Clinical Gait Analysis and Its Role in Treatment Decision-Making

Roy B. Davis, III, PhD, Sylvia Õunpuu, MSc, Peter A. DeLuca, MD, Mark J. Romness, MD

Disclosures

August 14, 2002

II. Indications of the Associated Muscle Activity

Although dynamic EMG has its limitations (ie, the amplitude information is limited unless directly related to a known force[11]), this technique is the only way to determine if a particular muscle is active during gait.[12] One can usually predict that a group of muscles is active, such as the knee extensors in a patient in crouch. However, the entire muscle group may not be active. In the majority of patients with cerebral palsy, the rectus femoris is active in mid swing and during the Duncan Ely test, but the vastus medialis and lateralis are not.[9] Similarly, in order to determine the cause of hind foot varus, all the potential contributors need to be assessed.[1] An examination of EMG data in conjunction with the joint kinetics can also provide more information about the cause of internal joint moments.

Determining Posterior Tibialis Activity During Gait

One common problem in cerebral palsy of the spastic hemiplegia type is varus deformity of the hind foot. Intramuscular (fine-wire) EMG helps determine the possible role of the tibialis posterior muscle in producing this deformity.

Video 6 depicts three children with a diagnosis of cerebral palsy with equinovarus deformities during gait. In all three patients, hind foot varus is noted throughout the gait cycle and in relaxed standing, the hind foot corrects to neutral. Clinical evaluation is similar in these patients, with spasticity of the tibialis posterior noted in all three cases, but with no fixed deformity of the hind foot. Hip flexion resulted in simultaneous dorsiflexion of the ankle with the forefoot in a supinated position. The passive ankle motion and dorsiflexion strength for the three patients are listed in Table 1 .

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Video 6. Close-up back views of the foot, ankle and shank for Patient 1, Patient 2 and Patient 3. In all patients, the hind foot is in varus during gait. Patient 1 has the most significant toe walking, followed by Patient 2 and then Patient 3.

The three patients underwent fine-wire EMG analysis to determine the function of the tibialis posterior and tibialis anterior in gait and during specific motor tasks ( Table 2 ). Although each patient had hind foot varus in gait and less than normal dorsiflexion in stance (less so in Patient 3), fine-wire EMG data (Figure 11) reveal three very different patterns of activity for both of these muscles in each patient.

Fine-wire EMG data in raw format for the tibialis posterior and tibialis anterior for four strides for: a) Patient 1, b) Patient 2 and c) Patient 3 (all shown in Video 6). Three distinct firing patterns for the posterior tibialis are illustrated; premature onset in swing (Patient 1), negligible activity (Patient 2) and continuous activity (Patient 3). Normal firing patterns are indicated by blue bars above each signal.

The gastrocnemius muscle is continuously active throughout the gait cycle in all three patients. The visual impression during gait implicates the tibialis posterior as responsible for the equinovarus deformity. However, in Patient 2, the varus position of the hind foot may be a result of the equinus alone, and not the tibialis posterior. In Patient 1, the tibialis posterior is implicated as contributing to poor pre-positioning of the hind foot in varus for initial contact in terminal swing. In Patient 3, the tibialis posterior also appears to contribute to a pre-positioning problem for the foot at initial contact, and the tibialis anterior contributes to the lateral weight-bearing position of the foot in stance. Patient 3, however, shows the least deformity and the most significant tibialis posterior activity of the three patients. The inconsistency of the EMG findings for relatively similar clinical (visual) presentations emphasizes the important role of EMG as an adjunct to visual gait analysis for determining the possible contribution of the various muscles in producing deformity.

Understanding Foot-Ankle Deformity Post Trauma

The treatment of a dynamic foot deformity requires knowledge of not only the abnormal motion, but the activity patterns of the agonistic and antagonistic muscles that contribute to the motion as well. For example, drop foot can be a result of absolute weakness of the ankle dorsiflexors or relative weakness due to the co-contraction of the antagonistic ankle plantar flexors.

Video 7 depicts a 25-year-old female with a mild left forefoot inversion-supination and drop foot problem in mid swing. This is due to multiple left lower extremity injuries, including an open fracture of the femur and laceration of the popliteal artery and peroneal nerve. Clinical evaluation reveals no fixed deformity of the ankle with normal length for the left plantar flexors and normal muscle control with selected muscle weakness (3.5/5 ankle dorsiflexion, 1/5 toe extension, 4/5 ankle plantar flexion, 5/5 toe flexion, 5/5 forefoot inversion and 0/5 forefoot eversion).

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Video 7. Close-up front view of the foot, ankle and shank of a 25-year-old female three years post lower extremity trauma including open femoral fracture, femoral artery and peroneal nerve laceration. The forefoot is in supination in early swing through initial contact and in a normal position in stance. There is a drop foot in swing.

Electromyography reveals some interesting findings during gait (Figure 12) and in specific voluntary motions of the ankle that would not have otherwise been appreciated. During voluntary plantar flexion, there is simultaneous activity of the tibialis anterior, a finding not typical in normal function. During voluntary dorsiflexion, there is activity of the tibialis anterior only, as expected. During gait, there is continuous activity of the tibialis anterior in stance as well as swing, again a finding not typical of normal function. Fine-wire monitoring of the tibialis posterior also revealed that this muscle is not contributing to the foot deformity in swing. Also, the normal activation pattern of the gastrocnemius in stance with no antagonistic activity in swing does not implicate this muscle as a contributor to the drop foot. The abnormal activation of the anterior tibialis during both voluntary activity and in gait suggests abnormal nerve healing after the trauma. These data indicate that the primary cause of the drop foot is weakness in the tibialis anterior and toe extensors and the primary cause of forefoot supination is a relative strength imbalance in swing between the tibialis anterior and toe extensors.

Surface and fine-wire EMG data in raw format for the tibialis posterior, tibialis anterior and gastrocnemius for the left side of a patient three years post left open femoral fracture and femoral artery and peroneal nerve laceration (Video 7). The posterior tibialis shows a biphasic pattern in stance and variable to no firing in swing. The anterior tibialis is on continuously throughout the gait cycle. The gastrocnemius shows normal function.

Summary

Without understanding the potential causes of the deforming forces and associated abnormal motion, treatment decision-making can be, at best, an educated guess. Electromyographic data can provide information about possible contributors to the abnormal motion. These data, in combination with joint motion and kinetics, can help determine if deforming forces are associated with the abnormal EMG.

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