1st Joint ESMAC-GCMAS Meeting - Análise de Marcha
1st Joint ESMAC-GCMAS Meeting - Análise de Marcha
1st Joint ESMAC-GCMAS Meeting - Análise de Marcha
Create successful ePaper yourself
Turn your PDF publications into a flip-book with our unique Google optimized e-Paper software.
O-46<br />
ABNORMAL EMG-ACTIVITY IN PATHOLOGICAL GAIT IN PATIENTS<br />
WITHOUT NEUROLOGICAL DISEASES<br />
Brunner Reinald (Prof), Romkes Jacqueline (M.Sc.)<br />
Laboratory for Gait Analysis, Children’s University Hospital, Basel, Switzerland<br />
Summary/conclusion<br />
The abnormal electromyographic (EMG) activity during gait seen in patients with cerebral<br />
palsy (CP) was also found in orthopaedic patients without neurological involvement. The<br />
abnormal EMG activity correlated best with muscle weakness. Weakness is a well recognised<br />
problem in patients with CP, too. The results of this study suggest that muscle weakness may<br />
be more important than spasticity to explain the pathological gait pattern, even in patients with<br />
spasticity.<br />
Introduction<br />
Abnormal muscle activity in patients with CP during gait is commonly taken as of spastic<br />
origin. Mimicking the individual gait pattern of a given patient with hemiplegic CP, however,<br />
produced similar EMG abnormalities in normals [1]. This study investigates the inci<strong>de</strong>nce and<br />
possible causes of abnormal EMG patterns in patients without neurological diseases.<br />
Statement of clinical significance<br />
In patients without neurological disease, abnormal muscle activity is either an indicator for a<br />
compensation strategy or a physiological variety. If the pattern found in CP is found in<br />
neurologically normals as well, the question of the origin of this pattern in CP rises. This study<br />
contributes to the un<strong>de</strong>rstanding of gait in CP.<br />
Methods<br />
All patients (n=39) without any neurological disease who were referred to the gait laboratory<br />
between January 2003 and March 2005 were inclu<strong>de</strong>d in this study. The primary pathologies<br />
varied wi<strong>de</strong>ly (club feet, ACL-ruptures, Perthes disease, ECF, unclear pain syndromes and<br />
more). Since January 2003 the routine of assessment in the gait laboratory was unchanged: the<br />
clinical examination of the lower extremities comprised of a test of range of motion (RoM)<br />
including all lengths of bi-articular muscles, a manual testing of muscle strength, and an<br />
assessment of spasticity (modified Ashworth scale). Instrumented gait analysis was performed<br />
(VICON 460, 2 Kistler force plates) including surface EMG of gastrocnemius medialis, tibialis<br />
anterior, rectus femoris, and semitendinosus bilaterally. Two data sets were exclu<strong>de</strong>d for<br />
artefacts. Raw EMG was analysed for abnormal activity. Any EMG activity duration<br />
prolonged more than half of maximal activity out of the normal range [2] was consi<strong>de</strong>red<br />
(figure 1: grey areas):<br />
A) Plantar flexor hyperactivity (gastrocnemius medialis, figure 1a): Too early onset of<br />
activation in terminal swing or at latest at initial contact in continuation till foot contact,<br />
prolonged activity in stance, usually accompanied by a shut off of the tibialis anterior muscle.<br />
B) Knee extensor hyperactivity (rectus femoris, figure 1b): Activity at mid-stance or later in<br />
stance.<br />
C) Hip extensor hyperactivity (semitendinosus, figure 1c): Hamstring activity reaching or<br />
exceeding mid-stance.<br />
- 160 -