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Most Post-Polio Syndrome May Be Normal Aging


ROCHESTER, Minn. -- Most so-called post-polio syndrome may be the effect of muscle weakness that comes with age rather than an exacerbation of the disease decades later, according to researchers here.

ROCHESTER, Minn., Aug. 22 -- Most so-called post-polio syndrome may be the effect of muscle weakness that normally occurs with age rather than an exacerbation of the disease decades later, according to researchers here.

Although most patients described a progressive decline in strength more than four decades after a polio infection, clinical findings indicated only modest changes similar to what would be expected in their peers, found a small study reported Eric J. Sorenson, M.D., of the Mayo Clinic, and colleagues, in the Journal of the Peripheral Nervous System.

The prospective, population-based study found no association between patient-reported symptoms and the magnitude of decline in neuron loss that causes post-polio syndrome weakness.

Rather, individuals were more likely to be symptomatic during the 15 year follow-up period if they had greater residual deficits in strength after the initial infection.

Dr. Sorenson said that these patients likely lost so much strength during their illness that any later change is very noticeable to them, but that most patients who have had childhood polio can expect years of stability without the need for major lifestyle modifications.

"Given the associations identified in this study, it appears that the severity of the residual deficits is the strongest predictor of its development rather than the rate of decline late in life," Dr. Sorenson and colleagues wrote.

The polio virus attacks specific neurons in the brainstem and anterior horn cells of the spinal cord. Although new nerve terminals may sprout from neurons that survive the attack to compensate and restore muscle function, these neurons may become overtaxed or degenerate and gradually die off.

In the study, the investigators followed 50 representative polio survivors, chosen randomly from 298 patients, for a mean of 15 years. The cohort had polio a mean of 40 years earlier. Electrophysiologic testing revealed that motor unit number estimates and compound muscle action potentials measures of neuron loss declined only modestly.

The summated compound muscle action potential amplitude declined from a mean of 26.0 at baseline in 1987 to 19.0 at the 15-year follow-up (P<0.001). The summated motor action unit number also significantly dropped from a mean of 407 at baseline to 226 (P<0.001).

Therefore, the polio survivors lost 2.9% of their motor units per year. The authors cited another study in a normal population in the same age range that found a loss rate of about 2% to 3% per year.

Amplitude decreased at 1.8% per year in these polio survivors, average age 53 at baseline, while the other study in a normal population found a similar 1.6% decrease per year.

"While the methods of these two studies differ, the similarity of these results suggests that our polio cohort did not age any differently than a normal population," the investigators wrote. "This suggests that the most likely cause for the decline in our polio survivors is aging alone."

Furthermore, there was no association between neuronal loss rate and patient-reported symptom progression over time. The amplitude decline was 6.8 mV for the asymptomatic patients compared to a mean decrease of 7.2 mV for the symptomatic group (P=0.90). Likewise, motor unit loss was 229 for the asymptomatic group compared to 120 for the symptomatic group (P=0.09).

Instead, the symptomatic group had more baseline residual damage than the asymptomatic group: 24.8 mV versus 31.8 mV for amplitude (P=0.08) and 376 versus 540 for motor units (P=0.04).

The researchers previously reported a modest decline in strength, timed walking tests and hand manipulation tests for these patients over time.

By the end of the 15 years, only 38 were available for follow up testing and only seven patients remained asymptomatic.

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