Research Review By Dr. Ceara Higgins©


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Date Posted:

April 2021

Study Title:

Effects of Tibiofibular and Ankle Joint Manipulation on Hip Strength and Muscle Activation


Lawrence MA, Raymond JT, Look AE et al.

Author's Affiliations:

University of New England, Portland, ME; Raymond Chiropractic and Sports Injury Center, Portland, ME; University of Hartford, West Hartford, Connecticut, USA.

Publication Information:

Journal of Manipulative and Physiological Therapeutics 2020; 43(5): 406-417.

Background Information:

Ankle sprains are one of the most common musculoskeletal injuries, accounting for more than 1 million visits to physicians each year in the United States (1). A history of lateral ankle sprains has been found to be associated with altered arthrokinematics and restrictions in the talocrural and distal tibiofibular joints (2). Loss of the normal posterior glide of the talus on the mortise during dorsiflexion and concurrent posterior glide of the of the distal fibula on the tibia with anterior displacement of the distal fibula relative to the tibia have been demonstrated after an ankle sprain (3). This may be due to lengthening or disruption of the anterior tibiofibular ligament (2). Altered motion of these joints could also affect the surrounding musculature. Up to 40% of individuals who have experienced an ankle sprain demonstrate recurrent symptoms of ankle instability despite receiving conservative treatment, possibly due to altered muscle activation around the ankle joint (4).

Individuals with a history of ankle sprain have also demonstrated decreased muscle activity (5), altered latency of the ankle, knee, and hip musculature during functional tasks (6) and altered proximal function during balance tasks (7).

Arthrogenic muscle inhibition (AMI) is defined as ongoing reflex inhibition of musculature around a joint after distension or damage to the structure of that joint, leading to altered afferent signals and decreased motoneuron pool excitability (8). Delayed firing and decreased firing ratios in ankle musculature after lateral ankle sprain are suggestive of AMI. Further, diminished firing of the hip extensors and ipsilateral weakness of the hip abductors has been found after ankle sprains. Overall, this suggests that damage to the lateral ankle ligaments causes neuromuscular alterations that are not limited to the ankle joint, often affecting proximal structures.

Most studies on high-velocity, low-amplitude (HVLA) manipulation of joints have focused on it as an intervention for pain or decreased range of motion. Joint manipulation has been shown to induce beneficial neurophysiological effects which may address the deficits associated with AMI by increasing sensory afferent input via stimulation of sensory receptors (9). Afferent signals from these receptors then synapse at the spinal level on interneurons and influence the motoneuron pool and efferent motor output which can promote the facilitation of inhibited musculature.

This study aimed to investigate whether a combination of HVLA manipulations of the talocrural, subtalar, proximal tibiofibular, and distal tibiofibular joints would influence hip muscle function in individuals with unilateral TFL weakness and a history of lateral ankle sprain.

Pertinent Results:

25 subjects participated in this study. 20 of the participants were assessed as having moderate mobility restrictions in the ankle, 3 as having severe restrictions, and 2 as having mild restrictions. No significant changes were found in maximal force production during TFL or rectus femoris MVIC testing from before manipulation to immediately after manipulation. However, significant improvements in TFL force production with a moderate effect size were seen from before manipulation to 48 hours after intervention. There was significant activity increase seen in Gmed with a moderate effect size immediately after manipulation.

The combination of talocrural, subtalar, distal and proximal tibiofibular joint manipulations increased the average force production during an MVIC in the TFL MMT position by 18.5% and the maximal force production at 48 hours after manipulation by 14.2%. Average Gmed activation on sEMG increased by 12.2% and maximal Gmed sEMG activation increased by 9.8% immediately after manipulation. This indicates that the Gmed activation could be contributing to the increased force production of the TFL from before manipulation to 48-hour post manipulation. The authors originally hypothesize that there was inhibitory weakness of the TFL, however, it is possible that the Gmed is in part or wholly responsible for the change in force production. The anterior fibers of Gmed function in identical ways to the MMT position of the TFL as described by Kendall and therefore may result in a similar weakness pattern. Therefore, it is possible that the authors’ initial hypothesis was mistaken, as the AMI may influence the anterior fibers of Gmed rather than the TFL. As the anterior fibers of Gmed have been shown to be active during narrow base of support tasks (12) and the anterior and middle portions help to initiate hip abduction, this might help to explain the latency of hip abduction function seen after ankle sprains (13).

No matter which muscle is involved, this study demonstrated that a combination of ankle joint manipulations has a positive effect on proximal hip abductor musculature force production, 48 hours after manipulation. This may be due to improved lower extremity kinematics, improved recruitment of proximal musculature during functional tasks and the resulting improvements in hip abductor muscle strength, and/or altered distal arthrokinematics no longer having an inhibitory effect on proximal muscle function. However, the results seen in this study may be best explained by the reflexogenic effect of manipulation where afferent input stimulated by manipulation is thought to result in changes in motor neuron excitability and local or regional muscular changes around the site of manipulation. This then evokes reflexes (likely from muscle spindles) which alter central or peripheral neural pathways (10). It is also possible that the body takes time to adapt to changes in arthrokinematics and load distribution after manipulation and that the changes seen at 48 hours are the result of improved motor control and recruitment in the absence of abnormal inhibitory input from the ankle joint complex.

Of note, all participants with unilateral hip abduction weakness showed restricted mobility of the involved ankle joint complex. It is plausible that the ipsilateral weakness results from the underlying mobility restrictions. Therefore, individuals with hyperlaxity may not show the same altered kinematics. Because of the relatively short time between the initial strength testing, manipulation, and immediate post-manipulation strength testing, the hip abductors may have been fatigued. This may account for no change being found until 48 hours post-manipulation.

Clinical Application & Conclusions:

The use of HVLA ankle joint and proximal/distal tib-fib manipulations may improve hip abductor muscle function in individuals with a history of ankle sprain and a presentation of unilateral weakness on a TFL muscle test. Contrary to the initial hypothesis, TFL activation did not increase, however, Gmed showed increases in muscular activation. It is important to note that the increased Gmed activation in a static muscle testing position may not translate to increased Gmed activation during functional movements.

Overall, a combination of HVLA manipulations to the ankle joint appeared to improve hip abductor strength at 48 hours after intervention. Further research is needed to clarify the effect of joint manipulation on muscle activity and determine why the increases in force production, which were not immediately seen, were present 48 hours post-manipulation.

Study Methods:

Recruitment of volunteers between 18 and 64 was undertaken from a local university and chiropractic practice. Subjects were screened using a self-reported medical history and a detailed clinical examination.

Exclusion criteria:
  • History of any ankle or hip fractures or surgeries
  • Limited passive knee flexion
  • Weakness of the psoas muscle during manual muscle testing
Inclusion criteria:
  • History of at least one ankle sprain
  • Unilateral TFL weakness ipsilateral to the side of the ankle sprain(s) as determined by a manual muscle break test (MMT)
  • Full, pain-free hip and knee flexion
Participants were not controlled for the number of prior ankle sprains or the frequency of their current ankle symptoms.

25 participants were selected. Wireless surface electromyography (sEMG) with bipolar electrodes was used to assess muscle activation of the TFL, gluteus medius (Gmed) and rectus femoris during all maximum voluntary isometric contraction (MVIC) trials. Subjects were positioned on a table with a frame with a force transducer attached. Participants were placed in a supine position with the contralateral side of the body aligned with the edge of the table. The test limb was positioned in approximately 20-30 degrees of hip flexion, 10-20 degrees of hip abduction, and maximal hip internal rotation with the force transducer aligned 12 cm superior to the lateral malleolus. This positioning was selected to isolate the force vector of the TFL. A mark was made on the lower limb to indicate the alignment of the force transducer and the participants were instructed not to wash the mark off until completion of testing at the 48-hour follow-up session.

In the first testing session, MVIC trials were performed bilaterally for the rectus femoris and Gmed prior to manipulation to provide baselines for muscle activation. MVIC testing of the TFL was performed bilaterally before manipulation (force and EMG), immediately following manipulation (force and EMG), and 48 hours after manipulation (force only). 2 practice trials were allowed to familiarize the subjects with the testing setup. 3, 5-second MVIC trials were performed in each session with a 1-minute rest period between trials. Alignment consistency was verified by a trained examiner between each trial to minimize variability.

HVLA manipulations were performed to the proximal tibiofibular, distal tibiofibular, talocrural, and subtalar joints of the limb determined to have TFL weakness by a chiropractor with 18 years of experience. Prior to manipulation the clinician assessed the mobility of the tibiofibular and talocrural joints and classified them as significantly restricted, moderately restricted, slightly restricted, normal, or lax. Each manipulation was performed up to 2 times, regardless of audible cavitation. Manipulations were deemed successful in the presence of cavitation or if the clinician determined that there was significant improvement in joint mobility.

Treatment Techniques:
  • Proximal Tibiofibular Manipulation: This manipulation was used to improve anterior glide of the proximal fibula on the tibia. The clinician placed one hand within the popliteal fossa, contacting the head of the fibula with their first metacarpal phalangeal joint and the opposite hand on the anterior aspect of the ankle. The patient was placed in end-range hip and knee flexion with slight tibial external rotation to increase contact between the fibular head and the clinician’s hand. Once a firm end-range was reached the clinician applied an HVLA thrust with the distal hand in a downward direction toward the ipsilateral buttock.
  • Distal Tibiofibular Manipulation: This manipulation was used to improve posterior glide of the distal fibula on the tibia. The patient’s affected leg was placed below the clinician’s centre of mass. The clinician cupped one hand around the calcaneus and placed the other hand on the anterior distal aspect of the lateral malleolus so that the contact was made with the thenar eminence. The clinician held the limb between their legs, level with their knees and applied a posterior force on the lateral malleolus. Once a firm end-range was reached a superior-to-inferior HVLA force was applied by thrusting with the legs and the hand in contact with the distal fibula.
  • Talocrural Manipulation: This manipulation was used to restore mobility of the talus within the talocrural joint and elicit neurophysiological effects by providing a distraction force on the talus (11). The clinician clasped both hands over the dorsum of the foot, inferior to the neck of the talus with both thumbs on the plantar aspect of the metatarsals to provide counterpressure. An HVLA thrust was then applied using a long-axis distraction force in a caudal direction with force generated by the clinician’s legs.
  • Subtalar Manipulation: This manipulation was used to improve mobility of the subtalar joint. The clinician placed the patient’s rear foot in the position of least resistance (inversion or eversion) and then cupped one hand around the posterior aspect of the calcaneus, applying a long-axis distraction force. Their other hand was cupped around the first to reinforce their grasp. An HVLA distraction thrust manipulation was applied to the calcaneus, pulling the calcaneus into eversion and abduction while extending the foot.

Study Strengths / Weaknesses:

  • This study was one of the first attempts to investigate the proximal effects of distal HVLA extremity manipulation (prior studies have looked at proximal HVLA manipulation effects on distal function).
  • Participants were selected based on a prescreening to determine the presence of hip weakness during a TFL muscle test. Therefore, the results may not be transferable to patients with other findings.
  • No control group was used for this study. Therefore, it not possible to extrapolate to effectiveness or causation.
  • There is no established minimal clinically important difference (MCID) for improvements in hip strength, making it impossible to determine if the changes seen in this study would result in clinically important changes in function.

Additional References:

  1. Wolfe MW. Management of ankle sprains. Am Fam Physician 2001; 63(1): 93-104.
  2. Denegar CR, Hertel J, Fonseca J. The effect of lateral ankle sprain on dorsiflexion range of motion, posterior taller glide, and joint laxity. J Orthop Sports Phys Ther 2002; 32(4): 166-173.
  3. Fukuhara T, Sakamoto M, Nakazawa R, et al. Anterior positional fault of the fibula after sub-acute anterior talofibular ligament injury. J Phys Ther Sci 2012; 24(1): 115-117.
  4. Zampagni ML, Corazza I, Molgora AP, et al. Can ankle imbalance be a risk factor for tensor fascia late muscle weakness. J Electromyogr Kinesiol 2009; 19(4): 651-659.
  5. Feger MA, Donovan L, Hart JM, et al. Lower extremity muscle activation during functional exercises in patients with and without chronic ankle instability. PM R 2014; 6(7): 602-611.
  6. Van Deun S, Staes FF, Stappaerts KH, et al. Relationship of chronic ankle instability to muscle activation patterns during the transition from double-leg to single-leg stance. Am J Sports Med 2007; 35(2): 274-281.
  7. Gribble P, Hertel J, Denegar C. Chronic ankle instability and fatigue create proximal joint alterations during performance of the Star Excursion Balance Test. Int J Sports Med 2007; 28(3): 236-242.
  8. Hopkins JT, Ingersoll CD. Arthrogenic muscle inhibition: a limiting factor in joint rehabilitation. J Sports Rehabil 2000; 9(2): 135-159.
  9. Colloca CJ, Keller TS, Harrison DE, et al. Spinal manipulation force and duration affect vertebral movement and neuromuscular responses. Clin Biomech (Bristol, Avon) 2006; 21(3): 254-262.
  10. Pickar JG. Neurophysiological effects of spinal manipulation. Spine J 2002; 2(5): 357-371.
  11. Kamali F, Sinaei E, Bahadorian S. The immediate effect of talocrural joint manipulation on functional performance of 15-40 years old athletes with chronic ankle instability: a double-blind randomized clinical trial. J Body Mov Ther 2017; 21(4): 830-834.
  12. Boudreau SN, Dwyer MK, Mattacola CG, et al. Hip-muscle activation during the lunge, single-leg squat, and step-up-and-over exercises. J Sport Rehabil 2009; 18(1): 91-103.
  13. Beckman SM, Buchanan TS. Ankle inversion injury and hyper mobility: effect on hip and ankle muscle electromyography onset latency. Arch Phys Med Rehabil 1995; 76(12): 1138-1143.