Exercícios Neuropraxia Nervo Radial e Mediano FRATURA do ÚMERO Clínica Fisioterapia Dr. Robson Sitta

▼ Contact: (11) 2528.4661 - www.fisiositta.com.br Dr. ROBSON SITTA PHYSIOTHERAPY CLINIC Rua Coriolano 1480 - Vila Romana (Lapa), São Paulo (SP) - Brazil FOLLOW US ON SOCIAL MEDIA: ▼ YOUTUBE: https://www.youtube.com/channel/UCb7a... ▼ INSTAGRAM:   / robson.sitta   ▼ FACEBOOK: https://www.facebook.com/fisiositta?f... ▼ LINKEDIN:   / robson-sit.  . ▼ WEBSITE: www.fisiositta.com.br PHYSIOTHERAPY SPECIALIZED in ORTHOPEDICS & MANUAL THERAPY Fracture Humeral Diaphyseal Injury with Neuropraxia of the Radial and Median Nerves Neuropraxia Neuropraxia is considered a first-degree injury and results from a blockage of nerve impulse transmission at the injured site, usually caused by a short-term process of intrinsic or extrinsic compression that causes local anoxia in neurons due to compression of blood vessels. This type of conduction block is considered physiological (biochemical changes) because the macroscopic structure of the nerve is virtually preserved. However, edema and subsequent thinning of the nerve fiber, with focal demyelination, may be observed at the injured site. Nerve conduction is preserved both above and below the injured site, with no Wallerian degeneration occurring, allowing for a muscular response to an electrical stimulus applied distally to the injured site. This blockage of stimulus conduction can be partial or complete, and as a result, a diminished response or even no motor response to stimulation proximal to the injury may occur. In neuropraxia, motor function is more compromised than sensory function, and the sensations carried by thicker fibers (proprioception and touch) are more affected than those carried 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 full recovery of function. Some examples of neuropraxia are partial palsies of the peroneal nerve that can occur after prolonged cross-legged positioning, palsies of the posterior cord of the brachial plexus or radial nerve resulting from prolonged head support on the back of a chair, and palsy 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 injury site and, to a lesser extent, proximal to the injury, with thinning of the axons within 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 inflow 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 nerve segment proximal to the injury, but stimulation of the distal segment may elicit a motor response for a few days, after which it disappears. The clinical picture of axonotmesis is complete sensory and motor paralysis. Due to the reduction in axonal caliber, conduction velocity is reduced in the segment proximal to the injury. Electromyography shows denervation potentials detected 2 or 3 weeks after injury. Insertion potentials disappear, and there are no action potentials when voluntary contraction is attempted. 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 the axon must travel between the injury site and the effector organ, as well as other factors. Because the endoneurial tubes are preserved in axonotmesis, the regeneration of each axon occurs within its respective tube, which ensures the reinnervation of the structures within the original pattern, guaranteeing complete recovery from the injury. Neurotmesis Neurotmesis includes third- to fifth-degree injuries, in which there is some impairment of the nerve's connective tissue support structure associated with axonal injury. Third-Degree Injury A third-degree injury occurs within the nerve fascicle, where the endoneurial tube is also severed. Fourth-Degree Injury A fourth-degree injury occurs when the fascicle is severely compromised or severed, with rupture of the perineurium. Fifth-Degree Injury This involves complete rupture of the nerve trunk, including the epineurium.