What Is Proximal Neuropathy?
A neurotoxicity caused by severe organophosphate poisoning. At present, it is believed that its pathogenesis and cholinesterase activity are inhibited for a long time, so that a large amount of acetylcholine accumulated in the synaptic space continues to act on N2 on the postsynaptic membrane Receptors desensitize them, causing transmission disorders at nerve and muscle junctions, and skeletal muscle paralysis occurs.
Proximal muscle and respiratory paralysis of the extremities
- Dysfunction of the post-synaptic neuromuscular junction causes a group of syndromes of proximal limb muscles, muscles III-, and X innervating cranial nerves and respiratory paralysis.
- Affected area
- Limbs
- Related diseases
- Phosphorus poisoning pesticide poisoning organophosphorus pesticide poisoning children organophosphorus pesticide poisoning paralysis
- Related symptoms
- Respiratory failure, coma, tearing, salivation, cerebral palsy, cerebral edema, weakness, circulation failure, organophosphate poisoning, delirium
- Affiliated Department
- Department of Internal Medicine
- Related inspections
- Cholinesterase serum cholinesterase (CHE) electromyogram
- A neurotoxicity caused by severe organophosphate poisoning. At present, it is believed that its pathogenesis and cholinesterase activity are inhibited for a long time, so that a large amount of acetylcholine accumulated in the synaptic space continues to act on N2 on the postsynaptic membrane. Receptors desensitize them, causing transmission disorders at nerve and muscle junctions, and skeletal muscle paralysis occurs.
- After the symptoms of poisoning improved significantly, there were sudden manifestations of acute organophosphorus pesticide poisoning such as tearing, salivation, sweating, muscle tremor, and pupil shrinkage, but there was no phenomenon of cerebral palsy, and the effect of increasing atropine was significant.
- Intermediate syndrome needs to be distinguished from rebound and atropine poisoning during the treatment of organophosphate poisoning. In the former, symptoms of acute organophosphorus pesticide poisoning such as tearing, drooling, sweating, muscle tremor, and pupil diminishment suddenly appear after the symptoms of poisoning have improved significantly, but there is no phenomenon of cerebral palsy, and the effect of increasing atropine is significant; the latter is often effective After high-dose application of atropine, symptoms such as delirium, coma, breathing, and circulatory failure appeared, and symptoms improved after atropine was reduced or discontinued. Secondly, it should be distinguished from central respiratory failure and delayed peripheral neuropathy. When central respiratory failure occurs in acute organophosphorus poisoning, it often indicates that the central nervous system is severely damaged, and often has a coma and pathological reflex. Most of the intermediate syndromes occur in the awake state. After rescue, the consciousness becomes clear, but there is still no spontaneous breathing, which indicates that respiratory failure is peripheral, but sometimes it can be mixed due to cerebral edema. Delayed peripheral neuropathy, which mostly occurs after 2-3 weeks of poisoning, mainly involves the distal limb muscles, and does not involve the cerebral nerves and respiratory muscles. Although the manifestations of the intermediate syndrome are diverse, most of the muscles dominated by the cerebral nerves are cervical flexion and respiratory muscles. Respiratory muscle paralysis is the most serious manifestation and the main cause of death.
- After the symptoms of poisoning improved significantly, there were sudden manifestations of acute organophosphorus pesticide poisoning such as tearing, salivation, sweating, muscle tremor, and pupil shrinkage, but there was no phenomenon of cerebral palsy, and the effect of increasing atropine was significant.
- The treatment of intermediate syndrome is mainly aimed at respiratory failure caused by respiratory muscle paralysis. The data in this group show that most of the respiratory arrests occur within a short period of time after muscle weakness and paralysis of the respiratory muscles occur. Therefore, effective artificial respiration should be established quickly, which is the key to successful rescue. At the same time continue to give antidote and supportive treatment to reduce mortality. In recent years, it has been found that rejuvenating agents can not only restore the physiological activity of poisoning enzymes, but also directly resist neuromuscular conduction block caused by cholinesterase inhibitors and improve nerve and muscle transmission. Some people also believe that the occurrence of intermediate syndrome may be related to insufficient application of resuscitation agents, so it is advocated that once a respiratory muscle palsy occurs, an assault dose of clodoxidine can be used for treatment.