The declining number of motor units in the normal individual may have little or no consequences until a very advanced age. In the post-polio individual, however, having had significant deficits in strength and functional capabilities from the initial poliomyelitis illness, any further loss of strength due to a loss of motor units may be readily apparent. Research suggests that normal age-related losses of anterior horn motor neurons reduces the size of the pool of functioning anterior horn cells, a pool that was already markedly diminished by the original poliomyelitis, and that these reductions lead to new muscle weakness. It is a remarkable fact the persons who had spinal poliomyelitis were shown to have normal muscle function even after loss of 60% of their anterior horn cells. Since normal anterior horn cell loss is suggested to occur at a rate of 5% per decade after age twenty, aging-related losses of spinal motor neurons could reduce the total number of anterior horn cells to below 40% and thereby cause decreased muscle functioning. (3) The enlarged, surviving, motor units may also have a limited capacity for re-innervation as compared to what normally occurs in the aging muscle. This may lead to a gradual loss in the number of myofibers innervated by the surviving enlarged motor units. The surviving motor units of a postpolio patient can have up to a seven-fold increase in size. (9) A hypothesis is that one mechanism by which muscle function is restored following the acute infection is by surviving motor neurons producing axonal sprouts. Through the growth of these sprouts, remaining motor neurons innervate not only their own muscle fibers but also thousands of additional muscle fibers orphaned when surrounding motor neurons died. Electromyographic studies indicate that the number of sprouts and their ability to function are decreased in a person who had polio, decreases that correlate with the number of years since polio's onset and not chronological age. (3) It has also been suggested that the transient muscle weakness that follows exercise may be caused by the metabolic fatigue of polio virus-damaged or extensively sprouted anterior horn cells. These motor neurons may become unable to meet the metabolic demands of functioning after years of operating in a damaged state or supplying more muscle fibers when they were designed to innervate. (3)

There is certainly ample electrophysiological and histological evidence documenting an ongoing process of denervation and re-innervation within the surviving motor units in polio survivors. (9) It is known that long after recovery from acute poliomyelitis, many polio survivors will continue to have abnormalities on conventional EMG regardless of whether or not they are experiencing new symptoms. These include persistence of the spontaneous fibrillation and fasciculation potentials, enlarged motor unit axon potentials and decreased recruitment. (8)

A simplified explanation of the process is that the motor neurons become exhausted. The exhaustion may be exacerbated by death of motor neurons, a process that begins in normal persons after approximately age 60. In motor neurons handicapped by a patients original polio, functional compensation is overreached, and postpolio syndrome occurs. (5)

Based on current understanding of the pathophysiology of postpolio motor units, a real cure seems unlikely and the goal of medical care is to minimize and control decline of strength over the life course. (10)

A number of functional etiologies may also lead to an apparent loss of neuromuscular function. These include progressive loss in strength and or endurance from disuse or overuse, weight gain, and chronic weakness of which the individual was perhaps unaware until the postpolio syndrome became well known. Disuse leads to a decrease in muscle strength and cardiorespiratory fitness in young, healthy individuals. There is no reason to believe that disuse does not play a role in the loss of neuromuscular function, at least in some postpolio individuals. (11)

The Institute of Medicine recently proposed a model for understanding secondary disability development. In this model a secondary condition is defined as any new condition that develops in the life course of a person with a primary disabling condition. Life-style/behavioral and biological risk factors interact with the primary disability to influence the process of further disablement from the secondary condition. New pathologies may progress to greater impairment, more functional limitation or additional disability. The process of secondary disablement then interacts with quality of life. The life-course paradigm for understanding secondary disablement emphasizes developmental and aging processes that can be expected during a persons life to increase chronic impairment and evolve into more functional limitation, thus requiring frequent readaptation to avoid additional disability. If the life-course model of secondary disablement is applied to people with a past history of polio, PPS is a secondary condition that postpolio people are at risk of developing. Inasmuch as the diagnostic criteria for PPS are inherently subjective symptoms, PPS cannot be defined objectively, and individualized criteria must be used. A more quantifiable criterion for diagnosing PPS is the presence of a new, or greater degree of, functional limitation resulting from the level of symptoms that a person is experiencing. This definition of PPS permits a clinician to consider diagnosis and management of a person with a past history of polio holistically because many new health problems may occur during the life of a post polio person that affects the neuromusculoskeletal systems and functional abilities. (12)