The Experts below are selected from a list of 453 Experts worldwide ranked by ideXlab platform

Martin Koltzenburg - One of the best experts on this subject based on the ideXlab platform.

  • the changing sensitivity in the life of the nociceptor
    Pain, 1999
    Co-Authors: Martin Koltzenburg
    Abstract:

    Abstract Plasticity of the central nervous system has been shown to be an important correlate in the generation of chronic pain. However, there is now also increasing evidence for profound changes of the primary sensory neurons including nociceptors throughout the life of an organism and these changes account for clinically relevant alterations of pain perception. During development sensory neurons require one or more growth factors that rescue neurons during critical periods of programmed cell death and growth factors also play an important role for the development of the appropriate phenotype. Neurotrophin-3 may initially have an effect on proliferation of many subtypes of sensory neurons including cells destined to become nociceptors during early development. During a critical period of late prenatal development nerve growth factor (NGF) signalling through its cognate high affinity receptor trkA has been shown to be the main survival factor during a critical period of prenatal development. Humans deficient of trkA suffer from the rare disorder of Congenital Analgesia. Postnatally, the subpopulation of non-peptidergic nociceptors lose their ability to respond to NGF, start to express receptor element for and begin to respond to glial cell line-derived neurotrophic factor (GDNF). Both NGF and GDNF have also been shown to regulate the sensitivity of nociceptors to heat and capsaicin in the adult. Changes in the levels of endogenous trophic factors have also been implicated for the generation of ongoing activity and sensitisation to heat that are the hallmark of nociceptors innervating inflamed tissue. Whereas the development of ongoing activity correlates with the intensity of ongoing pain, sensitisation of nociceptors to heat can explain the hyperalgesia to heat that typically accompanies inflammatory lesions in the skin. Dramatic changes of nociceptor phenotype occur following nerve injury. Sensory neurons, including nociceptors, start to express adrenoceptors and become responsive for catecholamines and these changes appear to be responsible for the development of sympathetically maintained pain in some patients.

Serratrice G - One of the best experts on this subject based on the ideXlab platform.

  • Congenital indifference and Congenital insensitivity to pain
    Bulletin de l'Academie nationale de medecine, 1992
    Co-Authors: Serratrice G
    Abstract:

    Congenital indifference to pain is often mistaken for Congenital insensitivity. It is characterized by the occurrence since childhood of lesions, mainly cutaneous and osteoarticular secondary to strictly painless traumas. However, despite the lack of pain, the patient is able to discriminate a painful stimulus. Autopsy shows no abnormality of the nervous system. A dysfunction of the central endomorphinic systems has been suggested. Congenital Analgesia is associated with anhidrosis in Swanson's syndrome (in which Lissauer the tractus is absent in the spinal cord) and with dysautonomia in Riley-Days's disease (in which there is a lack of amyelicinic fibres). On account of these data, some authors refuse the autonomy of Congenital indifference and classify it in the group of the various autonomic and sensory neuropathies. However it seems justified to acknowledge the Congenital Analgesia with two varieties: Congenital indifference in which there is no sensation of pain but normal sensory pathway and tonic function of endomorphinic system, Congenital insensitivity in which the painful stimulus is not transmitted to the central nervous system.

  • Polyneuritis, polyradiculoneuritis, polyneuropathies: development of a concept
    La Revue du praticien, 1992
    Co-Authors: Serratrice G
    Abstract:

    The concept of polyneuritis, polyradiculoneuritis and polyneuropathy has changed considerably since the last century. Charcot-Marie-Tooth disease has been dismembered into hypertrophic, neuronal and spinal forms. Within the group of hereditary sensory neuropathies, to Thevenard's ulcero-multilating acropathy have been added recessive forms of early onset and various types of Congenital Analgesia. Other hereditary polyneuropathies result from inborn errors of metabolism; in adults, these are chiefly Refsum disease, Fabry's disease, porphyria, amyloidosis and adrenoleucodystrophy. Guillain-Barre acute primary polyradiculoneuritis has come to be associated with chronic and recurrent forms and, more recently, with multifocal demyelinating neuropathy with persistent conduction blocks and antibodies to GM1. Young and Adams acute pandysautonomia is close to polyradiculoneuritis. Finally, many polyneuropathies, formerly labelled polyneuritis, are subsequent to an ever increasing number of known causes, notably infections (e.g. borreliosis or HTLV viruses) and drug-induced or industrial toxicity. Advances in explatory techniques have generated new concepts, including small and large fibre neuropathy, distal and central degenerations, myelin diseases and neuronal diseases.

  • Indolent arthropathies of the lower limbs
    Revue du rhumatisme et des maladies ostéo-articulaires, 1991
    Co-Authors: Serratrice G
    Abstract:

    : The didactic lecture deals with four questions: What is the origin of an isolated indolent arthropathy? diabetes, amylose, leprosis. What diagnosis in an adult familial form? Thevenard's disease when amylosis has been excluded. What are the varieties of Congenital indolent arthropathies? An early recessive form of Thevenard's disease and the Congenital Analgesia. How to deal with a unilateral indolent arthropathy? First of all, look for dysraphism.

Rohner P - One of the best experts on this subject based on the ideXlab platform.

  • Osteomyelitis in Congenital Analgesia
    Swiss dent, 1992
    Co-Authors: Rohner P
    Abstract:

    Presentation of a case of a Congenital analgia, who showed as a complication a chronical osteomyelitis of the mandible with formation of sequester and fracture. Partial resection of the mandible and immediate reconstruction was done performing simultaneously a rebuilding of the atrophied alveolus by the use of split ribs and fixation with a long miniplate.

Marko Anderluh - One of the best experts on this subject based on the ideXlab platform.

  • Isoform Selective Voltage-Gated Sodium Channel Modulators and the Therapy of Pain
    Current Medicinal Chemistry, 2013
    Co-Authors: Marko Jukič, Danijel Kikelj, Marko Anderluh
    Abstract:

    Voltage-gated sodium channels are large transmembrane protein complexes responsible for the propagation and transmission of electrical impulses through nerve, muscle and endocrine cells and cell systems. Dysregulated expression and/or functional changes of ion channel isoforms are found in many associated pathological conditions. In such cases, modulation of voltage gated sodium channels (Na V channels) is a recognised approach in medicinal chemistry. Multiple small-molecule active compounds are used for a plethora of Na V channel-linked indications, for example epilepsy and CNS disorders, arrhythmia, stroke and pain states such as Congenital Analgesia/hyperalgesia and neuropathic pain. As existent Na V channel modulators suffer mainly from selectivity issues and thus exert significant side effects, novel and selective Na V channel modulators would be beneficial. Consequently, the increased research on voltage-gated sodium channels has led to a large number of novel compounds that exploit classic binding site selectivity with state-dependence or functional selectivity. Such compounds offer selective targeting and new possibilities for studying the physiology of Na V channels and pathophysiology of the associated ailment conditions. This review consolidates the recent literature on Na V 1.3, 1.7 and 1.8 channel isoform selective and/or state-dependent modulators. In particular, their structure-activity relationship is illustrated, especially in the context of selectivity on a particular isoform, and their applicability in the therapy of neuropathic pain is described.

Vallede G Lascurain - One of the best experts on this subject based on the ideXlab platform.

  • Congenital Analgesia report of 2 cases
    Acta ortopedica mexicana, 2018
    Co-Authors: O Ruizmejia, J A Oribiogallegos, J Pimentelrangel, Vallede G Lascurain
    Abstract:

    Congenital Analgesia is a rare condition, reporting in the international literature in rare cases since 1932, when it was first described. Its cause has been the subject of development of multiple theories and studies through the years. Currently various studies and experiments as its origin point mutation in the gene encoding SC9NA sodium channels, which have an important role in nociceptive transmission signals in the human body. The purpose of this study is to present two cases that were valued in the department of pediatric orthopedics at UMAE HTYOLV, patients whose insensitivity to pain has produced significant injuries that were once cause for valuation of the hospital.