maier

2002

Physiological Reviews

656

433

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Chronic pain can occur after peripheral nerve injury, infection, or inflammation. Under such neuropathic pain conditions, sensory processing in the affected body region becomes grossly abnormal. Despite decades of research, currently available drugs largely fail to control such pain. This review explores the possibility that the reason for this failure lies in the fact that such drugs were designed to target neurons rather than immune or glial cells. It describes how immune cells are a natural and inextricable part of skin, peripheral nerves, dorsal root ganglia, and spinal cord. It then examines how immune and glial activation may participate in the etiology and symptomatology of diverse pathological pain states in both humans and laboratory animals. Of the variety of substances released by activated immune and glial cells, proinflammatory cytokines (tumor necrosis factor, interleukin-1, interleukin-6) appear to be of special importance in the creation of peripheral nerve and neuronal hyperexcitability. Although this review focuses on immune modulation of pain, the implications are pervasive. Indeed, all nerves and neurons regardless of modality or function are likely affected by immune and glial activation in the ways described for pain.

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Section: Animal Modelsmentioning

confidence: 96%

Beyond Neurons: Evidence That Immune and Glial Cells Contribute to Pathological Pain States

Watkins

Maier

2002

Physiological Reviews

656

433

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“…The extensive early demyelination contrasts with the demyelination noted in other models of ischemic nerve injury such as those induced by photochemical injury where demyelination was evident at 7 days after the insult ( Wietholter et al, 1993; Yu et al, 2000 ) or by ischemia‐reperfusion injury where demyelination appeared between 7 and 14 days after injury ( Iida et al, 2003 ) . This apparent discrepancy is best explained by a dual neural damage produced by phenol, both an ischemic insult and a caustic effect.…”

Section: Discussionmentioning

confidence: 88%

Nerve root degeneration and regeneration by intrathecal phenol in rats: a morphologic approach

Figueroa

Aldrete

Martínez-Cruz

et al. 2006

J Peripheral Nervous Sys

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Intrathecal injection of phenol (ITP) has been used to control intractable pain and spasticity. Direct caustic nerve damage has been postulated as the mechanism of analgesia. Sensation is commonly recovered, suggesting that a spontaneous regeneration process takes place. There is, however, a lack of mechanistic information on ITP therapy. To define morphologically the neurolysis and regeneration phenomena produced by ITP, anesthetized rats were subjected to laminectomy at L5; 5 microl of 22% phenol in saline solution or vehicle (control) was injected. Light and electron microscopy studies of nerve roots were performed at 2, 14, and 60 days after injection. Rats given ITP showed at the early stage a variable amount of roots with signs of infarction characterized by loss of axon-myelin units and thrombosis of intra-root vessels. At 14 days, abundance of macrophages removing debris, open vessels, and nerve sprouts was identified in damaged roots. At this time, non-myelinating glial fibrillary acidic protein-positive Schwann cells were observed in both damaged and apparently undamaged roots. At 60 days, abundance of 2',3'-cyclic nucleotide 3'-phosphodiesterase-positive Schwann cells myelinating newly formed axons was observed in damaged roots. Control rats did not show signs of neural or vascular pathology. Attempting to prevent thrombosis, another group of rats received heparin before ITP; these anti-coagulated rats developed radicular thrombosis, neurolysis, and hemorrhage. In conclusion, neurolysis produced by ITP is associated with acute ischemia (not prevented by heparin) and is followed by vascular, nerve, and myelin regeneration. Our results help understand the lack of efficacy of and some complications by ITP clinical therapy.

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“…Infarction of the sciatic nerve is a rare clinical entity, but is well described in experimental animal models (9). Large myelinated fibres appear to be more resistant to ischaemia than smaller myelinated or unmyelinated fibers (10).…”

Section: Discussionmentioning

confidence: 99%

Sciatic Palsy after Total Hip Arthroplasty Associated with Vascular Graft Occlusion

2011

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Sciatic nerve palsy is a well-recognised complication of total hip arthroplasty, and causes include direct injury during surgery (crushing or electrocautery), compression or stretching of the nerve, thermal damage caused by leaked bone cement, trauma during dislocation or reduction of the hip, haematoma, traction caused by leg lengthening or inadvertent intraneural injection from nerve blocks. We describe what we believe to be a case of sciatic nerve ischemia due to intra-operative arterial occlusion, and we discuss the vascular anatomy which may have contributed.

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Photochemically induced experimental ischemic neuropathy: A clinical, electrophysiological and immunohistochemical study

Cited by 9 publications

References 33 publications

Beyond Neurons: Evidence That Immune and Glial Cells Contribute to Pathological Pain States

Beyond Neurons: Evidence That Immune and Glial Cells Contribute to Pathological Pain States

Nerve root degeneration and regeneration by intrathecal phenol in rats: a morphologic approach

Sciatic Palsy after Total Hip Arthroplasty Associated with Vascular Graft Occlusion

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