Poliovirus replication in the CNS leads to paralysis through which mechanism?

Study for the Poliovirus and Poliomyelitis Test. Prepare with engaging flashcards and detailed multiple-choice questions, each with hints and explanations. Ace your exam with confidence!

Multiple Choice

Poliovirus replication in the CNS leads to paralysis through which mechanism?

Explanation:
Poliovirus causes paralysis by destroying motor neurons in the anterior horn of the spinal cord. The virus can reach the CNS after initial infection of the gut, and it preferentially infects lower motor neurons. When these neurons die, the muscles they innervate lose their neural input, leading to flaccid weakness, loss of reflexes, and eventual atrophy, often with visible fasciculations. Sensation stays intact because sensory neurons are not primarily affected, which is a hallmark of poliomyelitis. This mechanism differs from demyelination of peripheral nerves (which would disrupt nerve conduction along myelin), from causing weakness by blocking neuromuscular junctions (which would affect transmission at the synapse rather than neuron survival), and from increasing cortical excitability (which would imply a central, not motor-neuron–driven, process). The key idea is the direct destruction of motor neurons in the spinal cord’s anterior horn.

Poliovirus causes paralysis by destroying motor neurons in the anterior horn of the spinal cord. The virus can reach the CNS after initial infection of the gut, and it preferentially infects lower motor neurons. When these neurons die, the muscles they innervate lose their neural input, leading to flaccid weakness, loss of reflexes, and eventual atrophy, often with visible fasciculations. Sensation stays intact because sensory neurons are not primarily affected, which is a hallmark of poliomyelitis.

This mechanism differs from demyelination of peripheral nerves (which would disrupt nerve conduction along myelin), from causing weakness by blocking neuromuscular junctions (which would affect transmission at the synapse rather than neuron survival), and from increasing cortical excitability (which would imply a central, not motor-neuron–driven, process). The key idea is the direct destruction of motor neurons in the spinal cord’s anterior horn.

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