General Session: Cervical Degenerative - Hall F

Presented by: J. Cox

Author(s):

R. Haddas(1), J. Cox(1), R. Arakal(2), T. Belanger(3), S. Hochschuler(2), A. Boah(4), K. Ju(3)

(1) Texas Back Institute, Research Foundation, Plano, TX, United States
(2) Texas Back Institute, Plano, TX, United States
(3) Texas Back Institute, Rockwall, TX, United States
(4) Texas Back Institute, Denton, TX, United States

Abstract

Background: Cervical Spondylotic Myelopathy (CSM) is a degenerative condition of the cervical spine leading to a spectrum of neurological dysfunction. Gait impairment is one hallmark of CSM and has been shown to affect quality of life and ability to work. Currently, the gait disturbance in CSM is poorly understood. Some studies described the gait as spastic, while others suggest a paretic component. One study has shown impaired electromyographic (EMG) amplitude and the need for proximal muscle co-activation in patients with CSM. Further EMG characterization of the gait cycle may help elucidate the true neuromuscular pathology with implications on patient prognosis and rehabilitation techniques.

Purpose: The purpose of this study was to compare spine and lower extremity neuromuscular activity in patients with CSM prior to surgical intervention to healthy age-matched controls.

Study Design: A non-randomized, prospective, concurrent control cohort study.

Patient Sample: Twenty-five patients with symptomatic CSM who have been deemed appropriate surgical candidates along with 25 healthy controls.

Outcome Measures: Spine and lower extremity of integrated electromyography (iEMG) and max root mean square (RMS) EMG. iEMG activity is a graphic representation of the sum total EMG activity over a defined period of time.

Methods: Clinical gait analysis was performed the week before surgery. External Oblique (EO), Multifidus (Mf) at the level of L5, Erector Spinae (ES) at the level of L1, Gluteus Maximus (GM), Rectus Femoris (RF), Semitendinosus (ST), Tibialis Anterior (TA), and Medial Gastrocnemius (MG) neuromuscular activity were measured and recorded during the gait analysis session. Each subject performed a series of over-ground gait trials at a comfortable self-selected speed. One-way ANOVA analysis was used to determine differences on neuromuscular control in gait patterns in CSM patients compared to healthy controls.

Results: Compared to controls, patients with CSM demonstrated significantly less activation of the EO (2.09±13.5 vs 0.07±0.8 mV; p=0.049), GM (2.6±3.7 vs 0.09±0.1 mV; p=0.038), and MG (8.70±8.1 vs 4.15±6.8 mV; p=0.047). There was significantly higher muscle activation of the Mf in patients with CSM compared to controls (7.40±2.1 vs 3.40±0.04 mV; p=0.050). Peak EMG muscle activity was significantly lower in the EO (0.02±0.01 vs 0.03±0.01 mV; p=0.040), GM (0.03±0.01 vs 0.12±0.3; p=0.050), and Mf (0.45±1.1 vs 0.12±0.1 mV; p=0.048) of patients with CSM compared to healthy controls. Patients with CSM also had a significantly higher peak muscle activation of the Mf compared to controls (0.45±1.1 vs 0.12±0.1; p=0.048).

Conclusions: Patients with CSM often present with a gait disturbance that is poorly understood and has a significant impact on patients' morbidity and mortality. The results of this study demonstrate higher resting baseline EMG in multiple muscles with poor peak amplitude during recruitment of these muscles. Over-activation of the multifidus was also demonstrated. The results of this study suggest recruitment of the multifidus to counteract poor control of proximal muscles in an effort to keep the patient erect with a horizontal gaze. In addition to our findings, this study contributes to existing knowledge on muscle activity in patients with untreated CSM and will be useful in future studies investigating neuromuscular function of patients with CSM after surgical intervention.