Abstract

Post-polio muscular atrophy (PPMA) is characterized by new onset or increased weakness in patients with prior poliomyelitis after a stable period of time. Loss of highly reinnervated motor units during ageing has been accused for the development of this syndrome which is also known as “unstable-polio”. These patients have less number of motor units that can be estimated by conventional electrophysiological methods. By showing the large steps, CMAP scan provides information about the amount of collateral reinnervation in the construction of total muscle response (CMAP). As well as the number of motor units, their territory is also an object of curiosity. It is possible to record bioelectrical activity of motor unit lengthwise by scanning EMG and depict the temporal and spatial features of motor unit action potential (MUAP). This presentation aims to combine the findings in CMAP scan with scanning EMG and draw attention to reinnervation status of 2 PPMA patients whose tibialis anterior (TA) muscles were affected in different degrees. Two patients aged 39and 41 years were included. Patient 1 had PPMA for 8 years and his TA muscle strength was 3-/5, whereas Patient 2 showed PPMA findings for 1 year and his TA strength was 4/5. CMAP scan of TA muscle on recently affected side was performed with a commercially available software. In scanning EMG, MU territories were scanned with a concentric needle electrode (CNE) which is attached to a stepper motor. Another CNE is used for sweep triggering with the rate of selected motor units’ firing frequency. Acquired signals were processed by the dedicated software designed by the authors. CMAP scan of Patient 1 revealed a 1.65 mV CMAP constituting of 4 very large steps and Patient 2 revealed a 5.5 mV CMAP containing a few smaller steps. In scanning EMG, both patients’ motor units showed increased voltage in different parts corresponding to dense areas arisen from collateral reinnervation. Interestingly, the patient with more pronounced weakness for a longer period revealed both huge steps in his CMAP scan and also showed electrically silent areas in his scanned motor units. On the other hand, the patient with stronger TA muscle did not show very large steps or silent areas in his CMAP scan and MU scan, respectively. Loss of dense motor units leads to PPMA. However, in PPMA patients with severe weakness which is depicted by less number of motor units and presence of huge steps in CMAP scan, loss of fractions in motor unit territory might be a principal contributing factor which can only be demonstrated by scanning EMG.

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