KS> From: keith@actrix.gen.nz (Keith Stewart) KS>My wife has become interested through an acquaintance in Post-Polio Syndrome KS>This apparently is not recognised in New Zealand and different symptons ( eg KS>chest complaints) are treated separately. Does anone have any information  I'm not sure that this condition is "recognised" anywhere (in the sense of a disease with diagnostic criteria, clear boundaries between it and other diseases, unique pathologic or physiologic features, etc), but here goes with what many neurologists agree on.  Post-polio syndrome patients have evidence of motor neuron disease by clinical examination, EMG, and muscle biopsy.  The abnormalities are mostly chronic (due to old polio) but there is evidence of ongoing deterioration.  Clinically, the patients complain of declining strength and endurance with everyday motor tasks. Musculoskeletal pain is a nearly universal feature that doubtless contributes to the impaired performance.  The examination shows muscle weakness and atrophy.  The EMG shows evidence of old denervation with reinnervation (giant and long-duration motor unit action potentials) *and* evidence of active denervation (fibrillation potentials).  The biopsy also shows old denervation with reinnervation (fiber-type grouping) *and* evidence of active denervation (small, angulated fibers with dense oxidative enzyme staining) - but curiously, little or no group atrophy.  Post-polio patients do not have ALS.  In ALS, there is clinically evident deterioration from one month to the next.  In post-polio, the patients are remarkably stable in objective findings from one year to the next.  Of course, there are patients who had polio before who develop genuine ALS, but ALS is no more common among polio survivors than among people who never had polio.  The cause of post-polio syndrome is unknown.  There is little evidence that post-polio patients have active polio virus or destructive immunologic response to virus antigen.  There is no solid evidence that patients with post-polio have anything different happening to the motor unit (anterior horn cells, motor axons, neuromuscular junctions, and muscle fibers) than patients with old polio who are not complaining of deterioration. Both groups can have the same EMG and biopsy findings.  The reason for these "acute" changes in a "chronic" disease (old polio) is unknown.  Possibly spinal motor neurons (that have reinnervated huge numbers of muscle fibers) start shedding the load after several years.  There are a couple of clinical features that distinguish post-polio syndrome patients from patients with old polio who deny deterioration.  The PPS patients are more likely to have had severe polio.  The PPS patients are *much* more likely to complain of pain. They also tend to score higher on depression scales of neuropsychologic tests.  My take on this (I'm sure some will disagree):  after recovery from severe polio there can be abnormal loading on muscles, tendons, ligaments, bones, and joints, that leads to inflammatory and/or degenerative conditions affecting these structures.  The increasing pain, superimposed on the chronic (but unchanging) weakness, leads to progressive impairment of motor performance and ADL.  I am perhaps biased by personal experience of having never seen a PPS patient who was not limited in some way by pain.  I do not believe that PPS patients have more rapid deterioration of motor units than non-PPS patients (i.e., those with old polio of similar severity but without PPS complaints).