Peripheral Injury and CRPS

2021 ◽  
pp. 23-32
Author(s):  
Miroslav Backonja ◽  
Victor Wang
Keyword(s):  
Peripheral Injury

2. Peripheral injury in the rat: behavioural and neuronal correlates

1985 ◽  
Vol 308 (1136) ◽  
pp. 408-408
Keyword(s):  
Tissue Injury ◽  
Primary Afferents ◽  
Peripheral Tissue ◽  
Peripheral Injury ◽  
Induced Changes

Peripheral tissue injury alters dramatically the relation between a cutaneous stimulus and the sensation experienced by producing both a decrease in the threshold necessary to elicit pain and an increase in the pain resulting from suprathreshold stimuli (hyperalgesia). We have now investigated whether these injury-induced changes result from alterations in the properties of primary afferents (sensitization) (Lynn 1977) or whether the injury triggers a change within the c.n.s. (Woolf 1983).

scholarly journals Serum Neurofilament Light as a Biomarker of Traumatic Brain Injury in the Presence of Concomitant Peripheral Injury

2021 ◽  
Vol 16 ◽  
pp. 117727192110534
Author(s):  
Ker Rui Wong ◽  
William T O’Brien ◽  
Mujun Sun ◽  
Glenn Yamakawa ◽  
Terence J O’Brien ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Elevated Serum ◽  
Serum Levels ◽  
Long Bone ◽  
Post Injury ◽  
Neurofilament Light ◽  
Peripheral Injury ◽  
Long Bone Fracture ◽  
Severe Tbi

Introduction: Serum neurofilament light (NfL) is an emerging biomarker of traumatic brain injury (TBI). However, the effect of peripheral injuries such as long bone fracture and skeletal muscle injury on serum NfL levels is unknown. Therefore, the aim of this study was to determine whether serum NfL levels can be used as a biomarker of TBI in the presence of concomitant peripheral injuries. Methods: Rats were randomly assigned to one of four injury groups: polytrauma (muscle crush + fracture + TBI; n = 11); peripheral injuries (muscle crush + fracture + sham-TBI; n = 12); TBI-only (sham-muscle crush + sham-fracture + TBI; n = 13); and triple-sham (n = 7). At 2-days post-injury, serum levels of NfL were quantified using a Simoa HD-X Analyzer. Results: Compared to triple-sham rats, serum NfL concentrations were higher in rats with peripheral injuries-only, TBI-only, and polytrauma. When compared to peripheral injury-only rats, serum NfL levels were higher in TBI-only and polytrauma rats. No differences were found between TBI-only and polytrauma rats. Conclusion: Serum NfL levels did not differ between TBI-only and polytrauma rats, indicating that significant peripheral injuries did not affect the sensitivity and specificity of serum NfL as a biomarker of moderate TBI. However, the finding of elevated serum NfL levels in rats with peripheral injuries in the absence of a TBI suggests that the presence of such injuries may limit the utility of NfL as a biomarker of less severe TBI (eg, concussion).

scholarly journals Increased calcium-mediated cerebral processes after peripheral injury: possible role of the brain in complex regional pain syndrome

2020 ◽  
Vol 33 (2) ◽  
pp. 131-137
Author(s):  
Francis Sahngun Nahm ◽  
Jae-Sung Lee ◽  
Pyung-Bok Lee ◽  
Eunjoo Choi ◽  
Woong Ki Han ◽  
...  
Keyword(s):  
Complex Regional Pain Syndrome ◽  
Pain Syndrome ◽  
Peripheral Injury ◽  
The Brain

Evidence That Long-Term Hyperexcitability of the Sensory Neuron Soma Induced by Nerve Injury in Aplysia Is Adaptive

2005 ◽  
Vol 94 (3) ◽  
pp. 2218-2230 ◽  
Author(s):  
Xavier Gasull ◽  
Xiaogang Liao ◽  
Michael F. Dulin ◽  
Cynthia Phelps ◽  
Edgar T. Walters
Keyword(s):  
Sensory Neuron ◽  
Sensory Input ◽  
Aplysia Californica ◽  
Afferent Pathway ◽  
Sensory Deficits ◽  
Diverse Species ◽  
Peripheral Injury ◽  
Adaptive Consequences ◽  
Neuron Soma

Peripheral axotomy induces long-term hyperexcitability (LTH) of centrally located sensory neuron (SN) somata in diverse species. In mammals this LTH can promote spontaneous activity of pain-related SNs, and such activity may contribute to neuropathic pain and hyperalgesia. However, few axotomized SN somata begin to fire spontaneously in any species, and why so many SNs display soma LTH after axotomy remains a mystery. Is soma LTH a side effect of injury with pathological but no adaptive consequences, or was this response selected during evolution for particular functions? A hypothesis for one function of soma LTH in nociceptive SNs in Aplysia californica is proposed: after peripheral injury that produces partial axotomy of some SNs, compensation for sensory deficits and protective sensitization are achieved by facilitating afterdischarge near the soma, which amplifies sensory input from injured peripheral fields. Four predictions of this hypothesis were confirmed in SNs that innervate the tail. First, LTH of SN somata was induced by a relatively natural axotomizing event—a small cut across part of the tail in the absence of anesthesia. Second, soma LTH was selectively expressed in SNs having axons in cut or crushed nerves rather than nearby, uninjured nerves. Third, after several weeks soma LTH began to reverse when functional recovery of the interrupted afferent pathway was shown by reestablishment of a centrally mediated siphon reflex. Fourth, axotomized SNs developed central afterdischarge that amplified sensory discharge coming from the periphery, and the afterdepolarization underlying this afterdischarge was enhanced by previous axotomy.

scholarly journals Another perspective on fasciculations: when is it not caused by the classic form of amyotrophic lateral sclerosis or progressive spinal atrophy?

2014 ◽  
Vol 6 (3) ◽  
Author(s):  
Marco Antonio Araujo Leite ◽  
Marco Orsini ◽  
Marcos R.G. De Freitas ◽  
João Santos Pereira ◽  
Fábio Henrique Porto Gobbi ◽  
...  
Keyword(s):  
Amyotrophic Lateral Sclerosis ◽  
Motor Neuron ◽  
Motor Neuron Disease ◽  
Neurological Examination ◽  
Dendritic Spines ◽  
Motor Nerve ◽  
Normal Subjects ◽  
Peripheral Injury ◽  
Classic Form ◽  
Lateral Sclerosis

Fasciculations are visible, fine and fast, sometimes vermicular contractions of fine muscle fibers that occur spontaneously and intermittently. The aim of this article is to discuss the main causes for fasciculations and their pathophysiology in different sites of the central/peripheral injury and in particular to disprove that the presence of this finding in the neurological examination is indicative of amyotrophic lateral sclerosis. Undoubtedly, most fasciculations have a distal origin in the motor nerve both in normal subjects and in patients with motor neuron disease. Most of them spread to other dendritic spines often producing an antidromic impulse in the main axon. The clinical and neurophysiological diagnosis must be thorough. It may often take long to record fasciculations with electroneuromyography. In other cases, temporal monitoring is necessary before the diagnosis. The treatment, which may be adequate in some cases, is not always necessary

Acute and Chronic Craniofacial Pain: Brainstem Mechanisms of Nociceptive Transmission and Neuroplasticity, and Their Clinical Correlates

2000 ◽  
Vol 11 (1) ◽  
pp. 57-91 ◽  
Author(s):  
Barry J. Sessle
Keyword(s):  
Future Research ◽  
Peripheral Sensitization ◽  
Nociceptive Transmission ◽  
Somatosensory Information ◽  
Peripheral Injury ◽  
Strategic Role ◽  
Therapeutic Procedures ◽  
The Face ◽  
Craniofacial Pain ◽  
Organizational Features

This paper reviews the recent advances in knowledge of brainstem mechanisms related to craniofacial pain. It also draws attention to their clinical implications, and concludes with a brief overview and suggestions for future research directions. It first describes the general organizational features of the trigeminal brainstem sensory nuclear complex (VBSNC), including its input and output properties and intrinsic characteristics that are commensurate with its strategic role as the major brainstem relay of many types of somatosensory information derived from the face and mouth. The VBSNC plays a crucial role in craniofacial nociceptive transmission, as evidenced by clinical, behavioral, morphological, and electrophysiological data that have been especially derived from studies of the relay of cutaneous nociceptive afferent inputs through the subnucleus caudalis of the VBSNC. The recent literature, however, indicates that some fundamental differences exist in the processing of cutaneous vs. other craniofacial nociceptive inputs to the VBSNC, and that rostral components of the VBSNC may also play important roles in some of these processes. Modulatory mechanisms are also highlighted, including the neuro-chemical substrate by which nociceptive transmission in the VBSNC can be modulated. In addition, the long-term consequences of peripheral injury and inflammation and, in particular, the neuroplastic changes that can be induced in the VBSNC are emphasized in view of the likely role that central sensitization, as well as peripheral sensitization, can play in acute and chronic pain. The recent findings also provide new insights into craniofacial pain behavior and are particularly relevant to many approaches currently in use for the management of pain and to the development of new diagnostic and therapeutic procedures aimed at manipulating peripheral inputs and central processes underlying nociceptive transmission and its control within the VBSNC.

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