Case Presentation: An 84-year-old female with history of pediatric paralytic polio, heart failure with preserved EF, atrial fibrillation, coronary artery disease presented with progressive shortness of breath (SOB). Four months prior, she had presented to the emergency department with similar SOB and generalized weakness. At that time EKG, CT angiography chest and transthoracic echocardiogram were unremarkable. A follow up pharmacologic stress test was low risk for ischemia. One month prior, the patient presented with SOB, dull, retrosternal chest pain, and ongoing weakness. At that time right heart catheterization showed normal volume status and coronary angiography was normal. On her current presentation, she reported the additional symptom of dysphagia to solids and liquids that had apparently started 4 months previously. Her vital signs were unremarkable with oxygen saturation 98% on room air. A full neurologic exam revealed reflexes 1+ throughout, generalized decreased bulk and tone, strength 4/5 for left upper and lower extremities, and 4-/5 for right upper and lower extremities. Given her progressive dysphagia and SOB without clear etiology, a primary neurologic process was considered and vitamin B12, folate, syphilis, autoimmune panel, TSH, Lyme, and acetylcholine receptor antibodies were assessed and normal. Electromyography (EMG) finally showed an active and chronic process with intraspinal canal lower motor axon loss of the cervical and lumbosacral areas, suggestive of a primary motor neuron disease. Given the patient’s history of polio and the isolation of findings to lower motor neurons, her disease was most likely a post-polio syndrome (PPS) with mild respiratory involvement. She was discharged with low-intensity physical therapy and repeat EMG if any progression of symptoms occurred.

Discussion: PPS is a clinical entity characterized by new weakness and pain secondary to lower motor neuron axon loss, with onset decades after acute paralytic polio. It affects 28.5% of patients with history of paralytic polio. Given the polio epidemic of the 1950s, PPS is expected to be quite frequent in the current geriatric population and remains an underrecognized cause of weakness.The most important risk factors of PPS are female sex, respiratory symptoms during acute polio infection, older age at diagnosis, higher severity of disease, rapid recovery from the acute polio. The pathophysiology of PPS is not fully understood; however, axonal loss appears confined to the neurons affected during the primary illness.PPS can be confused with other more common causes of generalized weakness and myalgias. It is crucial to consider the patient’s history when it includes polio, even if diagnosed during infancy. Once suspected, it is important to keep in mind that there is not a diagnostic test: EMG can guide the diagnosis, but it does not reliably distinguish patients with prior paralytic polio, those with new weakness, or other lower motor neuron diseases. PPS remains a clinical diagnosis. The management of PPS is highly dependent on patient-physician relationship as reassurance and trust become fundamental in dealing with it. Low-intensity physical therapy, weight loss, respiratory support and orthotic supports are recommended.

Conclusions: Despite USA polio eradication in 1979, PPS may still occur given the significant lag-time to presentation. Also, familiarity with PPS should be enforced as the growing global trend against infant immunization risks the return of previously eradicated diseases.