Trench Foot

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Peter Misra - One of the best experts on this subject based on the ideXlab platform.

  • Trench Foot or Non-Freezing Cold Injury As a Painful Vaso-Neuropathy: Clinical and Skin Biopsy Assessments.
    Frontiers in Neurology, 2017
    Co-Authors: Praveen Anand, Rosario Privitera, Yiangos Yiangou, Philippe Donatien, Rolfe Birch, Peter Misra
    Abstract:

    Background: Trench Foot, or non-freezing cold injury (NFCI), results from cold exposure of sufficient severity and duration above freezing point, with consequent sensory and vascular abnormalities which may persist for years. Based on observations of Trench Foot in World War II, the condition was described as a vaso-neuropathy. While some reports have documented nerve damage after extreme cold exposure, sensory nerve fibres and vasculature have not been assessed with recent techniques in NFCI. Objective: To assess patients with chronic sensory symptoms following cold exposure, in order to diagnose any underlying small fibre neuropathy, and provide insight into mechanisms of the persistent pain and cold hypersensitivity. Methods: Thirty soldiers with cold exposure and persistent sensory symptoms (> 4 months) were assessed with quantitative sensory testing (QST), nerve conduction studies, and skin biopsies. Immunohistochemistry was used to assess intraepidermal (IENF) and subepidermal (SENF) nerve fibres with a range of markers, including the pan-neuronal marker PGP9.5, regenerating fibres with GAP43, and nociceptor fibres with TRPV1, SNSR and CGRP. Von Willebrand factor (vWF), eNOS, and VEGF were used for assessing blood vessels, and TRPA1, P2X7 for keratinocytes, which regulate nociceptors via release of Nerve Growth Factor (NGF). Results: Clinical examination showed pinprick sensation was abnormal in the feet of 20 patients (67%), and between 67% and 83% had abnormalities of thermal thresholds to the different modalities. 7 patients (23%) showed reduced sensory action potential amplitude of plantar nerves. 27 patients (90%) had decreased calf skin PGP9.5 IENF (p

  • Trench Foot or non freezing cold injury as a painful vaso neuropathy clinical and skin biopsy assessments
    Frontiers in Neurology, 2017
    Co-Authors: Praveen Anand, Rosario Privitera, Yiangos Yiangou, Philippe Donatien, Rolfe Birch, Peter Misra
    Abstract:

    Background: Trench Foot, or non-freezing cold injury (NFCI), results from cold exposure of sufficient severity and duration above freezing point, with consequent sensory and vascular abnormalities which may persist for years. Based on observations of Trench Foot in World War II, the condition was described as a vaso-neuropathy. While some reports have documented nerve damage after extreme cold exposure, sensory nerve fibres and vasculature have not been assessed with recent techniques in NFCI. Objective: To assess patients with chronic sensory symptoms following cold exposure, in order to diagnose any underlying small fibre neuropathy, and provide insight into mechanisms of the persistent pain and cold hypersensitivity. Methods: Thirty soldiers with cold exposure and persistent sensory symptoms (> 4 months) were assessed with quantitative sensory testing (QST), nerve conduction studies, and skin biopsies. Immunohistochemistry was used to assess intraepidermal (IENF) and subepidermal (SENF) nerve fibres with a range of markers, including the pan-neuronal marker PGP9.5, regenerating fibres with GAP43, and nociceptor fibres with TRPV1, SNSR and CGRP. Von Willebrand factor (vWF), eNOS, and VEGF were used for assessing blood vessels, and TRPA1, P2X7 for keratinocytes, which regulate nociceptors via release of Nerve Growth Factor (NGF). Results: Clinical examination showed pinprick sensation was abnormal in the feet of 20 patients (67%), and between 67% and 83% had abnormalities of thermal thresholds to the different modalities. 7 patients (23%) showed reduced sensory action potential amplitude of plantar nerves. 27 patients (90%) had decreased calf skin PGP9.5 IENF (p<0.0001), the remaining 3 patients had decreased nerve markers in subepidermis or Foot skin. There were marked increases of all vascular markers (for vWF in calf skin, p<0.0001), and increased sensory or regenerating SENF (for calf skin, GAP43, p=0.002). TRPA1 (p = 0.0012) and P2X7 (p<0.0001) were increased in basal keratinocytes. Conclusion: A range of skin biopsy markers and plantar nerve conduction studies are useful objective assessments for the diagnosis of peripheral neuropathy in NFCI. Our results suggest that an increase in blood vessels following tissue ischaemia/hypoxia could be associated with disproportionate and abnormal nerve fibres (irritable nociceptors), and may lead to NFCI as a "painful vaso-neuropathy"

Praveen Anand - One of the best experts on this subject based on the ideXlab platform.

  • Trench Foot or Non-Freezing Cold Injury As a Painful Vaso-Neuropathy: Clinical and Skin Biopsy Assessments.
    Frontiers in Neurology, 2017
    Co-Authors: Praveen Anand, Rosario Privitera, Yiangos Yiangou, Philippe Donatien, Rolfe Birch, Peter Misra
    Abstract:

    Background: Trench Foot, or non-freezing cold injury (NFCI), results from cold exposure of sufficient severity and duration above freezing point, with consequent sensory and vascular abnormalities which may persist for years. Based on observations of Trench Foot in World War II, the condition was described as a vaso-neuropathy. While some reports have documented nerve damage after extreme cold exposure, sensory nerve fibres and vasculature have not been assessed with recent techniques in NFCI. Objective: To assess patients with chronic sensory symptoms following cold exposure, in order to diagnose any underlying small fibre neuropathy, and provide insight into mechanisms of the persistent pain and cold hypersensitivity. Methods: Thirty soldiers with cold exposure and persistent sensory symptoms (> 4 months) were assessed with quantitative sensory testing (QST), nerve conduction studies, and skin biopsies. Immunohistochemistry was used to assess intraepidermal (IENF) and subepidermal (SENF) nerve fibres with a range of markers, including the pan-neuronal marker PGP9.5, regenerating fibres with GAP43, and nociceptor fibres with TRPV1, SNSR and CGRP. Von Willebrand factor (vWF), eNOS, and VEGF were used for assessing blood vessels, and TRPA1, P2X7 for keratinocytes, which regulate nociceptors via release of Nerve Growth Factor (NGF). Results: Clinical examination showed pinprick sensation was abnormal in the feet of 20 patients (67%), and between 67% and 83% had abnormalities of thermal thresholds to the different modalities. 7 patients (23%) showed reduced sensory action potential amplitude of plantar nerves. 27 patients (90%) had decreased calf skin PGP9.5 IENF (p

  • Trench Foot or non freezing cold injury as a painful vaso neuropathy clinical and skin biopsy assessments
    Frontiers in Neurology, 2017
    Co-Authors: Praveen Anand, Rosario Privitera, Yiangos Yiangou, Philippe Donatien, Rolfe Birch, Peter Misra
    Abstract:

    Background: Trench Foot, or non-freezing cold injury (NFCI), results from cold exposure of sufficient severity and duration above freezing point, with consequent sensory and vascular abnormalities which may persist for years. Based on observations of Trench Foot in World War II, the condition was described as a vaso-neuropathy. While some reports have documented nerve damage after extreme cold exposure, sensory nerve fibres and vasculature have not been assessed with recent techniques in NFCI. Objective: To assess patients with chronic sensory symptoms following cold exposure, in order to diagnose any underlying small fibre neuropathy, and provide insight into mechanisms of the persistent pain and cold hypersensitivity. Methods: Thirty soldiers with cold exposure and persistent sensory symptoms (> 4 months) were assessed with quantitative sensory testing (QST), nerve conduction studies, and skin biopsies. Immunohistochemistry was used to assess intraepidermal (IENF) and subepidermal (SENF) nerve fibres with a range of markers, including the pan-neuronal marker PGP9.5, regenerating fibres with GAP43, and nociceptor fibres with TRPV1, SNSR and CGRP. Von Willebrand factor (vWF), eNOS, and VEGF were used for assessing blood vessels, and TRPA1, P2X7 for keratinocytes, which regulate nociceptors via release of Nerve Growth Factor (NGF). Results: Clinical examination showed pinprick sensation was abnormal in the feet of 20 patients (67%), and between 67% and 83% had abnormalities of thermal thresholds to the different modalities. 7 patients (23%) showed reduced sensory action potential amplitude of plantar nerves. 27 patients (90%) had decreased calf skin PGP9.5 IENF (p<0.0001), the remaining 3 patients had decreased nerve markers in subepidermis or Foot skin. There were marked increases of all vascular markers (for vWF in calf skin, p<0.0001), and increased sensory or regenerating SENF (for calf skin, GAP43, p=0.002). TRPA1 (p = 0.0012) and P2X7 (p<0.0001) were increased in basal keratinocytes. Conclusion: A range of skin biopsy markers and plantar nerve conduction studies are useful objective assessments for the diagnosis of peripheral neuropathy in NFCI. Our results suggest that an increase in blood vessels following tissue ischaemia/hypoxia could be associated with disproportionate and abnormal nerve fibres (irritable nociceptors), and may lead to NFCI as a "painful vaso-neuropathy"

Giorgio Terenghi - One of the best experts on this subject based on the ideXlab platform.

  • neuropathy in non freezing cold injury Trench Foot
    Journal of the Royal Society of Medicine, 1997
    Co-Authors: Michael S Irwin, R Sanders, Colin J Green, Giorgio Terenghi
    Abstract:

    Non-freezing cold injury (Trench Foot) is characterized, in severe cases, by peripheral nerve damage and tissue necrosis. Controversy exists regarding the susceptibility of nerve fibre populations to injury as well as the mechanism of injury. Clinical and histological studies (n = 2) were conducted in a 40-year-old man with severe non-freezing cold injury in both feet. Clinical sensory tests, including two-point discrimination and pressure, vibration and thermal thresholds, indicated damage to large and small diameter nerves. On immunohistochemical assessment, terminal cutaneous nerve fibres within the plantar skin stained much less than in a normal control whereas staining to von Willebrand factor pointed to increased vascularity in all areas. The results indicate that all nerve populations (myelinated and unmyelinated) were damaged, possibly in a cycle of ischaemia and reperfusion.

Colin J Green - One of the best experts on this subject based on the ideXlab platform.

  • neuropathy in non freezing cold injury Trench Foot
    Journal of the Royal Society of Medicine, 1997
    Co-Authors: Michael S Irwin, R Sanders, Colin J Green, Giorgio Terenghi
    Abstract:

    Non-freezing cold injury (Trench Foot) is characterized, in severe cases, by peripheral nerve damage and tissue necrosis. Controversy exists regarding the susceptibility of nerve fibre populations to injury as well as the mechanism of injury. Clinical and histological studies (n = 2) were conducted in a 40-year-old man with severe non-freezing cold injury in both feet. Clinical sensory tests, including two-point discrimination and pressure, vibration and thermal thresholds, indicated damage to large and small diameter nerves. On immunohistochemical assessment, terminal cutaneous nerve fibres within the plantar skin stained much less than in a normal control whereas staining to von Willebrand factor pointed to increased vascularity in all areas. The results indicate that all nerve populations (myelinated and unmyelinated) were damaged, possibly in a cycle of ischaemia and reperfusion.

Rolfe Birch - One of the best experts on this subject based on the ideXlab platform.

  • Trench Foot or Non-Freezing Cold Injury As a Painful Vaso-Neuropathy: Clinical and Skin Biopsy Assessments.
    Frontiers in Neurology, 2017
    Co-Authors: Praveen Anand, Rosario Privitera, Yiangos Yiangou, Philippe Donatien, Rolfe Birch, Peter Misra
    Abstract:

    Background: Trench Foot, or non-freezing cold injury (NFCI), results from cold exposure of sufficient severity and duration above freezing point, with consequent sensory and vascular abnormalities which may persist for years. Based on observations of Trench Foot in World War II, the condition was described as a vaso-neuropathy. While some reports have documented nerve damage after extreme cold exposure, sensory nerve fibres and vasculature have not been assessed with recent techniques in NFCI. Objective: To assess patients with chronic sensory symptoms following cold exposure, in order to diagnose any underlying small fibre neuropathy, and provide insight into mechanisms of the persistent pain and cold hypersensitivity. Methods: Thirty soldiers with cold exposure and persistent sensory symptoms (> 4 months) were assessed with quantitative sensory testing (QST), nerve conduction studies, and skin biopsies. Immunohistochemistry was used to assess intraepidermal (IENF) and subepidermal (SENF) nerve fibres with a range of markers, including the pan-neuronal marker PGP9.5, regenerating fibres with GAP43, and nociceptor fibres with TRPV1, SNSR and CGRP. Von Willebrand factor (vWF), eNOS, and VEGF were used for assessing blood vessels, and TRPA1, P2X7 for keratinocytes, which regulate nociceptors via release of Nerve Growth Factor (NGF). Results: Clinical examination showed pinprick sensation was abnormal in the feet of 20 patients (67%), and between 67% and 83% had abnormalities of thermal thresholds to the different modalities. 7 patients (23%) showed reduced sensory action potential amplitude of plantar nerves. 27 patients (90%) had decreased calf skin PGP9.5 IENF (p

  • Trench Foot or non freezing cold injury as a painful vaso neuropathy clinical and skin biopsy assessments
    Frontiers in Neurology, 2017
    Co-Authors: Praveen Anand, Rosario Privitera, Yiangos Yiangou, Philippe Donatien, Rolfe Birch, Peter Misra
    Abstract:

    Background: Trench Foot, or non-freezing cold injury (NFCI), results from cold exposure of sufficient severity and duration above freezing point, with consequent sensory and vascular abnormalities which may persist for years. Based on observations of Trench Foot in World War II, the condition was described as a vaso-neuropathy. While some reports have documented nerve damage after extreme cold exposure, sensory nerve fibres and vasculature have not been assessed with recent techniques in NFCI. Objective: To assess patients with chronic sensory symptoms following cold exposure, in order to diagnose any underlying small fibre neuropathy, and provide insight into mechanisms of the persistent pain and cold hypersensitivity. Methods: Thirty soldiers with cold exposure and persistent sensory symptoms (> 4 months) were assessed with quantitative sensory testing (QST), nerve conduction studies, and skin biopsies. Immunohistochemistry was used to assess intraepidermal (IENF) and subepidermal (SENF) nerve fibres with a range of markers, including the pan-neuronal marker PGP9.5, regenerating fibres with GAP43, and nociceptor fibres with TRPV1, SNSR and CGRP. Von Willebrand factor (vWF), eNOS, and VEGF were used for assessing blood vessels, and TRPA1, P2X7 for keratinocytes, which regulate nociceptors via release of Nerve Growth Factor (NGF). Results: Clinical examination showed pinprick sensation was abnormal in the feet of 20 patients (67%), and between 67% and 83% had abnormalities of thermal thresholds to the different modalities. 7 patients (23%) showed reduced sensory action potential amplitude of plantar nerves. 27 patients (90%) had decreased calf skin PGP9.5 IENF (p<0.0001), the remaining 3 patients had decreased nerve markers in subepidermis or Foot skin. There were marked increases of all vascular markers (for vWF in calf skin, p<0.0001), and increased sensory or regenerating SENF (for calf skin, GAP43, p=0.002). TRPA1 (p = 0.0012) and P2X7 (p<0.0001) were increased in basal keratinocytes. Conclusion: A range of skin biopsy markers and plantar nerve conduction studies are useful objective assessments for the diagnosis of peripheral neuropathy in NFCI. Our results suggest that an increase in blood vessels following tissue ischaemia/hypoxia could be associated with disproportionate and abnormal nerve fibres (irritable nociceptors), and may lead to NFCI as a "painful vaso-neuropathy"