Degeneration and regeneration of cutaneous sensory nerve formations

Dubový, Petr; Aldskogius, Håkan

doi:10.1002/(sici)1097-0029(19960701)34:4<362::aid-jemt7>3.0.co;2-q

Cited by 24 publications

(9 citation statements)

References 101 publications

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“…Meissner corpuscles were severely reduced and in the few still present there was a wide range of abnormalities suggesting an ongoing degenerative process. Moreover, we observed some Meissner corpuscles abnormally placed to the base of the papilla; this aspect has been described in reinnervated Meissner corpuscles 26…”

Section: Discussionsupporting

confidence: 74%

Small fibers involvement in Friedreich's ataxia

Nolano

Provitera

Crisci

et al. 2001

Annals of Neurology

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Although the involvement of large myelinated sensory fibers in Friedreich's ataxia (FA) is well documented, an impairment of unmyelinated fibers has not been described. We demonstrate an involvement of cutaneous unmyelinated sensory and autonomic nerve fibers in FA patients. We performed a morphological and functional study of cutaneous nerve fibers in 14 FA patients and in a population of control subjects. We used immunohistochemical techniques and confocal microscopy applied to punch skin biopsies from thigh, distal leg, and fingertip, and compared the density of epidermal nerve fibers (ENFs) with the results of mechanical pain sensation and thermal and tactile thresholds performed on hand dorsum, thigh, distal leg, and foot dorsum. We observed in our patients a statistically significant loss of ENFs, a reduced innervation of sweat glands, arrector pilorum muscles and arterioles, and an impairment of thermal and tactile thresholds and mechanical pain detection.

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Section: Discussionsupporting

confidence: 74%

Small fibers involvement in Friedreich's ataxia

Nolano

Provitera

Crisci

et al. 2001

Annals of Neurology

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“…Studies on corpuscular changes following injuries of the nerves supplying them are also abundant and have been so far addressed mainly to structural (for references see Zelena, 1994) and histochemical (see Dubový and Aldskogius, 1996) aspects. More recently (for references see Má rquez et al, 1997) this topic has been addressed by means of immunohistochemical techniques.…”

Section: Discussionmentioning

confidence: 99%

“…Peripheral nerve lesions cause a series of morphological (see Zelena, 1994) and biochemical Ramieri et al, 1995;Dubový and Aldskogius, 1996;Már-quez et al, 1997) modifications in cutaneous sensory corpuscles, including upregulation of p75 (Yamamoto et al, 1992). Nevertheless, whether injury of the central (spinal cord transection) or peripheral (entrapment or section graft) processes of primary neurons modify the expression of neurotrophin receptors in human cutaneous sensory corpuscles has not been studied.…”

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confidence: 99%

p75 and TrkA neurotrophin receptors in human skin after spinal cord and peripheral nerve injury, with special reference to sensory corpuscles

et al. 1998

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Human skin, including nerves and sensory corpuscles, displays immunoreactivity (IR) for low-(p75) and high-affinity (TrkA-like) receptors for nerve growth factor (NGF), the best characterized member of the family of neurotrophins. This study was designed to analyze the changes induced by spinal cord and peripheral nerve injuries in the expression of neurotrophin receptors in digital skin, with special reference to nerves and sensory corpuscles.Skin biopsy samples were obtained from 1) the hand and toes of normal subjects, 2) below the level of the lesion of patients with spinal cord injury affecting dorsal and lateral funiculi, 3) the cutaneous territory of entrapped peripheral nerves (median and ulnar nerves), and 4) the cutaneous territory of sectioned and grafted nerves (median nerve). The pieces were formalinfixed and paraffin-embedded, cut in serial sections, and processed for immunohistochemistry using antibodies against human p75 and TrkA proteins. The percentage of sensory corpuscles displaying IR for p75 and TrkA-like, as well as the intensity of IR developed within them, was assessed using quantitative image analysis.Spinal cord severance causes a decrease in p75 IR in Meissner and Pacinian corpuscles, whereas TrkA-like IR did not vary. In other nonnervous tissues (i.e., epidermis, sweat glands), both p75 and TrkA-like IR was diminished or even absent. Similar but more severe changes were encountered in the skin from the territory of entrapped nerves. Finally, in subjects with sectioned-grafted nerves, p75 IR was found close to controls in nerves, reduced in Meissner corpuscles, and absent in the inner core of the Pacinian ones; TrkA-like IR was in the perineurium, a small percentage of Meissner corpuscles (about 7%), and the outer core and capsule of the Pacinan corpuscles. In the nonnervous tissues, p75 IR was practically absent, whereas TrkA-like IR did not change. No changes in the expression of neurotrophin receptors were observed in Merkel cells of the different groups.Present results show the following: 1) expression of nerve p75 IR in human cutaneous sensory corpuscles is sensitive to central deafferentation, to blockade or difficulty in axonal transport, and to disruption of axonal

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“…Within hours of implanting an empty tube it becomes filled with a fluid enriched with neurotrophic factors, extracellular matrix and other molecules which exert neurotrophic [86,202,203], and neurotropic influences [204]. During days 3-7 the fluid is replaced by an acellular fibronectin positive, laminin negative fibrous matrix, which is critical for Schwann cell proliferation and for Schwann cells to migrate into the tube [57,58,196,205,206].…”

Section: Empty Nerve Tubesmentioning

confidence: 99%

Promoting Axon Regeneration and Neurological Recovery Following Traumatic Peripheral Nerve Injuries

Kuffler¹

2015

Int J Neurorehabilitation Eng

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Repairing Peripheral Nerves following Traumas Nerve crushWithin several days of crushing a peripheral nerve, the injured axons begin to regenerate through their distal pathway until they reach their original targets with which they restore neurological function. The larger the number of axons that regenerate through the distal nerve, the greater the extent of neurological recovery [1][2][3]. The number of axons that regenerate, and thus neurological recovery, is influenced by the physiological state of the distal denervated nerve pathway [4][5][6][7].Following a peripheral nerve crush, the injured axons begin to regenerate within 2 days of injury [8]. They may regenerate to their targets through their original pathway in association with and promoted by its Schwann cells, the neurotrophic factors they release, and the Schwann cell extracellular matrix [1,4,[9][10][11][12][13][14]. Thus, the distal nerve provides a simple means for promoting and directing the regenerating axons to their original targets [15][16][17][18]. However, when a nerve has a gap, the gap must be bridged with a material that is permissive to and promotes axon regeneration across the entire gap to reach the distal nerve stump, through which the axons must then be able to regenerate.The Schwann cells in the denervated distal nerve release neurotrophic factors that promote axon regeneration, but also release extracellular matrix components that promote and inhibit axon regeneration [19][20][21][22][23][24][25][26]. Thus, regeneration through the distal nerve is a balance of the influences of factors that both promote and inhibit regeneration. If the Schwann cells are present, such as after a simple nerve crush, virtually 100% of the axons regenerate and they innervate all the denervated synaptic sites. If the Schwann cells within the distal nerve pathway are killed, leaving only the extracellular matrix intact, the number of axons that regenerates to their targets decreases by 94%. This is because the factors required to trigger the regenerating axons to branch at extracellular matrix branch points are missing, axons do not branch, and therefore each axon reinnervates only a single denervated muscle fiber. Thus, Schwann cells along the distal nerve pathway and a AbstractFollowing a peripheral nerve crush, or when a peripheral the nerve is transected and the nerve stumps anastomosed, neurological recovery is generally excellent. This is because the axons merely have to regenerate through the distal portion of the nerve through the existing extracellular matrix of the denervated Schwann cells that direct and promote them to their distant denervated motor and sensory targets. However, when a length of a peripheral nerve is destroyed, and anastomosis is not possible, the standard surgical repair technique is to graft a length/s of autologous sensory nerve into the gap. Neurological recovery is generally good if the nerve gap is <2 cm in length, the repair is performed <4 months post trauma, and the patients are <25 years of age. Because the nerve ...

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Degeneration and regeneration of cutaneous sensory nerve formations

Cited by 24 publications

References 101 publications

Small fibers involvement in Friedreich's ataxia

Small fibers involvement in Friedreich's ataxia

p75 and TrkA neurotrophin receptors in human skin after spinal cord and peripheral nerve injury, with special reference to sensory corpuscles

Promoting Axon Regeneration and Neurological Recovery Following Traumatic Peripheral Nerve Injuries

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