The most widely accepted diagnostic tool used to evaluate patients with MS is Kurtzke’s Expanded Disability Status Scale, or EDSS.¹,² The EDSS evaluates the severity of impairment due to MS using a 10-point scale ranging from 0, the least severe cases of MS, to 10, death resulting from MS.² Steps 1.0 through 4.5 refer to patients who are ambulatory without the use of a walking aid. The precise steps within this range are determined by a subscale called the Functional System (FS) score, which include pyramidal (motor function), cerebellar, brainstem, sensory, bowel and bladder, visual, cerebral or mental, and other functions. The FS subscale ranges from 0 to 5 or 6. An EDSS score between 1.0 and 4.5 should not change by 1.0 step unless there is also a change in the same direction in at least one FS.³ A patient’s ability to walk plays a critical role in determining the EDSS score because the difference between grades 4.0 through 6.0 are assigned based on how far a patient can walk without ambulatory assistance, with the differences between 4.0, 4.5, 5.0, and 5.5 being the ability to walk 500, 300, 200, or 100 m, respectively.³,⁴ Patients with an EDSS score between 1.0 and 6.5 stand to gain the most from orthopedic interventions to improve balance and mobility.

About 84% of patients with MS are affected by spasticity, a disabling symptom of MS associated with reduced mobility, painful spasms, and sleep disturbances.⁵ The Modified Ashworth Scale (MAS) measures muscle resistance during passive movement. Resistance is scored on a six-point scale (0, 1, 1+, 2, 3, 4), where 0 indicates no increased resistance and 4 indicates rigid flexion or extension.⁶,⁷ The MAS is the preferred measure of spasticity because of its clinical interrater consistency. Knowledge of a patient’s level of spasticity can help clinicians determine a treatment plan. The key to successful spasticity management is striking a balance between the beneficial and negative aspects of treatment, specifically with pharmacological interventions.⁸

Another method of monitoring the disability status of patients with MS is the 25-Foot Walk (T25FW), a test of maximum walking speed on a short distance. When compared with other clinical measurements of ambulation, the results of the T25FW correlated strongly with those of the EDSS.⁹ The T25FW is among the most commonly used standardized measurements of MS patient walking ability due to the ease of administration.

Spinal somatosensory conduction and central integration within the brain are closely related in coordinating balance and movement. Each of these is affected in individuals with MS.²⁵,²⁹,³⁰ Lesions in the dorsal column of the spinal cord are responsible for slowed somatosensory conduction. Regarding lower extremity motor control, slowed somatosensory conduction within the spinal cord results in the delayed transmission of proprioceptive information from the lower extremity to the brain. Consequently,
the brain is given less time to integrate proprioceptive information and produce an appropriate motor response. In a study assessing somatosensory conduction, individuals with MS exhibited delayed somatosensory evoked potentials within the cerebellum in response to an external stimulus perturbing balance in comparison with healthy controls. This was shown to result in larger postural response latencies as well as exacerbated and asymmetric movement scaling during compensatory movements.²⁹ Slower postural response latencies have also been correlated with poorer measures of balance, such as increased postural sway.³¹ Additionally, the degree of MS lesions in the dorsal column has been correlated with poorer measures of sensation.³²

Individuals with MS have been shown to recruit alternative neural circuitry in additional regions of the cerebellar and cerebral cortices for postural motor learning and rely more heavily on feed-forward control for balance involving other senses.²⁸,³³ This is supported by the findings that individuals with MS may require higher cognitive demands during ambulation. This is evidenced by the observations that they perform poorly on dual tasks involving motion than healthy controls³⁴,³⁵ and that individuals with MS rely more heavily on sight for balance than healthy controls.³⁶,³⁷,³⁸,³⁹ It is hypothesized that this is an adaptation to allow more proactive maintenance of balance to correct for impaired movement compensation ability stemming from corticocerebellar conduction impairment.³³ Owing to the reliance on proactive balance management, individuals with MS exhibit a more cautious gait pattern to avoid positions of instability and reduce the necessity of compensatory postural adjustments.

Impaired proprioception receptors within the foot and ankle of individuals with MS contribute to a deficit in sensory information available to coordinate body position and maintain balance. Muscle spindles and other mechanoreceptors around the ankle joint are of particular importance for reducing body sway while standing and for maintaining overall balance.⁴⁰ In MS, lack of dorsiflexion with a limited range of motion at the ankle joint from spasticity and muscle weakness reduces the amount of proprioceptive information provided from the ankle.³⁵,⁴¹,⁴²,⁴³ Individuals with MS therefore often compensate for reduced ankle mobility by increasing motion at the hip.⁴²,⁴⁴ Additionally, mechanoreceptor sensitivity along the plantar surface of the foot, particularly beneath the heel and first metatarsal head, is often reduced in MS. Individuals with MS have been shown to score significantly worse on two-point discrimination tests along the plantar surface of the foot, indicating decreased light touch sensitivity, and degree of sensitivity has been correlated with balance performance and EDSS score.⁴⁵ It is unclear, however, if this lack of sensitivity is reflective of truly impaired peripheral sensation or impaired relay of sensory information via the spinal cord.³² Regardless, because plantar surface mechanoreceptors provide important proprioceptive information,
abnormal sensation also likely contributes to sensorimotor dysfunction via decreased proprioceptive information from the lower extremity. Thus, not only is proprioception information delayed via slowed somatosensory conduction, but it is also often incomplete owing to deficits in peripheral proprioceptive sensation.

Impaired muscle control and spasticity in patients with MS stem from acquired imbalances between the intrinsic and extrinsic muscles of the foot due to the varying degrees of inflammatory involvement, progressive nerve demyelination, axonal disruption, interruption of efferent nerve conduction, and decreased inhibitory interneuron modulation. With disease progression, spasticity can lead to contractures, starting first with extensor spasms then later affecting flexor tone.⁴⁶,⁴⁷ From these dynamic muscle imbalances comes the influence of equinus as a primary deforming force and its various compensations. Equinus is when the foot is in a more plantarflexed position (in relation to the lower leg) with limited ankle dorsiflexion and the subtalar joint in a neutral position.⁴⁸ Although contractures and deformities tend to occur later on in the disease progression, the most common site for contracture in patients with MS was noted to be at the ankle joint.⁴⁹ The ankle joint is a prime sagittal plane dominant joint (e.g., dorsiflexion/plantarflexion) of the distal extremity and is most capable of compensating for sagittal plane forces (e.g., equinus). When paired with an extended double support time as seen in MS,⁵⁰ equinus with spasticity and/or contracture affects the forefoot and medial aspects of the foot by increasing average ground reaction forces during mid to late stance and uncoupling the opposite “swing limb” during the swing phase of gait.¹⁰,¹⁸,⁵¹ The degree of these imbalances is often determined by the level, extent, and areas of brain and spinal cord involvement. For example, lesions in the pyramidal tracts can cause varied weakness and spasticity, whereas lesions in the dorsal columns and cerebellar lesions can cause varied loss of coordination and proprioception (e.g., ataxia and postural sway).¹ Owing to the fact that the possible pedal deformities found in MS assume a more rigid or contracted attitude over time, stressing supination or mass flexion/adduction toward the midline of the body, the foot is never allowed to properly transition to an effective “mobile adaptor” during midstance to “accept” the ground and effectively. The combination of spasticity and/or contractures, equinus, postural balance/proprioceptive discoordination, and increased shearing ground reaction forces (especially vertical and horizontal/linear) creates an environment that is both destructive and kinesthetically inefficient to the maintenance of proper joint mechanics and bipedal ambulation in an already compromised individual.

Instability caused by the aforementioned factors results in overall movement impairment and a constant effort to remain balanced through compensatory movements. These strategies are generally aimed at better controlling the body’s center of mass (COM) during gait, avoiding positions of instability imposed by motion, and allowing additional time for integration of sensory information and execution of compensatory movements. As the disease progresses, these compensatory strategies become increasingly noticeable clinically and contribute to decreased quality of life. However, even if there appears to be an absence of disability upon clinical presentation, motion analysis tools can be used to detect minute gait abnormalities in MS patients, leading to a more precise EDSS score.²,⁵² Beyond disease progression, movement impairment has also been shown to correlate with increased incidence of falls and subsequent fear of falling in MS. Therefore, patients who have a history of falls in MS often exhibit more cautious movement strategies.¹⁶,¹⁷,²¹,²⁵

There are several general alterations in gait that are commonly employed by patients with MS. These alterations are characterized by decreased walking velocity, shorter stride length, and wider step width. Additionally, individuals with MS exhibit a higher proportion of time in the double stance phase of gait, in which both feet are in contact with the ground. These alterations can be noticed clinically at later stages of disease progression and can also be detected in the absence of clinical disability through motion analysis tools. As the disease progresses, gait often becomes more variable owing to increasing difficulty controlling the body’s COM within the region of stability.⁵³,⁵⁴ The sum of these general alterations serves three purposes: (1) to allow increased time for somatosensory integration and planning of an appropriate response to maintain balance; (2) to control the COM within the margins of stability of the body and avoid unnecessary positions of imbalance; (3) to limit energy expenditure on compensation and therefore limit fatigue.