Neuropatia Periférica / Neuropraxia Nervo Radial EVOLUÇÃO Clínica de Fisioterapia Dr. Robson Sitta

▼ (11)2528.4661 Call and schedule your appointment Rua Coriolano 1480 - Vila Romana (Lapa), SP. Dr. Robson Sitta Physiotherapy Clinic ▼ SUBSCRIBE to our YouTube channel and receive all the news in real time: https://www.youtube.com/channel/UCb7a... ▼ Visit the official website and learn more: www.fisiositta.com.br ▼ LIKE Dr. Robson Sitta Physiotherapy Clinic on Facebook: https://www.facebook.com/fisiositta?f... ▼ ADD Robson Sitta on LinkedIn:   / robson-sit.  . SPECIALIZED PHYSIOTHERAPY in ORTHOPEDICS & MANUAL THERAPY Clinical Evolution Peripheral Neuropathy / Radial Nerve Neuropraxia Neuropraxia Neuropraxia is considered a first-degree injury and is caused by a blockage of nerve impulse transmission at the injured site, usually caused by a process of intrinsic compression or extrinsic, of short duration and which causes local anoxia in neurons, due to compression of blood vessels. This type of conduction block is considered physiological (biochemical changes), since the macroscopic structure of the nerve is practically preserved, but at the site of the injury, edema and subsequent thinning of the nerve fiber can be observed, with focal demyelination. Nerve conduction is preserved both above and below the site of the injury, and Wallerian degeneration does not occur, allowing for a muscular response to an electrical stimulus applied distally to the site of the injury. This blockage to stimulus conduction may be partial or complete, and because of this, there may be a diminished response or even no motor response to stimulation proximal to the injury. In neuropraxia, motor function is more compromised than sensory function, and the sensitivities conducted by thicker fibers (proprioception and touch) are more affected than those conducted by thin fibers (pain and temperature), contributing to local impairment of the myelin sheath. When the compressive process is removed, the remyelination process occurs and nerve conduction returns in approximately 6 weeks, with complete recovery of function. Some examples of neuropraxia are partial paralysis of the fibular nerve that may appear after a long period of cross-legged lying, paralysis of the posterior cord of the brachial plexus or radial nerve resulting from prolonged support of the head on the back of a chair, and paralysis of the dorsal interosseous nerve due to compression when sleeping with the head resting on the forearm. Axonotmesis Axonotmesis is considered a second-degree injury and is characterized by Wallerian degeneration distal to the site of the injury and, to a small extent, proximal to the injury, with thinning of the axons in a few centimeters of the proximal stump. It usually occurs due to more intense or prolonged compression of the arterioles and neural venous drainage, causing an increase in intraneural pressure sufficient to completely block the passage of nutrient inflows through the axoplasm. This compression triggers the degenerative process of the axon, called axonotmesis, and of the myelin sheath, but with preservation of the endoneurial tube. In this type of situation, no muscular response is observed to stimulation of the segment of the nerve proximal to the injury, but stimulation of the distal segment can provoke a motor response for a few days, and then disappears. The clinical picture of axonotmesis is complete sensory and motor paralysis. Due to the reduction in axonal caliber, the conduction velocity is reduced in the segment proximal to the injury. Electromyography shows denervation potentials that are detected 2 or 3 weeks after the injury, and the insertion potentials disappear and there are no action potentials when there is an attempt at voluntary contraction. If the compression is removed, axonal and myelin sheath regeneration occurs, with spontaneous recovery of the injury. The regeneration process is variable and can last from weeks to months, mainly depending on the distance to be traveled by the axon between the site of the injury and the effector organ, in addition to other factors. Since in axonotmesis the endoneurial tubes are preserved, the regeneration of each axon occurs within its respective tube, which guarantees the reinnervation of the structures within the original pattern, ensuring complete recovery from the injury. Neurotmesis Neurotmesis comprises third to fifth degree injuries, in which there is some impairment of the structure of the connective support of the nerve associated with the axonal injury. Third degree injury A third degree injury occurs within the nerve fascicle, where the endoneurial tube is also sectioned. Fourth degree injury A fourth degree injury occurs when the fascicle is severely compromised or sectioned, with rupture of the perineurium. Fifth-degree injury Presents complete rupture of the nerve trunk, including the epineurium.