REVISTA

Alodinia mecánica

Valoración Valoración: 3 Estrellas

Descripción: Artículo que revisa los procesos fisiopatológicos que intervienen en el desarrollo de alodinia mecánica y su complejidad.

TITULO FUENTE ORIGINAL:

Mechanical allodynia

AUTORES:

Lolignier S, Eijkelkamp N, Wood JN.

REVISTA ABREV.:

Pflugers Arch

AÑO:

2015

REFERENCIA:

467(1):133-9

DOI:

10.1007/s00424-014-1532-0.

RESUMEN ORIGINAL:

Mechanical allodynia (other pain) is a painful sensation caused by innocuous stimuli like light touch. Unlike inflammatory hyperalgesia that has a protective role, allodynia has no obvious biological utility. Allodynia is associated with nerve damage in conditions such as diabetes, and is likely to become an increasing clinical problem. Unfortunately, the mechanistic basis of this enhanced... + Leer más

Mechanical allodynia (other pain) is a painful sensation caused by innocuous stimuli like light touch. Unlike inflammatory hyperalgesia that has a protective role, allodynia has no obvious biological utility. Allodynia is associated with nerve damage in conditions such as diabetes, and is likely to become an increasing clinical problem. Unfortunately, the mechanistic basis of this enhanced sensitivity is incompletely understood. In this review, we describe evidence for the involvement of candidate mechanosensitive channels such as Piezo2 and their role in allodynia, as well as the peripheral and central nervous system mechanisms that have also been implicated in this form of pain. Specific treatments that block allodynia could be very useful if the cell and molecular basis of the condition could be determined. There are many potential mechanisms underlying this condition ranging from alterations in mechanotransduction and sensory neuron excitability to the actions of inflammatory mediators and wiring changes in the CNS. As with other pain conditions, it is likely that the range of redundant mechanisms that cause allodynia will make therapeutic intervention problematic.

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Descarga gratuita: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4[...]