Weakness or paralysis

Myelopathy. Damage to the spinal cord results in weakness or paralysis of voluntary muscles. 

Bronchoconstriction and secretion, muscular weakness or paralysis, CNS depression, including respiratory centers Inhibition of acetylcholinesterase (reversible or irreversible)... 

Ocular findings, including nystagmus (horizontal or vertical), weakness or paralysis of the lateral recti muscles, and weakness or paralysis of conjugate gaze Korsakoff s psychosis is most characterized by the following ... 

The outcome of stroke depends on the area of neurones involved and may include weakness or paralysis of muscles, numbness, visual or speech disturbances and coma. 

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... 

The cause of death is attributed to anoxia resulting from a combination of central respiratory paralysis, severe bronchoconstriction, and weakness or paralysis of the accessory muscles for respiration. 

Atropine administered repeatedly as necessary and pralidoxime (2-PAM Cl) are antidotes for nerve agent toxicity. Although atropine has no effect on nicotinic receptors, and therefore will not reverse muscle weakness or paralysis, it can reduce morbidity and mortahty by reversing some of the muscarinic effects such as bron-chospasm, bradycardia, sahvation, diaphoresis, diarrhea, and vomiting (2). These antidotes may not be available in the field, especially in or near the site of attack. If mihtary Mark 1 kits are available, they provide autoinjectors that automatically dehver 2mg of atropine and 600mg pralidoxime (9). 

Other cases have since been reported49 52 and in some, the weakness or paralysis lasted for days to weeks. One suggestion was that lack of early oxime therapy might contribute to the development of the syndrome,53 but it has occurred with adequate amounts of oxime.49,50,54 The cause of this neuromus-... 

Mixed cholinergic syndrome. Because both nicotinic and muscarinic receptors are stimulated, mixed effects may be seen. The pupils are usually miotic (of pinpoint size). The skin is sweaty, and peristaltic activity is increased. Fasciculations are a manifestation of nicotinic stimulation and may progress to muscle weakness or paralysis. (Examples organophos-phate and carbamate insecticides and physostigmine.)... 

Ingestion abdominal pain, diarrhea, vomiting, trembHrrg, feeling of weakness or paralysis in arms ar>d legs. rinse mouth, take immediately to hospital. 

Nervous system Anterior spinal cord syndrome is a rare condition involving weakness or paralysis of the extremities, often accompanied by pain, frequently without a history of trauma. A case has been attributed to atenolol [5 ]. 

In addition to Mellanby s results with dogs, Aberle and Setterfield and Sutton have described degeneration of medullary sheaths of sensory tracts at the periphery of the cord. In some cases this degeneration was found in the posterior columns, and in others the posterior roots were involved. These changes were found to be associated with marked weakness or paralysis of the extremities. These authors were able to obtain a clinical cure of this condition with cod-liver oil while it was still possible to demonstrate lesions in the nervous system. Aberle suggests that this result may be due to the fact that the regenerated axis cylinder functions before remyelination of the fiber is complete. He points out that stimulation of the motor cortex in embryonic animals may elicit motor responses before the corticospinal tracts are myelinated. Modern research on nerve regeneration supports Aberle s explanation. 

Signs of potassium deficiency are primarily those of decreased muscular irritability and disturbances of conduction and contractility in the heart muscle. Muscular weakness or paralysis are characteristic and may be accompanied by lethargy and coma. Cardiac dilatation, hypertension, congestive failure, and cardiac arrest may occur. Death may result from respiratory or cardiac failure or from paralytic ileus. 

Motor pathways in the brain consist of an upper motor neuron and a lower motor neuron. The upper motor neuron is located in the cerebral cortex and the lower motor neuron in the brain stem. A lesion of the upper motor neuron will result in muscle weakness or paralysis, with no muscle atrophy early and a disuse atrophy developing after a period of time. If a body part is bilaterally represented in the cortex, this would not be as noticeable. Increased muscle tone may be present along with increased tendon reflexes. The lower motor neuron is located in the brain stem. A lesion of the lower motor neuron is generally manifested as muscle weakness, flaccid paralysis, loss of reflexes, and an atrophy of the muscles. 

TABLE 7-6. Toxicants Inducing Muscle Weakness or Paralysis ... 

The answer is S [1C 1 a-b, HI b (1)]. Salivation, miosis, bradycardia, and dyspnea are muscarinic signs of organophosphate cholinesterase inhibition that are counteracted by atropine. Paresis is a nicotinic (neuromus-cuiar) effect and is not altered by atropine. As a result, even though the parasympathetic signs of organophosphate toxicosis are coiv trolled by atropine animals may still have muscle tremors, weakness, and even dyspnea (as a result of weakness or paralysis of the striated muscles of respiration). 

Another classic feature of acute lead poisoning is a motor neuropathy giving rise to weakness or paralysis, most commonly of the external muscles of the dominant hand, to produce the classical wrist-drop. Lead palsy less frequently affects the lower limbs giving rise to foot-drop, a condition seen more often in children than in adults. 

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