1 NEUROMOTOR FUNCTION FOLLOWING WHOLE BODY VIBRATION IN INDIVIDUALS WITH CHR ONIC ANKLE INSTABILI TY By DANA M. OTZEL A DISSERTATION PRESENTED TO THE GRADUATE SCHOOL OF THE UNIVERSITY OF FLORIDA IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF DOCTOR OF PHILOSOPHY UNIVERSITY OF FLORIDA 2012
2 2012 Dana Marie Otzel
3 To my parents, I would not have been able to pursue this work without their support
4 ACKNOWLEDGMENTS I thank my pa rents for their never ending love and support as I pursue d a doctorate degree I thank Dr. Mark Tillman for his continued support and mentorship during my academic development. I also thank my committee members, Dr. Chris Hass, Dr. Mark Bishop, Dr. Erik Wi kstrom and Dr. Paul Borsa for their patience and feedback. I thank Curtis Weldon for his contribution to the set up and design of a program to enable the Hoffman n r eflex testing. A special thanks to Ryan Roemmich for contributing a program to analyze the H offman n reflex data. Finally, I would like to thank Hector and my friends for their encouragement and understanding throughout my time as a student.
5 TABLE OF CONTENTS page ACKNOWLEDGMENTS ................................ ................................ ................................ .. 4 LIST OF TABLES ................................ ................................ ................................ ............ 7 LIST OF FIGURES ................................ ................................ ................................ .......... 8 LIST OF ABBREVIATIONS ................................ ................................ ........................... 10 ABSTRACT ................................ ................................ ................................ ................... 11 CHAPTER 1 INTRODUCTION ................................ ................................ ................................ .... 13 2 LITERATURE REVIEW ................................ ................................ .......................... 16 Classification of Chronic Ankle Instability ................................ ................................ 16 Ankle Pathoanatomy/Neuroanatomy ................................ ................................ ...... 17 Ankle Sprain Patho mechanics ................................ ................................ ................ 20 Abnormal Ankle Mechanics Post Injury ................................ ................................ .. 22 Sensorimotor System Deficits ................................ ................................ ................. 24 Arthrogenic Muscle Inhibition and the Hoffmann Reflex ................................ ......... 34 Whole Body Vibration ................................ ................................ ............................. 39 Purpose ................................ ................................ ................................ .................. 43 3 METHODS ................................ ................................ ................................ .............. 48 Participants ................................ ................................ ................................ ............. 48 Instrumentation ................................ ................................ ................................ ....... 49 Hoffmann Reflex ................................ ................................ ............................... 49 Joint Position Sense ................................ ................................ ......................... 49 Whole Body Vibration ................................ ................................ ....................... 50 Procedures ................................ ................................ ................................ ............. 50 H reflex Testing ................................ ................................ ................................ 50 Joint Position Sense ................................ ................................ ......................... 51 Whole Body Vibration Training ................................ ................................ ......... 52 Data Analysis ................................ ................................ ................................ .......... 53 4 RESULTS ................................ ................................ ................................ ............... 62 Participants ................................ ................................ ................................ ............. 62 Neuromotor Function ................................ ................................ .............................. 62 H reflex ................................ ................................ ................................ ............. 62 JPS ................................ ................................ ................................ ................... 63
6 Absolute Error ................................ ................................ ............................ 63 Constant Error ................................ ................................ ............................ 63 5 DIS CUSSION ................................ ................................ ................................ ......... 97 Arthrogenic Muscle Inhibition ................................ ................................ .................. 97 Whole body Vibration ................................ ................................ ............................ 102 Proprioception ................................ ................................ ................................ ....... 108 Limitations ................................ ................................ ................................ ............. 113 Conclusion ................................ ................................ ................................ ............ 115 APPENDIX A FOOT AND ANKLE DISABILITY INDEX ................................ .............................. 116 Foot and Ankle Disability Index ................................ ................................ ............. 116 Foot and Ankle Disability Index Sport ................................ ................................ ... 117 B PHYSICAL ACTIVITY AND DIETARY RECALL QUESTIONNAIRE .................... 118 LIST OF REFERENCES ................................ ................................ ............................. 119 BIOGRAPHICAL SKETCH ................................ ................................ .......................... 135
7 LIST OF TABLES Table page 4 1 H:M ratio ANOVA results ................................ ................................ .................... 65 4 2 Mean (+SD) H:M Ratio ................................ ................................ ....................... 72 4 3 ANOVA results for JPS AE at 15 inversion ................................ ....................... 73 4 4 ANOVA results for JPS AE at 20 inversion ................................ ....................... 74 4 5 Mean (+SD) JPS AE at 15 and 20 ................................ ................................ ... 84 4 6 ANOVA results for JPS CE at 15 inversion ................................ ....................... 85 4 7 ANOVA results for JPS CE at 20 inversion ................................ ....................... 86 4 8 Mean (+SD) JPS CE at 15 and 20 ................................ ................................ ... 96
8 LIS T OF FIGURES Figure page 2 1 The talocrural axis of rotation. ................................ ................................ ............ 45 2 2 The subtalar axis of rotation. ................................ ................................ .............. 46 2 3 H reflex and M wave response following a single im pulse. ............................... 47 3 1 H reflex experimental set up ................................ ................................ ............... 55 3 2 Whole body vibration platforms ................................ ................................ ......... 56 3 3 Time line of laboratory visits. ................................ ................................ .............. 57 3 4 H reflex testing po sitio n. ................................ ................................ ..................... 58 3 5 Participant set up for joint position sense. ................................ .......................... 59 3 6 Participant positioning on the Power P ................................ .................... 60 3 7 Participant positioning on the Ju ................................ ............................. 61 4 1 Mean H:M ratio means between groups ................................ ............................. 66 4 2 Mean H:M ratios by condition. ................................ ................................ ............ 67 4 3 Mean H:M ratios by time. ................................ ................................ .................... 68 4 4 Mean H:M ratios for each condition across time ................................ ................ 69 4 5 Mean H:M ratio by group and condition. ................................ ............................. 70 4 6 Mean H:M ratios by group and time. ................................ ................................ ... 71 4 7 JPS AE mean values at 15 and 20 of inversion. ................................ .............. 75 4 8 JPS mean AE values at 15 for condition. ................................ .......................... 76 4 9 JPS mean AE values at 15 for time. ................................ ................................ .. 77 4 10 JPS mean AE values at 15 for group and condition. ................................ ......... 78 4 11 JPS mean AE value s at 15 for group and time. ................................ ................ 79 4 12 JPS mean AE values at 20 for condition ................................ ........................... 80 4 13 JPS mean AE values at 20 for time. ................................ ................................ .. 81
9 4 14 JPS mean AE values at 20 for group and condition. ................................ ......... 8 2 4 15 JPS mean AE values at 20 for group and time. ................................ ................ 83 4 16 JPS CE mean values at 15 and 20 of inversion. ................................ .............. 87 4 17 JPS mean CE values at 15 for condition. ................................ .......................... 88 4 18 JPS mean CE val ues at 15 for time ................................ ................................ .. 89 4 19 JPS mean CE at values at 15 for group and condition. ................................ ..... 90 4 20 JPS mean CE values at 15 for group an d time ................................ ................. 91 4 21 JPS mean values in degrees CE at 20 for condition. ................................ ........ 92 4 22 JPS mean CE values at 20 for time. ................................ ................................ 93 4 23 JPS mean CE values in degrees a t 20 for group and condition ........................ 94 4 24 JPS mean CE values at 20 for group and time. ................................ ................ 95
10 LIST OF ABBREVIATION S AE absolute error AI ankle instability AMI arthrogenic muscle inhibition CAI c hronic ankle instability CE constant error FAI f unctional ankle instability H max maximum H reflex peak to peak amplitude H reflex Hoffman n Reflex JPS joint position sense M max m aximum direct muscle peak to peak amplitude MN motoneuron WBV whole body vibration
11 Abstract of Dissertation Presented to the Graduate School of the University of Flori da in Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy NE UROMOTOR FUNCTION FOLLOWING WHOLE BODY VIBRATION IN INDIVIDUALS WITH CHR ONIC ANKLE INSTABILI TY By Dana M. Otzel December 2012 Chair: Mark D. Tillman Major: Health and Human Performance Upwards of 73 % of individuals develop chronic ankle instability (CAI), characterized by recurrent injury and repeated episodes of a giving way sensation, following an initial lateral ankle sprain. Deafferentation due t o mechanoreceptor damage following the injury is suggested to play a role in the development of arthrogenic muscle inhibition (AMI). Reducing the risk of recurrent ankle sprains is paramount in preventing degenerative osteoarthritic changes of the ankle co mplex which can lead to reduced physical activity. While traditional rehabilitation serves to promote returning to pre injury activity levels, not all sensorimotor deficits may be vanquished in individuals with CAI. Alternatively, whole body vibration (WBV ) is a modality that has the potential to address neurophysiologic deficits accompanied by CAI and prevent re injury Mechanical vibration promotes blood flow to tissue and is suggested to stimulate the neuromuscular system by increasing excitability of se nsory receptors. Our goal was to determine if an acute bout of WBV can improve AMI and proprioception in individuals with CAI. The Hoffman n reflex (H reflex) was used to assess motoneuron (MN) pool recruitment, serving as an estimate of alpha MN excitabili ty. Proprioception was assessed using ankle joint position sense (JPS) without visual cues at 15 and 20 of inversion. Ten
12 young adults with CAI and ten age matched healthy controls participated. Everyone underwent a control, sham, and WBV condition over three separate visits in randomized order. H reflex and JPS were assessed prior to, immediately following and 30 minutes after the condition (time p, 0, and 30, respectively). Separate 2x3x3 (group [CAI, Control]; condition [1, 2, 3]; time [p, 0, 30] analy ses of variance were used to determine the effects of WBV on soleus muscle H:M ratios and JPS angle errors. The CAI group presented with lower H:M ratios compared to controls (0.467 vs. 0.619, p = 0.028) collapsed across condition and time. No differences were found between groups or across conditions f or JPS (2.75 vs. 2.75 at 15, p = 0.886, 2.50 vs. 3.00 at 20, p = 0.331). Those with CAI have a lower MN drive compared to healthy individuals A single bout of WBV did not improve AMI or proprioception in those with CAI nor did it have a benefit to healthy individuals. Furthermore, WBV deteriorated JPS performance, although not to a statistically significant level. The acute performance improvements that have been observed by researchers following WBV ar e not due enhanced neural drive as many have suggest given that the H reflex was not potentiated F urther research is warranted to evaluate the cumulative effects of WBV training during the recovery of balance and proprioception following injury.
13 CHAPTE R 1 INTRODUCTION More than 25,000 ankle sprains occur each day in the United States [ 1 2 ] with medical costs reaching $3.65 billion annually [ 3 ] Furthermore, residual symptoms can interfere with normal activities of daily living, as well as, athletic performance. Recu rrent ankle sprains are the most common cause of posttraumatic ankle osteoarthritis [ 4 ] involving greater occurrences of articular lesions, degeneration and ankle defects [ 2 5 6 ] Upwards of 73% of individuals develop chronic ankle instability (CAI) [ 7 12 ] characterized by recurrent in jury and repeated episodes of a giving way sensation, following the initial sprain [ 13 ] Deafferentation due to mechanoreceptor damage following injury is suggested to play a role in the development of arthrogenic muscle inhibition (AMI). AMI is the diminished ability to contract the musculature surrounding a compromised joint which ca n reduce the dynamic support of the ankle. Reducing the risk of recurrent ankle sprains is paramount in preventing degenerative osteoarthritic changes of the ankle complex which can lead to reduced physical activity and not being active over time can lesse pre injury activity levels, not all sensorimotor deficits may be vanquished in individuals with CAI. For instance, postural control impairments can persist in those wi th both a s hort and long history of CAI [ 14 ] Alternatively, whole body vibration (WBV) is a modality that has the potential to address neurophysiologic deficits accompanied by CAI and prevent re injury. WBV delivers oscillatory motion vertically through the entire body as a person stands on a plat form and is being utilized in rehabilitation clinics and fitness center settings. The mechanical vibration promotes blood flow to tissue and is suggested to stimulate the
14 neuromuscular (NM) system by increasing excitability of sensory receptors [ 15 ] Recent evidence has demonstrated enhancements in power, strength, and neuromuscular perf ormance after WBV train ing [ 15 16 ] WBV has the potential to improve NM function by enhancing NM excitability and recruitment patter ns by stimulating sensory receptors, specifically the muscle spindles [ 15 ] Although improvements in postu ral control and disease, multiple sclerosis, and the elderly, no research is available examining the effects of WBV on individuals with CAI. Given that AMI may accompany CA I and WBV has the potential to increase neural drive excitability, investigation of the effects of WBV in individuals who have experienced ankle injury is warranted. The aim of this study will be to evaluate the neuromotor and functional effects of WBV tra ining in individuals who have CAI. The potential benefits of WBV may be quantified via the Hoffmann reflex (H reflex) and joint position sense (JPS) to evaluate AMI and proprioception, respectively. The H reflex serves as a valuable procedural means in det ermining muscle inhibition caused by joint damage. H reflex can be used to assess motoneuron (MN) pool recruitment, serving as an estimate of alpha MN ( MN) excitability. This indirect measure is achieved by percutaneously sending an electric impulse to a mixed peripheral nerve in order to elicit two electromyographic responses in the muscle of interest, the H Reflex and M wave. The H reflex is a monosyna ptic reflex that begins at the point of electric stimulation and results in action potentials traveling along afferent fibers until they reach and synapse on MNs. The efferent portion of the H reflex pathway results from action potentials, generated by th e MNs, to travel along efferent fibers until they reach the neuromuscular junction which produces a twitch response in
15 the electromyograph (EMG). Electric stimulation of the peripheral nerve also elicits direct activation of the efferent fibers, sending a ction potentials directly from the point of stimulation to the neuromuscular junction. This efferent arc produces a response in the EMG known as the muscle response (M wave). The maximal H reflex (H max ) recruited represents an estimate of the number of MNs one is capable of activating in a given state, whereas the maximal M wave (M max ) recruited represents activation of the entire MN pool, or maximum muscle activation, and serves as a stable measure [ 17 18 ] Therefore, comparing the H max /M max ratio indicates the proportion of the entire MN pool capable of being recruited. Using this technique, AMI has been identi fied in both the soleus and peroneal musculature of the involved limb of patients exhibiting unilateral functional ankle instability (FAI) [ 19 ] AMI of the peroneals and soleus muscles hinders the dynamic protective mechanism to p revent lateral ankle re injury. A reorganization of feedback and feedforward neuromuscular control may be taking place in people with CAI based on the evidence of the altered gait patterns and bilateral postural contro l deficits that develop in this population. Given that the likelihood of recurrent a nkle sprain is high after an initial ankle sprain and that balance plays an important role in preventing such an injury, the principal focus during rehabilitation should be on re establishing effective postural stability and proper feedback neuromuscular control. Our overall goal is to evaluate and compare the effects of WBV on proprioception and AMI between individuals with CAI and healthy controls Specifically, we will te st the hypotheses that introducing WBV will improve 1) AMI by examining H reflex and 2) joint position sense
16 CHAPTER 2 LITERATURE REVIEW More than 25,000 ankle sprains occur each day in the United States [ 1 20 ] and many people who sustain the injury do not seek formal rehabilitation. Furthermore, residual symptoms can interfere with athletic performance and normal activities of daily living. Lateral sprains, which result from forced inversion of the ankle, make up 80% of ankle ligamentous injuries with a hi gh incidence rate in athletics [ 10 12 21 ] Previous research has indicated that 40 73% of individuals develop CAI fol lowing the initial sprain [ 7 12 ] Recurrent ankle sprains are the most common cause of posttraumatic ankle osteoarthritis [ 4 ] involving greater occurrences of articular lesions, degeneration and ankle defects [ 2 5 6 22 ] Reducing the risk of recurrent ankle sprains is paramount to preventing the degenerative changes of the ankle complex that accompany the condition. While rehabilitation serves to promote returning to pre injury activity levels, not all sensorimotor deficits may be vanquished. WBV is a training modality that has t he potential benefit of addressing sensorimotor deficits accompanied by CAI. WBV delivers mechanical vertical vibration to the body. While the exact mechanism is unknown, mechanical vibration promotes blood flow to tissue and is suggested to stimulate the neuromuscular system by increasing excitability of sensory rece ptors [ 23 25 ] The following sections will review pathoanatomy of the ankle, pathology of CAI includ ing abnormal mechanics, sensorimotor disturbances involving AMI and postural control deficits. Classification of Chronic Ankle Instability CAI is characterized by repeated episodes of a giving way sensation and recurrent injury [ 13 26 ] and the symptoms can persist indefinitely. CAI may develop as a
17 result of mechanical ankle instability (MAI) or functional ankl e instability (FAI). Although both can occur in isolation, researchers have proposed that a combination of MAI and FAI develops in individuals with CAI [ 27 ] MAI is identified when motion exceeds normal physiologic limits as a result of ligament rupture. Patients who experience mechanical instability do not necessarily develop r ecurrent an kle hypersupination [ 28 ] FAI involves joint motion going beyond voluntary control but does no t necessitate joint translation that exceeds normal physiologic al motion [ 13 ] In fact, a high proportion of individuals with FAI do not present with physiological laxi ty on examination [ 26 ] With arthroscopi c assessment, Takao et al. [ 29 ] found that all patients with FAI, despite absence of lateral laxity, had morphological ligamentous abnormality, serving as a contributor to the underlying instability. Individuals who have experienced a single lateral ankle sprain and do not develop res idual ankle instabili ty are known as copers [ 14 30 ] Copers are able to return to high level physical activ ities that include jumping and pivoting without loss of function. This special population may adopt appropriate neuromuscular responses that prevent recurrent ankle sprain [ 30 33 ] Ankle Pathoanatomy/Neuroanatomy The ankle complex consists of three articulations that allow for triplanar range of motion of the rearfoot. The talocrural joint, or ankle mortise, is formed by the articulations between the distal malleoli of the tibia and fibula and the inferior surface of the tibia with the dome of the talus. This articulation forms an oblique axis for this uniaxial hinge joint with the majority of motion occurring in the sagittal plane. The axis runs slightly anterior to the frontal plane from the medial malleolus and extends downward and just posterior to the frontal plane through the lateral malleolus (Figure 2 1). Rather than isolated extension and flexion occurring around the oblique axis, small
18 amounts of rotation ab out the transverse and frontal planes a ccompany the sagittal movement [ 34 ] Physiologic dorsiflexion is accompanied by external rotation and eversion while internal rotation and inversion accompanies plantarflexion. The articulation between the talus and calcaneus forms the subtala r joint (STJ). The two separate joint cavities that compose the STJ are the inferior posterior facet of the talus with the superior posterior facet of the calcaneus and the head of the talus with the anterior superior facets of the calcaneus, the sustentac ulum tali of the calcaneus, and the concave proximal surface of the tarsal navicular. The complex bony arrangement results in the posterior articulation lying more lateral with a lower center of rotation than the anterior joint; even so a single oblique ax is is though t to be shared (Figure 2 2). The orientation of the axis varies across the population but typically has a 40 degree upward tilt a nd 20 degree medial angulation [ 35 ] More recent research suggests that the STJ has multiple axes of rotation with different spatial locations due to the articulating surfaces of the t alus and calcaneus [ 36 ] The triplanar motions of pronation and supination occur at the STJ. The tibiofibul ar syndesmosis is the third articulation of the ankle complex allowing for accessory gliding motion that is necessary for full physiologic range of motion while the thick interosseous membrane connecting the distal tibia and fibula and the anterior and pos terior inferior tibiofibular ligaments provide static stability to the ankle. In general, stability of the ankle complex i s provided by bony articulation congruency, static ligaments and stiffness generated by the musculature surrounding the foot a nd ankle [ 37 ] In a full weight bearing position, the bony congruency provi des resistance to translation and rotational s tress [ 37 ] The anter ior talofibular ligament
19 (ATFL), calcaneofibular ligament (CFL), and posterior talofibular ligament (PTFL) originate and attach on the lateral aspect of the ankle providing the ankle with static stability. The deltoid ligament attaches medially providing r esistance to eversion stress. The ATFL resists anterior translation of the talus and excessive inversion and internal rotation of the talus on the tibia and becomes tauter when the ank le is plantarflexed [ 38 ] The CFL resists excessive supination at the talocrural and subtalar joints, excess ive inversion and internal rotation of the rearfoot, and is taut when the ankle is dorsiflexed. The PTFL resists inversion and in ternal rotation when loaded [ 37 ] The cervical and interosseous ligaments are referred to as the cruciate ligaments of the ankle and stabilize the STJ. Although not fully understood, the cruciat e ligaments together provide stability to the two STJs during supination and pronation [ 39 40 ] Deep fibers of the extensor retinaculum are suggested to provide support to the STJ and when compromised may lead to sinus tarsi syndrome [ 41 ] Located lateral and superficial, the lateral talocalcaneal (LTCL) and fibulotalocalcaneal ligaments (FTCL) provide additional resistance to supination The peroneal l ongus and brevis muscles are primary movers of rearfoot supination and dynamic restraints against inversion providing defense against lateral ankle sprain s Additional joint stiffening is provided by the anterior tibialis, extensor digitorum longus, extens or digitorum brevis, and peroneus tertius as the muscles eccentrically contract. The cervical ligament, CFL, peroneus longus and brevis, and the sustentaculum tali striking the talar tubercle act together to limit inversion. The lumbar and sacral plexes su pply motor and sensory function to the ankle. The tibial, deep peroneal, and superficial peroneal nerves are mixed nerves supplying
20 motor function and sensory information to the muscles crossing the ankle joint while the sural and saphenous nerves su pply s ensory function only Joint capsules of the mortise and STJ and the lateral ligaments are endowed with mechanoreceptors providing proprioceptive feedback. The tension detecting muscle spindles distributed throughout the peroneal muscles and tendons add to proprioception of the ankle complex. Ankle Sprain Pathomechanics The magnitude of load and positioning of the ankle will determine the extent of ligamentous injury. Excessive supination of the rearfoot while the shank is externally rotated bears stress to the lateral ankle ligaments [ 20 42 ] The tension in this inverted position is increased as body weight is accepted during the initial contact of gait or descent from a jump. Fuller [ 43 ] suggests that lateral ankle sprains occur due to the location and magnitude of the GRF relative to the STJ axis at initial foot contact with the ground. The medial shift o supination moment at the S TJ [ 43 ] which can result simply by stepping on a pebble at the medial heel or landing on an A foot that has a COP lo cated medial to the STJ axis will endure greater supination moments from GRF (longer supination moment arm is created) compared to a foot with less area medial to the STJ axis (or a laterally deviated STJ axis) [ 35 43 44 ] When the rearfoot is supinated, STJ inversion and internal rotation occurs and when coupl ed with greater amounts of plantarflexion the stress on the ATFL is increased [ 38 ] The static support of the ATFL prevents anterior displacement of the talus and excessive inversion and internal rotation of the talus on the tibia [ 38 ] The ATFL has the lowest load and energy to failure under tension compared to the CFL and PT FL, and based on its fiber orientation and location is the first ligament to fail when placed in a supinated and
21 plantarflexed position [ 45 ] The CFL is the second most common sprained lateral ankle ligament [ 46 ] Ankle sprains are subjectively classified into three grades based on severity of injury and typically two grading scales are used. Linde nfeld [ 47 48 ] have described a three grade system based on a trauma to a single ligament, wher eas others have based the grading on number of ligaments involved. Grade I sprains are defined as ligament stretching without a full rupture and typically involve mild swelling and tenderness with little to no functional loss [ 47 48 ] Grade II sprains are characterized by partial rupture of the ligament accompanied by moderate swelling, pain, and tenderness with palpation, range of motion loss and functional deficits. Grade III sprains involve comp lete ligament rupture, severe swelling and tenderness, and loss of function and range of motion. The muscles surrounding the talocrural and STJ provide postural adjustments that counteract the external torques created from ground contact of the stance limb as [ 49 ] During normal gait, ground reaction forces (GRFs) ac t lateral to the STJ axis and anterior to the talocrural joint axis causing ankle eversion and dorsiflexion [ 49 ] The plantar flexors a nd inverter m uscles act against this torque [ 50 ] The STJ axis of the stance limb continues to move medially and laterally as the foot everts and inverts respectively during gait [ 44 ] Inversion in a weight bearing ankle is thought to overpower the peroneals [ 49 ] The COM and inert ia will collectively determine the line of action of the GRF [ 36 49 ] If a greater amount of inversion occurs just prior to ground contact, external inversion torque is applied to the ankle and if the compensatory pronation moment generated by
22 the peroneal muscles and lateral ligaments is not great enough to counteract the force, the supination torque will cause e xcessive inversion and internal rotation [ 43 ] Furthermore, the latency (or electromechanical delay) of the evertors may be too long to counteract the torque increasing the likelihood of injury if further perturbed [ 51 53 ] H owever, Vaes et al. [ 54 ] failed to find a difference in latencies when inverting the ankle to 50 when comparing healt hy ankles and CAI. The authors [ 54 ] suggest that the motor response time is shorter than the total inver sion time providing enough time for the protection by the peroneals bef ore the ankle reaches 50 Preparatory activity in the muscles crossing the STJ including the peroneal muscles can produce stiffness prior to foot contact with the ground and may explai n the protection of the ankle against hyperinversion in weight bearing activities [ 51 ] Abnormal Ankle Mechanics Post Injury Hypermobility as well as hypomobility at the talocrural and subtalar joints can r esult from the initial injury [ 55 ] Ligamentous laxity can result in alter ed proprioception and subsequent hypermobility [ 27 56 59 ] Decreased ligamentous tautness of the anterior talofibular, calcaneofibular, cervical or interosseous ligaments of the subtalar joint, or the inferior tibiofibular interosse ous ligaments may result in increased accessory motion in which excessive gliding and rolling of the talus on the mortise may occur, creating an abnormal instantaneous axis of rotation during physiologic motion [ 60 ] Generally, once the ATFL is torn, the static restraint against transverse plan e motion is weakened and greater amounts of internal rotation are allowed [ 40 ] In contra st, the talus can become fixed in a more anterior position not allowing normal arthrokinematic accessory motion of the talus gliding posteriorly on the calcaneus which results in limitation of full dorsiflexion. Similarly, the fibula can displace anteriorl y, moving the axis of rotation of
23 the joint and limiting m otion [ 55 ] Therefore, hypomobility can create an abnormal axis of rotation whic h influences both physiologic and accessory motion [ 60 ] However, functional amounts of dorsiflexion can still be reached most likely due to increased motion at nearby joints or an abnormal instantaneous axis of rotation at the talocrural joint [ 30 60 ] In fact, Brown et al. [ 30 ] found that individuals with MAI had greater dorsiflexion during walking after initial contact than those with FAI or healthy controls. Brown and colleagues [ 30 ] found differences in ankle kin ematics for various dynamic movements (walk, run, step down, drop jump, and stop jump) between individuals with MAI compared to copers and functionally unstable groups in which greater eversion and dorsiflexion motion was observed during some movements ind icating an altered kinematic pattern to prevent injury. For instance, having greater dorsiflexion during a drop jump may serve as a protective mechanism in which the reliance on bony stability increases and the reliance on the compromised lateral ligaments is reduced in a mechanically unstable ankle [ 30 ] Furthermore, greater frontal plane motion was detected in both the FAI and MAI groups compared to copers when wa lking in addition to larger standard deviations of frontal plane movement which may indicate greater movement variability [ 30 ] When landing from a single leg jump Caulfield and Garrett [ 61 ] also found that individuals with FAI landed with greater amounts of dor siflexion compared to healthy controls. Spaulding et al. [ 62 ] found greater variability in gait characteristics for CAI individuals compared to healthy control s. One potentially harmful difference in those with CAI is having greater amounts of plantar flexion prior to ground contact given the stress of the lateral ligaments with plantar flexion [ 62 ]
24 Altered neuromuscular control may lead to the changes seen in ankle kinematics due to the multiple degrees of freedom of the lower extremity One possible explanation of how the copers manage the injury is by overcoming a rthrokinematic restrictions, neuromuscular control impairments, or AMI; something that individuals with CAI are unable to do. Therefore, establishing differences between copers and CAI patients and then developing effective rehabilitation techniques to ove rcome deficits is of fundamental importance to clinicians and patients alike Wikstrom and colleagues [ 31 ] set out to identify which clinical tools could detect differences among CAI, coper and uninjured groups. The authors [ 31 ] have identified clinical differences between individuals with CAI and copers as well as uninjured controls based on self assessed disability instruments. However, the CAI group performed no differently than the copers and uninjured controls on hop tests, which are routinely used a s functional performance measures in rehabilitation. Interestingly, when asked about ankle stability, the CAI group reported that they perceived greater amounts of ankle instability than the copers and uninjured con trols [ 31 ] Sensorimotor System Deficits Evidence exists confirming that once ankle joint integrity is lost, the sensorimotor system becomes compromised [ 11 51 53 63 93 ] Intact and properly functioning afferent pathways are critical for providing accurate feedback that is necessary for a functioning motor control s ystem. Joint injury may influence afferent feedback that leads to ankle stability. Proprioception, a component of the sensorimotor system which includes both kinesthesia and joint position sense (JPS), is mediated by skin, articular, and muscle mechanorece ptors that send afferent information to the appropriate cerebral centers. When the neuromuscular feedback system is disrupted, motor control is co mpromised.
25 Freeman et al. [ 13 ] suggested that damaged mechanoreceptors in the capsule and ligaments are responsible for the development of FAI. The articular deafferentation results in a slow ed response of the evertor muscles that are needed to protect the ankle when a sudden inversion perturbation occurs. However, recent research has also implicated the involvement of feed forward motor control that becomes hindered in the dynamic defense of sudden ankle inversion [ 51 64 67 94 95 ] Sudden inversion perturbations while standing in experimental lab settings have revealed that ankle everter muscle latencies go beyond the time required to protect ligamentous integrity [ 51 93 96 ] The f forcefully inverted suggests that there are other features of the surface interface of realistic foot to ground interactions that may slow the inversion motion providing enough time fo r the evertor s and other centrally coordinated activity from proximal and contralateral limb musculature to protect the ankle [ 51 ] Preprogrammed co contraction of muscles surrounding the ankle just before heel strike increases joint stiffness which enhances dynamic defense against ligament injury [ 67 ] However, most study designs involve an inversion perturbation with a trapdoor while in a static standing position. Hopkins et al. [ 66 97 ] compared muscle activity in individuals with FAI and healthy active people following sudden ankle inversion under t he common experimental condition where a trapdoor drops while standing in addition to a functional experimental model in which a platform would drop during the dynamic task of walking. The authors found [ 66 ] that the time to reach maximal inversion was greater under the walking condition along with greater peak peroneal muscle activity as opposed to the standing condition in healthy controls. The muscle preactivation and increased muscle spindle sensitivity
26 observed when walking pr ovides an appropriate representation of neuromuscular activity and the increased dynamic protecti on of the ankle when perturbed [ 66 97 ] Individuals with FAI failed to activate the muscles to the same extent when perturbed during walking which was demonstrated by increased peroneal latencies and electromechanical delay compared to the uninv olved limb and to t he controls [ 97 ] The fact that individuals with C possibly due to decreased sensitivity from the muscle spindles, may help to explain the reoccurrence of injury. Decreased kinesthesia [ 70 72 ] reduced joint positi on sense [ 68 69 98 99 ] impaired cutaneus sensation [ 76 77 ] impaired neuromuscul ar firing patterns [ 52 53 64 73 78 ] decre ased nerve conduction velocity [ 90 100 ] decre ased postural control [ 79 85 87 89 ] and decreased strength [ 11 56 69 86 101 ] have all been associated with CAI. The superficial peroneal nerve is stretched when the ankle is inverted and the deep peroneal nerve is stretched with plantarflexion [ 90 91 ] A combination of ankle inversion and plantarflexion is common when landing from a jump and can result in ankle sprain. Similarly, when walking or ru nning, an uneven surface can cause the ankle to invert with slight plantarflexion. The anterior talofibular ligament and calcaneofibular ligament are stressed under these motions and depending on the degree of stress may result in ligament failure. Further more, the primary evertor s are often strained, leading to muscle tendon mechanoreceptor damage [ 26 ] Whether or not a peroneal strain is sustained following an ankle sprain, evertor strength is often compromised. Muscle strength is commonly assessed by measuring maximum voluntary contraction (MVC), and is typically reported as peak torque. Eve rtor
27 weakness has been detected in individuals with unilateral CAI c ompared to the uninvolved limb [ 11 8 6 101 ] when compared to healthy controls and copers [ 69 ] However, other studies have failed to find such weakness in the peroneal muscles [ 56 102 103 ] Baumhauer et al. [ 20 ] prospectively studied risk factors for lateral ankle sprains in which an increased ratio of eversion to inversion strength, increased ratio of plantar flexion to dorsiflexion strength, and increased plantar flexion strength all increased the risk of ankle sprain. When w eakness of the peroneal and the triceps surae muscles persists, the risk of an inversion ankle sprain rises [ 1 65 ] In addition to possible muscle strain, with forceful ankle inversion the superficial peroneal nerve becomes at risk for traction injury and additional risk is presented with sp rains of greater severity or with a deficient anterior talofibular ligament [ 91 ] The superficial fibular nerve innervates the primary evertor muscles inclu ding the peroneus longus and brevis; while the deep peroneal nerve innervates the peroneus tertius and extensor digitorum longus, all of which are responsible for dynamic su pport of the lateral ankle The importance of lateral ankle ligament mechanorecepto rs is undetermined based on conflicting findings Feuerbach et al. [ 104 ] observed that JPS is not compromised when lateral ankle ligaments are under local an esthesia On the contrary, McKeon et al. [ 105 ] observed postural control deficits when the lateral ankle ligaments were anest hetized The mechanoreceptors in the muscle tendon structures are major contributors to proprioception. Konradsen et al. [ 106 ] provided evidence of this by blocking the afferent input from the ligaments and capsule of the ankle and foot complex and measuring pa ssive and active JPS. Although passive JPS of the ankle was compromised under anesthesia, active joint positions sense was not compromised
28 suggesting that muscle and tendon receptors proximal to the block were engaged, diminishing the neuromuscular deficit s. Based on the findings of Konraden et al. [ 106 ] trauma to the muscle tendon mechanoreceptors may have a greater impact on proprioception than ligament or joint capsule mechanoreceptors. When evaluating JPS in individuals with AI, there is conflicting evidenc e on whether proprioceptive deficits exist. Some researchers [ 68 69 98 99 107 108 ] have found impaired performance with JPS while other s [ 109 111 ] have shown equivalent execution when compared to healthy individuals. Methodology for evaluating JPS differs among the studies including speed of mov ement, test angles, and whether the movement is passive or active during recall. Reliability of the measure was found to be high using an isokinetic dynamometer when assessing passive JPS Intraclass correlation coefficients were .94 and .98 at testing ang les of 10 and 20 with three to five days between testing session s [ 108 ] Konradsen and Mag nusson [ 98 ] found that the absolute error during active JPS was significa ntly greater in the affected ankle of individuals with unilateral AI (2.5 ) compared to the uninjured side (2.0 ) as well as when compared to healthy controls (1.7 ) Similarly, Nakasa et al [ 112 ] found side to s ide differences of 1.0 for those with AI compared to 2 in the healthy group and an overall statistically significant deficit in the AI group Boyle and Negu s [ 107 ] found active and passive JPS deficits in those with AI compared to uninjured participants. Willems et al. [ 69 ] reported that those with FAI underestimated the inversion angle during active JPS to a greater extent than c ontrols did. Yokoyama and colleagues [ 113 ] looked at combined plant arflexion angles with either 10 or 20 of inversion and also found that those with FAI underestimated the plantarflexion angle. Functionally, this is important when considering landing kinematics
29 if the person has a lower perce ption of plantarflexion. Following a six week isokinetic strengthening protocol, Sekir et al [ 114 ] found improvements in passive JPS at 10 and 20 in which absolute error decreased by a degree at both testing angles These results demonstrate the importance of re establishing proprioception following i njury and that JPS measures are reliable Postural control deficits: Postural control impairments are well documented in individuals with CAI [ 14 ] Bilateral postural deficits lasting up to three weeks after the ankle sprain and decreased bilateral proprioception have been revealed in CAI [ 76 79 92 115 ] Furthermore, central neural adaptations may take place as opposed to peripheral deficits alone; as seen in altered recruitment patterns of hip musculature and anticipatory postural control alterations [ 32 76 92 94 116 ] When balancing on a single leg, pronation and supination occur at the subtalar joint to maintain stability and are referred to as using an ankle strategy for postural control. Individuals with CAI have also been observed to use a less efficient hip strategy which may develop as a result of altered neuromuscular control of the involved limb [ 85 88 117 ] Wikstrom et al. [ 118 ] has established differences in postural control between individuals with CAI and copers u sing various stabilometric postural control measures to analyze performance during single leg stance. In addition to evaluating the traditional COP displacement characteristics and time to boundary, a spatiotemporal assessment that estimates the time an in dividual has to make a postural correction while maintaining upright stance within thei r base of support, the authors [ 118 ] also assessed center of pressure center of mass (COP COM) moment arm characteristics. CO P COM moment arm measures represent the distance between the COP and COM in the transverse
30 plane and accounts for movements of individual segments present in the multilinked human body that are absent when using a single inve rted pendulum approach [ 119 ] COP velocities in the mediolateral and anteroposterior directions were greater in individuals with CAI compared to copers and controls as well as peak COP COM moment arm in the anteroposteri or direction and resultant mean COM COP moment arm were larger in those with CAI relative to copers. Moreover, Wikstrom et al. [ 118 ] found that all four COP COM measures detected impairments in postural control i n the CAI group and suggests that those with CAI may adopt an alternative postural control strategy and may explain the basis of the instability. Another explanation that could account for the postural control differences are the possible changes in the me chanical properties of the musculotendinous unit which are in part regulated by motor control programs that have also been shown to be altered in individuals with CAI [ 94 118 ] Postural instability serves as a predictor of ankle sprain and ankle stability [ 28 81 87 120 121 ] Balance training may hel p to prevent re injury. Holme et al. [ 122 ] found that individuals who did not partake in rehabilitation had a recurrent sprain rate of 29% compared to 7% in thos e who went through rehabilitation. Other research has shown that there are improvements of proprioception and neuromuscular control as indicated by improved postural stability during single leg stance [ 28 84 115 121 123 126 ] and dynamic conditions [ 121 125 126 ] Dynamic postural control has been widely used to differentiate between individuals with CAI and uninjured controls [ 82 83 127 ] For example, certain jump protocols require an individual to transition from a dynamic to a static state during which the time to stabilization (TTS) is calculate d based on the time required to minimize the
31 resultant GRFs following a jump landing to a static baseline stance [ 83 ] Successful differentiation between CAI and individuals with no history of lower extremity injury have been made using a jump protocol in which C AI individuals had longer TTS than healthy controls [ 82 83 110 127 ] Wikstrom and colleagues (2007) measured various TTS components of dynamic stability in a single leg hop stabilization model and established the dynamic postural stability index ( DPSI). TTS measures provide three separate directional indices of forces, although multidirectional control can be determined, global changes cannot be monitored. Therefore, Wikstrom [ 83 ] developed the DPSI to make up for the shortcomings of the TTS measures. DSPI is ca lculated by measuring stability indices in three principal directions: anterior posterior (APSI), medial lateral (MLSI) and vertical (VSI) [ 83 ] Wikstrom and colleagues [ 128 ] found differences in the vertical stability index, the anteroposterior component of dynamic stab ility, as well as overall DPSI between patients with CAI and healthy controls, suggesting the importance of preparatory actions that may help to protect injury in those with CAI Additionally, DPSI can detect differences between individuals with stable ank les and individuals with FAI [ 128 ] Other differences have been found while assessing dynamic postural control related to gait. Altered kinematics and kinetics during self selected walking speeds have been reported in individuals with CAI when compared to healthy controls [ 65 96 ] These changes may be responsible for increased stress ap plied to the ankle joint duri ng heel strike and loading response phases of the gait cycle where increased inversion was observed [ 65 9 6 ] Patients with CAI exhibited a concentric evertor moment versus an eccentric inverter moment produced by the controls [ 96 ] Delahunt and colleagues [ 96 ]
32 hypothesized that the increased inverted position just prior to heel contact along with the increased activity of the evertor s operates as a feed forward protective mechani sm in individuals with ankle instability. Furthermore, McLoda et al. [ 129 ] found increased evertor preactivation prior to foot to ground contact during walking, jogging, and drop landing in comparison to quiet standing in healthy individuals. Centrally mediated motor programming appears to accomp any different movemen t patterns [ 129 ] Du ring the early stance phase of gait spindle sensitivity is increased as the weight of the body is transferred to the stance leg helping to stiffen the joint [ 13 0 131 ] The joint stiffness developed at the ankle was reinforced by the longer time taken to reach full inversion during walking in the Hopkin s et al. [ 66 ] study. Consid ering this research, the adaptations that take place may help to explain why individuals with unstable ankles experience lateral ankle ligament injury when subjected to a n unanticipated ground contact [ 65 96 129 ] Altered kinematics and kinetics have also been found during a single leg drop jump in ind ividuals with CAI compared to healthy controls [ 61 132 ] Individuals with CAI were less efficient at reaching the closed packed position of the ankle after initial contact compared to the healthy controls. Just prior to initial contact, decreased peroneus longus integrated electromyography ( EMG ) activity and increased ankle inversion were observed. Joint angular displacement just before ground contact differed between patients with CAI and controls, suggesting that the centrally mediated feed forward motor program was altered possibly by a learned adaptation following the injury in which greater dorsiflex ion was used to decrease the effects of the landing forces on the ligamen ts [ 61 ] Lateral and anteri or force peaks occurred significantly earlier in
33 patients with CAI. Furthermore, the force peaks occurred before reflex corrections of the forces could take place, suggesting deficits in the feed forward motor control system. Planned and unplanned gait te rmination ( GT ) provide an experimental model that possesses known and repeatable set of neuromuscular responses that can be constructed to challenge both feed forward and feedback neuromuscular control [ 94 95 133 ] Both feed forward and feedback control of GT strategies were shown to be altered in patient s with CAI during planned and unplanned GT resulting in inefficient COM control [ 95 ] CAI subjects did not reduce their propulsive forces during GT trials (planned and unplanned) to the same extent as healthy subjects. Subsequently, braking forces were found to be higher in CAI subjects than healthy subjects. Moreover, these changes were seen bilaterally in those with CAI and the findings indicate that an altered motor program and slower neuromuscular response exists in CAI subjects during planned and unplanned GT. CAI subjects were shown to be less stable when going from a dynamic to a static state as indicated by poorer APSI and DPSI scores observed compared to healthy controls. While planned GT challenges feed forward motor control activity, unplanned stopping challenges feed back responses because the person must react to an external stimulus. Feed back activity occurs as a response to sensory detection of motion [ 134 ] whereas, feed forward control is the anticipatory action that occurs prior to the sensory detection of a homeostatic disruption [ 134 135 ] Hass et al. [ 94 ] compared individuals with CAI and uninjured controls using a gait initiatio n model. The CAI group demonstrated reduced COP excursions towards the unaffected stepping limb based on the perceived stability of the initial stance limb. The authors [ 94 ] suggest that those with CA I are adopting an altered supraspinal motor control mechanism to reduce the
34 postural demands of the involved extremity. Overall, the results suggest that ankle instability may alter feed forward control whether transitioning from quiet stance to steady sta te gait or decelerating the COM to quiet stance [ 94 95 ] The work b y Wikstrom and colleagues [ 31 ] in esta blishing reliable and valid instruments to distinguish participants with ankle instability and the recent research that has improved our understanding of the motor responses in individuals with CAI have enabled us to look towards the next step in addressin g the unfavorable neuromuscular control adaptations that occur and ultimately prevent the osteoarthritic changes that may develop later in life. Arthrogenic Muscle Inhibition and the Hoffmann Reflex Arthrogenic muscle response is an ongoing reflex reactio n of the muscles surrounding a joint after distention or damage to joint structures as a part of a natural joint protective response [ 136 ] The response can be inhibition or excitation of voluntary muscle activation. AMI is a diminished ability to contract the intact musculature surrounding a compromised joint [ 136 137 ] Pain is thought to contribute to AMI, although, simulated knee joint effusion experiments have revealed the presence of AMI in the absence of pain [ 138 139 ] Effusion [ 140 ] and altered afferent feedback [ 137 ] are considered to be other contributors of AMI. Altered afferent feedback results f rom the proposed deafferentation that occurs as a consequence of the damage to capsular and ligamentous mechanoreceptors due to injury and is suggested to be a mechanism for AMI development [ 137 ] The deafferentation alterations of the CNS following ankle injury are suggested to play a role in AMI in peop le with FAI [ 19 ] There are a few techniques to measure AMI, voluntary force productio n from the motoneuron (MN) pool of interest or the product of neuromuscular recruitment of the
35 MN pool. Voluntary force output is often measured by comparing pre injury MVC to post injury MVC values or by evaluating the differences among the injured limb, contralateral limb and healthy controls. There are several limitations to the use of MVC including participant motivation to perform the MVC, inability to isolate muscles during voluntary contraction, difficulty in obtaining baseline MVC if subjects are ev aluated only after the injury has occurred, and inability to use the contralateral limb for comparison due to crossover effect to the uninvolved side [ 136 ] The technique of twitch interpolation is commonly used to determine whether human muscles are activated fully during maximal voluntary efforts (also referred to as extrapolation) [ 141 ] Twitch interpolation can be used in the absence of baseline force output measures in which a supramaximal electrical stimulus is delivered t o the muscle compared to a maximal voluntary isometric contraction (MVIC). The MVIC relies on central neural drive to the muscle, whereas the maximal superimposed electrically evoked contraction is independent of the central nervous system [ 142 ] Inferences can be made of t he level excitability of motorneurons or neural drive with the measurement of voluntary activation via tw itch interpolation [ 143 ] The ratio of peak force output during a voluntary maximal effort to the same measure during an electrically evoked involuntary maximal contraction is known as the central activation ratio (CAR), and is used to assess th e central inhibition i n the muscle of an individual. Incomplete motor unit activation of a muscle (i.e., CAR < 100%) is an indicator of inhibition of the neural drive within the central nervous system during a maximal isometric contraction [ 144 ] An alternative to using the twitch inter polation technique, the Hoffman n reflex (H reflex) can be used to assess MN pool recruitment. H reflex serves as an estimate of
36 alpha MN ( MN) excitability, which is a valuable procedural means in determining muscle inhibition cau sed by joint damage. By percutaneously delivering an electric stimulus to a mixed peripheral nerve two EMG responses can be elicited: 1. afferent sensory action potentials are transmitted through the MN pool, synapse with the MN, and efferent motor respon ses extend to the neuromuscular junction (H Reflex) and/or 2. direct efferent motor response starting from the point stimulation to the neuromuscular junction (M wave) [ 18 145 ] If electrical stimulation of the nerve exceeds the threshold for activation of Ia afferents and the afferent terminals are sufficiently depolarized to cause neurotransmitter release at the Ia afferent/alpha motoneuron synapse, excitatory postsynaptic potentials (EPSPs) will be elicited and an H reflex will be recorded [ 18 145 ] If enough neurotransmitter is released from the primary afferent terminals, postsynaptic depolarization of alpha MNs occurs, and if postsynaptic depolarization is above threshold, then the MNs will fire action potentials that will cause neurotransmitter release of acetylcholine at the neuromuscular junction. The resulting depolarization and subsequent contraction of the muscle fibers will then be recorded as an H reflex via surface electrom yography (EMG) electrodes placed over the muscle. Additional Ia afferent and motor axons are recruited by increasing the level of electrical stimulation resulting in a larger refle x response and a larger M wave [ 146 ] The larger diameter Ia afferents are recruited before the smaller dia meter motor axons [ 147 ] The H reflex traces will increase in size as the stimulation intensity increases until the H reflex reaches its maximum (H max ), greater stimulation after this maximum will result in a trace that disappears from the EMG reco rding. Continuing to increase the stimulus intensity beyond that required for an H reflex results in direct stimulation of the motor efferent
37 fibers and an M wave is recorded with EMG. The process of increasing stimulus intensity by small increments until the maximum M wave (M max ) amplitude is obtained is known as achieving a recruitment curve. H reflex is sensitive measure but there are methodological concerns that must be considered when using the technique. Subject positioning, stimulation setup, stimulu s duration, intensity and frequency, and recording electrodes placement are some of the factors that must be attended to. H reflex measures during quiet standing are found to be reliable measur es within and between sessions [ 148 150 ] H max serves as an estimate of the number of MNs one is capable of activating in a given state [ 145 ] M max represents activation of the entire MN pool, or maximu m muscle activation, and therefore should be a stable measure [ 18 ] The H max /M max ratio is interpreted as the proportion of the entire MN pool capable of being recruited based on the stability of the M max measu re. Smaller ratios (indicating decreased excitability of the MN pool) would indicate greater muscle inhibition. Using thi s technique, McVey et al. [ 19 ] identified AMI in the soleus and peronea l musculature and not in the tibialis anterior in the involved limb of patients exhibiting unilateral FAI. The diminished muscle drive may be responsible for a decreased nerve conduction velocity, impaired neuromuscular firing, and subsequent muscle weakne ss. The feed forward changes that are observed in CAI may develop as the body tries to overcome the muscles that become inhibited. To assess the influence of activation history on MN pool excitability, a paired reflex depression (PRD) technique can be used in which a double pulse stimulation is given to the nerve eliciting two H reflexes. PRD is measured by comparing the percent depression of the conditioned H reflex peak relative to the nonconditioned H reflex
38 peak. Individuals with CAI are unable to modul ate PRD in the soleus while in a single leg stance to the same extent that healthy individuals could and may help explain why postural control is compromised [ 151 ] Additionally, CAI participants demonstrate higher overall levels of postsynaptic inhibition when compared with healthy match ed controls, suggesting that segmental spinal reflex modulation is used as a CNS adaptation of CAI [ 151 ] Sefton et al. [ 151 ] observed the influence of activation history on MN pool excitability in the soleus of individuals with CAI; a PRD technique was used under two stance conditions: single and double legged stance. T hose with CAI had no change in PRD levels when going from double to single leg stance, whereas healthy controls had a 15% change, signifying that individuals with CAI were less able to modulate PRD in a single leg stance compared to healthy individuals. Th e authors suggest that segmental spinal reflex modulation is used as a CNS adaptation of CAI [ 151 ] Furthermore, correlations have been found between reduced postural control and a decreased ability to modulate spina l reflexes [ 151 ] Interestingly, a few studies have shown that those with poor reflex modulation can be tr ained in order to improved modulation result ing in better postural control [ 152 153 ] Sefton et al. [ 151 ] additionally, CAI participants s howed higher overall levels of recurrent inhibition (postsynaptic inhibition) when compared with healthy matched controls. The au thors [ 151 ] suggest that segmental spinal reflex modulation is used as a CNS adaptation of CAI. Proximal motoneuron pool excitability appears to be altered in individuals with unilateral CAI compared to healthy individuals. Bilateral hamstring inhibition and ipsilateral quadriceps facilitation were found in those with CAI using a cent ral activation ratio technique [ 154 ] Given that a re ciprocal relationship exists between the soleus and
39 quadriceps muscles [ 136 154 156 ] quadriceps facili tation is likely to occur because the soleus is i nhibited due to CAI [ 154 ] Reciprocal inhibition occurs between the quadriceps and hamstrings for smooth coordinated movement to occur The findings of hamstring inhibition due to q uadriceps facilitation associated with CAI are reasonable. The crossover effect of hamstring inhibition to the contralateral extremity coupled with the occurrence of bilateral postural control deficits observed with CAI indicates the need to rehabilitate t he lower extremities concurrently after injury. Van Deun et al. [ 116 ] compared the onset of and recruitment order of muscle activation patterns of individuals with CAI and healthy controls during a transition from double leg to a single leg stance position using surface EMG. The authors found that individuals with CAI not only activated their muscles later, they were less likely to change the recruitment order from an eyes open to an eyes closed condition compared to healthy controls [ 116 ] Anticipatory feed forward responses are essential in overcoming the inherent reflex pathway delays as balance is perturbed. These anticipatory postural adjustments which are important to avoid injury appear to be disrupted. CAI subje cts reacted to voluntary movement and relied on feedback when transitioning from two legs to one, whereas healthy subjects used feed forward mechanisms and recruited muscles before the voluntary moveme nt began [ 116 ] The neuromuscular sy ability to adapt to different equilibrium disturbances may lead to risk of r e injury [ 116 ] One therapeutic intervention that shows promise in overcoming the sensorimotor deficits that cause altered feedback motor contr ol is WBV. Whole Body Vibration Recent evidence of enhancements in power, strength, and neuromuscular perf ormance after WBV training (WBVT) has been found [ 16 25 157 158 ] In young healthy
40 adults, improvements in strength are not seen in conjunct ion with improvements in postural control [ 16 159 ] In contrast, clinical populations have shown improve ments [ 160 162 ] Specifically, in addition to benefits related to athletic performance, WBV is a potential therapeutic tool in th e treatment of motor disor ders [ 163 166 ] and bone mineral loss [ 160 167 ] Bruyere et al. [ 162 ] reported improved health related quality of life and a decline in the risk of falls through improved gait and balance in elderly people who underwent a 6 week WBV intervention 3 times a week. Similarly, Bogaerts et al. [ 161 ] found improvements in postural control following a year long WBV training protocol compared to healthy controls who did n ot receive WBV. Cloak e t al. [ 126 ] d ivided a group of individuals with FAI into a control group and another that went through six weeks of WBV T The authors [ 126 ] found improvements in both static and dynamic balance following WBVT. Bautmans et al. [ 168 ] found postural control improvements in elderly nursing home residents when compared to controls who did not have WBV training. Roelents and colleagues [ 169 ] found increased isometric and dynamic knee strength, speed of movement, and improvement in countermovement jump performance in o lder women after a 24 week WBV training program in which most of the gains were achieved after week 12. Verschueren et al. [ 160 ] found increased hip muscul ature strength, increased bone mineral density, and improved postural control in older women. Based on the overall improvements in strength and the rate of force development following WBV training that have been found in older populations, the risk of fall s would be inherently reduced. WBV is commonly delivered while semi squatting on a vibrating platform that oscillates up to 50 times per second and delivers oscillatory motion vertically through
41 the entire body. The exact mechanism of how mechanical vibrat ion might produce benefits for the body is not fully understood. The prevailing theory is that vibration stimulates the nervous system and creates a stretch reflex in the body that causes the muscles to contract [ 158 ] Repeated rapid muscle contractions promote blood flow to t he muscles, bones, and tissues [ 170 ] WBV can improve neuromuscular function by enhancing neuromuscular excitability and recruitment patterns by stimulating sensory receptors, specifically the muscle spindles. The mechanisms underlying the improvements associated with WBV are suggested to result from reflex muscle contractio ns as a tonic vibration reflex [ 24 25 171 ] Excitation of muscle spindles causes the r eflex contraction which leads to enhanced activity of the Ia loop, specifically an MNs by feedback from muscle spindles while depressing the function of golgi tendon organs (GTO) which inhibit muscle action [ 24 25 171 172 ] Inc reased EMG activity was found in the vastus lateralis and biceps femoris when maintaining an isometric semi squat as well as performing dynamic squats while on the WBV platform compa red to an overground condition [ 173 ] Similarly, Roelents et al. [ 174 ] found increased muscle activity in the rectus femoris, vastus lateralis, vastus medialis, and gastrocnemius during an unloaded isometric high squat, low squat, and one legged squat positions while on a WBV platform compared to a n o vibration control condition. Recently, Melnyk and colleagues [ 175 ] investigated the effect of WBV on stretch reflexes involved in knee joint control. Stretch reflexes of the hamstrings were evoked by inducing an anterior tibial translation while standing before and after a single bout of WBV in the treatment group compared to controls. Using EMG, increased size of short latency respo nse was found along with a reduced maximal tibial translation after WBV
42 compared to the controls. Reflexive joint protection was enhanced in the hamstrings which protect the ACL by limiting anterior translation of the tibia on the femur after WBV training [ 175 ] Based on the protective nature of the short term neuromuscular response following WBV at the knee, further investigation is wa rranted in people with ankle instability. In contrast to the previous study, Hopkins et al. [ 176 ] found no differences in electromechanical delay or reaction time in the peroneal longus after a single five minute bout of WBV suggesting muscle sp indle sensitivity is not enhanced with WBV. However, the WBV platform used in that study was designed to pivot around a fulcrum so that the feet reciprocally oscillate instead of having a uniform vertical vibration like the design of a Power Plate The m echanical vibration that is delivered in a platform that teeters side to side may not have the same effect as one that delivers uniform vertical vibration. Hopkins et al. [ 177 ] similarly found that the stretch reflex was not potentiated with a single five minute bout of WBV. The timing and amplitude of the quadriceps stretch reflex were statistically the same between the WBV and control groups [ 177 ] Althoug h WBV platforms can be commonly found in physical therapy clinics as a part of variety of rehabilitation protocols, little evidence based research exists to confirm or explain the effects of WBV during recovery from inj ury. Moezy and colleagues [ 178 ] investigated such effects in patients who have undergone anterior cruciate ligament r econstruction. Greater improvements in postural control and proprioception recovery occurred in ACLR patients who were enrolled in a WBV training program were found compared to conventio nal therapy [ 178 ] WBV training began 12 weeks postoperatively with both the control and WBV training groups enrolling in physical therapy immediately
43 after surgery. The authors suggest that the postural control improvements may be due to improved synchronization of firing of motor units and cocontraction of synergist muscles wi th the mechanical vibration [ 178 ] Armstrong et al. [ 179 ] investigated the acute effects of WBV on soleus MN excitability f ollowing WBV. A single one minute bout of WBV 40 Hz at low amplitude (2 4 mm) was used and considered as moderately high intensity. Successive measurements of the H reflex were recorded at the test intensity of 30% of M max every 30 seconds for 30 minutes immediately following WBV. All subjects displayed a significant suppression of the H reflex during the first minute post WBV. Four distinct recovery patterns were observed among the participants as the H reflex returned to baseline values Based on how a participant recovered, he/she was assigned to one of the four groups All but one group had H reflex es values return to pr e WBV levels; one group remained suppressed. Some showed depressed H reflex es up to 30 minutes after WBV while others showed potentiation. No gender differences were found. A limitation of the study is only having a single, one minute bout of WBV when typi cally five to ten minutes are spent on the modality for therapeutic and exercise based training. In this study we investigate d the acute effects on spinal reflex modulation immediately following a five minute session of WBV. Purpose The aim of this study w as to evaluat e the neuromotor effects of WBV training in individuals who have CAI. Given that AMI may accompany CAI and WBV has the potential to increase neural drive excitability, investigation of the effects of WBV in individuals who have experienced ank le injury is warranted. A reorganiz ation of feedback control may be taking place in people with CAI based on the evidence of the
44 altered gait patterns ( increased inversion at heel strike ) as well as central adaptations (altered recruitment patterns of hip musculature bilateral postural control deficits and anticipatory postural control alterations ) that can develop in this population. Given that the likelihood of recurrent ankle sprain is high after an the initial ankle sprain and proprioception plays an important role in preventing such an injury, the principal focus during rehabilitation should be on re establishing effective n euromuscular control. Our goal was to determine if WBV can improve AMI and proprioception in individuals with CAI. Specifically, we test ed the hypot heses that introducing WBV would improve 1) AMI by examining H reflex and 2) joint position sense in individuals with history of lateral ankle insta bility. The present study compare d JPS and AMI measures in individuals with CAI with thos e of healthy controls prior to and following an intervention proposed to affect neuromuscular function.
45 Figure 2 1 The talocrural axis of rotation.
46 Figure 2 2 The subtalar axis of rotation.
47 Figure 2 3 H reflex and M wave response followi ng a single impulse. SA = stimulation artifact SA M wave H reflex
48 CHAPTER 3 METHODS Participants Ten individuals with CAI (age 18 35 yrs) and ten healthy age matched controls were recruited to participate in this study. Inclusion criteria for the CAI participants were as follows: history of at least one moderate ankle sprain which compromised the integrity of the lateral ligaments and required immobilization in the past, no formal rehabilitation, at least one recurrent ankle sprain between three and six months prior to par ticipation in the study, and perceiving pain, instability, and/or weakness of the involved ankle. The Foot and Ankle Disability Index (FADI) and Foot and Ankle Disability Index Sport (FADI S) which are 26 and eight item self reported questionnaires respect ively, were used to ensure that the participants met the criteria to be included in the CAI group (see appendix A). All activity items are scored from 0 (unable to do) to 4 (no difficulty at all) in addition to the four pain items of the FADI which are sco red from 0 (none) to 4 (unbearable). These questionnaires yield 104 and 32 point scales in which lower percent scores indicate great er disability. S core s < 90% for both the FADI and FADI S are typically used to c lassify one as having CAI [ 121 180 ] The FADI and FADI S have been proven to be valid, reliable and precise measures capable of identifying individual s with AI among college aged, recreationally active individuals [ 31 180 ] A ll participants were free of an y lower extremity or head injury three months prior to testing. Furthermore, participants were excluded if they ha d a history of lower extremity fracture or surgery or ha d any acute or chronic orthopedic compli cation in which weight bearing wa s contraindic ated. Other exclusions included vestibular, visual, and balance
49 hypertension, diabetes, or cancer w ere excluded from the study. Additionally, participants were asked to mai ntain their normal hydration state, not to drink caffeine on testing days, and not to advance or increase their current fitness routine to avoid introducing muscle fatigue and soreness, all of which can alter the H reflex. (Appendix B) Instrumentation Ho ffmann Reflex H reflexes were induced with a GRASS S48 muscle stimulator and GRASS stimulus isolation unit, model SIU8T (Grass Technologies, Astro Med Inc., W. Warwick, RI) in order to produce and amplify electrical impulses. A unipolar electrode set up wa s used in which a reusable silver/silver chloride biopotential skin electrode (Model F E9M 90; Gereonics Inc. Mission Viejo, CA) served as the cathode to deliver the impulses percutaneously while a dispersal pad placed superior to the patella served as the anode. Ambu blue sensor M (Ballerup, Denmark) surface electrodes were placed on the soleus and peroneal muscles to detect changes in muscle activity. EMG leads were connected from the sensors to an electrode board (Model F 15EB/B1) as the signals were am plified by a GRASS physiodata amplifier system (Model 15LT) (Figure 3 1). Data w ere recorded with a custom LabVIEW Real Time software (National Instruments Corporation 2010) program which captured peak peak amplitudes of M waves and H reflexes as well as the onset of muscle response following stimulation. Joint Position Sense A Kinetic Communicator (KINCOM) dynamometer (Chattanooga Group, Inc. Hixson, TN) was used to measure JPS. The passive mode with constant speed and no
50 minimum force effort required fo r motion to occur was utilized for ankle inversion range of motion. Whole Body Vibration A Power Plate vibration platform (Personal Power Plate; Power Plate International Limited; Northbrook, IL, 2004) was used for all WBV sessions, while the Juvent 100 0 platform ( Juvent, Inc. 2007; Somerset, NJ ) was used as a sham vibration condition (Figure 3 2). Procedure s A repeated measures pre intervention/post intervention experimental model was utilized. Participants visited the laboratory three times with one visit including the WBV training, a sham training, and the third as a control condition. Condition order was randomized. An example of a typical visit schedule is outlined in Figure 3 3. Each participant was tested on acute neuromotor function via H reflex and joint position sense. To avoid any cumulative training from occurring, a 72 hour rest period was given between sessions. H reflex Testing H reflex testing was performed to indirectly measure AMI. We percutaneously sent an electric impulse to a mixed peripheral nerve to elicit two EMG responses in the muscle of interest, the H Reflex and M wave (Figure 3 4). Single one millisecond duration square wave pulses were delivered to attain a recruitment curve. Stimulation intensity began at 0 volts a nd was in creased by increments of .2 volts with ten second rest periods given between impulses to prevent postactivation depression. H/M recruitment curves [ 18 145 ] were mapped for each muscle by increasing the stimulation intensity until reaching a maximum H reflex (H max ). The stimulation intensity was
51 continuously increased, resulting in direct stimulation of motor e fferent fibers, to acquire a maximum M wave (M max ) amplitude. H max and M max amplitudes were used to estimate the excitability of the neuronal pool given that H max serves as an estimate of the number of MNs one is capable of activating in a given state. Pe ak to peak amplitudes of the H reflex and M wave were measured for electrical stimulations at each testing period Participants were positioned in a slightly reclined seated position on the KINCOM with the knee close to full extension (5 10 flexion ), hi ps flexed approximately 30 and the ankle in a neutral position, during all H reflex testing (Figure 3 4 ). The stimulating electrode was positioned superior to the popliteal fossa on the tibial nerve in order to elicit muscle responses in the soleus muscle The dispersal pad was placed just superior to the patella. Bilateral soleus and peroneal cutaneous areas were shaved if needed then cleansed with rubbing alcohol prior to recording electrode placement. EMG electrodes were placed 2 cm distal to the medial gastrocnemius and 2 cm medial to the posterior midline of the leg for recording electrical activity of the soleus muscle. A ground electrode was placed over the ipsilateral lateral malleolus. EMG signals were band pass filtered from 10 to 500 Hz and colle cted at 2000 Hz. Baseline recruitment curves were recorded for the soleus muscle in each participant. H/M recruitment curves were collecte d immediately before WBV (time p ) and immediately follow ing the training at 0 minutes (time 0 ) and again 30 minutes (t ime 30) later for all conditions. Joint Position Sense Directly after the H reflex assessment conclude d the participant w as situated for JPS testing. Participants wer e positioned on the KINCOM in a slightly recli ned position (seat back angle 45), hip fle xed approximately 45 knee fl exed at approximately 45 and ankle in a subta lar neutral position (Figure 3 5 ). The foot was securely strapped into
52 the ankle attachment which connect ed to the lever arm that allow ed for the ankle to move in both inversion a nd eversion directions. One strap crossed over the forefoot which secured it to the platform while the other strap sat just proximal to the talocrural joint holding the heel in place. Passive joint positioning was assessed at two testing positions, 15 and 20 of in version. Participants wore blinder glasses to eliminate visual cues therefore allowing for a true sense of ankle position supplied by receptors in and surrounding the joint. Three trials at each target angle were performed. A trial began in the s ubtalar neutral position ( 0 ) then the ankle was slowly moved passively by the examiner toward the target angle. Once the target angle was reached, the position was held for 10 seconds allowing the participant to remember that position. The ankle was then moved five to ten more into inversion and then ba ck to the neutral position. T he joint moved again toward the target angle at a constant five/ second this time by the dynamometer lever arm. As soon as the participant perceived the ankle had reached the ta rget angle, he/she was instructed to exert a quick forceful contraction in the opposite direction that the lever arm is moving (into eversion). This resulted in a spike in force recorded on the KINCOM indicating the angle at which the participant believed was the position to be remembered. Absolute and constant e rror measures served as performance outcome scores to detect the magnitude and direction of the error respectively Similar techniques have been used to test passive JPS in individuals with FAI. [ 69 108 ] Whole Body Vibration Training During each WBV session, the participant stood on the platform and r eceive vertical sinusoidal WBV at 35 Hz, 3 mm displacement, and 54 m/s 2 acceleration. Training included five 60 second increments on the platform with a 60 second rest
53 period between each bout. Similar protocols ha ve been used with WBV training [ 181 183 ] Participants were instructed to maintain a static squat at 70 degree knee flexion angle while grasping the handles without pushing or pulling with the arms (Fi gure 3 6) During the sham condition, the participant was instructed to hold the same squat position and the same training protocol was used with one minute on and one minute off the platform (Figure 3 7) Participants were told that the vibration from the sham condition was subsensory so not to influence performance during JPS task. A handheld goniometer was used to ensure that the participant held the 70 degree squat position for both the vibration and sham conditions. During the control condition partici pants comfortably stood for 10 minutes. Data Analysis Data Reduction. M aximum values of the H reflex and M waves for the soleus muscle w ere examined for analysis using a custom Matlab program. The average of three H maxes and M maxes were used to calculate H:M ratios at each time point. JPS a ngle error data was analyzed using EXCEL Absolute error (AE) and constant error (CE) were calculated and averaged over the three trials in each of the two testing angles. Statistical Analysis. A 2x3x3 (group [CAI invol ved limb/control limb]; condition [1, 2, 3]; time [p 0 30] a nalyses of variance (ANOVA) with repeated measures on the last two factors was used to determine if soleus muscle H:M ratios differ ed between the C AI and healthy control groups. Dependent variab les include d average peak to peak amplitudes measured in millivolts following stimulation of the H reflex Four separate 2x3x3 (group [CAI involved limb /control limb], condition [1, 2, 3], time [p 0, 30]) ANOVA with repeated measures on the last two fact ors examined differences among average
54 JPS AE and CE at 15 and 20 of inversion Significance was set at .05. Bonferoni p ost hocs were performed when appropriate.
55 Figure 3 1. H reflex experimental set up. Photo courtesy of author.
56 Figure 3 2. Whol e body vibration platforms. Juvent on left, Power P my3 on right Photo courtesy of author.
57 Figure 3 3. Time line of laboratory visits.
58 Figure 3 4. H reflex testing position Photo courtesy of author.
59 Figure 3 5. Participan t set up for joint position sense. Photo courtesy of author.
60 Figure 3 6. Participant positioning on the Power Plate Photo courtesy of author.
61 Figure 3 7. Participant positioning on the Juvent Photo courtesy of author.
62 CHAPTER 4 RESULTS Par ticipants Ten participants with AI (s ix fema les, four males; 20.7 + 1.3 yrs, 169.4 + 10.7 cm, 66 .0 + 10.1 kg) were included the ankle instability group Ten age matched participants (seven females, three males; 19.8 + 0 .7 yrs, 165.6 + 9.2 cm, 59.1 + 10.7 kg ) served as the control group. Individuals in the ankle instability group scored below 95% on the FADI and below 85 % on the self reported FADI S questionnaire and experienced a previous ankle sprain within six months but more than three months prior to tes ting. Neuromotor Function H reflex Soleus H:M ratios were analyzed with a mixed design 2x3x3 ANOVA with repeated measures on the last two factors Sphericity for the condition by time interaction was violated ( p = .005) Ther efore Greenhouse Geisser values were used based on the conservative nature of the test. A main effect for group was found for mean H:M ratios (Table 4 1 ). Specifically, m ean H:M ratios for the AI group were lower than that of the healthy control group (Fi gure 4 1 ). Within subject analysis revealed no main effects for condition or time (Table 4 1 ; Figure 4 2; Figure 4 3 ) However, a tre nd was found (p = .072) for the condition by t ime interaction (Table 4 1 ; Figure 4 4 ) The Bonferroni post hoc indicated an increase in H:M ratios between the pre test (time p) and second post test (time 30) thirty minutes after the sham treatment (p = .005) Mean H:M ratios for the remaining nonsignificant two way interactions are presented in Figures 4 5 and 4 6, while means for three way interactions are displayed in Table 4 2.
63 JPS Absolute Error Separate mixed 2x3x3 ANOVA with repeated measures on the last two factors were used to evaluate differences in JPS AE at 15 and 20 The first ANOVA (15) revealed no main effect between gr oups. Similarly, n o main effects or interactions were found for within subject comparisons for JP S AE at 15 of inversion (Table 4 3 ). Likewise, T he ANOVA performed on JPS AE at 20 of inversion did not reveal a group main effect. A main effect f or conditio n was revealed but no interactions were observe d (Table 4 4 ). Overall group means for JPS AE at 15 an d 20 can be found in Figure 4 7 Main effects and t wo way interactions for JPS AE means at 15 and 20 are displayed in Figures 4 8 to 4 1 5 M eans regarding the t hree way interactions are shown in Table 4 5 Constant Error Separate mixed 2x3x3 ANOVA with repeated measures on the last two factors were used to evaluate differences of JPS CE at 15 and 20 Results from the ANOVA for JPS CE at 15 and 20 are reported in Tables 4 6 and 4 7 Between subjects comparisons revealed no main effect for group at 15 (Figure 4 16) A main effect for time (p = 001 ) was seen for JPS at 15 (Table 4 6) The Bonferroni post hoc procedure revealed that error at time p was less than the error at time 30 (p = .002) (Figure 4 18 ) Similarly, a trend was found between time p and time 0 (p = .064 ) in whi ch the error was greater at time 30 A time by group interaction ( p = 001 ) for JPS CE was also revealed at 15 (Fi gure 4 20 ) The Bonferroni post hoc procedure revealed that p erformance decreased from time p to time 0 (p = .001) in the AI group Similarly, performance decreased from time p to time 30 (p < .001) in the AI group (Figure 4 20 ) Main effects
64 and two way i nteractions for JPS mean error at 15 are displayed in Figures 4 16 to 4 2 0 Means for three way interactions are displayed in Table 4 8 N o main effect for group was found for JPS CE at 20 Furthermore, no main effects for condition or time were discover e d. A c ondition by group interaction was observed for JPS at 20 (Table 4 7) The Bonferroni post hoc procedure revealed that during the sham condition the AI group differed from the control group (p = .036) (Figure 4 23 ) More specifically, t he AI group o vershot the targ et angle whereas the control group undershot the t arget Additionally, the AI group performance decreased (p = .007) between the control condition and the sham condition. A trend was revealed (p = 053) in which performance worsen ed betwe en the control and the WBV condition. A condition by time by group interaction was found for JPS at 20 (Table 4 7 ) The Bonferroni post hoc procedure revealed that groups performed differently during the sham condition at time 0 ( p = .016 ) in which the AI group overshot the target and the control group undershot the target (Table 4 8) Analogously groups performed differently during the sham condition at time 30 in which the AI group overshot the t arget Main effects and two way interactions for JPS mean error at 20 are displayed in Figures 4 21 to 4 2 4 Means for three way interactions are display in Table 4 8
65 Table 4 1 H:M ratio ANOVA results Variable F value (df) p 2 Group 5.700 (1,18) 0 .028 0 .241 Condition 0.475 (2,36) 0 .6 11 0 .026 Time 1.373 (2,36) 0 .266 0 .071 Condition*Group 0.736 (2,36) 0 .47 6 0 .039 Time*Group 1.231 (2,36) 0 .30 3 0 .064 Condition*Time 2.600 (4,72) 0 .072* 0 .126 Condition*Time*Group 1.361 (4,72) 0 .2 6 7 0 .070 group main effect; trend; significance set at alpha = .05
66 Figure 4 1. Mean H:M ratio means between groups; p < .05
67 Figure 4 2. Mean H:M ratios by condition
68 Figure 4 3. Mean H:M ratios by time
69 Figure 4 4 Mean H:M ratio s for each condition across time
70 Figure 4 5 Mean H :M ratio by group and condition
71 Figure 4 6 Mean H:M ratios by group and time
72 Table 4 2. Mean ( + SD) H:M Ratio Ankle Instability Healthy Group Control time p 0.483 (0.182) 0.610 (0.152) Control time 0 0.497 (0.156) 0.593 (0.109) Control tim e 30 0.480 (0.185) 0.623 (0.147) Sham time p 0.457 (0.162) 0.595 (0.156) Sham time 0 0.466 (0.185) 0.639 (0.160) Sham time 30 0.489 (0.185) 0.659 (0.159) WBV time p 0.460 (0.168) 0.607 (0.135) WBV time 0 0.437 ( 0.149) 0.632 (0.128) WBV time 30 0.433 (0.166) 0.614 (0.135)
73 Table 4 3 A NOVA results for JPS AE at 15 inversion Variable F value (df) p 2 Condition 0.126 (2,36) .882 .007 Time 2.153 (2,36) .131 .107 Condition*Group 0.701 (2,36) .503 .038 Time*Group 0.948 (2,36) .397 .050 Condition*Time 1.148 (4,72) .341 .060 Condition*Time*Group 0.307 (4,72) .873 .017 significance set at alpha = .05
74 Table 4 4. ANOVA result s for JPS AE at 20 inversion Variabl e F value (df) p 2 Condition 3.475 (2,36) .042 .162 Time 0.326 (2,36) .724 .018 Condition*Group 0.813 (2,36) .452 .043 Time*Group 0.932 (2,36) .403 .049 Condition*Time 0.714 (4,72) .585 .038 Condition*Time*Group 0.217 (4,72) .928 .012 signifi cance set at alpha = .05
75 Figure 4 7 JPS AE mean values at 15 and 20 of inversion
76 Figure 4 8 JPS m ean AE values at 15 for condition
77 Figure 4 9 JPS m ean AE values at 15 for time
78 Figure 4 10. JPS mean AE values at 15 for group and co ndition
79 Figure 4 11 JPS mea n AE values at 15 for group and time
80 Figure 4 12 JPS m ean AE values at 20 for condition ; p < .05
81 Figure 4 1 3 JPS m ean AE values at 20 for time
82 Figure 4 14 JPS mean AE values at 20 for group and conditi on
83 Figure 4 15 JPS mean AE values at 20 for group and time
84 Table 4 5. Mean (+SD) JPS AE at 15 and 20 Ankle Instability Healthy Group Ankle Instability Healthy Group 15 15 20 20 Control time p 2.25 (1.50 ) 3.00 (3.25 ) 1.75 (0.75 ) 2.75 (1.50 ) Control time 0 3.00 (1.00 ) 3.25 (3.00 ) 2.00 (1.00 ) 2.75 (1.50 ) Control time 30 2.50 (1.00 ) 3.00 (2.75 ) 2.25 (1.25 ) 2.75 (1.50 ) Sham time p 3.00 (0.75 ) 2.50 (1.50 ) 2.75 (1.0 0) 3.50 (1.75 ) Sham time 0 3.25 (2.25 ) 2.25 (1.00 ) 2.75 (1.2 5 ) 3.00 (2.25 ) Sham time 30 3.00 (1.25 ) 3.00 (2.00 ) 2 .25 (1.25 ) 3.00 (2.00 ) WBV time p 2.25 (1.25 ) 2.25 (1.50 ) 2.25 (1.00 ) 3.00 (1.75 ) WBV time 0 3.50 (0.75 ) 3.00 (1.50 ) 3.00 (1.00 ) 2.75 ( 2.00 ) WBV time 30 2.75 (1.50 ) 2.25 (1.25 ) 2.50 (1.50 ) 2.50 (1.75 )
85 Table 4 6 A NOVA results for JPS CE at 15 inversion Variable F value (df) p 2 Group 0.590 (1,18) 0. 452 0.0 32 Condition 0.303 (2,36) 0 741 0 017 Time 8.260 (2,36) 0 001 0 315 Condition*Group 0.804 (2,36) 0 455 0 043 Time*Group 8.512 (2,36) 0 001 0 .321 Condition*Time 0.661 (4,72) 0 621 0 .0 35 Condition*Time*Grou p 0.433 (4,72) 0 784 0 .0 23 *significance set at alpha = .05
86 Table 4 7 ANOVA result s for JPS CE at 20 inversion Variable F value (df) p 2 Group 0. 339 (1,18) 0. 568 0. 018 Condition 0.720 (2,36) 0 494 0 038 Time 0.973 (2,36) 0 388 0 .0 5 1 Condition*Group 7 235 (2,36) 0 002 0 287 Time*Group 0.136 (2,36) 0 873 0 .008 Condition*Time 1.563 (4,72) 0 193 0 .0 8 0 Condition*Time*Group 2.986 (4,72) 0 024 0 1 4 2 *significance set at alpha = .05
87 Figure 4 16. JPS CE mean values at 15 an d 20 of inversion
88 Figure 4 17. JPS mean CE values at 15 for condition
89 Figure 4 18. JPS mean CE values at 15 for time ; time p is different than time 30 p < 05
90 Figure 4 19. JPS mean CE at values at 15 for group and condition
91 Figure 4 20 JPS mean CE values at 15 for group and time ; AI group performed differently at time p than time 0, AI group performed differently at time p than time 30, p< .05
92 Figure 4 21 JPS mean values in degrees CE at 20 for condition
93 Fig ure 4 22 JPS mean CE values at 20 for time
94 Figure 4 23 JPS mean CE values in degrees at 20 for group and condition AI group error differed from healthy group error during the sham condition; AI performance differed between the control and sham conditions
95 Figure 4 24. JPS mean CE values at 20 for group and time
96 Table 4 8 Mean ( + SD) JPS CE at 15 and 20 Ankle Instability Healthy Group Ankle Instability Healthy Group 15 15 20 20 Control time p 0.75 (2.00 ) 0.7 (4.00 ) 0.00 (1.00 ) 0.50 (3.25 ) Control time 0 1.5 0 ( 1. 5 0 ) 0.50 (3. 75) 0.75 (1.50 ) 1.00 (2.75 ) Control time 30 1.25 (1.7 5) 1.25 (3.50 ) 0.25 (2.25 ) 1.50 (2.00 ) Sham time p 1.00 (2.25 ) 0. 5 0 (2.50 ) 1.25 (2.00 ) 1.25 (2.75 ) Sham time 0 2.00 (3.2 5) 0.00 ( 1.50 ) 1.25 (2.00 ) 1.00 (1.50 ) Sham time 30 2.00 (2.25 ) 1.25 (3.25 ) 2.00 (1.50 ) ** 0. 5 0 (1.75 ) ** WBV time p 0.75 (1.75 ) 0.75 (2.00 ) 1.25 (1.75 ) 0.25 (3.00 ) WBV time 0 2.00 (2.7 5) 0.50 (2.75 ) 1.00 (2.50 ) 0.75 (2.00 ) WBV time 30 2.00 (2.00 ) 0. 5 0 ( 2.00 ) 1.50 (2.25 ) 0.50 (1.75 ) Groups differed in error at time 0 during the sham condition, p < .05 ; ** Groups differed in error at time 30 during the sham condition p < .05
97 CHAPTER 5 DISCUSSION The aim of the present study was to evaluate ne uromoto r function after WBV training in individuals who have CAI AMI may accompany CAI and WBV may have the potential to increase neural drive excitability therefore investigation of the effects of WBV in individuals who have experienced ankle injury was warrant ed. This is the only study to our knowledge to evaluate the effects of acute WBV on neural drive and proprioception in those with CAI. To address these aims, neuromotor function was evaluated in participants with and without ankle insta bility prior to and immediately following a single bout of WBV. In addition to the treatment condition each participant unde rwent identical evaluations under a control condition as well as a sham condition AMI was evaluated using the H reflex and JPS was observed to gauge p otential proprioceptive changes following treatment. In the following discussion I will address how AMI and proprioception may change with the introduction of WBV. Given that the likelihood of recurrent ankle sprain is high after an the initial ankle spra in and balance plays an important role in preventing such an injury, the principal focus during rehabilitation should be on re establishing effective postural stability and improve neuromuscular control. Our goal was to determine if WBV can improve AMI and postural control in individuals with CAI. Specifically, we tested the hypo theses that introducing WBV would improve 1) AMI by examining H reflex and 2) joint position sense in individuals with history of lateral ankle instability Arthrogenic Muscle Inhib ition The H reflex was used to assess MN pool recruitment, serving as an esti mate of the excitability at the 1a MN synapse One millisecond percutaneous electrical
98 stimulations over the tibial nerve were used to elicit the H reflex as well as direct mu scle stimulation known as an M wave. Maximum H reflexes and maximum M waves were recorded with surface electromyography over the soleus muscle with the knee close to full extension. H max represents an estimate of the number of MNs one is capable of activat ing in a given state, whereas the M max represents activation of the entire MN pool, or maximum muscle activation, and serves as a stable measure. Therefore, comparing the H max :M max ratio indicates the proportion of the entire MN pool capable of being recru ited. Higher ratios (indicating in creased excitability of the MN pool) would indicate reduced muscle inhibition. The fact that there were no differences between baseline H:M ratios among the three visits indicates that we were able to reliabl y measure the H reflex. Therefore, w e are confident that we were able to consistent ly measure the neural drive of the soleus muscle under each treatment condition. Furthermore, muscle length, limb position, and postura l orientation remained constan t for all laboratory v isits and testing sessions because we were able to set and save seat and lever arm position information in the isokinetic dynamometer. The H reflex has been evaluated under different tasks to see what changes occur at the 1a MN synapse level. The exc itability of a MN pool is adjustable for different postures and tasks. These spinal level reflexes are controlled by multiple mechanisms and different pathwa ys [ 184 ] Changing the amou nt of sensory feedback from peripheral afferents is known as gating of spindle afferents. This gating can be achieved by peripheral mechanisms and from supraspinal influences such as greater cortical control sent through descending vestibulospinal pathways Through both descending cortical and peripheral control the gating of afferent feedback is achieved
99 through presynaptic control mechanisms. The change in the gain of the soleus H reflex, which is a measure of the change of H reflex amplitude divided by t he change in background EMG, has been studied across different postures, during locomotion, and tasks of varying complexity [ 185 186 ] The findings indicate that reflex gain can be modulated in a functionally appropriate manner [ 185 186 ] For instance the soleus H reflex amplitude is suppressed in an unstable postural environment indicating greater cortical control over the task and less control at the spinal level to prevent unwanted postural oscillations [ 187 ] The soleus H reflex is depressed with greater muscle activation going from a prone to standing position [ 185 186 ] H reflex suppression increases further from standing to walking as the task complexity rises indicating the gain of the reflex [ 188 ] The adaptability of the reflexes at the spina l control level improve s our efficiency of executing the movement. The neurolo gical mechanisms responsible for modulating the H reflex change during different environmental conditions are presynaptic inhibition (PSI) reciprocal inhibition, recurrent inhib ition, and vestibular influences. PSI likely contributes to mediating change s for different stances given that background EMG increased during periods of postural instability at the same time H reflex was depressed [ 186 ] Under descending control this can involve depolari zation of primary afferents by inhibitory interne urons [ 184 ] The role of different sensory inputs to the MN is important to understand. Visual, somatosensory, and vestibular information all project to the cerebellum and a convergence of the information from these sources allows for inte gration of input from multiple sources to contribute to the H reflex modulation [ 186 ] Soleus H reflex gain is depressed when standing on one leg versus two and when the visual system is removed the H reflex is depressed even more [ 186 ] Pi nar
10 0 and colleagues [ 186 ] found a 24.4% reduction in the gain of soleus H reflex when vision was eliminated and a 68.8% d epression when task complexity increased. PSI may contribute by interrupting 1 a fiber connections to the MN and can be influenced from sensory systems and form supraspinal sites responsible for motor control such as the basal ganglia, motor cortex, and cerebellum [ 186 ] To avoid the effects of PSI, we collected the H reflex in a seated position instead of standing. Using the H reflex McVey et al. [ 19 ] identifi ed AMI in the soleus and peroneal musculature in the involved limb of patients exhibiting unilateral AI. Likewise Palmieri Smith [ 189 ] reported AMI i n the peroneal muscles in those with FAI. The above authors [ 189 ] used s imilar criteria to ours in order to determine whether FAI was present H:M rat io s for the AI group in our study were similar to those observed by McVey et al. [ 19 ] Palmieri Smith et al. [ 189 ] and Sefton et al. [ 151 ] Furthermore, our healthy group values are comparable to H:M ratios found in healthy individuals examined by Jeon and colleagues [ 184 ] in a prone position ( 0.58 ) P almieri Smith et al. [ 189 ] reported ov erall mean H:M ratios of .323 in the FAI group and 0 .4 4 2 in the control grou p. Moreover the se authors found sig nificantly smaller H:M ratios in the involved limb compared to the uninvolved limb ( 0 .32 3 compared to 0 .399 respectively ) indicating side to side differences In the present study the overall mean for H:M ratios in hea lthy controls were 0 .619 compared to 0 .4 67 in the AI group. The d iminished muscle drive appears to persist in those with AI and may be responsible for impaired neuromusc ular firing and muscle weakness and can lead to reinjury and ultimately result in compromised overall joint health [ 136 ]
101 Not all researchers have found lower H:M ratios in individuals with CAI. Sefton and colleagues [ 151 ] failed to find differences in H:M ratio in the soleus muscle of those with CAI. The m ean H:M ratio val ue for the CAI group was 0 .54 compared to 0.56 for the healthy controls Although H:M ratio did not vary among healthy and individ uals with CAI paired reflex depression ( PRD ) and recurrent inhibition were significantly different between the groups [ 151 ] Overall greater le vels of recurrent inhibition were found in th ose with CAI and those with CAI were not able to modulate PRD to the same extent as healthy controls when going from a double to a single limb stance. Based on previous research the nervous system adaptations are likely taking place due to the initial per ipheral joint injury. A possible mechanism for these adaptations is that the mechanoreceptors damaged at the time of the initial injury do not regenerate and their function is never fully regained which can lead to altered afferent exchange that persists. The feed forwar d changes that are observed in C AI may develop as the body tries to compensate for the muscles that become inhibited. Sefton and colleagues [ 151 ] suggest that segmental spinal re flex modulation is used as a central nervous system adaptat ion of CAI Furthermore, correlatio ns have been found between reduced postural control and a decreased ability to modulate spina l reflexes [ 151 ] Sefton et al. [ 151 ] additionally found that CAI participants showed higher overall levels of recurrent inhibition (postsynaptic inhibition) when compared with healthy matched controls. A f ew studies have shown t hat those with poor reflex modulation can be trained in order to improve modulation resulting in better postural control [ 152 153 ] Based on our data, no acute changes were made for MN drive following a single bout of WBV The neural
102 drive remained depressed in those with CAI and no change was found in the healthy group. Whole body Vibration WBV is suggeste d to improve neuromuscular function by enhancing neuromuscular excitability and recruitment patterns by stimulating sensory receptors, specifically the muscle spindles. The mechanisms underlying the improvements associated with WBV are suggested to result from reflex muscle contractions as a ton ic vibration reflex [ 24 25 171 ] Excitation of muscle spindles caus e s reflex contraction leading to e nhanced activity of the Ia loop in which MNs increases by feedback from muscle spindles and the functi on of golgi tendon organs (GTO), which inhibit muscle action are depressed [ 24 25 171 172 ] Researchers have evaluated the effects of WBV on strength and power, as well as ne uromuscular function by measuring muscle activation, electromechanical delay following reflexes and H reflex Acute effects of increased power and strength following a single bout of WBV have been observed [ 190 191 ] Torvinen et al. [ 191 ] found improvements in power strength and balance after a four minute bout of WBV. Long term benefits have also been found ; for instance a fter a 12 week WBV training period, Del e cluse and colleagues [ 192 ] found knee extensor strength increases and countermovement jump height improvements. The se power increases following WBV training could be explained by increases in the ra te of force development which can be measured with explosiv e activities such as jumping. In addition to power, muscle activity has been evaluated during WBV. Increased EMG activity was found in the vastus lateralis and biceps femoris when maintaining an isometric semi squat and while performing dynamic squats whil e on the WBV platform compared to an overground
103 condition [ 173 ] Roelents et al. [ 174 ] found increased muscle activity in the rectus femoris, vastus lateralis, vastus medialis, and gastrocnemius during an unloaded isometric hig h squat, low squat, and one legged squat with WBV compared to a no vibration control condition. Performance improvements are evident with WBV and the enhancements are often thought to be the result of neural changes, specifically increasing muscle spindle sensitivity, however, t here are mixed results of whether the excitability of neuromuscular system changes following WBV Armstrong and authors [ 179 ] investigated the acute effects of WBV on soleus MN excitability f ollowing a single bout of WBV in healthy individuals ; a one minute bout of WBV at 40 Hz was implemented The authors considered the bout to be a moderately high intensity exercise and enough to cause fatigue H reflex was recorded at the test intensity of 30% of M max every 30 seconds for 30 minutes immediately following WBV. All subjects displayed a significant suppression of the H reflex during the first minute post WBV. A limitation of that study is only having a single, one minute bout of WBV when typically five to ten minutes are spent on the modality for therapeutic and exercise based training. In the present study, the acute e ffects on spinal reflex modulation immediately following a five minute session of WBV and measurements were made immediately after and 30 minutes after the training. McB ride and colleagues [ 181 ] evaluated an acute bout of WBV on triceps surae muscle force and MN excitability. Muscle force increased at eigh t minutes following WBV but no differences were found for H:M ratios among the pretest and post tests. The se authors [ 181 ] believe postactivation potentiation (PAP) in which pre exercise muscle contractions lead to subsequent enhanced muscle force output may have led to strength improvements
104 given the MN e during maximal volitional contractions) stayed the same Acute changes to motor output with WBV are thought to be associated with neural factors. One being an increase in sensitiv ity of muscle spindle afferent fibers and facilitation of MN by increasing motor unit recruitment, increasing firing rate, and/or improving synchronization [ 25 ] The improvements seen in muscle performance after WBV train ing appear to occur without an increase in the excitation of the stretch reflex or H reflex [ 177 183 ] The excitation of the patellar tendon stretch reflex remained unchanged [ 177 183 ] and the soleus H reflex was depressed during and [ 182 ] following [ 179 ] WBV This contradicts the notion that improved functional outcome is due to potentiation of reflex activity. In the present study, we did not find a significant reduction in the H:M ratio following WBV. Melnyk and colleagues [ 175 ] investigated the effect of WBV on stretch reflexes involved in knee joint control. Stret ch reflexes of the hamstrings were evoked by inducing an anterior tibial translation while standing before and after a single bout of WBV in the treatment group co mpared to controls. I ncreased size of the short latency response was found along with a reduc ed maximal tibial translation aft er WBV compared to the controls suggesting that the r eflexive joint protection was enhanced in the hamstrings which limit anterior translation of the tibia on the femur after WBV training [ 175 ] Rittweger and colleagues [ 193 ] found potentiation of the patellar stretch reflex following WBV with a simultaneous squat exercise to exhaustion I n contrast Hopkin s et al. [ 176 ] found no differences in electromechanical delay or reaction time in the peroneus longus after a single five minute bout of WBV suggesting muscle spindle
105 sensitivity is not enhanced with WBV. However, the WBV platform used in that study was designed to pivot around a fulcrum so that the feet reciprocally oscillate d instead of having a uniform vertical vibration like the design of a Power Plate used in the current investigation Similar to the present study, Hopkins et al. [ 177 ] did not find improvement in neuromotor control. The se authors [ 177 ] found that the stretch reflex was not potentiated with a single five minute bout of WBV. T he timing and amplitude of the quadriceps stretch reflex were statistically the same between the WBV and control groups [ 177 ] Cochrane and colleagues [ 183 ] examined muscle twitch and patellar reflex properties simultaneously following a five minute bout of WBV in a static squat position. Thr ee conditions were evaluated : WBV with squat, static squat without WBV, and stationary cycling. Peak force, rate of force development and patellar tendon reflex were measured prior to WBV, 90 seconds after and fiv e and ten minutes after each condition. Pea k force and rate of force development was significantly greater with WBV than without WBV or cycling. The patellar tendon reflex was not potentiated after WBV. These authors [ 183 ] therefore concluded that WBV result ed in PAP Further the authors [ 183 ] suggest that the PAP is due to muscle twitch potentiation or an greater myogenic response that occurs with WBV rather than a neural mediated effect that wo u ld be seen with reflex potentiation. The increase in intramuscular temperature from WBV may be a contributing factor of greater muscular effort immediately following WBV [ 194 ] Similar to Cochrane and authors [ 183 ] our investigation did not re veal any change in neural drive at the spina l level We discovered no changes in MN pool recruitment following WBV treatment. However, a trend was found for the sham condition in which H:M rat ios increased from
106 baseline testing to testing 30 minutes later. The sham condition involved maintaining f ive 70 static squats for one minute intervals with one minute of rest between. Although neural drive did not increase immediately following the squats, by thirty minutes it was higher. Due to testing constraints, the Hoffman n reflex was only assessed at t wo time points following the condition, therefore greater increases in neural drive may have taken place between zero and 30 minutes following the squats. Using an active warm up of static squats may have a favorable neuromuscular effect for performan ce. B ased on our findings, WBV combined with static squats does not potentiate the H reflex. Trimble et al. [ 195 ] investigated the effects of an intense bout of volitional resistance exercise on H reflex and detected an acute depression f ollowed by a longer potentiation of the soleus H reflex. Eight sets of ten repetitions of concentric and eccentric muscle contractions of the triceps surae served as the physiological stimuli. Further research is necessary to conclude whether neural drive is increased following a short bout of isometric exercise ( static squats ) Additionally the effects of long term WBV training on neural drive have yet to be determined. Moezy and colleagues [ 178 ] investigated the effects of WBV in patients with anterior cruciate ligament reconstruction. Greater improvements in postural control and proprioception recovery occurred in ACLR patients who were enrolled in a WBV training program compared to conventional therapy [ 178 ] Identi cal rehabilitation programs bega n immediately after surgery, the only difference was the introduction of WBV training at 12 weeks postoperatively. Improvements in postural control were found and w ere suggested to be due to better synchronization of motor unit firing and cocontraction of synergist muscles with the mechanical vibration [ 178 ] Although enhanced neural drive
107 following WBV was not evident in our study, future research should evaluate introducing WBV training earlier in the rehabilitation process after experiencing a lateral ankle sprain. All of our participants that had AI were at least a year out from the initial lateral ankle sprain thereby allowing for potential neuromuscular feedback adjustments to set in WBV tr aining may have potential to overcome propriocepti ve deficits due to impaired neural drive after the initial injury if implemented in a similar fashion to Moez y and colleagues [ 178 ] approach to incorporate the WBV early on during rehabilitation. Our investigation used WBV oscillating at 35 Hz at a depth of approximately four mm, settings that have been used in previous research F in ding optimal training frequency, duration, intensity and platform amplitude of WBV training to match rehabilitation goals should be the focus of treatment studies in the future One factor to consider regarding typical WBV training is that the most common body orientation to be in while on the platform is a squat During a squat the ankle is dorsiflexed thereby putting the gastrocnemius and soleus on stretch. H:M ratios have been shown to be depressed during a stretch [ 196 197 ] Little research has been done evaluating MN excitability following a static stretch Following a static stretch training program of 30 sessions H:M ratios were reduced after the 30 th session but no changes were seen after the first 10 or 20 sessions. The neural effects were transient and H:M ratios returned back to baseline when a retention test was administered 30 days later [ 198 ] Avela et al. [ 199 ] identified immediate reduction in the H reflex ( 43%) following repeated prolonged active stretching lasting an hour The re duction of the H:M ratio was much less at 15 and 30 minutes following the stretch protocol [ 199 ] Stretching may have a inhibitory effect on the drive and may decrease the overall MN excitability. If this
108 is the case, it would serve as a possible explanation of the lack of increase in MN excitability. Proprioception Proprioception provides afferent sensory information about body movement and location. JPS is a reliable gauge to evaluate proprioceptio n in both healthy and clinical populations. Our study assessed ankle proprioception with a passive JPS method using an isokinetic dynamometer. Both absolute and constant errors were calculated in order to thorough ly evaluate the magnitude and direction of error individuals with CAI were making. There are mixed findings regarding whether individuals with C AI have JPS deficits [ 200 ] Our study is the first to evaluate proprioception following WBV in individuals with CAI. We found only one other study which has measured ankle JPS after WBV training in healthy individuals. Similar to our study, Pollock et al. [ 201 ] evaluated JPS after five one minute bouts of WBV at 30 Hz taking measurements before, immediately 15 a nd 30 minutes following the treatment. Dorsiflexion JPS at 5 10 and 15 was not affected by the single bout of WBV Mean absolute angle error was approximately 1.5 for the healthy population The present study revealed no differences in JPS performance between the CAI and healthy group The mean AE in our study was 2.43 and 2.82 for the CAI group versus 2.89 and 2. 75 in the healthy group at 15 and 20 respectively Sekir et al. [ 114 ] found higher passive JP S error in the involved ankle of individuals with AI (2.35 at 10 and 3.10 At 20 ) compared to the uninvolved side (1.50 at 10 and 1.79 at 20 ). Similar procedures were implemented in our study in which JPS was assessed with an isokinetic dynamometer usi ng continuous passive mode. Furthermore, the authors [ 114 ] calculated the reliability for the JPS procedure that yielded intraclass coefficients of 0.90 and 0.94 at 10 and 20 respectively. Following a 6 week
109 isok inetic strengthening program, JPS at 10 and 20 degrees improved in the injured ankle by approximately 1 at both target angles [ 114 ] R e establishing proprioception following injury may facilitate the improvement o f postural control and foot positioning at foot strike during gait The mean inversion JPS error values we observed in the CAI and healthy groups are comparable to the values of several other studies. Konradsen and Magnusson [ 98 ] f ou nd that the AE during active JPS was significantly greater in the affected ankle of individuals with unilateral AI (2.5 ) compared to the uninjured side (2.0 ) as well as when compared to healthy controls (1.7 ). Similarly, Nakasa et al [ 112 ] found side to s ide diffe rences of 1.0 for those with AI compared to .2 in the healthy group and an overall statistically significant deficit in the AI group. When looking at constant error, Willems et al. [ 69 ] reported that both the FAI and contr ol groups underestimated the passive inversion angle to a greater extent than controls did. Mean CE for the FAI and control groups were 7. 90 and 7. 68 respectively, somewhat higher than the mean CE found in our study Similarly, Brown et al. [ 110 ] found larger mean AE for passive JPS of 5.90 in FAI group and 5.13 in the controls. Like our study, Brown et al. [ 110 ] failed to find differences between the CAI group and healthy group. The mean CE we discovered was 1.32 and 0.80 in the CAI group versus 0.68 and 0.43 in the healthy g roup at 15 and 20 respectively When taking direction of the error into consideration, our study revealed that both groups overshot the target angles Similarly, Sefton et al. [ 111 ] reported that both the CA I and healthy groups overshot the inversion target angle of 15 with no significant differences between the group means In our study, reference angles were passively introduced and replication of the target angle was passive
110 Electromechanical delay may h ave contributed to overestimation of the target angle since the participant actively produced a counterforce once t he target angle was perceived. Conversely Sefton et al. [ 111 ] used an active replication proce dure after a passive target was introduced and the participants in the CAI and healthy groups overshot the target with means of 1.70 and 0.64, respectively. Yokoyama and colleagues [ 113 ] evaluated combined plantarflexion angles with either 10 or 20 of inversion and found that those with FAI underestimated the plantarflexion angle. The clinical significance of someone who has AI and presents with impaired JP S is of interest. As suggested by Konradsen and Voigt [ 51 ] if the ankle is more inverted at foot strike during gait, one may be at greater risk to incur a sprain due to the improper foot positioning. This notion is further reinforced by the findings of Delah unt and colleagues [ 64 ] who found that those with AI had greater amounts of inversion just prior to foot strike. Interesti ngly t he WBV treatment had no effect on JPS AE or CE We chose the five minute duration of WBV so not to reach the threshold of fatigue [ 158 ] A few studies have evaluated the effects of fatigue on ankle JPS in healthy individuals [ 202 203 ] Sandrey et al. [ 202 ] found that postfatigue AE at inversion angles of 10 and 20 increased in young healthy adults. The fatigue protocol involved performing concentric and eccentric exercise of the ankle evertor s using an isokinetic dynamometer at speeds of 60 /second until force was half of the maximum voluntary contraction JPS AE increased from a mean of 1.56 to 2.44 at 10 and 2.00 to 3.12 at 20 [ 202 ] These values are in line with the error that both groups presented with following WBV in our study. Prior to WBV, AE was 2.25 in the CAI group and 2.25 in the healthy group when tested at 15 and 2.25 and 3.0 0 at 20, respectively. AE in creased to 3.50 at
111 15 and 3.00 at 20 in the CAI group immediately following WBV then decreased to 2.75 and 2.50 at 30 minutes after WBV however still remained slightly elevated Proprioception performance statistically remained the same following a single bout of WBV in both groups. On a case by case basis, WBV actually caused a decline in performance. The differences in AE were not statistically significant which may in part by due to low effect sizes. H owever clinically it may be meaningful that those with CAI had worse performance following WBV For CE, the CAI group overestimated the amount of inversion at 15 immediately following and 30 mi nutes after WBV, increasing from 0.78 to 2.02 and 1.92 of error, respectively. Concerning CE at 20, the CAI group went from a baseline of 1.36 error to 0.99 immediately after WBV. Performance then decreased to 1.54 of error 30 minutes following WBV. The peroneal muscles eccentrically contract and guard against excessive amounts of inversion. Whether walking, running, or landing from a jump, the amount of inversion detected at foot strike is important to avoid improper foot positioning that can lead t o a sprain. If someone with may put the person at greater ri sk of a lateral ankle sprain. Evaluating the variability of the error during the JPS task can give insigh t to the testing time We reviewed the standard deviations of AE and CE for both groups During the control condition mean AE at 15 ranged from 2.25 to 3.00 in both groups w ith corresp onding standard deviations ranging from 1.50 to 3.25 with variability exceeding the group mean s at times When compared to the WBV condition, baseline means and standard deviations were similar to the control condition in which both
112 groups ha d a mean error of 2.25 and standard deviations were 1.25 in the CAI group and 1.50 in the healthy group for JPS at 15 Immediately following WBV (time 0) mean AE increased while variability remained the same as pre test (time p) values (mean + standar d deviation: CAI 3.50 + 1.00, healthy 3.00 + 1.75). Likewise, at time 30 variability was similar to time p and time 0 ( mean + standard deviation: CAI 2.75 + 1.50 healthy 2.25 + 1.25 ) At 20, mean AE ranged from 1.75 to 2.75 in both groups with standard deviations ranging from 0.75 to 1.50 during the control condition. Variability did not increase across testing times during the WBV condition ( mean + standard deviation: time p CAI 2.25 + 1.00, healthy 3.00 + 1.50; time 0 CAI 3.00 + 1.00, healthy 2.75 + 2.00; time 30 CAI 2.50 + 1.50 healthy 2.50 + 1.75 ). When evaluating CE, variability more than doubled that of the mean error scores at times during the control condition ( mean + standard deviation: 15 time p CAI 0.75 + 2.00, healt hy 0.75 + 4.00; time 0 CAI 1.50 + 1.50, healthy 0.50 + 3 .50; time 30 CAI 1.25 + 1.75 healthy 1 25 + 3.50 ; 20 time p CAI 0.00 + 1.00, healthy 0.50 + 3.25; time 0 CAI 0.75 + 1.50, healthy 1.00 + 2.75; time 30 CAI 0.25 + 2.25 healthy 1 .50 + 2.00 ). Variability did not increase following WBV ( mean + standard deviation: 15 time p CAI 0.75 + 1.50 healthy 0.75 + 2.00 ; time 0 CAI 2.00 + 2.75 healthy 0.50 + 2.75 ; time 30 CAI 2.00 + 2.00 healthy 0.50 + 2.00 ; 20 time p CAI 1.2 5 + 1.75 healthy 0.25 + 3.00 ; time 0 CAI 1.00 + 2.50 healthy 0.75 + 2.00 ; time 30 CAI 1.50 + 2.25 healthy 0.50 + 1.75 ) Due to high variability of performance compared to the mean s cores statistical differences were not evident. Overall, WB V did not cause a rise in variability. More importantly, WBV did not result in improved proprioception.
113 Mohammadi et al. [ 203 ] evaluated active and passive JPS AE following a n evertor muscle fatigue protocol as we ll as playing soccer for 45 minutes in soccer players Active JPS error increased from 1.9 to 3.2 at of 15 and 1.7 to 2.9 at a target angle [ 203 ] Likewis e, passive JPS error increased from 2.8 to 4.7 and 2.3 to 3.9, respectively [ 203 ] Fatigue may influence the mechanorecptors in the muscles that provide dynamic support of the ankle [ 203 ] Furthermore, the ability to perceive ankle JPS and to make postural adjustments in response to the detected angles is thought to be crucial to prevent an ankle sprain [ 69 ] We do not believe to have indu ced fatigue with WBV in our investigation, but it is an important consideration when using WBV as a rehabilitative tool not to reach fatigue and then engage in activities where the ankle is vulnerable to the mechanisms of a sprain Limitations Multiple me asures of the H reflex among condition s and across condition s have inherent variability in the H max and M max peak to peak amplitudes. Although every effort was made to replicate limb position at each testing session, some variability may have occurred. P ar ticipants were asked to avoid caffeine intake on testing days as well as not to increase the intensity or difficulty of their current exercise regimen so not to induce muscle fatigue, both of which can affect the Hoffmann reflex. Although the participant s verbally said they complied with the requests, there is no way of knowing if they did in fact comply. Although the soleus muscle is a dynamic ankle stabilizer, it may not be the optimal choice to evaluate MN excitability for those with lateral AI given th e mechanism of injury involves mainly frontal motion However, the soleus is often assessed to gain
114 insight of changes in spinal control under different postures and varying tasks [ 184 187 ] Furthermore, AMI has been found in the soleus and peroneals in individuals with CAI indicating that both muscles are affected due to the injury. Sudden inversion combined with plantar flexion is the motion that typically result s in a lateral ankle sprain. Evaluation of the peroneal musculature, which primarily evert s the ankle and aid s in protecting against an inversion torque, may allow better insight to AMI in those with C AI. Given the ease of finding an H reflex in the soleus muscle the soleus was chosen for evaluation instead of the peroneal muscles. Furthermore, we evaluated proprioception in a single direction, inversion, which is a frontal plane motion Evaluating plantarflexion the primary action of the soleus, would ha ve better matched the sagittal proprioception measures with the AMI assessed in the soleus muscle Another limitation we encountered was having a l imited sample size for the AI and healthy groups Small sample sizes may have contributed to nonsignificant results for H:M ratios and JPS. The observed power that corresponded with the main effect for group for H:M ratios was 0.618 Observed p ower for several comparisons were below an optimal value of 0.80. Furthermore, effect size was less than optimal for mul tiple comparisons Another limitation in our investigation is a possible ceiling effect that may have occurred due to the inclusion of high functioning CAI participants Other researchers [ 121 204 ] have recruited individuals with CAI who score 85% or lower on the FADI Hale and Hertel [ 180 ] examined the FADI and FADI S and determined that both were sensitive to deficits associated with CAI. The au thors [ 180 ] observed scores of 90% for the FADI and 80% on the FADI S in those with CAI Five participants with CAI scored 95% on the
115 FADI while the other scores ranged from 77% to 93%. As for the FADI S, scores for our CAI participants ranged from 34% to 84%. Including h igh functioning CAI partic ipants may have reduced the chance of proprioceptive improvements. A final limitation of our study is the possible error in estimation associated with the electromechanical delay during the JPS testing. A lag may have occurred between the perception of the passively presented inversion target angle and the reaction time to produce a counteraction force with voluntary contraction which may account for the overestimation of the target angle However, as previously noted, Sefton et al. [ 111 ] also observed over estimation of the target angle using an active JPS procedure which does not rely on reaction time as the passive procedures implemented in our investigation. Co nclusion Neural drive is diminished in the invo lved limb of individuals with ankle instability. JPS performance was the same between those with CAI and healthy controls. A single bout of WBV did not improve AMI or proprioception in those with CAI nor did it have a benefit to healthy individuals. Furthe rmore, WBV deteriorated JPS performance, although not to a statistically significant level The acute performance improvements that have been observed by researchers following WBV are not due enhanced neural drive as many have suggest given that the H refl ex was not potentiated. While no gains were found with one bout, f uture research should evaluate introducing WBV training during rehabilitation especially when addressing the recovery of balance and proprioception WBV may have the potential to overcome t hese deficits as a result of strengthening the sensorimotor pathways that are intact. It is important that future studies focus on finding optimal training frequency, duration, intensity and platform amplitude of WBV training to match rehabilitation goals
116 APPENDIX A FOOT AND ANKLE DISABILITY INDEX Please answer every question with one response that most closely describes your condition within the past week. If the activity in question is limited by something other than your foot or ankle, mark N/A. Rate t he function as no difficulty at all (4), slightly difficult (3), moderately difficult (2), extreme difficulty (1), unable to do (0). Rate the pain as no pain (4), mild (3), moderate (2), severe (1), or unbearable (0). Foot and Ankle Disability Index Left Ankle Right Ankle Function Pain Function Pain ____ Standing ____ ____ Wal king on even ground ____ ____ Walking on even ground without shoes ____ ____ Walking up hills ____ ____ Walking down hills ____ ____ Going up stairs ____ ____ Going down stairs ____ ____ Walking on uneven ground ____ ____ Steppin g up and down curves ____ ____ Squatting ____ ____ Sleeping ____ ____ Com ing up on your toes ____ ____ Walking initially ____ ____ Walking 5 minutes or less ____ ____ Walking app roximately 10 minutes ____ ____ Walking 1 5 minutes or greater ____ ____ Ho me responsibilities ____ ____ Activit ies of daily living ____ ____ Personal care ____ ____ Light to moderate work (standing, wal king) ____ ____ Heavy work ____ (push/pulling, climbing, carrying) ____ Recr eational activities ____ ____ General level of pain ____ ____ Pain at rest ____ ____ Pain during your normal activity ____ ____ Pain first thing in the morning ____
117 Foot and Ankle Disability Index Sport Function Pain Function Pain ____ ____ Running ____ ____ ____ ____ Jumping ____ ____ ____ ____ Landing ____ ____ ____ ____ Squatting and stopping quickly ____ ____ ____ ____ Cutting, lateral movements ____ ____ ___ ____ Low impact activities ____ ____ ____ ____ Abi lity to perform activity with ____ ____ your normal technique ____ ____ Ability to particip ate in your desired ____ ____ sport as long as you would like.
118 APPENDIX B PHYSICAL ACTIVITY AND DIETARY RECALL QUESTIONNAIRE How many times a week do you exercise? What kinds of activities do you do when exerc ising (e.g. cardio, weight training)? Did you sleep a normal amount last night? How many hours a night do you normally sleep? Did you eat normally yesterday? Have you eaten normally today? Did you have breakfast this morning? What did you have for breakfas t and at what time did you eat? If applicable, what did you have for lunch today and at what time did you eat ? Did you have a normal amount of liquids yesterday? What did you drink yesterday? What have you had to drink today?
119 LIST OF REFERENCES 1. Kannus P, Renstrom P. Treatment for acute tears of the lateral ligaments of the ankle. Operation, cast, or early controlled mobilization. J Bone Joint Surg Am. 1991 Feb;73(2):305 12 2. Hintermann B, Boss A, Schafer D. Arthroscopic findings in patients with chronic ankle instability. Am J Sports Med. 2002 May Jun;30(3):402 9 3. Osborne MD, Rizzo TD, Jr. Prevention and treatment of ankle sprain in athletes. Sports Med. 2003;33(15):1145 50 4. Valderrabano V, Hintermann B, Horisberger M, Fung TS. L igamentous posttraumatic ankle osteoarthritis. Am J Sports Med. 2006 Apr;34(4):612 20 5. Harrington KD. Degenerative arthritis of the ankle secondary to long standing lateral ligament instability. J Bone Joint Surg Am. 1979 Apr;61(3):354 61 6. Gross P, Mar ti B. Risk of degenerative ankle joint disease in volleyball players: study of former elite athletes. Int J Sports Med. 1999 Jan;20(1):58 63 7. Staples OS. Ruptures of the fibular collateral ligaments of the ankle. Result study of immediate surgical treatm ent. J Bone Joint Surg Am. 1975 Jan;57(1):101 7 8. Verhagen RA, de Keizer G, van Dijk CN. Long term follow up of inversion trauma of the ankle. Arch Orthop Trauma Surg. 1995;114(2):92 6 9. Gerber JP, Williams GN, Scoville CR, Arciero RA, Taylor DC. Persist ent disability associated with ankle sprains: a prospective examination of an athletic population. Foot Ankle Int. 1998 Oct;19(10):653 60 10. Smith RW, Reischl SF. Treatment of ankle sprains in young athletes. Am J Sports Med. 1986 Nov Dec;14(6):465 71 11. Konradsen L, Olesen S, Hansen HM. Ankle sensorimotor control and eversion strength after acute ankle inversion injuries. Am J Sports Med. 1998 Jan Feb;26(1):72 7 12. Yeung MS, Chan KM, So CH, Yuan WY. An epidemiological survey on ankle sprain. Br J Sports Med. 1994 Jun;28(2):112 6 13. Freeman MA. Instability of the foot after injuries to the lateral ligament of the ankle. J Bone Joint Surg Br. 1965 Nov;47(4):669 77 14. Wikstrom EA, Naik S, Lodha N, Cauraugh JH. Balance capabilities after lateral ankle trau ma and intervention: a meta analysis. Med Sci Sports Exerc. 2009 Jun;41(6):1287 95
120 15. Bosco C, Colli R, Introini E, Cardinale M, Tsarpela O, Madella A, et al. Adaptive responses of human skeletal muscle to vibration exposure. Clin Physiol. 1999 Mar;19(2): 183 7 16. Mahieu NN, Witvrouw E, Van de Voorde D, Michilsens D, Arbyn V, Van den Broecke W. Improving strength and postural control in young skiers: whole body vibration versus equivalent resistance training. J Athl Train. 2006 Jul Sep;41(3):286 93 17. Pal mieri RM, Tom JA, Edwards JE, Weltman A, Saliba EN, Mistry DJ, et al. Arthrogenic muscle response induced by an experimental knee joint effusion is mediated by pre and post synaptic spinal mechanisms. J Electromyogr Kinesiol. 2004 Dec;14(6):631 40 18. Zeh r EP. Considerations for use of the Hoffmann reflex in exercise studies. Eur J Appl Physiol. 2002 Apr;86(6):455 68 19. McVey ED, Palmieri RM, Docherty CL, Zinder SM, Ingersoll CD. Arthrogenic muscle inhibition in the leg muscles of subjects exhibiting func tional ankle instability. Foot Ankle Int. 2005 Dec;26(12):1055 61 20. Baumhauer JF, Alosa DM, Renstrom AF, Trevino S, Beynnon B. A prospective study of ankle injury risk factors. Am J Sports Med. 1995 Sep Oct;23(5):564 70 21. Fong DT, Hong Y, Chan LK, Yung PS, Chan KM. A systematic review on ankle injury and ankle sprain in sports. Sports Med. 2007;37(1):73 94 22. Ferkel RD, Chams RN. Chronic lateral instability: arthroscopic findings and long term results. Foot Ankle Int. 2007 Jan;28(1):24 31 23. Burke D, Hagbarth KE, Lofstedt L, Wallin BG. The responses of human muscle spindle endings to vibration of non contracting muscles. J Physiol. 1976 Oct;261(3):673 93 24. Roll JP, Vedel JP, Ribot E. Alteration of proprioceptive messages induced by tendon vibration i n man: a microneurographic study. Exp Brain Res. 1989;76(1):213 22 25. Cardinale M, Bosco C. The use of vibration as an exercise intervention. Exerc Sport Sci Rev. 2003 Jan;31(1):3 7 26. Hertel J. Functional instability following lateral ankle sprain. Spor ts Med. 2000 May;29(5):361 71 27. Hertel J. Functional Anatomy, Pathomechanics, and Pathophysiology of Lateral Ankle Instability. J Athl Train. 2002 Dec;37(4):364 75
121 28. Tropp H, Ekstrand J, Gillquist J. Factors affecting stabilometry recordings of single limb stance. Am J Sports Med. 1984 May Jun;12(3):185 8 29. Takao M, Innami K, Matsushita T, Uchio Y, Ochi M. Arthroscopic and magnetic resonance image appearance and reconstruction of the anterior talofibular ligament in cases of apparent functional ankle instability. Am J Sports Med. 2008 Aug;36(8):1542 7 30. Brown C, Padua D, Marshall SW, Guskiewicz K. Individuals with mechanical ankle instability exhibit different motion patterns than those with functional ankle instability and ankle sprain copers. Clin Biomech (Bristol, Avon). 2008 Jul;23(6):822 31 31. Wikstrom EA, Tillman MD, Chmielewski TL, Cauraugh JH, Naugle KE, Borsa PA. Self assessed disability and functional performance in individuals with and without ankle instability: a case control study. J Ort hop Sports Phys Ther. 2009 Jun;39(6):458 67 32. Wikstrom EA, Tillman MD, Chmielewski TL, Cauraugh JH, Naugle KE, Borsa PA. Dynamic postural control but not mechanical stability differs among those with and without chronic ankle instability. Scand J Med Sci Sports. 2010 Feb;20(1):e137 44 33. Hubbard TJ. Ligament laxity following inversion injury with and without chronic ankle instability. Foot Ankle Int. 2008 Mar;29(3):305 11 34. Lundberg A, Svensson OK, Nemeth G, Selvik G. The axis of rotation of the ankle joint. J Bone Joint Surg Br. 1989 Jan;71(1):94 9 35. Inman V. The Joints of the Ankle. Baltimore, MD: Williams & Wilkins; 1976 36. Kirby KA. Subtalar joint axis location and rotational equilibrium theory of foot function. J Am Podiatr Med Assoc. 2001 Oct;9 1(9):465 87 37. Stormont DM, Morrey BF, An KN, Cass JR. Stability of the loaded ankle. Relation between articular restraint and primary and secondary static restraints. Am J Sports Med. 1985 Sep Oct;13(5):295 300 38. Renstrom P, Wertz M, Incavo S, Pope M, Ostgaard HC, Arms S, et al. Strain in the lateral ligaments of the ankle. Foot Ankle. 1988 Oct;9(2):59 63 39. Stephens MM, Sammarco GJ. The stabilizing role of the lateral ligament complex around the ankle and subtalar joints. Foot Ankle. 1992 Mar Apr;13(3 ):130 6 40. Kjaersgaard Andersen P, Wethelund JO, Helmig P, Soballe K. The stabilizing effect of the ligamentous structures in the sinus and canalis tarsi on movements in the hindfoot. An experimental study. Am J Sports Med. 1988 Sep Oct;16(5):512 6
122 41. Me yer JM, Lagier R. Post traumatic sinus tarsi syndrome. An anatomical and radiological study. Acta Orthop Scand. 1977 May;48(1):121 8 42. Balduini FC, Tetzlaff J. Historical perspectives on injuries of the ligaments of the ankle. Clin Sports Med. 1982 Mar;1 (1):3 12 43. Fuller EA. Center of pressure and its theoretical relationship to foot pathology. J Am Podiatr Med Assoc. 1999 Jun;89(6):278 91 44. Kirby RL, Price NA, MacLeod DA. The influence of foot position on standing balance. J Biomech. 1987;20(4):423 7 45. Attarian DE, McCrackin HJ, DeVito DP, McElhaney JH, Garrett WE, Jr. Biomechanical characteristics of human ankle ligaments. Foot Ankle. 1985 Oct;6(2):54 8 46. Renstrom PA, Konradsen L. Ankle ligament injuries. Br J Sports Med. 1997 Mar;31(1):11 20 47. Lindenfeld TN. The differentiation and treatment of ankle sprains. Orthopedics. 1988 Jan;11(1):203 6 48. Balduini FC, Vegso JJ, Torg JS, Torg E. Management and rehabilitation of ligamentous injuries to the ankle. Sports Med. 1987 Sep Oct;4(5):364 80 49. T ropp H. Commentary: Functional Ankle Instability Revisited. J Athl Train. 2002 Dec;37(4):512 5 50. Mann RA. Surgical implications of biomechanics of the foot and ankle. Clin Orthop Relat Res. 1980 Jan Feb(146):111 8 51. Konradsen L, Voigt M, Hojsgaard C. A nkle inversion injuries. The role of the dynamic defense mechanism. Am J Sports Med. 1997 Jan Feb;25(1):54 8 52. Lofvenberg R, Karrholm J, Sundelin G, Ahlgren O. Prolonged reaction time in patients with chronic lateral instability of the ankle. Am J Sports Med. 1995 Jul Aug;23(4):414 7 53. Karlsson J, Andreasson GO. The effect of external ankle support in chronic lateral ankle joint instability. An electromyographic study. Am J Sports Med. 1992 May Jun;20(3):257 61 54. Vaes P, Duquet W, Van Gheluwe B. Peron eal Reaction Times and Eversion Motor Response in Healthy and Unstable Ankles. J Athl Train. 2002 Dec;37(4):475 80 55. Hubbard TJ, Hertel J. Mechanical contributions to chronic lateral ankle instability. Sports Med. 2006;36(3):263 77
123 56. Bosien WR, Staples OS, Russell SW. Residual disability following acute ankle sprains. J Bone Joint Surg Am. 1955 Dec;37 A(6):1237 43 57. Anderson KJ, Lecocq JF, Lecocq EA. Recurrent anterior subluxation of the ankle joint; a report of two cases and an experimental study. J Bone Joint Surg Am. 1952 Oct;34 A(4):853 60 58. Erickson SJ, Smith JW, Ruiz ME, Fitzgerald SW, Kneeland JB, Johnson JE, et al. MR imaging of the lateral collateral ligament of the ankle. AJR Am J Roentgenol. 1991 Jan;156(1):131 6 59. Siegler S, Chen J, Sch neck CD. The effect of damage to the lateral collateral ligaments on the mechanical characteristics of the ankle joint -an in vitro study. J Biomech Eng. 1990 May;112(2):129 37 60. Denegar CR, Miller SJ, 3rd. Can Chronic Ankle Instability Be Prevented? Ret hinking Management of Lateral Ankle Sprains. J Athl Train. 2002 Dec;37(4):430 5 61. Caulfield BM, Garrett M. Functional instability of the ankle: differences in patterns of ankle and knee movement prior to and post landing in a single leg jump. Int J Sport s Med. 2002 Jan;23(1):64 8 62. Spaulding SJ, Livingston LA, Hartsell HD. The influence of external orthotic support on the adaptive gait characteristics of individuals with chronically unstable ankles. Gait Posture. 2003 Apr;17(2):152 8 63. Konradsen L. Se nsori motor control of the uninjured and injured human ankle. J Electromyogr Kinesiol. 2002 Jun;12(3):199 203 64. Delahunt E, Monaghan K, Caulfield B. Altered neuromuscular control and ankle joint kinematics during walking in subjects with functional insta bility of the ankle joint. Am J Sports Med. 2006 Dec;34(12):1970 6 65. Monaghan K, Delahunt E, Caulfield B. Ankle function during gait in patients with chronic ankle instability compared to controls. Clin Biomech (Bristol, Avon). 2006 Feb;21(2):168 74 66. Hopkins JT, McLoda T, McCaw S. Muscle activation following sudden ankle inversion during standing and walking. European Journal of Applied Physiology. 2007 Mar;99(4):371 8 67. Dietz V. Human Neuronal Control of Automatic Functional Movements Interaction between Central Programs and Afferent Input. Physiol Rev. 1992 Jan;72(1):33 69 68. Glencross D, Thornton E. Position sense following joint injury. J Sports Med Phys Fitness. 1981 Mar;21(1):23 7
124 69. Willems T, Witvrouw E, Verstuyft J, Vaes P, De Clercq D. P roprioception and Muscle Strength in Subjects With a History of Ankle Sprains and Chronic Instability. J Athl Train. 2002 Dec;37(4):487 93 70. Garn SN, Newton RA. Kinesthetic awareness in subjects with multiple ankle sprains. Phys Ther. 1988 Nov;68(11):166 7 71 71. Forkin DM, Koczur C, Battle R, Newton RA. Evaluation of kinesthetic deficits indicative of balance control in gymnasts with unilateral chronic ankle sprains. J Orthop Sports Phys Ther. 1996 Apr;23(4):245 50 72. Lentell G, Baas B, Lopez D, McGuire L, Sarrels M, Snyder P. The contributions of proprioceptive deficits, muscle function, and anatomic laxity to functional instability of the ankle. J Orthop Sports Phys Ther. 1995 Apr;21(4):206 15 73. Halasi T, Kynsburg A, Tallay A, Berkes I. Changes in joi nt position sense after surgically treated chronic lateral ankle instability. Br J Sports Med. 2005 Nov;39(11):818 24 74. Lynch SA, Eklund U, Gottlieb D, Renstrom PA, Beynnon B. Electromyographic latency changes in the ankle musculature during inversion mo ments. Am J Sports Med. 1996 May Jun;24(3):362 9 75. Brunt D, Andersen JC, Huntsman B, Reinhert LB, Thorell AC, Sterling JC. Postural responses to lateral perturbation in healthy subjects and ankle sprain patients. Med Sci Sports Exerc. 1992 Feb;24(2):171 6 76. Bullock Saxton JE, Janda V, Bullock MI. The influence of ankle sprain injury on muscle activation during hip extension. Int J Sports Med. 1994 Aug;15(6):330 4 77. Bullock Saxton JE. Sensory changes associated with severe ankle sprain. Scand J Rehabil Med. 1995 Sep;27(3):161 7 78. Konradsen L, Ravn JB. Ankle instability caused by prolonged peroneal reaction time. Acta Orthop Scand. 1990 Oct;61(5):388 90 79. Tropp H, Odenrick P. Postural control in single limb stance. J Orthop Res. 1988;6(6):833 9 80. R ose A, Lee RJ, Williams RM, Thomson LC, Forsyth A. Functional instability in non contact ankle ligament injuries. Br J Sports Med. 2000 Oct;34(5):352 8 81. Docherty CL, Valovich McLeod TC, Shultz SJ. Postural control deficits in participants with functiona l ankle instability as measured by the balance error scoring system. Clin J Sport Med. 2006 May;16(3):203 8
125 82. Ross SE, Guskiewicz KM. Examination of static and dynamic postural stability in individuals with functionally stable and unstable ankles. Clin J Sport Med. 2004 Nov;14(6):332 8 83. Wikstrom EA, Tillman MD, Borsa PA. Detection of dynamic stability deficits in subjects with functional ankle instability. Med Sci Sports Exerc. 2005 Feb;37(2):169 75 84. Goldie PA, Evans OM, Bach TM. Postural control fo llowing inversion injuries of the ankle. Arch Phys Med Rehabil. 1994 Sep;75(9):969 75 85. Perrin PP, Bene MC, Perrin CA, Durupt D. Ankle trauma significantly impairs posture control -a study in basketball players and controls. Int J Sports Med. 1997 Jul;18 (5):387 92 86. Hartsell HD, Spaulding SJ. Eccentric/concentric ratios at selected velocities for the invertor and evertor muscles of the chronically unstable ankle. Br J Sports Med. 1999 Aug;33(4):255 8 87. Friden T, Zatterstrom R, Lindstrand A, Moritz U. A stabilometric technique for evaluation of lower limb instabilities. Am J Sports Med. 1989 Jan Feb;17(1):118 22 88. Gribble PA, Hertel J, Denegar CR, Buckley WE. The Effects of Fatigue and Chronic Ankle Instability on Dynamic Postural Control. J Athl Trai n. 2004 Dec;39(4):321 9 89. Cornwall MW, Murrell P. Postural sway following inversion sprain of the ankle. J Am Podiatr Med Assoc. 1991 May;81(5):243 7 90. Kleinrensink GJ, Stoeckart R, Meulstee J, Kaulesar Sukul DM, Vleeming A, Snijders CJ, et al. Lowered motor conduction velocity of the peroneal nerve after inversion trauma. Med Sci Sports Exerc. 1994 Jul;26(7):877 83 91. O'Neill PJ, Parks BG, Walsh R, Simmons LM, Miller SD. Excursion and strain of the superficial peroneal nerve during inversion ankle spr ain. J Bone Joint Surg Am. 2007 May;89(5):979 86 92. Evans T, Hertel J, Sebastianelli W. Bilateral deficits in postural control following lateral ankle sprain. Foot Ankle Int. 2004 Nov;25(11):833 9 93. Isakov E, Mizrahi, J., Solzi, P., Susak, Z., Lotem M. Response of the Peroneal Muscles to Sudden Inversion of the Ankle During Standing. Journal of Applied Biomechanics. 1986;02(02):100 9 94. Hass CJ, Bishop MD, Doidge D, Wikstrom EA. Chronic ankle instability alters central organization of movement. Am J Spo rts Med. 2010 Apr;38(4):829 34
126 95. Wikstrom EA, Bishop MD, Inamdar AD, Hass CJ. Gait termination control strategies are altered in chronic ankle instability subjects. Med Sci Sports Exerc. 2010 Jan;42(1):197 205 96. Delahunt E, Monaghan K, Caulfield B. Cha nges in lower limb kinematics, kinetics, and muscle activity in subjects with functional instability of the ankle joint during a single leg drop jump. J Orthop Res. 2006 Oct;24(10):1991 2000 97. Hopkins JT, Brown TN, Christensen L, Palmieri Smith RM. Defic its in peroneal latency and electromechanical delay in patients with functional ankle instability. J Orthop Res. 2009 Dec;27(12):1541 6 98. Konradsen L, Magnusson P. Increased inversion angle replication error in functional ankle instability. Knee Surg Spo rts Traumatol Arthrosc. 2000;8(4):246 51 99. Konradsen L. Factors Contributing to Chronic Ankle Instability: Kinesthesia and Joint Position Sense. J Athl Train. 2002 Dec;37(4):381 5 100. van Cingel RE, Kleinrensink G, Uitterlinden EJ, Rooijens PP, Mulder P G, Aufdemkampe G, et al. Repeated ankle sprains and delayed neuromuscular response: acceleration time parameters. J Orthop Sports Phys Ther. 2006 Feb;36(2):72 9 101. Tropp H. Pronator muscle weakness in functional instability of the ankle joint. Int J Spor ts Med. 1986 Oct;7(5):291 4 102. Bernier JN, Perrin DH, Rijke A. Effect of unilateral functional instability of the ankle on postural sway and inversion and eversion strength. J Athl Train. 1997 Jul;32(3):226 32 103. Lentell G, Katzman LL, Walters MR. The Relationship between Muscle Function and Ankle Stability. J Orthop Sports Phys Ther. 1990;11(12):605 11 104. Feuerbach JW, Grabiner MD, Koh TJ, Weiker GG. Effect of an ankle orthosis and ankle ligament anesthesia on ankle joint proprioception. Am J Sports Med. 1994 Mar Apr;22(2):223 9 105. McKeon PO, Booi MJ, Branam B, Johnson DL, Mattacola CG. Lateral ankle ligament anesthesia significantly alters single limb postural control. Gait Posture. 2010 Jul;32(3):374 7 106. Konradsen L, Ravn JB, Sorensen AI. Propr ioception at the ankle: the effect of anaesthetic blockade of ligament receptors. J Bone Joint Surg Br. 1993 May;75(3):433 6 107. Boyle J, Negus V. Joint position sense in the recurrently sprained ankle. Aust J Physiother. 1998;44(3):159 63
127 108. Sekir U, Y ildiz Y, Hazneci B, Ors F, Saka T, Aydin T. Reliability of a functional test battery evaluating functionality, proprioception, and strength in recreational athletes with functional ankle instability. Eur J Phys Rehabil Med. 2008 Dec;44(4):407 15 109. Gross MT. Effects of recurrent lateral ankle sprains on active and passive judgements of joint position. Phys Ther. 1987 Oct;67(10):1505 9 110. Brown CN, Ross, S.E., Mynark, R., Guskiewicz, K.M. Assessing functional ankle instability with joint position sense, time to stabilization, and electromyography. J Sport Rehabil. 2004;13:122 34 111. Sefton JM, Hicks Little CA, Hubbard TJ, Clemens MG, Yengo CM, Koceja DM, et al. Sensorimotor function as a predictor of chronic ankle instability. Clin Biomech (Bristol, Avon ). 2009 Jun;24(5):451 8 112. Nakasa T, Fukuhara K, Adachi N, Ochi M. The deficit of joint position sense in the chronic unstable ankle as measured by inversion angle replication error. Arch Orthop Trauma Surg. 2008 May;128(5):445 9 113. Yokoyama S, Matsusa ka N, Gamada K, Ozaki M, Shindo H. Position specific deficit of joint position sense in ankles with chronic functional instability. J Sport Sci Med. 2008 Dec;7(4):480 5 114. Sekir U, Yildiz Y, Hazneci B, Ors F, Aydin T. Effect of isokinetic training on str ength, functionality and proprioception in athletes with functional ankle instability. Knee Surg Sports Traumatol Arthrosc. 2007 May;15(5):654 64 115. Gauffin H, Tropp H, Odenrick P. Effect of ankle disk training on postural control in patients with functi onal instability of the ankle joint. Int J Sports Med. 1988 Apr;9(2):141 4 116. Van Deun S, Staes FF, Stappaerts KH, Janssens L, Levin O, Peers KK. Relationship of chronic ankle instability to muscle activation patterns during the transition from double le g to single leg stance. Am J Sports Med. 2007 Feb;35(2):274 81 117. Pintsaar A, Brynhildsen J, Tropp H. Postural corrections after standardised perturbations of single limb stance: effect of training and orthotic devices in patients with ankle instability. Br J Sports Med. 1996 Jun;30(2):151 5 118. Wikstrom EA, Fournier KA, McKeon PO. Postural control differs between those with and without chronic ankle instability. Gait Posture. 2010 May;32(1):82 6 119. Winter DA, Patla AE, Prince F, Ishac M, Gielo Perczak K. Stiffness control of balance in quiet standing. J Neurophysiol. 1998 Sep;80(3):1211 21
128 120. McGuine TA, Greene JJ, Best T, Leverson G. Balance as a predictor of ankle injuries in high school basketball players. Clin J Sport Med. 2000 Oct;10(4):239 44 1 21. McKeon PO, Hertel J. Systematic review of postural control and lateral ankle instability, part I: can deficits be detected with instrumented testing. J Athl Train. 2008 May Jun;43(3):293 304 122. Holme E, Magnusson SP, Becher K, Bieler T, Aagaard P, Kj aer M. The effect of supervised rehabilitation on strength, postural sway, position sense and re injury risk after acute ankle ligament sprain. Scand J Med Sci Sports. 1999 Apr;9(2):104 9 123. Rozzi SL, Lephart SM, Sterner R, Kuligowski L. Balance training for persons with functionally unstable ankles. J Orthop Sports Phys Ther. 1999 Aug;29(8):478 86 124. Hale SA, Hertel J, Olmsted Kramer LC. The effect of a 4 week comprehensive rehabilitation program on postural control and lower extremity function in indi viduals with chronic ankle instability. J Orthop Sports Phys Ther. 2007 Jun;37(6):303 11 125. Bernier JN, Perrin DH. Effect of coordination training on proprioception of the functionally unstable ankle. J Orthop Sports Phys Ther. 1998 Apr;27(4):264 75 126. Cloak R, Nevill AM, Clarke F, Day S, Wyon MA. Vibration training improves balance in unstable ankles. Int J Sports Med. 2010 Dec;31(12):894 900 127. Ross SE, Guskiewicz KM, Yu B. Single leg jump landing stabilization times in subjects with functionally un stable ankles. J Athl Train. 2005 Oct Dec;40(4):298 304 128. Wikstrom EA, Tillman MD, Chmielewski TL, Cauraugh JH, Borsa PA. Dynamic postural stability deficits in subjects with self reported ankle instability. Med Sci Sports Exerc. 2007 Mar;39(3):397 402 129. McLoda TA, Hansen AJ, Birrer DA. EMG analysis of peroneal and tibialis anterior muscle activity prior to foot contact during functional activities. Electromyogr Clin Neurophysiol. 2004 Jun;44(4):223 7 130. Nakazawa K, Kawashima N, Akai M, Yano H. On t he reflex coactivation of ankle flexor and extensor muscles induced by a sudden drop of support surface during walking in humans. J Appl Physiol. 2004 Feb;96(2):604 11 131. Sinkjaer T, Andersen JB, Ladouceur M, Christensen LO, Nielsen JB. Major role for se nsory feedback in soleus EMG activity in the stance phase of walking in man. J Physiol. 2000 Mar 15;523 Pt 3:817 27
129 132. Caulfield B, Garrett M. Changes in ground reaction force during jump landing in subjects with functional instability of the ankle joint Clin Biomech (Bristol, Avon). 2004 Jul;19(6):617 21 133. Bishop MD, Brunt D, Pathare N, Patel B. The interaction between leading and trailing limbs during stopping in humans. Neurosci Lett. 2002 Apr 19;323(1):1 4 134. Johansson R, Magnusson M. Human post ural dynamics. Crit Rev Biomed Eng. 1991;18(6):413 37 135. Riemann BL. Is There a Link Between Chronic Ankle Instability and Postural Instability? J Athl Train. 2002 Dec;37(4):386 93 136. Hopkins JT, Ingersoll, C.,D. Arthrogenic muscle inhibition: a limiti ng factor in joint rehabilitation. J Sport Rehabil. 2000;9:135 9 137. Young A. Current issues in arthrogenous inhibition. Ann Rheum Dis. 1993 Nov;52(11):829 34 138. Young A, Stokes M, Iles JF. Effects of joint pathology on muscle. Clin Orthop Relat Res. 19 87 Jun(219):21 7 139. Spencer JD, Hayes KC, Alexander IJ. Knee joint effusion and quadriceps reflex inhibition in man. Arch Phys Med Rehabil. 1984 Apr;65(4):171 7 140. McNair PJ, Marshall RN, Maguire K. Swelling of the knee joint: effects of exercise on qu adriceps muscle strength. Arch Phys Med Rehabil. 1996 Sep;77(9):896 9 141. Hales JP, Gandevia SC. Assessment of maximal voluntary contraction with twitch interpolation: an instrument to measure twitch responses. J Neurosci Methods. 1988 Sep;25(2):97 102 14 2. Milner Brown HS, Stein RB, Yemm R. The orderly recruitment of human motor units during voluntary isometric contractions. J Physiol. 1973 Apr;230(2):359 70 143. Herbert RD, Gandevia SC. Twitch interpolation in human muscles: mechanisms and implications f or measurement of voluntary activation. J Neurophysiol. 1999 Nov;82(5):2271 83 144. Hunter S, White M, Thompson M. Techniques to evaluate elderly human muscle function: a physiological basis. J Gerontol A Biol Sci Med Sci. 1998 May;53(3):B204 16 145. Palmi eri RM, Ingersoll CD, Hoffman MA. The hoffmann reflex: methodologic considerations and applications for use in sports medicine and athletic training research. J Athl Train. 2004 Jul;39(3):268 77
130 146. Magladery JW. Some observations on spinal reflexes in ma n. Pflugers Arch. 1955;261(4):302 21 147. Li CL, Bak A. Excitability characteristics of the A and C fibers in a peripheral nerve. Exp Neurol. 1976 Jan;50(1):67 79 148. Williams LR, Sullivan SJ, Seaborne DE, Morelli M. Reliability of individual differences for H reflex recordings. Electromyogr Clin Neurophysiol. 1992 Jan Feb;32(1 2):43 9 149. Hopkins JT, Ingersoll CD, Cordova ML, Edwards JE. Intrasession and intersession reliability of the soleus H reflex in supine and standing positions. Electromyogr Clin Neurophysiol. 2000 Mar;40(2):89 94 150. Handcock PJ, Williams LR, Sullivan SJ. The reliability of H reflex recordings in standing subjects. Electromyogr Clin Neurophysiol. 2001 Jan Feb;41(1):9 15 151. Sefton JM, Hicks Little CA, Hubbard TJ, Clemens MG, Yen go CM, Koceja DM, et al. Segmental spinal reflex adaptations associated with chronic ankle instability. Arch Phys Med Rehabil. 2008 Oct;89(10):1991 5 152. Mynark RG, Koceja DM. Down training of the elderly soleus H reflex with the use of a spinally induced balance perturbation. J Appl Physiol. 2002 Jul;93(1):127 33 153. Voigt M, Dyhre Poulsen P, Simonsen EB. Modulation of short latency stretch reflexes during human hopping. Acta Physiol Scand. 1998 Jun;163(2):181 94 154. Sedory EJ, McVey ED, Cross KM, Inger soll CD, Hertel J. Arthrogenic muscle response of the quadriceps and hamstrings with chronic ankle instability. J Athl Train. 2007 Jul Sep;42(3):355 60 155. Koceja DM, Kamen G. Interactions in human quadriceps triceps surae motoneuron pathways. Exp Brain R es. 1991;86(2):433 9 156. Hopkins JT, Ingersoll CD, Krause BA, Edwards JE, Cordova ML. Effect of knee joint effusion on quadriceps and soleus motoneuron pool excitability. Med Sci Sports Exerc. 2001 Jan;33(1):123 6 157. Cormie P, Deane RS, Triplett NT, McB ride JM. Acute effects of whole body vibration on muscle activity, strength, and power. J Strength Cond Res. 2006 May;20(2):257 61 158. Cardinale M, Wakeling J. Whole body vibration exercise: are vibrations good for you? Br J Sports Med. 2005 Sep;39(9):585 9; discussion 9 159. Torvinen S, Kannus P, Sievanen H, Jarvinen TAH, Pasanen M, Kontulainen S, et al. Effect of four month vertical whole body vibration on performance and balance. Med Sci Sport Exer. 2002 Sep;34(9):1523 8
131 160. Verschueren SM, Roelants M, Delecluse C, Swinnen S, Vanderschueren D, Boonen S. Effect of 6 month whole body vibration training on hip density, muscle strength, and postural control in postmenopausal women: a randomized controlled pilot study. Journal of Bone and Mineral Research. 2 004 Mar;19(3):352 9 161. Bogaerts A, Verschueren S, Delecluse C, Claessens AL, Boonen S. Effects of whole body vibration training on postural control in older individuals: a 1 year randomized controlled trial. Gait Posture. 2007 Jul;26(2):309 16 162. Bruye re O, Wuidart MA, Di Palma E, Gourlay M, Ethgen O, Richy F, et al. Controlled whole body vibration to decrease fall risk and improve health related quality of life of nursing home residents. Arch Phys Med Rehabil. 2005 Feb;86(2):303 7 163. Schuhfried O, Mi ttermaier C, Jovanovic T, Pieber K, Paternostro Sluga T. Effects of whole body vibration in patients with multiple sclerosis: a pilot study. Clin Rehabil. 2005 Dec;19(8):834 42 164. Turbanski S, Haas CT, Schmidtbleicher D, Friedrich A, Duisberg P. Effects of random whole body vibration on postural control in Parkinson's disease. Res Sports Med. 2005 Jul Sep;13(3):243 56 165. Ahlborg L, Andersson C, Julin P. Whole body vibration training compared with resistance training: effect on spasticity, muscle strengt h and motor performance in adults with cerebral palsy. J Rehabil Med. 2006 Sep;38(5):302 8 166. van Nes IJ, Geurts AC, Hendricks HT, Duysens J. Short term effects of whole body vibration on postural control in unilateral chronic stroke patients: preliminar y evidence. Am J Phys Med Rehabil. 2004 Nov;83(11):867 73 167. Rubin C, Recker R, Cullen D, Ryaby J, McCabe J, McLeod K. Prevention of postmenopausal bone loss by a low magnitude, high frequency mechanical stimuli: a clinical trial assessing compliance, ef ficacy, and safety. Journal of Bone and Mineral Research. 2004 Mar;19(3):343 51 168. Bautmans I, Van Hees E, Lemper JC, Mets T. The feasibility of Whole Body Vibration in institutionalised elderly persons and its influence on muscle performance, balance an d mobility: a randomised controlled trial [ISRCTN62535013]. BMC Geriatr. 2005;5:17 169. Roelants M, Delecluse C, Goris M, Verschueren S. Effects of 24 weeks of whole body vibration training on body composition and muscle strength in untrained females. Int J Sports Med. 2004 Jan;25(1):1 5 170. Kerschan Schindl K, Grampp S, Henk C, Resch H, Preisinger E, Fialka Moser V, et al. Whole body vibration exercise leads to alterations in muscle blood volume. Clin Physiol. 2001 May;21(3):377 82
132 171. Burke D, Schiller HH. Discharge pattern of single motor units in the tonic vibration reflex of human triceps surae. J Neurol Neurosurg Psychiatry. 1976 Aug;39(8):729 41 172. Issurin VB, Tenenbaum G. Acute and residual effects of vibratory stimulation on explosive strength i n elite and amateur athletes. J Sports Sci. 1999 Mar;17(3):177 82 173. Hazell TJ, Jakobi JM, Kenno KA. The effects of whole body vibration on upper and lower body EMG during static and dynamic contractions. Appl Physiol Nutr Metab. 2007 Dec;32(6):1156 63 174. Roelants M, Verschueren SM, Delecluse C, Levin O, Stijnen V. Whole body vibration induced increase in leg muscle activity during different squat exercises. J Strength Cond Res. 2006 Feb;20(1):124 9 175. Melnyk M, Kofler B, Faist M, Hodapp M, Gollhofer A. Effect of a whole body vibration session on knee stability. Int J Sports Med. 2008 Oct;29(10):839 44 176. Hopkins T, Pak JO, Robertshaw AE, Feland JB, Hunter I, Gage M. Whole body vibration and dynamic restraint. Int J Sports Med. 2008 May;29(5):424 8 177. Hopkins JT, Fredericks D, Guyon PW, Parker S, Gage M, Feland JB, et al. Whole body vibration does not potentiate the stretch reflex. Int J Sports Med. 2009 Feb;30(2):124 9 178. Moezy A, Olyaei G, Hadian M, Razi M, Faghihzadeh S. A comparative study of whole body vibration training and conventional training on knee proprioception and postural stability after anterior cruciate ligament reconstruction. Br J Sports Med. 2008 May;42(5):373 8 179. Armstrong WJ, Nestle HN, Grinnell DC, Cole LD, Van Gilder EL, Warren GS, et al. The acute effect of whole body vibration on the hoffmann reflex. J Strength Cond Res. 2008 Mar;22(2):471 6 180. Hale SA, Hertel J. Reliability and Sensitivity of the Foot and Ankle Disability Index in Subjects With Chronic Ankle Instability. J Athl Train. 2005 Mar;40(1):35 40 181. McBride JM, Nuzzo JL, Dayne AM, Israetel MA, Nieman DC, Triplett NT. Effect of an acute bout of whole body vibration exercise on muscle force out put and motor neuron excitability. J Strength Cond Res. 2010 Jan;24(1):184 9 182. Sayenko DG, Masani K, Alizadeh Meghrazi M, Popovic MR, Craven BC. Acute effects of whole body vibration during passive standing on soleus H reflex in subjects with and withou t spinal cord injury. Neurosci Lett. 2010 Sep 20;482(1):66 70
133 183. Cochrane DJ, Stannard SR, Firth EC, Rittweger J. Acute whole body vibration elicits post activation potentiation. Eur J Appl Physiol. 2010 Jan;108(2):311 9 184. Jeon HS, Kukulka CG, Brunt D Behrman AL, Thompson FJ. Soleus H reflex modulation and paired reflex depression from prone to standing and from standing to walking. Int J Neurosci. 2007 Dec;117(12):1661 75 185. Koceja DM, Trimble MH, Earles DR. Inhibition of the soleus H reflex in sta nding man. Brain Res. 1993 Nov 26;629(1):155 8 186. Pinar S, Kitano K, Koceja DM. Role of vision and task complexity on soleus H reflex gain. J Electromyogr Kinesiol. 2010 Apr;20(2):354 8 187. Koceja DM, Markus CA, Trimble MH. Postural modulation of the so leus H reflex in young and old subjects. Electroencephalogr Clin Neurophysiol. 1995 Dec;97(6):387 93 188. Trimble MH, Brunt D, Jeon HS, Kim HD. Modulations of soleus H reflex excitability during gait initiation: central versus peripheral influences. Muscle Nerve. 2001 Oct;24(10):1371 9 189. Palmieri Smith RM, Hopkins JT, Brown TN. Peroneal activation deficits in persons with functional ankle instability. Am J Sports Med. 2009 May;37(5):982 8 190. Bosco C, Cardinale M, Tsarpela O, Colli R, Tihanyi J, von Duv illard SP, et al. The influence of whole body vibration on jumping performance. Biol Sport. 1998;15(3):157 64 191. Torvinen S, Kannus P, Sievanen H, Jarvinen TAH, Pasanen M, Kontulainen S, et al. Effect of a vibration exposure on muscular performance and b ody balance. Randomized cross over study. Clin Physiol Funct I. 2002 Mar;22(2):145 52 192. Delecluse C, Roelants M, Verschueren S. Strength increase after whole body vibration compared with resistance training. Med Sci Sport Exer. 2003 Jun;35(6):1033 41 19 3. Rittweger J, Mutschelknauss M, Felsenberg D. Acute changes in neuromuscular excitability after exhaustive whole body vibration exercise as compared to exhaustion by squatting exercise. Clin Physiol Funct Imaging. 2003 Mar;23(2):81 6 194. Cochrane DJ, St annard SR, Sargeant AJ, Rittweger J. The rate of muscle temperature increase during acute whole body vibration exercise. Eur J Appl Physiol. 2008 Jul;103(4):441 8 195. Trimble MH, Harp SS. Postexercise potentiation of the H reflex in humans. Med Sci Sports Exerc. 1998 Jun;30(6):933 41
134 196. Pinniger GJ, Nordlund M, Steele JR, Cresswell AG. H reflex modulation during passive lengthening and shortening of the human triceps surae. J Physiol. 2001 Aug 1;534(Pt 3):913 23 197. Guissard N, Duchateau J, Hainaut K. M echanisms of decreased motoneurone excitation during passive muscle stretching. Exp Brain Res. 2001 Mar;137(2):163 9 198. Guissard N, Duchateau J. Effect of static stretch training on neural and mechanical properties of the human plantar flexor muscles. Mu scle Nerve. 2004 Feb;29(2):248 55 199. Avela J, Kyrolainen H, Komi PV. Altered reflex sensitivity after repeated and prolonged passive muscle stretching. J Appl Physiol. 1999 Apr;86(4):1283 91 200. Munn J, Sullivan SJ, Schneiders AG. Evidence of sensorimot or deficits in functional ankle instability: a systematic review with meta analysis. J Sci Med Sport. 2010 Jan;13(1):2 12 201. Pollock RD, Provan S, Martin FC, Newham DJ. The effects of whole body vibration on balance, joint position sense and cutaneous se nsation. Eur J Appl Physiol. 2011 Dec;111(12):3069 77 202. Sandrey MA, Kent TE. The effects of eversion fatigue on frontal plane joint position sense in the ankle. J Sport Rehabil. 2008 Aug;17(3):257 68 203. Mohammadi F, Roozdar A. Effects of fatigue due t o contraction of evertor muscles on the ankle joint position sense in male soccer players. Am J Sports Med. 2010 Apr;38(4):824 8 204. McKeon PO, Paolini G, Ingersoll CD, Kerrigan DC, Saliba EN, Bennett BC, et al. Effects of balance training on gait paramet ers in patients with chronic ankle instability: a randomized controlled trial. Clin Rehabil. 2009 Jul;23(7):609 21
135 BIOGRAPHICAL SKETCH Dana Marie O tzel was born in Ocala, Florida She rec eived a Bachelor of Science in athletic t raining from Stetson U niversity in 2002. Gainesville has since been her home and is where she earned a Master of Science degree from the Department of Applied Physiology and Kinesiology majoring in health and human performance with a concentration in biomechanics at the Univers ity of Florida U nder the guidance of Dr. Mark Tillman she received her PhD in December 2012