After the acute spell of poliomyelitis, patients commonly suffers from sequelae of weakness. Some of these patients experience new weakness after a time period of stable symptoms.
The aim of this thesis was to evaluate the possible mechanisms for persistent weakness and development of new weakness in prior polio patients.
The usefulness of neurophysiologic methods to study prior polio was evaluated. Also two follow up investigations were performed in the attempt to investigate a possible relationship between development of weakness over time and possible failure in neuromuscular function and relation to muscular activity. In another investigation an evaluation of the exceptional finding of a history of paralytic poliomyelitis without neurophysiologic signs of anterior horn cell death was made. The last investigation dealt with reflex pattern in prior polio and it’s relation to weakness and anterior horn cell loss.
The weakness in prior polio is mainly due to loss of motor neurons with incomplete compensatory mechanisms of reinnervation. The new weakness is mainly due to exaggerated physiological age dependent loss of whole motor neurons, but also fragmentation of the motor unit is likely when these have reached an upper size. Defective neuromuscular transmission and failure in the central drive contribute to a lesser degree to weakness.
Neurophysiologic method of choice for the assessment of motor unit size and the micro-physiology of the motor unit is Macro EMG.
Muscular overuse may accelerate motor unit loss over time in prior polio. Extremely large motor units measured with Macro EMG predict new weakness and Macro EMG can be used for prognostication of development of new weakness in prior polio.