Paralysis, nerve block

Peripheral nerve block is created by injecting ethanol around the selected nerve. The effect of alcohol on nerve tissue has been examined in animal models and in postmortem specimens from patients who received neurolytic blocks (8,9). In general, alcohol causes destruction of nerve fibers, with subsequent Wallerian degeneration. The basal lamina around the Schwann cell usually remains intact. This leaves a tract available for axon regeneration without the formation of a neuroma. If the cell bodies are completely destroyed, regeneration will not occur. Contact of alcohol with unintended nerve roots underlies many of the more serious complications. Involvement of anterior rootlets sufficient to interrupt motor nerve function will result in muscle weakness or paralysis. Interruption of... 

Kaufman MR, Elkwood Al, Rose Ml, Patel T, Ashinoff R, Fields R, et al. Surgical treatment of permanent diaphragm paralysis after interscalene nerve block for shoulder surgery. Anesthesiology 2013 119(2) 484—7. 

Delayed-action paralytic neurotoxins that block the release of acetylcholine causing a symmetric, descending flaccid paralysis of motor and autonomic nerves. Paralysis always begins with the cranial nerves. Toxins are obtained from an anaerobic bacteria (Clostridium botulinum). Toxin A is a white powder or crystalline solid that is readily soluble in water. It is stable for up to 7 days as an aqueous solution. All toxins are destroyed by heat and decompose when exposed to air for more than 12 h. 

Local anesthesia involves the blockade of nerve conduction in order to stop sensation. Because local anesthetics act on all nerve fibers they may also temporarily create motor paralysis. The usefulness of local anesthetics is their ability to completely block axonal transduction, which is reversible and without any apparent lasting effects. 

Certain organic forms of mercury can elicit specific damage in the main cell body of peripheral neurons. Similar responses are associated with certain natural products called vincristine and vinblastine, both of which have been used as antileukemic medicines. The deadly botulinum toxins, mentioned earlier in this chapter, block transmission of nerve impulses at the synapses of motor neurons. This blockage results in muscular paralysis which, if sufficiently severe, can lead to death, usually because respiration is impaired. The once widely used pesticide, DDT, is an organic chemical that also acts on the nervous system at this site, although it can also mount an attack on areas of the CNS. 

Botulinum toxin from Clostridium botulinum is the most potent poison known. The lethal dose in an adult is approx. 3x10 mg. The toxin blocks exo-cytosis of ACh in motor (and also parasympathetic) nerve endings. Death is caused by paralysis of respiratory muscles. Injected intramuscularly at minuscule dosage, botulinum toxin type A is used to treat blepharospasm, strabismus, achalasia of the lower esophageal sphincter, and spastic aphonia. 

Blocks transmission of nerve signals by interactions with glutamate-gated chloride channels Depolarization and spastic paralysis... 

Paresthesias, weakness and paralysis of lower extremity, hypotension, high or total spinal block, urinary retention or incontinence, fecal incontinence, headache, back pain, septic meningitis, meningismus, arachnoiditis, shivering cranial nerve palsies due to traction on nerves from loss of CSF, and loss of perineal sensation and sexual function Rare... 

Effect on eye Atropine produces mydriasis by blocking the cholinergic nerves supplying the smooth muscles of sphincter of the iris on local administration into the eye. It also produces paralysis of accommodation or cycloplegia (the condition in which, one can see things... 

Since local anesthetics are capable of blocking all nerves, their actions are not limited to the desired loss of sensation from sites of noxious (painful) stimuli. Although motor paralysis can be desirable during surgery, it may also limit the ability of the patient to cooperate (ie, push) during obstetric delivery or ambulate without assistance after outpatient surgery. 

The toxin produced by the bacterium C. botulinum is a mixture of six large molecules and is one of the two most potent toxins known to humans. Each consists of two components, a heavy (100 kDa) and light (50 kDa) polypeptide chain. The toxin molecule is transported into nerve cells and destroys a synaptosomal protein, which prevents the release of the neurotransmitter acetylcholine. This blocks muscle contraction, causing paralysis. This can be fatal. 

By destroying the protein, the toxin prevents the release of the neurotransmitter acetylcholine from small packets at the ends of nerves by exocytosis. These nerves, attached to voluntary muscles, need acetylcholine to allow the flow of signals (impulses) between the nerve and the muscle. By preventing the release of acetylcholine, botulinum toxin blocks muscle contraction, causing paralysis and relaxation. The therapeutic action relies on relaxation of muscles, generally in the face. It is therefore used to treat blepharospasm (uncontrolled contractions) and stroke-induced permanent facial muscle contractions. 

Since Bayliss wrote these paragraphs, Lapicque has shown that curare changes the chronaxie of the muscle, thereby throwing it out of step with the nerves. It is a blocking effect and not a complete paralysis of the muscle. 

Efforts should be made to use these drugs sparingly, and to check that their effects have worn off before the patient leaves the operating room. In fact, electric stimulation of a peripheral nerve (e.g., ulnar nerve) can be used to objectively determine if there is residual muscle paralysis.1 The muscles supplied by the nerve must show an appropriate twitch response to a given electric stimulus to insure that the patient has recovered adequately from the neuromuscular blocking drug.20,31... 

When applied locally to nerve tissue in appropriate concentrations, local anesthetics (Figure 23.2) reversibly block the action potentials responsible for nerve conduction. They act on any part of the nervous system and on every type of nerve fiber. Thus, a local anesthetic in contact with a nerve trank can cause both sensory and motor paralysis in the area innervated. The necessary practical advantage of the local anesthetics is that their action is reversible at clinically relevant concentra-... 

Hughes R, Whaler BC (1962) Influence of nerve-ending activity and of drugs on the rate of paralysis of rat diaphragm preparations by cl. botulinum type a toxin. J Physiol 160 221-33 Humeau Y, Doussau F, Grant NJ, Poulain B (2000) How botulinum and tetanus neurotoxins block neurotransmitter release. Biochimie 82 427 16... 

The neurotoxin, tetrodotoxin, a highly potent poison from the puffer fish, blocks the conduction of nerve impulses along axons and so leads to respiratory paralysis by binding very tightly to the Na+ channel and blocking its action. 

Neuromuscular paralysis This side effect most often results after direct intraperitoneal or intrapleural application of large doses of aminoglycosides. The mechanism responsible is a decrease in both the release of acetylcholine from prejunctional nerve endings and the sensitivity of the postsynaptic site. Patients with myasthenia gravis are particularly at risk. Prompt administration of calcium gluconate or neostigmine can reverse the block. 

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