Biochemical and pharmacological properties of a neurotoxic protein isolated from the blood serum of heavily burned patients

Sepulchre, C.; Moati, F.; Miskulin, M.; Huisman, Olivier; Móczár, E.; Robert, A.M.; Monteil, R; Guilbaud, J

doi:10.1002/path.1711270306

Cited by 22 publications

(5 citation statements)

References 8 publications

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“…In 1979, Sepulchre et al postulated that circulating burn neurotoxin can lead to neuropathy at sites remote from the original burned area. 42 Monafo and Eliasson further proved these findings in a thermal injury rat model. Burn injury led to the accumulation of neurotoxic factors that lead to progressive conduction block and ultimately led to peripheral neuropathy at sites distant to the burn.…”

Section: Mechanismmentioning

confidence: 74%

Peripheral Neuropathy and Nerve Compression Syndromes in Burns

Strong

Agarwal

Cederna

et al. 2017

Clinics in Plastic Surgery

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Peripheral neuropathy and nerve compression syndromes lead to substantial morbidity following burn injury. Patients present with pain, paresthesias, or weakness along a specific nerve distribution or experience generalized peripheral neuropathy. The symptoms may manifest at various times from within one week of hospitalization to many months after wound closure. While current treatments require surgical release of entrapped or compressed nerves, additional studies are necessary to develop therapies for peripheral neuropathy when no detectable signs of nerve compression are present. Studies have shown that peripheral neuropathy may also be due to vascular occlusion of vasa nervorum, inflammation, neurotoxin production leading to apoptosis, and direct destruction of nerves from the burn injury. A better understanding of the molecular and cellular mechanisms underlying the pathogenesis of neuropathic pain following burn injury is essential to the development of novel interventions. Early and effective treatment to minimize the long-term sequela of peripheral neuropathy and nerve compression syndromes will lead to improved outcomes. In this review, we discuss the natural history, diagnosis, current treatments, and future directions for potential interventions for peripheral neuropathy and nerve compression syndromes as they relate to burn injury.

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Section: Mechanismmentioning

confidence: 74%

Peripheral Neuropathy and Nerve Compression Syndromes in Burns

Strong

Agarwal

Cederna

et al. 2017

Clinics in Plastic Surgery

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“…Post-burn neuropathy and nerve dysfunction distant to the injury site represented another field of investigation in the systemic reaction that follows the burn. Analysis of possible neurotoxic mediators identified elevated TNF alpha, serum nitrite [24,31,32], as well as c-AMP, c-GMP, PGE2, IgF1, and IGFB-3 as possible factors for the so-called nerve insult [35]. Another interesting thesis for altered conduction velocity and misperception at distant sites could be the theory of cortical threshold changes/reorganization [36].…”

Section: Discussionmentioning

confidence: 99%

“…These include age > 20 years, TBSA > 20%, and intensive care unit stay > 20 days [15,29,30]. Neurotoxins, released from the burn eschar and circulating in the blood stream, may also trigger neuropathies in areas distant from the cutaneous burn [31,32].…”

Section: Human Studiesmentioning

confidence: 99%

“Out of Touch”—Recovering Sensibility after Burn Injury: A Review of the Literature

Tsolakidis

Alharbi

Rennekampff³

et al. 2022

EBJ

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Background: Full-thickness burn injuries (FTBI) not only lead to a significant burden in multiple ways, including social life and self-esteem, but have also a tremendous impact on environmental interaction by reducing sensibility in manifold ways. On these grounds, possible ways and solutions to recover sensibility in burn wounds are essentials and should not be overlooked. Methods: A review of experimental, clinical studies and the related literature was performed with the aim to highlight post-burn nerve regeneration and discover ways for sensory re-integration to complement the therapeutic concept. Results: In human burn injuries, it has been hypothesized that grafted cells, partly multipotent stem cells, could be additionally responsible for nerve regeneration in burn wound areas. In addition, burn eschar excision, performed within a short post-burn time frame, can reduce or even avoid long-term nerve damage by reducing post-burn toxic mediator release. Various animal studies could demonstrate sensory reinnervation of different qualities in burn wounds. Post-burn scar tissue prevents, or at least decelerates, nerve reinnervation, but could be reduced by targeted mediators. Conclusion: Sensory loss is present in skin grafted areas following full-thickness burn-wound excision, thereby leading to a reduction in quality of life. In addition, various mediators might reduce or avoid nerve damage and should be considered at an early stage as part of a holistic burn-patient therapeutic approach. In addition, supportive multifaceted physical therapy strategies are essential.

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“…These events cause subsequent neuronal damage [ 16 ] and cerebral edema [ 17 , 18 ], and can result in critically increased intracranial pressure [ 19 ]. The pathophysiological events leading to this severe inflammatory downward spiral are depicted in Figure 2 .…”

Section: Breakdown Of the Blood–brain Barrier And Development Of Cerementioning

confidence: 99%

Bench-to-bedside review: Burn-induced cerebral inflammation – a neglected entity?

et al. 2009

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Severe burn injury remains a major burden on patients and healthcare systems. Following severe burns, the injured tissues mount a local inflammatory response aiming to restore homeostasis. With excessive burn load, the immune response becomes disproportionate and patients may develop an overshooting systemic inflammatory response, compromising multiple physiological barriers in the lung, kidney, liver, and brain. If the blood-brain barrier is breached, systemic inflammatory molecules and phagocytes readily enter the brain and activate sessile cells of the central nervous system. Copious amounts of reactive oxygen species, reactive nitrogen species, proteases, cytokines/chemokines, and complement proteins are being released by these inflammatory cells, resulting in additional neuronal damage and life-threatening cerebral edema. Despite the correlation between cerebral complications in severe burn victims with mortality, burn-induced neuroinflammation continues to fly under the radar as an underestimated entity in the critically ill burn patient. In this paper, we illustrate the molecular events leading to blood-brain barrier breakdown, with a focus on the subsequent neuroinflammatory changes leading to cerebral edema in patients with severe burns. IntroductionSevere burn injury remains a significant health issue for society and a life-threatening event for the victim. Each year, more than 1.2 million people in the United States alone suffer burn injuries [1]; some 100,000 of these patients are hospitalized, accounting for a total of 2 million hospital days [2]. Thermal injuries mainly affect patients younger than 50 years of age [3] and remain one of the leading causes of childhood deaths, according to the Children's Burn Awareness Program. While the overall mortality has been reported to be 5%, it rapidly increases with advancing age and burn size up to 96% [3]. Most fatalities (65%) seem to be linked to burn-induced multiple organ failure, and 93% of burn patients present with clinical signs of the systemic inflammatory response syndrome before succumbing to their injuries [4].One of the critically impaired yet frequently overlooked organs in severe burn victims is the brain, despite the fact that cerebral complications in severe burn victims have been shown to highly correlate with mortality [5]. Hypoxic brain injury has been found as a primary cause of death in up to 10% of severe burn patients in an age-dependent manner [6]. The present review focuses on the neuroinflammatory changes occurring after severe burn injury and on the molecular mechanisms involved in their pathogenesis. Breakdown of the blood-brain barrier and development of cerebral edemaUnder physiological conditions, the blood-brain barrier (BBB) tightly regulates the molecules that enter the brain tissue. During the systemic inflammatory response syndrome, sepsis, or severe burn injury, however, this physical barrier between the systemic circulation and the cerebral parenchyma can be seriously compromised.When peripheral tissues are ex...

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Biochemical and pharmacological properties of a neurotoxic protein isolated from the blood serum of heavily burned patients

Cited by 22 publications

References 8 publications

Peripheral Neuropathy and Nerve Compression Syndromes in Burns

Peripheral Neuropathy and Nerve Compression Syndromes in Burns

“Out of Touch”—Recovering Sensibility after Burn Injury: A Review of the Literature

Bench-to-bedside review: Burn-induced cerebral inflammation – a neglected entity?

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