lunes, 7 de agosto de 2017

Más de insensibilidad congénita al dolor/ More on congenital insensitivity to pain

Agosto 6, 2017. No. 2772






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Indiferencia congénita al dolor
Congenital Indifference to Pain Adelaida Álvarez C.*, Simón P. Aristizábal L.**, Luis E
Rev. Col. Anest. Noviembre 2010 - enero 2011. Vol. 38 - No. 4: 528-535
Resumen
Introducción. En la fase aguda, el dolor ejerce un mecanismo natural de protección. No obstante, existen dos trastornos congénitos cuya característica principal es una baja o nula reactividad al trauma: la insensibilidad congénita al dolor y la indiferencia congénita al dolor. Esta última es una condición poco común en la que a pesar de no existir anormalidades neurológicas en las vías del dolor, el individuo carece de una respuesta emocional a la lesión tisular. Objetivos. Presentar el caso de una niña con indiferencia congénita al dolor y hacer revisión de la fisiopatología y una aproximación diagnóstica. Metodología y resultados. Presentación de caso clínico. Conclusiones. El diagnóstico de indiferencia congénita al dolor es básicamente un diagnóstico de exclusión y dado que aún no se conoce cura para este trastorno, la prevención, la educación y el tratamiento interdisciplinario son lo primordial en estas entidades.
Las mutaciones NaV1.9 del canal de sodio asociadas con la insensibilidad al dolor disminuyen la excitabilidad neuronal.
Sodium channel NaV1.9 mutations associated with insensitivity to pain dampen neuronal excitability.
J Clin Invest. 2017 Jun 30;127(7):2805-2814. doi: 10.1172/JCI92373. Epub 2017 May 22.Abstract
Voltage-gated sodium channel (NaV) mutations cause genetic pain disorders that range from severe paroxysmal pain to a congenital inability to sense pain. Previous studies on NaV1.7 and NaV1.8 established clear relationships between perturbations in channel function and divergent clinical phenotypes. By contrast, studies of NaV1.9 mutations have not revealed a clear relationship of channel dysfunction with the associated and contrasting clinical phenotypes. Here, we have elucidated the functional consequences of a NaV1.9 mutation (L1302F) that is associated with insensitivity to pain. We investigated the effects of L1302F and a previously reported mutation (L811P) on neuronal excitability. In transfected heterologous cells, the L1302F mutation caused a large hyperpolarizing shift in the voltage-dependence of activation, leading to substantially enhanced overlap between activation and steady-state inactivation relationships. In transfected small rat dorsal root ganglion neurons, expression of L1302F and L811P evoked large depolarizations of the resting membrane potential and impaired action potential generation. Therefore, our findings implicate a cellular loss of function as the basis for impaired pain sensation. We further demonstrated that a U-shaped relationship between the resting potential and the neuronal action potential threshold explains why NaV1.9 mutations that evoke small degrees of membrane depolarization cause hyperexcitability and familial episodic pain disorder or painful neuropathy, while mutations evoking larger membrane depolarizations cause hypoexcitability and insensitivity to pain.

¿Podemos compartir un dolor que nunca sentimos? Correlaciones neuronales de empatía en pacientes con insensibilidad congénita al dolor.
Can we share a pain we never felt? Neural correlates of empathy in patients with congenital insensitivity to pain.
Neuron. 2009 Jan 29;61(2):203-12. doi: 10.1016/j.neuron.2008.11.023.
Abstract
Theories of empathy differ regarding the relative contributions of automatic resonance and perspective taking in understanding others' emotions. Patients with the rare syndrome of congenital insensitivity to pain cannot rely on "mirror matching" (i.e., resonance) mechanisms to understand the pain of others. Nevertheless, they showed normal fMRI responses to observed pain in anterior mid-cingulate cortex and anterior insula, two key regions of the so-called "shared circuits" for self and other pain. In these patients (but not in healthy controls), empathy trait predicted ventromedial prefrontal responses to somatosensory representations of others' pain and posterior cingulate responses to emotional representations of others' pain. These findings underline the major role of midline structures in emotional perspective taking and understanding someone else's feeling despite the lack of any previous personal experience of it--an empathic challenge frequently raised during human social interactions.

Dolor emocional sin dolor sensorial - ¿Sueño?
Emotional pain without sensory pain--dream on?
Neuron. 2009 Jan 29;61(2):153-5. doi: 10.1016/j.neuron.2009.01.003.
Abstract
The article by Danziger and colleagues in this issue of Neuron evaluates empathy in a unique population--individuals with congenital insensitivity to pain. As such, it provides insights into the brain's ability to evaluate others' feeling to observed pain without having a specific sensory experience of pain itself.

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