The most widely accepted model of new weakness in PPS-- that of peripheral disintegration of motor units--was originally proposed by Wiechers and Hubbell.[1] To elucidate their hypothesis, background information follows.

Immediately following APP, brain stem and spinal cord motor neurons that persist are capable of elaborating new branches called axonal sprouts. Sprouts may originate from the terminal axon, from a more proximal unmyelinated axon, or from nodes of Ranvier even more proximal to the motor point. Motor axonal sprouts are capable of reinnervating muscle fibers that have lost their motor innervation due to APP.

Motor axonal sprouting is associated with at least two changes in the structure of motor units (defined as motor neurons and the muscle fibers they innervate). First, axonal sprouting increases the size of the motor unit. In mammals, somatic motor neurons may innervate a variable number of muscle fibers, depending on the muscle studied. Thus, human hand muscles (requiring considerable fine control) are innervated by motor neurons that supply dozens to hundreds of muscle fibers, whereas large muscles such as the quadriceps are divided into motor units consisting of thousands of muscle fibers. After APP, motor unit size can increase by 7- to 8-fold. Thus, a motor neuron in the quadriceps designed to support 5000 muscle fibers may support 35,000 or 40,000 muscle fibers in its full capacity for reinnervation after poliomyelitis.

A second major change in motor unit structure relates to fiber type grouping. Muscle fibers comprise at least three histochemical types, depending on contraction characteristics. Ordinarily, muscle fibers from a single motor neuron are distributed in a mosaic pattern throughout a muscle fascicle. Because of local sprouting after APP, muscle fibers innervated by the same motor neuron may be clustered in groups. Because motor neurons determine histochemical muscle fiber type, this phenomenon gives rise to fiber type grouping on histochemical analysis of muscle biopsies.

Wiechers and Hubbell[1] proposed that the compensatory enlargement of motor units after APP is not indefinitely stable, and that terminal axonal sprouts degenerate over time (Figure 1). They were able to demonstrate that jitter on single-fiber electromyography (SFEMG), an indirect indicator of terminal axonal integrity (explained below), increased with the number of years after APP. Although no other investigator (including Wiechers in a separate study[2] of vaccine- related APP) was able to replicate these data, the theory proposed to explain the original data has received direct and indirect confirmation over the past 15 years.

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