ABSTRACT
Rupture of Achilles tendon is a common accident affecting professional and recreational athletes. Acute and chronic pain are symptoms commonly observed in patients with rupture. However, few studies have investigated whether Achilles tendon rupture is able to promote disorders in the central nervous system (CNS). Therefore, the current study aimed to evaluate nociceptive alterations and inflammatory response in the L5 lumbar segment of Balb/c mice spinal cord after Achilles tendon rupture. We found increased algesia in the paw of the ruptured group on the 7th and 14th days post-tenotomy compared with the control group. This phenomenon was accompanied by overexpression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase-2 (NOS-2) as well as hyperactivation of astrocytes and microglia in nociceptive areas of L5 spinal cord as evidenced by intense GFAP and IBA-1 immunostaining, respectively. Biochemical studies also demonstrated increased levels of nitrite in the L5 spinal cord of tenotomized animals compared with the control group. Thus, we have demonstrated for the first time that total rupture of the Achilles tendon induced inflammatory response and nitrergic and glial activation in the CNS in the L5 spinal cord region.
ABSTRACT
Os autores estudaram 24 pacientes, em clinica psiquiatrica, que apresentaram quadro clinico comparavel com distonia neurovegetativa. Os pacientes foram divididos em quatro grupos dispostos em quadrado latino sendo cada grupo tratado com placebo, clobazam AD e clobazam AD modificado. Os tratamentos foram administrados pelo metodo duplo-cego sendo a ordem de administracao definidos aleatoriamente. Os resultados sobre a sintomatologia avaliada pela escala de Hamilton para ansiedade mostram a superioridade da associacao clobazam + homatropina + ergotamina sobre os demais tratamentos utilizados. A tolerancia clinica foi excelente, nao tendo sido registrado qualquer efeito colateral relevante nos quatro grupos de tratamento