Peripheral sensory neuropathies – pain loss vs. pain gain
Autor: | C. Geoffrey Woods, Ingo Kurth, James J. Cox |
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Přispěvatelé: | Woods, Geoff [0000-0002-8077-2101], Apollo - University of Cambridge Repository |
Rok vydání: | 2020 |
Předmět: |
small fiber neuropathy
business.industry Sodium channel Sensory system medicine.disease Peripheral Anesthesia Hereditary sensory and autonomic neuropathy Genetics hereditary sensory and autonomic neuropathy Medicine Small Fiber Neuropathy business congenital insensitivity to pain sodium channels Genetics (clinical) Congenital insensitivity to pain |
Zdroj: | Medizinische Genetik. 32:233-241 |
ISSN: | 1863-5490 0936-5931 |
Popis: | Peripheral sensory neurons are afferent neurons that innervate the skin, joints, bones, muscles, and mucosal tissues. By converting different stimuli into action potentials, they transmit signals for the sensing of temperature, touch, pressure, or pain. This review discusses the known Mendelian disorders which affect pain sensing in humans. For painlessness, these disorders can be classified as developmental, neurodegenerative, or functional, where pain-sensing neurons (nociceptors) are present but cannot be activated or produce action potentials. Affected patients suffer from numbness with recurrent injuries, burns, and poorly healing wounds. For Mendelian disorders of excess pain, aberrant overactivity of nociceptors is a hallmark and leads to paroxysmal or continuous pain states. Again, the effect can be functional or, as in small fiber neuropathies, can be accompanied by degeneration of small unmyelinated nerve fibers in the skin. About 20 different genes are known to cause Mendelian pain disorders and the molecules involved are of general interest for human pain research and as analgesic targets. Comprehensive genetic testing is the key to early diagnosis and adaptation of clinical management. |
Databáze: | OpenAIRE |
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