ABSTRACT
The continuous pandemic coronavirus disease 2019(COVID-19)caused by severe acute respiratory syndrome coronavirus-2(SARS-CoV-2)is a serious threat to human life and health because of high infectious pathogenicity, and it also has posed a new challenge to the current medical model. Many literatures have shown that these changes range from the more common ocular surface diseases such as inflammation of the cornea, conjunctiva, and sclera, to the relatively rare paracentral acute middle maculopathy and acute macular neuroretinopathy. For patients with ocular symptoms as the first or accompanying symptoms of SARS-CoV-2 infection, how to identify the correlation between ocular manifestations and SARS-CoV-2 infection is undoubtedly a serious challenge for ophthalmologists. In this review, the ocular pathology caused by both SARS-CoV-2 infection and vaccination was discussed, covering pathological changes in the ocular surface, uvea, retina and macula, and cranial nerves.
ABSTRACT
El dolor neuropático es un síndrome de muy difícil manejo en la práctica clínica. Suele originarse a consecuencia de lesiones o enfermedades que afectan al sistema somatosensorial. Lesiones de nervios periféricos, la diabetes, el virus herpes zoster, entre otras, son ejemplos de entidades clínicas que causan dolor neuropático. Este tipo de dolor supone modificaciones de la fisiología normal de las neuronas que integran la vía de transmisión nociceptiva y que operan tanto a nivel periférico, como central. Entre estos mecanismos se incluye la generación de descargas ectópicas, cambios en el genoma de las neuronas involucradas, alteración de canales iónicos, pérdida de las actividades inhibitorias endógenas, activación anormal del sistema inmunitario y sensibilización tanto periférica, como central. Este artículo resume los mecanismos moleculares y neuroplásticos que ocurren en situaciones de dolor neuropático y revisa diferentes modelos experimentales para su estudio. El desarrollo de estos modelos ha permitido dilucidar los mecanismos subyacentes de esta patología, el diseño de nuevas estrategias terapéuticas y el diagnóstico acertado de la enfermedad
Neuropathic pain is a very complex clinical syndrome that results as a consequence of lesions or diseases affecting the somatosensory system. Lesion of peripheral nerves, diabetes, herpes zoster virus, among others, are clinical entities that may cause neuropathic pain. Neuropathic pain also reflects changes of the normal physiology of the nociceptive transmission neurons that may happen at peripheral and central levels. These mechanisms include the generation of ectopic discharges, genomic changes of the neurons involved, alterations of ionic channels and of the endogenous inhibition of pain, abnormal activation of the immune system as well as peripheral and central sensitization. This article review the molecular and neuroplastic mechanisms associated to neuropathic pain and discuss different experimental models for its study. The development of these models has been helpful to understand the subjacent mechanisms of this pathology, and has contributed to design new therapeutical approaches and the correct diagnose of the disease