Hemiplegic Gait and the Role of the Ankle-Foot Orthosis

Abstract

The goal of this paper is to gain insight into the stroke patient and the effect stroke has on gait. A general overview of stroke, normal gait, and hemiplegic gait will be reviewed. The effect that the ankle foot orthosis has on gait and variations in its design will be discussed as well.

Introduction

Cerebral Vascular Accident is a complicated injury that presents with many different deficits. Functions of the brain may be permanently or temporarily impaired depending upon the severity of the injury. Neuromuscular function impairment can result in a variety of different presentations and the effect on gait can be slight to severe. Hemiplegia, the paralysis of the side of the body opposite the lesion, and hemiparesis, weakness on the opposite side of the lesion, are symptoms of stroke (Sullivan, 335). The ankle foot orthosis (AFO) is commonly prescribed as a rehabilitation or permanent aid to assist the CVA patient with mobility. Orthotic design can be altered to best serve patients who present with different gait deviations.

Mechanisms of Stroke

Different mechanisms cause stroke. The three most common causes include thrombus, embolism, and hemorrhage secondary to aneurysm or developmental abnormalities (O'Sullivan 335). A thrombus is a clot in the cardiovascular system formed during life from constituents of blood (Stedman's, 1597). Cerebral thrombi lead to occlusion of an artery in the brain and tissue death results (Sullivan, 336). Embolism is a plug composed of a detached thrombus or vegetation, mass of bacteria, or other foreign body, occluding a vessel (Stedman's 501). Cerebral emboli are commonly associated with cardiovascular disease. Hemorrhage is the escape of blood through a ruptured or unruptured vessel wall. An aneurysm is the circumscribed dilation of an artery (Stedman's, 77). Intracerebral hemorrhage is a rupture of one of the brain vessels, which results with bleeding into the brain. Tissue death is a result of chemicals in the blood, increased pressure, or restriction of distal blood flow (O'Sullivan, 336). A common precursor to strokes is transient ischemic attack (TIA). TIA is a temporary interruption of blood flow to the brain. Symptoms of localized neurologic dysfunction may last a few minutes to a few hours. When the attack is over there is no evidence of permanent neurologic dysfunction. TIA's are clinically significant because 30 percent of major stroke victims experience TIA's prior to a major stroke (O'Sullivan 336).

Where the occlusion of blood flow occurs in the brain determines the clinical presentation. Sullivan discusses common presentations of occlusion of five different arteries. These arteries are the anterior cerebral, middle cerebral, posterior cerebral, internal carotid, and the vertebral basilar.

The anterior cerebral artery supplies blood to the medial aspects of the frontal and parietal lobes. The frontal lobe functions include initiating voluntary movement of skeletal muscle, analyzing sensory experiences, responses related to memory, emotions, reasoning, judgement, planning and verbal communication. The parietal lobe responds to stimuli from cutaneous and muscular receptors in the body (Van De Graaff, 326). Damage to these areas of the brain may result in contralateral hemiparesis and sensory loss, with greater involvement in the lower extremity than the upper extremity. Aphasia, dysfunction in linguistic communication, apraxia, the disorder of voluntary movement, and agraphia, the inability to write, are commonly attributed to anterior cerebral artery occlusion (O'Sullivan, 339). Occlusion of this artery is uncommon.

The middle cerebral artery is the most common sight of stroke. This artery supplies blood to the lateral aspect of the frontal and parietal lobes as well as the temporal lobe. The temporal lobes primary functions are involved with hearing (O'Sullivan, 329). Occlusion of the middle cerebral artery may result in drowsiness, contralateral hemiplegia, sensory loss of the face, arm and leg, deficits in vision, aphasia, and apraxia (O'Sullivan, 339).

The posterior cerebral artery supplies blood to the occipital lobe and the medial and inferior temporal lobes. The occipital lobes principal function concerns vision (Van DeGraaff, 329). Occlusion of this artery may result in contraleteral sensory loss, affecting mostly pain and temperature, and persistent contralateral pain from any sensory input. Vision disorders and movement disorders also present with posterior cerebral artery occlusion (O'Sullivan, 339).

Internal carotid artery occlusion produces symptoms similar to both anterior and middle cerebral artery occlusions (O'Sullivan, 339). Vertebral-Basilar artery occlusions generally produce loss of conciousness, brainstem and cranial nerve damage, and hemiplegia or quadriplgia with decerebrate posturing (O'Sullivan, 339). Decerebrate posturing is considered a coma like state.

Recovery, Spasticity, Synergy, and Sensory Impairment

Recovery from stroke follows a sequential series of events. Brunnstrom defined six general, sequential stages of recovery. A patient may achieve a full recovery, or plateau at any stage, depending on the severity of the stroke and the patient's adaptiveness (O'Sullivan, 343). Stage 1 is characterized as a period of flaccidity following the acute episode. No movement of the limbs can be elicited. Stage 2 presents with minimal voluntary movement and components of limb synergies may appear. Spasticity begins to develop. During Stage 3 of recovery the patient gains some voluntary control of movement synergies. Spasticity further develops and may become severe. Movement combinations not associated with either synergy pattern are mastered in Stage 4. Mastering these movements is initially difficult and progressively easier. Also, spasticity begins to decline at this stage. At Stage 5, the patient masters more difficult movement combinations and basic limb synergies become less apparent. Stage 6 of recovery presents with the disappearance of spasticity and coordination approaches normal (O'Sullivan, 343). Stroke patients tend to show the greatest amount of improvement in the first 6 weeks following the CVA and progress will plateau six to eight months post-acute injury (Atlas, 379).

Spasticity is described as the overreaction to stretch (Perry, 179). Spasticity occurs in approximately 90 percent of stroke patients, and the anti-gravity muscles are most commonly effected. In the lower extremity this group of muscles includes pelvic retractors, hip adductors and internal rotators, hip and knee extensors, plantar flexors, supinators and toe flexors (O'Sullivan, 343). Five functional deficits result from spasticity. 1) Selective control is impaired. 2) Primitive locomotor patterns appear. These include flexion and extension synergy patterns. 3) The timing of muscular contractions during gait are altered when compared to normal gait. 4) Proprioception becomes altered. 5) Muscular control becomes altered due to limb position and body alignment (Perry, 179).

Synergy patterns are stereotyped primitive movement patterns associated with the presence of spasticity (O'Sullivan, 343). The two synergies involved with each limb are flexion and extension synergies. These synergies are patterned volitional movements which consist of mass extension or flexion at the hip, knee and ankle simultaneously during movement (Atlas, 380). This loss of selective volitional control of the lower extremity impairs the gait of the stroke patient. Interestingly, the only muscle group of the lower extremity not associated with either synergy pattern are the ankle evertors. This makes this muscle group difficult to rehabilitate due to its non-association with a synergy pattern (O'Sullivan, 343).

Sensory impairment also is effected by stroke. In a study by Gamble, 43 percent of her experimental group had abnormal sensation. Of this 43 percent, 29 percent had gross loss, which was defined as loss of three or more of the following: light touch, heavy pressure, temperature, pain, vibration and proprioception (Gamble, 270). Perry states that proprioception loss obstructs gait because it prevents the patient from knowing the position of the hip, knee, ankle and foot in reference to the floor. This results in the patient being unaware of when the limb contacts the floor, making transfer of body weight unsafe (Perry, 175). To compensate for this deficit patients may hyperextend the knee with floor contact to emphasize initial contact. This also results in slow, cautious walking (Perry, 176).

Normal Gait

Dr. Jacquelin Perry, Chief of Pathokinesiology at Rancho Los Amigos Medical Center, is the sole source of information regarding gait in this research paper. She is responsible for developing the gait analysis laboratory at Rancho in 1968, and has been involved with research in this field since that time. Thanks to Dr. Perry, a systematic method of gait analysis has been developed to help the rest of us understand the complexities of gait.

In order to understand the deficits of hemiplegia, it is imperative to understand normal gait. The normal gait cycle is defined as a single sequence of events between two sequential initial contacts of the same limb (Perry, 497). Normal gait consists of two periods, stance and swing, which can be further broken down into eight phases. These are: 1) initial contact 2) loading response 3) mid-stance 4) terminal stance 5) pre-swing 6) initial swing 7) mid-swing 8) terminal swing. The sequential combination of these eight phases allows the limb to perform three vital tasks. These are weight acceptance, single limb support, and limb advancement (Perry, 10).

The first two phases, initial contact and loading response are the phases during which the task of weight acceptance occurs. For weight acceptance to occur, three functional patterns are needed. These are shock absorption, initial limb stability, and preservation of progression (Perry, 11). Initial contact occurs in the first 2% of the gait cycle. The posture of the joints at this time determine the limbs loading response pattern (Perry, 11). The objective of this phase is to position the limb with a heel rocker (Perry, 11). Loading response consists of the first 10% of the gait cycle. During this period both limbs are in contact with the floor. The objectives of this phase are shock absorption, weight bearing stability, and preservation of progression (Perry, 11).

The next two phases, mid stance and terminal stance, are the phases during which the task of single limb support occurs. During this interval, one limb is responsible for supporting the body. Mid stance occurs at 10-30% of the gait cycle. This phase is defined as the period in which the opposite foot is lifted and continues until body weight is aligned over the forefoot (Perry, 12). The objectives of this phase are progression over the stationary foot and limb, and trunk stability (Perry, 12). Terminal stance occurs at 30-50% of the gait cycle. During this phase single limb support is completed. It begins with heel rise and ends with double limb support. Throughout this phase body weight progresses over the forefoot (Perry, 12). The objective of this stage is progression of the body past the supporting foot (Perry, 12).

The next four phases, pre-swing, initial swing, mid-swing and terminal swing are the phase during which the task of limb advancement occurs. The limb assumes three postures during this period. It lifts itself, advances, and prepares for the next stance interval (Perry, 13). Pre-swing occurs at 50-60% of the gait cycle. Double limb support begins this phase and ipsilateral toe off completes it (Perry, 13). The objective of this phase is to prepare the limb for swing (Perry, 14). Initial swing occurs at 60-73% of the gait cycle. It begins when the foot lifts from the floor and ends when the foot is opposite the stance foot. The objectives of this phase are foot clearance of the floor and advancement of the limb from its trailing position (Perry, 14). Mid-swing occurs at 73- 87% of the gait cycle. This phase begins with the swinging limb opposite the stance limb and ends when the swinging limb is forward and the tibia is vertical (Perry, 15). The objectives of this phase are limb advancement and foot clearance of the floor (Perry, 15). Terminal swing occurs at 87- 100% of the gait cycle. This phase begins with the tibia vertical and ends with the foot striking the floor. The objectives of this phase are limb advancement and preparation for stance (Perry, 16).

Three forces act on joints. These are falling body weight, ligamentous tension and muscular activity (Perry, 24). Body weight is the dominant force acting on joints. Muscular activity is the response of the body to control the joint whose action is determined by body weight. During walking the effect of body weight is identified by the ground reaction force (GRF). As body weight falls to the ground an equal but opposite force counteracts it. GRF can be thought of as a vector that originates from the ground as an opposing force to body weight (Perry, 24). It is the relationship of this force to a joint that creates motion in a joint. Joints are inherently unstable because they are designed to move. For example, if the GRF is posterior to the ankle, the ankle will plantar flex. The ankle is a lever and if an upward directed force acts on the heel, the opposite end of the lever, the toes, will be directed downwards.

Ankle, Knee, and Hip Function during the Phases of Gait

Hemiplegia results in altered positions of the joints of the leg during the phases of gait. Joint position in normal walking provides functional positioning of the limb to provide shock absorption, bear weight, and advance the limb. To understand the effect altered joint angulation has on walking, it is important to understand the purpose of joint angulation in normal gait.

Initial Contact

The ankle is at a neutral 90 degrees position at initial contact. This prepares the limb for loading response by being in a position that allows for heel rocker (Perry, 61).

At initial contact the knee is extended because its function is to be stable for weight bearing. The ground reaction force anterior to the knee as well as muscle activity in the quadriceps produces a stable knee for initial contact (Perry, 100).

At initial contact the hip is flexed 30 degrees. This position is an inherently unstable one because the GRF is anterior to the hip, and forward momentum of the trunk naturally want to flex the hip. Hip extensor action and hamstrings are active at this moment to prevent further hip flexion (Perry122).

Loading Response

During loading response the ankle experiences 10 degrees of plantar flexion. At 2% of the gait cycle GRF is posterior to the ankle joint, forcing plantar flexion. The pretibial muscles decelerate the foot toward the floor, and the tibia is drawn forward. These actions contributes to limb progression as well as shock absorption (Perry, 62).

During loading response the knee flexes 15 degrees. This action provides shock absorption. As the ankle plantar flexes the GRF is posterior to the knee, creating this flexion moment. The quadriceps act eccentrically to control the extent of knee flexion (Perry, 100).

During initial loading response all five hip extensors, and hamstrings actively maintain hip stability. The hip progressively extends from its 30 degrees flexed position during mid-stance. As the limb progresses forward the GRF vector changes alignment posterior to the knee and close to the hip. Relative hip extension occurs as the heel rocker advances the tibia and femur and the quadriceps act to stabilize the knee. Hip extensor musculature ceases in response to this change in GRF since the joint is no longer inherently unstable (Perry, 123).

Mid Stance

During mid stance the ankle experiences 10-15 degrees of dorsiflexion. The GRF advances anterior to the joint due to the forward progression of body weight. Soleus muscle activity controls the rate of deceleration of the advancing tibia (Perry, 63).

During mid stance the knee is extending from its flexed position to increase its stability. Knee flexion is reduced by the action of the soleus slowing the progression of the tibia, and the faster forward progressing femur (Perry, 102). As the knee extends and the ankle dorsiflexes, body weight moves forward and the GRF moves from posterior to anterior of the knee joint, providing a knee extension moment.

During mid stance the hip progressively extends. Body weight progresses forward and the foot moves posterior in relationship to the hip. The GRF moves posterior to the hip, which provides an extension force.

Terminal Stance

The motion of the ankle at terminal stance is heel rise with continued ankle dorsiflexion. By the end of mid-stance the GRF lies in the forefoot. This makes the forefoot the sole support of body weight and it acts as a rocker to progress the limb (Perry, 64). Triceps surae have locked the ankle as dorsiflexion reaches its peak angulation. By the end of terminal stance the triceps surae musculature is free to planter flex the foot as the opposite limb is contacting the floor.

The knee reaches full extension during terminal stance. Three factors facilitate this action. Strong ankle plantar flexion provides a stable tibia over which the femur continues advancing (Perry, 103). The forefoot rocker facilitates forward fall of body weight over the leg. The GRF is anterior to the knee producing knee extension (Perry, 103). Restraint of the hip by the tensor fascia lata tenses the iliotibial band to produce some knee extension force (Perry, 103). By the end of terminal stance the knee starts to flex. The anterior position of the GRF, producing a stable knee, allows the triceps surae to fire to allow knee flexion. 5 degrees of knee flexion are obtained before the end of terminal stance (Perry, 103).

Hip hyperextension occurs during terminal stance. Body weight rolls over the forefoot rocker and the limb is now in a trailing position. The GRF is posterior to the hip. The thigh is pulled into extension, followed by hyperextension (Perry, 125).

Pre-swing

During pre-swing the opposing limb makes contact with the floor which assists with body balance and transfer of body weight (Perry, 66). Since the opposing limb is now responsible for body support, the ipsilateral limb is prepared to unload and advance. 20 degrees of ankle plantar flexion occurs during pre-swing. This functions to allow the knee to flex, as the GRF is now posterior to the knee.

Knee flexion during swing occurs due to three mechanisms. GRF advances anterior to the metatarsophalangeal joints removing the force that previously held the mid-foot close to the ground. Foot stability is lost and the tibia is free to roll forward. Triceps surae muscle action accelerates heel rise and tibial advancement. The gastrocnemius and popliteus also actively flex the knee. This results in 40 degrees of knee flexion, which prepares the limb for toe clearance and swing (Perry, 104).

Hip flexion occurs in pre-swing. The advancing tibia produces knee flexion, which also carries the thigh forward. Quadriceps muscle action to restrain the flexing knee also produces force to flex the hip (Perry, 125).

Initial Swing

The function of the ankle during initial swing is to clear the foot of the floor for limb advancement. At the moment of toe-off the foot is in 20 degrees of plantar flexion. This position does not impede forward progression because of the tibia's trailing position. For the tibia to advance it is necessary to raise the foot to avoid contact with the floor. The pretibial muscles activate and raise the foot to 5 degrees of plantar flexion by the time the swing foot is opposite the stance limb (Perry, 67).

Knee flexion during initial swing is necessary for the foot to clear the floor. The 15 degrees of dorsiflexion gained at the ankle alone is not enough for limb clearance because the foot is still maintained in an equinus position. Knee flexion angle of 60 degrees is necessary for foot clearance (Perry, 105).

The hip is actively flexing during initial swing. Momentum started in pre-swing continues into initial swing and the hip rapidly flexes 20 degrees in 0.1 seconds (Perry, 126). This synergy is desirable in aiding the knee to flex during initial swing.

Mid Swing

The ankle continues to dorsiflex during mid swing. As the tibia becomes neutral the weight of the foot creates a stronger downward torque. The pretibial muscles increase their muscle action in response to the increased force and the foot obtains a neutral position (Perry, 68).

The knee passively extends during mid-swing. This aids in advancing the limb and preparing it for initial contact (Perry, 106).

The hip flexes an additional 10 degrees during mid swing. This continues the advancement of the limb. This action can be considered passive as hip flexors action is absent or minimal (Perry, 127).

Terminal Swing

The ankle remains dorsiflexed and pretibial group muscle activity increases in preparation for initial contact.

The knee becomes fully extended. This action advances the limb and prepares it for initial contact.

During terminal swing hip flexion is ceased. This prepares the limb for stance. The hamstrings contract to decelerate the femur (Perry, 128).

Gait is a tri-planar activity. For the sake of simplicity, this review of joint motion covers analysis of the sagittal plane only. Sagittal plane devaitons with the stroke patient will be the most evident and perhaps the most detrimental to the gait cycle. The effectiveness of the AFO will be most evident in the sagittal plane.

Hemiplegic Gait

Hemiplegic gait can be characterized as slow and stiff with poorly coordinated movements of the affected limb, requiring compensatory actions by the unaffected limb (J Lehmann, 763). Lehmann found in his study that hemiplegic gait speed ranged from 8 to 55 meters/minute. That compared to 49 to 79 meters/minute in able bodied individuals of the same age (Lehmann, 766). Hemiplegic patients also showed an increase in asymmetry during gait when compared to their able bodied counterparts. Hemiplegic patients walked with a shorter stance and longer swing phase on their affected side. This may be explained by the fact that the instability of the affected limb prompts the patient to shift his weight to the unaffected side as early as possible. Perry states that this presentation can be attributed to impaired proprioception, and increased spasticity (Perry, 312). Patients may also depend on synergy patterns to advance the hemiplegic limb.

Proprioception impairment obstructs walking because the person does not know the position of the hip knee, ankle and foot in relation to the floor (Perry, 175). This results in the patient being unaware of when it is safe to transfer weight onto the effected limb. The patient walks slow and cautiously since they are unaware of the effected limb's position.

Spasticity leads to the loss of natural progression of the limb due to the unyielding eccentric muscle contraction. Plantar flexion and knee extensor spasticity are common characteristic of hemiplegic gait during stance.

Plantar flexion spasticity is the most common, and hence, the most influenced deformity effected by utilizing an AFO. The excessive muscle action of the soleus and gastrocnemius is a component of the extensor synergy pattern. The ankle becomes plantar flexed at terminal swing in preparation for initial contact. This position of the ankle will effect all of stance phase, and in some individuals swing phase as well.

Every individual that has suffered a stroke is going to present with different gait deviations. The following section will discuss the effect the plantar flexed foot has on phases of gait since this is the most detrimental deformity of hemiplegic gait.

Initial Contact

During initial contact two abnormal modes of floor contact may result. These are low heel contact and forefoot contact (Perry, 187). Low heel contact occurs when the ankle is in 15 degrees of plantar flexion and the knee is fully extended. The heel still makes initial contact with the floor, but the forefoot is almost parallel with the floor (Perry, 187). 15 degrees of plantar flexion is the most common angle of plantar flexion deformity because this is the position of minimal joint tension (Perry, 193). Forefoot contact results from the combination of ankle plantar flexion and knee flexion. 20 degree angulation at each joint is sufficient to place the forefoot lower than the heel for initial contact (Perry, 187).

Loading Response

Low heel contact reduces the heel rocker since the foot only travels through 10 degrees of arc rather than the normal 25 to 30 degrees. As a result the knee flexion thrust is reduced and progression of the limb is lost (Perry, 187).

Forefoot contact results in three different loading patterns. If ankle mobility is present, the heel will rapidly drop to the floor and the tibia will stay vertical. A rigid plantar flexed ankle can result in two results. First, the heel will not make contact with the floor. Secondly, the heel will make contact with the floor and the tibia will be driven backwards (Perry, 187).

The knee loses the 15 degree arc of motion normally occurring during loading response. Therefore, the limb loses the main shock absorption method of loading response as well as limb advancement.

Mid Stance

Excessive plantar flexion in mid stance inhibits tibial progression. If the ankle is limited to less than five degrees of motion by 30% of the gait cycle, the ankle rocker is loss (Perry, 188). Three characteristic substitutions are used to continue progression. These are premature heel off, knee hyperextension, and forward trunk lean.

Premature heel rise is the mechanism used by vigorous walkers with no other major disability (Perry, 188). The patient is able to advance their weight from the hindfoot to the forefoot. Heel rise now occurs in mid stance rather than terminal stance. The duration of foot flat is limited and a reduction in walking speed corresponds to this (Perry, 188).

Knee hyperextension occurs if ligamentous laxity is present. The knee hyperextends as the femur progresses forward over the posteriorly aligned tibia. This is commonly seen with the stroke patient.

Forward lean of the trunk with anterior tilt is a substitution used during mid stance. This method results less in progression of the limb as it does in helping maintain balance over the plantar flexed foot. This characteristic is seen with very slow walkers who are more disabled (Perry, 189).

Terminal Stance

The effects of excessive ankle plantar flexion on terminal stance phase depend on the patient's ability to roll onto the forefoot. If the patient cannot attain a heel rise, the advancement of the body is limited to the extent the knee can hyperextend, or trunk lean and hip rotation can improve the forward progression of the stance limb to the other limb (Perry, 190). As a result step length is shortened. If the patient can roll onto the forefoot they will appear to have a normal terminal stance. Heel rise will be excessive, but hard to notice (Perry, 190).

Initial Swing

Unless, the degree on ankle plantar flexion is extreme, the effect on initial swing is insignificant. The trailing position of the tibia minimizes the effect of excessive plantar flexion.

Mid Swing

Toe drag will present itself in mid swing if there is excessive plantar flexion. Swing of the limb is inhibited unless there is substitution by other muscle groups. Increased hip flexion lifts the limb, the knee flexes in response to gravity, and the toe will clear the floor. Increased knee flexion without hip flexion would actually increase toe drag. This happens because the tibia would be directed backwards and increases the foots equinus position (Perry191).

Perry identifies four patterns of dysfunction with the stroke patient. These are drop foot, dynamic varus (swing), stance equinus, and stiff knee gait (Perry, 312).

Drop Foot

The mildly effected stroke patient may present with a drop foot. Initial contact is made with the foot flat position. Some tibial advancement is loss due to the decreased heel rocker, but terminal stance and heel rise are appropriate (Perry, 314). Mid swing is the only phase where the disability is apparent. Some patients will be able to clear the foot by increasing hip flexion. A patient who cannot clear the foot suffers from hip flexion weakness.

Dynamic Varus (Swing)

The hemiplegic foot may display varying amounts of varus during gait. The cause is strong tibialis anterior action as part of the flexor synergy pattern, while the long toe extensors are inactive (Perry, 314). Initial contact is made with the lateral side of the foot. Loading response involves a rapid drop of the medial side of the foot into a safe weight bearing position. Tibialis anterior muscle action discontinues as extensor synergy patterns emerge. Triceps surae muscle action during mid stance inhibits ankle dorsiflexion and the forefoot rocker is lost. As a result, pre-swing knee flexion is also loss. During initial swing, the foot inverts. This signifies that the anterior tibialis is the dominant ankle dorsiflexor. Limited knee flexion results in toe drag (Perry, 316).

Stance Equinus

Equinus during stance eliminates shock absorbing knee flexion and inhibits progression of the limb (Perry, 317). Initial contact is made with the forefoot due to a plantar flexed ankle, and limited knee and hip flexion. During mid stance the knee hyperextends due to the loss of the heel and ankle rockers and the femur advancing over the vertical tibia. A short contralateral step occurs during pre-swing, indicating that the weight bearing limb can progress no further (Perry, 317). There is inadequate knee flexion due to the low heel rise and relatively neutral position of the ankle. The lack of ankle dorsiflexion and knee flexion, combined with the patients slow gait velocity, results in the inability to transfer the weight onto the forefoot (Perry, 319). The patient needs to transfer all his weight to the opposite limb to unlock the knee and advance the leg. During the initial swing the patient drags his toe due to inadequate knee and hip flexion. In mid swing the patient has adequate clearance of the foot from the floor. There is the minimal amount of flexion needed at the hip, knee, and ankle to accomplish this. The knee extends and the ankle plantar flexes during terminal swing to prepare the limb for stance. These actions exhibit dependence on the extensor synergy pattern for gait.

Stiff Knee Gait

This patient experiences genu recurvatum due to a rigidly plantar flexed foot. Initial contact is by the forefoot due to excessive ankle plantar flexion, a fully extended knee and limited hip flexion. During loading response heel contact is delayed due to the rigidly plantar flexed foot. The knee hyperextends to accomplish foot flat. During mid- stance the contralateral limb is unable to advance past the stance limb. The stance limb is relieved of knee hyperxtension since it is not bearing full body weight, but no knee flexion results to advance the limb. Since the stance limb is not trailing the contralateral limb during initial swing, there is no need for the large knee flexion arc. The patient needs sufficient hip and knee flexion to clear the plantar flexed foot of the floor. During mid swing the patient clears the foot of the floor by utilizing a lateral trunk lean. In terminal swing the patient regains full extension of the knee in preparation for initial contact.

Overall, hemiplegic gait can be characterized as being slower than normal gait. A study by Burdett et al, states their hemiplegic patient walked at 15% of normal speed. They also noted a 37% shorter stride length, and a 250% longer stride time (Burdett, 1202).

The Ankle Foot Orthosis

A common attribute to all of the hemiplegic gait patterns discussed is a plantar flexed foot. The Atlas of Orthotics lists four indications for use of an AFO for the stroke patient. These are, 1) inadequate dorsiflexion during midswing through terminal swing resulting in a problem with foot clearance. 2) Inadequate dorsiflexion to allow heel fist at initial contact. 3) Mediolateral ankle/foot instability during stance and swing phase. 4) Insufficient tibia control during stance (Atlas, 381). The AFO is effective at treating these symptoms of hemiplegic gait because it acts directly on the ankle joint and indirectly on the knee and hip.

Studies have shown that the AFO is effective at improving certain aspects of gait. Generally, the use of the AFO creates a more balanced and dynamic gait. It has been shown that patients wearing an AFO have longer relative single stance on the affected side and better swing symmetry (Hesse, 1860). Since there is longer single stance on the affected side, double limb support is decreased during the gait cycle. This phenomenon can be contributed to the patients increased confidence in bearing weight on the paretic limb. Lehmann states that patients are able to increase their self selected walking speed when wearing an AFO. Walking also is a more efficient activity with an AFO. Lehmann found that energy consumption per meter walked per kilogram body weight improved (Lehmann, 106 '93).

By simply addressing plantar flexion at the ankle the patient is able to achieve heel contact at initial contact. This may be the single most important effect of the AFO because this event begins the stance period of gait in the normal manner. Hesse noted a decrease in plantar flexor activity during initial contact (1855). The AFO may not only aid in control of plantar flexor spasticity, but extensor synergy as a whole.

The AFO helps control the knee during loading response by decreasing extension, and increasing the shock absorbing effect of knee flexion during loading response (Burdett, 1202). It is important to note that a patient must have adequate quadriceps strength to stabilize the knee flexion caused by the AFO. Hesse noted increased quadriceps activity during loading response and midstance in his hemiplegic patients while wearing an AFO compared to gait without the AFO (1855).

Hesse notes a decrease in tibialis anterior activity during initial swing. He states that this decrease in muscle activity may suppress the flexor synergy. It also aids in controlling inversion of the foot during swing. This results in a foot being better aligned for weight acceptance during initial contact and reduces the risk of ankle sprain (Hesse, 1856).

Swing symmetry also improved with use of the AFO (Hesse, 1860). This may be a result of increased hip and knee flexion as well as a decreased amount of plantar flexion at the ankle.

AFO Design

AFO design can vary markedly. Variations in orthotic designs amongst different orthotic laboratories are common. Although each laboratory will apply the same principles to the fabrication of orthotics, different materials and techniques of fabrication are widespread.

A more traditional design is the conventional double adjustable ankle joint AFO. This design includes two metal uprights connected to a leather calf band proximally. Distally a metal stirrup is connected to a shoe and this is connected to adjustable joints that are riveted to the double uprights. Advantages to this design are that the joints can be adjusted to provide free range of motion, dorsiflexion or plantar flexion stops, or dorsiflexion or plantar flexion assist (Atlas, 384). Since this design contacts less skin than a polymer AFO, it is cooler to wear. Disadvantages are cosmesis, and the patient is limited to wearing one style of shoe. Since it is not a total contact device it is harder to control a deformity such as calcaneal varus. A leather strap, called a t-strap can be incorporated to help control deformity (Atlas, 386). This strap is riveted to the shoe, which the AFO is constructed on. The strap wraps around the patient's ankle and applies a resistive force against the deformity. This design, although still present, is not commonly used in the United States. In societies where high temperature thermoplastics are less readily available, the double adjustable ankle joint AFO may be more common place.

The most common AFO design used in the United States currently is the polymer AFO. This style of orthosis is lighter, more cosmetic, and can be worn with a variety of shoes when compared to the conventional AFO design. Polymer AFOs are total contact systems. The benefit to total contact is that deformities of the leg can be better controlled because the force is dispersed over a greater surface area. To prevent skin breakdown and increase control, variations in padding and strapping are included in the design. These are constructed from polypropylene or a similar high temperature thermo-formable polymer. Two subcategories of polymer AFO's are solid ankle, and articulated. Solid ankle AFO's incorporate variations in rigidity by varying the trim line of the plastic. For example, an anterior trim line design AFO would have plastic extending anterior to the malleoli of the patient's leg. A posterior trim line would have plastic trimmed behind the malleoli. These two variations in design would present with different resistance to force in all three planes. The anterior trim line AFO will resist motion greater in the sagittal, coronal, and transverse plane than the posterior trim line. A patient who presents with an equinovarus deformity will be better served by an anterior trim line AFO because the design will offer greater resistance against the deformity. A patient with a drop foot deformity will be better served with a posterior trim line because this design will provide resistance against unwanted plantar flexion during swing phase, yet is flexible enough to bend during stance.

Articulating AFOs incorporate joints into their structure. A wide variety of joints are available on the market today. Most are applied to the cast before the plastic is thermoformed over the cast. Other designs allow a joint to be added to the plastic after the orthosis has been thermoformed. Each style has benefits and disadvantages and each orthotists weighs these options prior to choosing a design for a patient. Some styles of joints provide greater rigidity to the overall structure, and some are more flexible. The advantage to articulated polymer AFOs is that motions of the ankle may be controlled in a manner similar to the double adjustable ankle joint used in the conventional system. Another advantage to articulated AFOs is that deformity may be controlled with a total contact articulating design.

In conclusion, cerebral vascular accident is a complicated medical condition that effects a person's cognitive and neuromuscular control. The CVA patient may have slight to severe dysfunction. Restoring a patient's ability to walk independently plays an important part in the rehabilitation process of the whole patient. The Ankle Foot Orthosis may play a key role in this rehabilitation process and should be considered an integral part of restoring patient's lives.

Works Cited

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