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Motor unit potential analysis in the cases with hemifacial spasm and postparalytic facial hyperactivity
Meral Erdemir Kiziltan1, Nurten Uzun, Feray Karaali Savrun
1Istanbul University Cerrahpasa Medical School, Department of Neurology, Istanbul-Turkey.
Abstract:
This study seeks to find an answer to whether the damage caused by the focal demyelinated focus in hemifacial spasm (HFS) causes a deviation from normal in MUP's. The study evaluated MUP parameters of orbicularis oculi (o.oc) and orbicularis oris (o.or) muscles in the total of 76 cases, 41 of whom had a history of peripheral facial paralysis (PFP) and postparalytic facial hyperactivity (PPFHA) and 35 of whom had HFS. Control data was obtained from healthy sides 22 of 76 cases. "t test" and multiple comparisons were used for statistical evaluations. For o.oc muscle; when compared with the normal group, PPFHA group had significantly increased motor unit durations (p < 0.001), phase (p < 0.05), area (p < 0.05), turn (p < 0.05) and polyphasic potential numbers (p < 0.05) and HFS group had significantly increased amplitudes (p < 0.05), area (p < 0.05) and polyphasic potential numbers (p < 0.05). When patients groups were compared for the same muscle, PPFHA group had significantly increased MUP durations (p < 0.001) and number of turns (p < 0.05) as compared to HFS group. When o.or muscle values were compared with the normal group, PPFHA group had significantly increased durations (p < 0.001), phase (p < 0.05), area (p < 0.05) and turn numbers (p < 0.001) and polyphasic potential rates (p < 0.05) and area/amplitude values (p < 0.05), HFS group had significantly increased durations (p < 0.05), phase (p < 0.05), area (p < 0.05) and turn numbers (p < 0.05). When patient groups were compared for the same muscle, MUP duration was significantly increased (p < 0.05) in the PPFHA group as compared to HFS group. In conclusion, with the quantitative method, there is neurogenic involvement in the facial muscles of upper and lower halves in cases of HFS although lesser than PFP cases. This suggests that focal demyelination causes secondary axonal loss at least in some of the cases.
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