Abstract

Myofascial release (MFR) is a technique for resolving fascial restriction; i.e., the fascia trapped with moderate pressure is continuously expanded to expand collagen fibers as well as fascial elastin fibers. In recent years fascia has increasingly been studied, as the roles and importance of fascia have become apparent. In many case reports pain and postural alignment have been designated as the outcome, and changes before and after MFR have been observed. Controlled studies have included a variety of researches for the presence or absence of the effects of MFR on patients with certain diseases, comparison of MFR with other techniques, and basic studies on the effects of MFR in healthy persons. It has been believed, however, that systematic reviews are of various quality levels because of the obscure content of intervention and insufficient exclusion of bias in spite of the favorable effects and the moderate quality of MFR techniques. The future task confronting us is thought to accumulate controlled studies, which will allow acquiring definite blinding and distinctly explaining fascial changes by detailed intervention methods.

Introduction

Myofascial release (MFR) is a technique for relieving fascial restriction; i.e., the fascia trapped with moderate pressure is expanded continuously, by which collagen fibers, as well as fascial elastin fibers, are expanded. Since MFR yields no any pain to the person treated by MFR without use of any specific tool, it can be used for every disease over all age groups; i.e., it is available for acute/chronic pain, restricted range of motion (ROM), conditioning in children and the aged, sports injury, and so on [1]. Some investigators have reported the origin of MFR. MFR is a fruit of soft tissue mobilization according to an American physical therapist, John F. Barnes [2], one of the Structural Integration (Rolfing®) techniques developed by an American biochemist, Ida P. Rolf [3], and a product of the technique developed by Thomas W. Myers [4], the author of “Anatomy Train”, who directly received training from Ida P. Rolf.

In recent years the roles and importance of fascia have become apparent, and at the same time fascia is being increasingly studied. Despite that MFR exerts the effects non-invasively on fascia via the superficial skin and fat layer, many MFR researches have designated changes in physical function, including changes in alignment and ROM, as the outcome. For this reason, the questions of whether fascia can be actually found or not and of how fascia changes remained. In recent years, however, imaging-out of fascia by an ultrasound imaging diagnostic device and observation of changes in the properties of fascia have become possible. This article introduces some previous researches for MFR with the author’s case reports. Self-MFR and foam roller MFR are excluded from the present study.

Previous Researches

Case reports

Barnes has reported treatment of a 35-year-old female patient who has suffered from thoracic outlet syndrome for 2 years. The 30-minute treatment including expansion of her upper limbs and MFR of the iliac muscle was conducted twice to three times a day for 2 weeks. Her pain was reduced, swing of her upper limbs during walking was normalized, kyphosis was improved, her body trunk and pelvis were restored to a median position, and the right-to-left load became even [5]. Le Bauer et al. have reported treatment of an 18-year-old female patient, who has suffered from bimodal scoliosis for 6 years. The 60-minute treatment including MFR involving her body trunk and expansion of her both lower limbs was conducted twice a day for 2 weeks. Postural alignment, X-ray images, pain, the condition with scale 22 based on the Scoliosis Research Society, and ROM of thoracolumbar rotation were markedly improved [6].

Martin has reported treatment of a female patient with diffuse systemic sclerosis. The treatment included 11 sessions of MFR involving the head and neck and 9 sessions of MFR involving her body trunk, and it took 60 minutes for each session. The treatment was conducted for 5 months, and symptoms of Raynaud’s phenomenon, thoracic mobility, and orificial distance were improved [7]. Walton has reported treatment of a 35-year-old female patient with primary Raynaud’s phenomenon. The 45-minute treatment including MFR of the region ranging from the neck to the dorsal surface of the chest and expansion of her upper limbs was conducted for 3 weeks. The duration and frequency of the appearance of Raynaud’s phenomenon and the severity of pain were decreased [8]. Many case reports have designated pain and postural alignment as the outcome and observed changes before and after MFR.

Controlled studies

Barnes et al. have divided 10 orthopedic outpatients into an MFR group of 6 patients who were treated with MFR [of the quadriceps muscle of thigh (QMT), iliopsoas muscle, and the contralateral iliopsoas muscle] for 10 minutes and a control group of 4 patients who were subjected only to lie on a bed for 10 minutes, and compared both groups concerning lateral tilt angle of the pelvis [the mean difference in the distance between the right and left anterior superior iliac spine (ASIS) and the central point at patient’s feet]. The difference in the distance was significantly reduced in MFR group, increasingly showing the symmetric form of the pelvis [9]. Takeda et al. have conducted MFR of the greater pectoral muscle and smaller pectoral muscle in 25 patients with retentive hemiplegia, and compared the angle of abduction of the shoulder on the affected side, speed and the degree of easiness of patients’ daily living lives, and 10-meter walking speed before and after MFR. They have reported the significant improvement in the abduction angle and the speed of the patients’ daily living lives [10]. Marszaiek has conducted MFR of the head, neck, upper limbs, and the upper body trunk in 40 patients who have undergone total laryngectomy. The esophageal pressure was significantly decreased after MFR, having led to easy training of esophageal phonation [11]. Some other reports have shown that MFR of the head and neck in patients with the forward head posture has induced the significant improvement in the craniospinal angle, neck disability index, and cervical ROM [12, 13] and that MFR of the body trunk involving the low back in low back pain patients has induced significant improvement in pain and the influence of low back pain on daily living activities [14–16].

Kain et al. have compared each ROM of flexion, extension, and abduction of the shoulder between an MFR group of 18 healthy subjects who underwent precordial MFR for 3 minutes and a hot pack group of 13 healthy subjects who underwent hot pack for 20 minutes. Both groups showed significantly increased ROM, compared to that before the implementation, except that only the flexion angle was significantly higher in the MFR group than in the hot pack group [17]. Henley et al. have compared heart rate on a tilt (50°) table, normalized ECG, and respiration rate between an MFR group of 17 healthy subjects who underwent MFR of the neck for 2 minutes and a pseudo-MFR group of 17 healthy subjects with their neck only touched by rater’s hands. Tachycardiac rate and normalized ECG were significantly increased in both groups, compared to those at rest, whereas the tachycardiac rate and the normalized ECG were lower in the MFR group than in the pseudo-MFR group [18].

Kuruma et al. have compared ROM of knee joint flexion, muscle stiffness, and reaction time among a QMT-MFR group of 10 healthy subjects who underwent MFR of the QMT for 8 minutes, a hamstrings (H)-MFR group of 10 healthy subjects who underwent MFR of H for 8 minutes, and a stretching group of 10 healthy subjects who underwent stretching of QMT. All groups significantly showed improvement in ROM, while reaction time was significantly reduced in the QMT-MFR and H-MFR groups [19]. Ichikawa et al. have compared muscle stiffness and the fascial transmission distance on ultrasonic images among an MFR group of 12 healthy subjects who underwent MFR of the lateral great muscle for 4 minutes, 10-min-hot-pack group of 12 healthy subjects who underwent hot pack for 10 minutes, and 20-min-hot-pack group of12 healthy subjects who underwent hot pack for 20 minutes. There were significant changes in muscle stiffness and the fascial transmission distance only in the MFR group [20].

We have compared angles of active and passive extension and elevation of lower limbs and muscle strength (extension/flexion of the knee joint) before intervention and for 6 days after intervention among an H-MFR group of 10 healthy subjects who underwent MFR of hamstrings (H), a QMT (re-education)-MFR group of 10 healthy subjects who underwent muscle re-education exercises of QMT (40 times at muscle strength of 40% of 1 repetition maximum) following MFR of H, and an H (re-education)-MFR group of 10 healthy subjects who underwent muscle re-education exercises of H following MFR of H. Improvements in the extension and elevation angles for the lower limbs and the muscle strength of knee flexion were much more in the H (re-education)-MFR group than in two other groups. There were also significant differences between those 6 days after and before the implementation. In the H-MFR group there were significant differences in the angle of extension and elevation of lower limbs and muscle strength of knee flexion between those for 4 days after and before MFR [21]. To investigate the fascial properties after MFR, we clarified intra-rater reliabilities [ICC (1, 1)] 4 days after measurements of superficial and deep fascial transmission distances on ultrasound images of lateral head of the gastrocnemius muscle by using an ultrasound imaging diagnostic device and measurement of muscle stiffness according to real-time tissue elastographic function (superficial layer: 0.89; deep layer: 0.98; muscle stiffness: 0.90) [22]. We compared ROM of ankle dorsal flexion, muscle strength of ankle plantar flexion, fascial transmission distance, and muscle stiffness before and after intervention and for 4 days after intervention between an MFR group of 17 healthy subjects who underwent MFR of the lateral head of gastrocnemius muscle for 3 minutes and a stretching group of 17 healthy subjects who underwent static stretching for 3 minutes. In both groups, ROM and fascial transmission distance were increased and muscle stiffness was decreased immediately after the intervention, compared to those before intervention. Immediately after the intervention muscle strength was increased in the MFR group and decreased in the stretching group, while ROM, muscle strength, and fascial transmission distance were increased and muscle stiffness was decreased 4 days after the intervention than those before the intervention only in the MFR group [23]. Thus, there have been a variety of controlled studies including comparative studies on the presence/absence of the effects of MFR on patients with certain diseases and between MFR and other techniques, as well as basic researches of the effects of MFR on healthy persons.

Systematic reviews

Yang et al. [24] have inspected 1329 references in the literature concerning chest physiotherapy for pneumonia in adults in 2010, which included 6 references of randomized controlled trials (434 subjects). As a result, it was revealed that osteopathic therapy including MFR allowed admission period and the duration required for intravascular and systemic antibiotic treatment having been decreased, although any symptom of pneumonia or X-ray finding was not improved [22]. Yuan et al. have investigated minutely 532 references in the literature concerning treatment for fibromyalgia in 2015, and 2 references about randomized trials of MFR (145 subjects) were included in meta-analysis. As a result, it was revealed that MFR had moderate evidence of its effects particularly on pain, anxiety, and depression [25]. McKenney et al. have examined closely 88 references in the literature to investigate the quality and reliability of MFR in 2013, and 10 references of randomized trials were included. Ajimsha et al. have also investigated 3 systematic reviews in 2019. The thus-described researchers’ studies have provided evidence of the favorable effects of MFR and the moderately technical quality, but according to them, it has various degrees of quality for the reason that the intervention contents are obscure and that bias is insufficiently removed. They have brought their researches to a conclusion by saying that individual systematic review will become a beginning toward future investigation of higher quality [26, 27].

Case reports

The author encountered 2 patients who acquired characteristic improvement as a result of MFR. These cases are introduced below. The first case was a male patient in his 50s, a physician, whose chief complaint was low back pain. When he tried to stand up after morning medical examination, he could not stand up because of low back pain. As for sites of low back pain, he had both lumbar regions, but the pain was particularly severe in the right region. He had no idea of any event by which low back pain was manifested in his recent daily activities. According to inquiries about his past history, he had right second metatarsal capital fracture 6 months ago. He has been unable to bear any load on the affected site and shown claudication because of pain for a while. At present, he had no pain in the right second metatarsal bone. He felt low back pain in getting-up and standing positions and during walking. Since he had pain when load was given to the affected site, evaluation was started with his feet on the assumption that the right second metatarsal capital fracture was responsible for low back pain. Subsequently, high-density regions were recognized in the right long extensor muscle of great toe, right anterior tibial muscle, lateral head of the right gastrocnemius muscle, right biceps muscle of thigh, right iliac muscle, bilateral lumbar iliocostal muscle, and bilateral lumbar quadrate muscles. Except for the lumbar quadrate muscles, it was considered that claudication to avoid using the second metatarsal bone resulted in the condition in which fascial dysfunction has spread along the anterior and posterior motion arrangement (referred to the concept of fascia and fascial approach) (Figure 1). Faced with this situation, we considered the feet as the cause of the condition, and we conducted MFR on each of the right long extensor muscle of great toe, right anterior tibial muscle, and lateral head of the right gastrocnemius muscle for 3 minutes. After MFR, low back pain was reduced from score 8 to score 3 based on the Numerical Rating Scale. When MFR was conducted on each of the bilateral lumbar iliocostal muscles for 2 minutes, low back pain disappeared and he felt no physical disorder at his low back. His subsequent course also appeared favorable.

Figure 1. Fascia showing the ascending spread of high-density areas.

The second case was a male patient in his 80s, and diagnosed as having had left middle cerebral arteriosclerosis. Owing to (rt-PA) thrombolysis, paralysis was improved from complete paralysis to moderate right hemiplegia. It was improved even to mild paralysis by 3-week rehabilitation, and he acquired retentive self-supporting in a standing position and walking without support with light assistance. However, improvement of function of swallowing was worse than that of physical function. It was assumed from postural evaluation that anterior cephalic presentation and unbalance between the right and left postural alignments (effortive on the non-affected side) inhibited movements of the masticatory muscle and muscles of tongue. On this assumption, MFR of the suboccipital muscles, left sternocleidomastoid muscle, suprahyoid muscles, posterior region of neck, and upper fibers of left trapezius muscle, and expansion of the left upper limb were conducted for 40 minutes a day for 3 days. As a result, the anterior cephalic presentation was improved (Figure 2), the right and left postural alignments showed symmetric balance (Figure 3), and the swallowing function was also improved (Table 1).

Figure 2. Postural alignment on the sagittal plane (rightward motion) before and after the treatment.

Figure 3. Postural alignment on the frontal plane (ante-motion) before and after the treatment.

Table 1. Evaluation of the swallowing function before and after the treatment.

Conclusion

Establishment of evidence of the effects of MFR seems to be delayed, while approach to fascia is increasingly spreading along with the increasing recognized importance of fascia. The future task confronting us is thought to accumulate controlled studies, which will allow distinctly explaining fascial changes under the condition of definite blinding by detailed intervention methods.

References

1. Takei H (2001) Myofascial Release. Rigakuryoho Kagaku. Apr: 103–107 (Japanese).
2. Barnes JF (1990) How It Bagan Myofascial Release the search for excellence. Washington, USA: National Library of Medicine Pg No: 1–2.
3. Yasushi F (2005) An Outline of Rolfing. Japanese Journal of Complementary and Alternative Medicine. Feb: 37–43(Japanese).
4. Earls J, Myers TW (2010) An Introduction to Fascial Release Technique Fascial Release for Structural Balance Chichester, UKB: Lotus Publishing Pg No: 4–16.
5. Barnes JF (1996) Myofascial release in treatment of thoracic outlet syndrome. J Bodyw Mov Ther  Jan: 53–57.
6. LeBauer A, Brtalik R, Stowe K (2008) The effect of myofascial release (MFR) on an adult with idiopathic scoliosis. J Bodyw Mov Ther 12: 356–363. [crossref]
7. Martin MM (2008) Effects of the myofascial release in diffuse systemic sclerosis. J Bodyw Mov Ther Apr: 1–9.
8. Walton A (2008) Efficacy of myofascial release techniques in the treatment of primary Raynaud’s phenomenon. J Bodyw Mov Ther Pg No: 274–280.
9. Barnes MF, Gronlund RT, Little MF, Personius WJ (1997) J Bodyw Mov Ther. Oct: 289–296.
10. Takeda S, Takahashi K, Kawasaki T, Kaneko T, et al. (2005) Ijikinouso cchuukatamahi kanja Mahisoku kyoubukingunn henokinnmakuriri- sunoouyou [abstract] Rigakuryouhougaku  32(Suppl 2): ID-868 (Japanese).
11. Marszaiek S (2009) Estimation of influence of myofascial release techniques on esophageal pressure in patients after total laryngectomy. Eur Arch Otorhinolaryngol May: 1305–1308.
12. Kim J, Kim S, Shim J, Kim H (2018) Effects of McKenzie exercise, Kinesio taping, and myofascial release on the forward head posture. J Phys Ther Sci Pg No: 1103–1107.
13. Aggarwal A, Shete AV, Palekar TJ (2018) Efficacy of Suboccipital and Sternocleidomastoid Release Technique in Forward Head Posture Patients With Neck Pain: A Randomized Control Trial. Int J Physiother Pg No: 149–155.
14. Tozzi P1, Bongiorno D, Vitturini C (2011) Fascial release effects on patients with non-specific cervical or lumbar pain. J Bodyw Mov Ther 15: 405–416. [crossref]
15. Ajimsha MS, Daniel B, Chithra S (2014) Effectiveness of myofascial release in the management of chronic low back pain in nursing professionals. J Bodyw Mov Ther 273–281.
16. Arguisuelas MD, Lison JF, Domenech-Fernandez J, Martinez-Hurtado I (2019) Effects of myofascial release in erector spinae myoelectric activity and lumbar spine kinematics in non-specific chronic low back pain: Randomized controlled trial. Clin Biomech (Bristol, Avon) 27–33.
17. Kain J, Martorello L, Swanson E, Sego S (2010) Comparison of an indirect tri-planar myofascial release (MFR) technique and a hot pack for increasing range of motion. J Bodyw Mov Ther 63–67.
18. Henley CE, Ivins D, Mills M, Wen FK, et al. (2008) Osteopathic manipulative treatment and its relationship to autonomic nervous system activity as demonstrated by heart rate variability a repeated measures study. Osteopath Med Prim Care 2–7.
19. Kuruma H, Takei H, Nitta O, Furukawa Y, et al. (2006) Kinmakuriri-su to sutorecchingu womochiita rigakuryouho ukouka no hikakukentou [abstract] Rigakuryouhougaku 2006; 34 (Suppl 2) ID-259 (Japanese).
20.  Ichikawa K, Takei H, Usa H, Mitomo S, et al. (2015) Comparative analysis of ultrasound changes in the vastus lateralis muscle following myofascial release and thermotherapy: a pilot study. J Bodyw Mov Ther 327–336.
21. Katsumata Y, Takei H, Hori T, Hayashi H (2016) Influences of muscle re-education exercises for myofascial extensibility and muscle strength after myofascial release. Rigakuryoho Kagaku 99–106.
22. Katsumata Y, Takei H, Hayashi H, Ichikawa K (2017) Intra- and Inter-rater Reliabilities of measurements of fascial displacement and muscle stiffness by using ultrasound images. Rigakuryoho Kagaku 215–220 (Japanese).
23. Katsumata Y, Takei H, Sasaki Y, Watanabe K (2019) Ultrasonographic changes in fascial properties over time after myofascial release. Integr J Orthop Traumato 1–6.
24. Yang M, Yuping Y, Yin X, Wang BY, et al. (2010) Chest physiotherapy for pneumonia in adults. Cochrane Database Syst Rev CD006338.
25. Yuan SL, Matsutani LA, Marques AP (2015) Effectiveness of different styles of massage therapy in fibromyalgia: a systematic review and meta-analysis. Man Ther 257–264.
26. McKenney K, Elder AS, Elder C, Hutchins A (2013) Myofascial release as a treatment for orthopaedic conditions: a systematic review. J Athl Train 522–527.
27. Ajimsha MS, Shenoy PD (2019) Improving the quality of myofascial release research – A critical appraisal of systematic reviews. J Bodyw Mov Ther 561–567.

Summary

A 41-year-old female patient, who developed trigger finger after she repeated cervical sprain several times, underwent myofascial evaluation and treatment, which were based on Fascial Manipulation^®, in addition to evaluation by physical therapy, and favorable results were obtained. She showed symptoms of trigger finger, which suddenly occurred, for 5 months. Palliative treatment was the only method for the symptoms, and they did not reach improvement. The site and tissue, which are responsible for the condition, were specified first on evaluation by physical therapy. Subsequently addition of exercise test and palpation test for fascia in view of a past history and timeline may appropriately approach to problems with high-density sites and force transmission of the fascia related to pain.

Introduction

Many cases of trigger finger have been believed to be idiopathic, and the symptoms occur spontaneously. Some reports have indicated the relevance to occupational or repetitive activities [1]. For the pathogeneses, much attention was paid to specification of sites of myofascial dysfunction in view of a past history and living activity level and routes of force transmission, as well as conventional tests and evaluation. This article describes favorable results of the myofascial evaluation and treatment, which were based on Fascial Manipulation^® (FM^®) and conducted in addition to evaluation by physical therapy, in a patient who developed trigger finger after she repeated cervical sprain several times.

Roles of fasciae

Fascia has been explained at the International Conference of Scientific Research of Fascia, as follows: “Fascia, a soft tissue constituent of the connective tissue system all over the human body, forms a 3-D matrix in the whole body to support structures “[2]. Fascia spread over all organs, muscles, bones, and nerve fibers to cover them. The definition of fascia includes aponeurosis, ligament, tendon, retinaculum, articular capsule, capsules of organs and vessels, epineurium, meninges, periosteum, and intra- and intermuscular fibers of all fasciae. All of them indicate that fasciae have important roles in muscular biomechanics, coordination of muscular peripheral movements, and maintenance of proprioceptor and postures.

Some muscle fibers of epimysium enter the deep fascia; i.e., 37% of muscle origins and insertions enter the deep fascia and intermuscular septum (myofascial expansion) without insertion and the inserted tendon [3]. When fascial dysfunction occurs, muscle spindle and nociceptor are stimulated, spreading along the fascial arrangement via the deep fascia. For instance, aponeurotic fasciae cover the whole muscles of the upper limb, and collagen fiber bundles are arranged in different directions in the aponeurotic fasciae. The thoracic muscles receive tension at a proximal site by insertion of various fasciae, enabling to slide between them and inferior muscles. The brachial fasciae are connected at a proximal site to axillary fascia, greater pectoral fascia, deltoid fascia, and dorsolateral fascia, while they are connected to antebrachial fascia at a distal site. The mediolateral intermuscular septum is originated from the brachial fascia, by which the upper arm is divided into the front and the rear parts as segments. At the elbow the brachial fascia is reinforced by the anterior and rear retinacula, and the anterior retinaculum is composed of the brachial biceps aponeurosis. The brachial biceps aponeurotic expansion branches off two directions. In one direction a fiber bundle extends like a bow obliquely and medially below and binds at the antebrachial fascia. Inside the elbow many muscle fibers of the round pronator muscle and radial carpal flexor are inserted into the antebrachial fascia from the inside. In the other direction collagen fiber bundles are running in parallel to a median line of the forearm in a longitudinal direction. This fibrous expansion reaches the antebrachial fascia between the radial carpal flexor and the humeroradial muscle. Therefore, when the brachial biceps (muscle) tendon is extended at a proximal site, two force lines appear in a medial direction corresponding to the coved fibers and in a direction longitudinally running along the central part of the forearm.

On movements of the upper limbs in various directions, fascial expansion activates fascial proprioceptor with a specific moving pattern and extends a specific site of the brachial fascia, connecting different sites to transmit force. Owing to the relationship between the muscle and fascia coordinative movement to the periphery is realized by performance of movement in a correct direction and correct recognition [2, 4].

Fascia has a role in enhancement of muscle sliding. There is hyaluronic acid in loose connective tissue between deep fascial layers and between epimysium and endomysium, which acts as a lubricant [5]. When hyaluronic acid aggregation is induced by trauma, overuse, etc., fascial layer sliding is restricted. Contraction of the epimysium causes tendon extension due to high density of epimysium, and the extension stimulates the articular receptor to lead to its excitement and pain around the joint. When the body has pain, it responds to the pain with secondary compensation by a posture to avoid the pain. The change in base tension due to the compensation will be controlled by up-and-down tension on the competitive or ipsilateral side, leading to increased complication of the symptoms [6].

FM^®

The subjects of FM^® treatment include the point [referred to by Centre of Coordination (CC)] on the epimysium, to which one-way muscle strength converges, and the point [referred to by Centre of Fusion (CF)], to which force of adjacent two deep fascia (aponeurotic fascia) units converges. The body is divided into 14 segments, and a functional unit related to movement in each direction is called as fascial unit. All the segments include 6 CC points. There are 6 directions of movement: Sagittal plane (antemotion: AN and retromotion: RE); frontal plane (lateromotion: LA and mediomotion: ME); and horizontal plane (extrarotation: ER and intrarotation: IR). Each fascial unit is designated from the movement direction and segment. For example, the fascial unit of anterior movement of CU (elbow) is designated as AN-CU. There are 4 directions of movement of CF: Anterio-lateral (Ante-Latero: AN-LA); anterior-medial (Ante-Medio: AN-ME); retrolateral (Retro-Latero: RE-LA); and retromedial (Retro-Medio: RE-ME) [6,7]. CC forms the one-way continuous arrangement (called as fascial arrangement) associated with movement direction along the sagittal, frontal, and horizontal planes [8]. For example, the facial arrangement of anterior movement of the upper limbs is composed of 5 fascial units, i.e., AN-SC (scapula), AN-HU (upper arm), AN-CU, AN-CA (carpus), and AN-DI (finger), and anterior movement of the upper limbs is induced by the arrangement. CF has a fascial diagonal line, which appears on a diagonal line of fascial arrangement, and a fascial spiral, which integrates articular elements with retinaculum to influence wide-range pain. It comes to be important for treatment which arrangement has a problem [6, 7].

Pathogeneses of Trigger Finger (Snapping Finger)

Trigger finger is tenosynovitis of the flexor tendon due to imbalance between the tendon sheath and the flexor tendon passing the sheath. Transmission disorder occurs in the tendon sheath to lead to pain, swelling, and heat sensation of fingers. It has been reported that thickening of the tendon sheath, ligamentous intrathecal narrowing, edematous enlargement of the tendon itself, and so on are responsible for these conditions [9]. The augmentation of the symptoms early in the morning and amelioration of the symptoms by day are frequently observed. When they advance, a snapping phenomenon develops, and it may ultimately result in secondary contracture of the Proximal Inter Phalangeal (PIP) joint. The symptoms also frequently appear in a plurality of fingers. It has been believed that the phenomenon is one of the most common causes of hand pain in adults. It has also been reported that the prevalence is ca. 2% of the general population, and tends to be high in women in their fifties or sixties. The prevalence in women in the later stages of pregnancy is also high, and the condition is also characterized by its frequent occurrence due to overuse of hand and as sports injury. It frequently occurs in patients with diabetes, rheumatoid arthritis, or those under the conditions such as amyloidosis, in which systemic accumulation of proteins occurs. As for the treatment, some investigators have reported evidence of moderate efficacy of conservative intervention including the short-term use of Non-Steroidal Anti-Inflammatory drug (NSAID) [10]. The orthotic treatment has also been widespread [11]. In case of conservative therapy, surgical treatment may also be selected when any improvement is not achieved by conservative therapy.

Treatment case

1. General information

A patient is a 41-year-old woman, housewife.

The chief complaints included flexion contracture of and resting pain in the left thumb MP joint and thumb movement pain, and she grasped with difficulty because of pain.

Approximately 5 months ago she suddenly had left thumb pain and restricted Range of Motion (ROM) at the time of rising from her bed. In the early stage the pain was gradually reduced by day, but in the next morning she repeated pain and restricted ROM. The pain gradually augmented even by day. She visited a hospital, and received intrathecal steroid injection with a diagnosis of trigger finger. Even so, the symptoms were not improved. Subsequently she had an attempt to receive acupuncture as well, but the pain augmented. Her left thenar swelling also appeared, and she could do daily living activities (ADL), including clothespin pinching, taking out coins, grasping dish and mobile phone, etc., with difficulty. Thus, she came to interfere with the whole range of housework.

Diagnosis: Trigger finger (snapping finger)

Past history:

20 years of age: Cervical sprain-due to numbness in the region ranging from neck to left hand (traffic accident)

25 years of age: Surgery for right inguinal hernia

30 years of age: Cervical sprain-due to numbness in the region ranging from neck to left hand (traffic accident). Treated by cervical collar fixation

36 years of age: Cervical sprain-due to numbness in the region ranging from neck to both hands (traffic accident)

38 years of age: Right 5th metatarsal fracture

39 years of age: Cervical sprain (a violent fall)

In her late thirties she repeated pain around the scapula once or twice a year.

41 years of age: Lt Thumb trigger finger (snapping finger)

2. Evaluation by physical therapy

Pain: Resting pain (+), movement pain (+), numbness (-)

Active movement: ROM restriction in all directions of left thumb CM joint, in association with pain with score 8 based on the Numerical Rating Scale (NRS).

Passive movement: ROM restriction in all directions of left thumb CM joint, in association with NRS 8 pain.

Neurological test: Various neurological tests (-)

End feel: Empty

Joint play test: Hypermobility of C4th/5th and 5th/6th; low mobility of TH1st/2nd.

Muscle tightness: Brachioradial muscle, long palmar muscle, round pronator muscle, biceps muscle of arm, scalenus, and smaller pectoral muscle.

Observation of posture: Round back and forward head.

Observation of motion: Difficult movements of grasping and pinching.

3. Hypothesis

This patient developed numbness in her both upper limbs after she sustained cervical sprain several times. Since she had a past history of cervical collar fixation, her cervical vertebrae were examined. Various neurological tests are negative at present. She repeated cervical sprain, and had the imbalanced trunk because of coexistence of hypermobility of the cervical vertebrae with low mobility of the thoracic vertebrae. The patient may have been forced to have compensation for various postures under the situation with her unstable neck. It was further considered that the poor alignment accelerated excessive tension of her neck and chest to have led to tension stress to her left thumb through fascial arrangement and expansion from the trunk to the upper limbs. On the hypothesis that the stress spread from the cervicothoracic vertebrae downward, fascia was evaluated.

4. Palpation test [High density level (*~***)]: Comparative palpation test was conducted in TH (thorax), SC, and CA. LT LA-CA***, Bi LA-TH***, Lt LA-SC**, Rt LA-CL (neck)**, Lt ME-CA**, and Lt ME-CU**.

Palpation test revealed high density at the above-described sites, indicating remarkable areas of high density on the frontal plane arrangement.

5. Treatment

First treatment: Lt LA-CA (Figure 1), Lt LA-CU, Lt LA-DI (Figure 2), Lt ME-DI (Figure 3), and Lt ME-CA (Figure 4) (++).

Figure 1. Lt LA-CA.

Figure 2. Lt LA-DI.

Figure 3. Lt ME-DI.

Figure 4. Lt ME-CA.

Second treatment: Lt LA-CA, Lt LA-SC (Figure 5), Rt LA-CL, Lt ME-CU, and Bi LA-TH (Figure 6) (+++).

Figure 5. Lt LA-SC.  

Figure 6. Lt LA-TH.

6. Treatment results

Although pain on grasping movement was reduced and ROM was improved after the first treatment, she complained of tension on her neck and upper back. One week later she received the second treatment, and pain on pinching movement, restricted ROM, and a sensation of tension on her upper back disappeared.

Discussion

The patient repeated cervical sprain, and had numbness in the region ranging from her neck to fingers. However, the region was not consistent with the dermatome of the C4th/5thor 5th/6th, which showed cervical hypermobility, and the site of numbness varied day by day. The patient’s condition repeated remission and exacerbation. Her life in such a situation is presumed to have caused various compensatory postures and activities. One of these causes is fascial compensation. Excessive tension of her trunk, which is originated from cervical instability, is considered to have received stress through fascial expansion to the hand along the arrangement of fascial connection. For this reason arrangement of fascial balance between the proximal and distal positions may have led to reduction in symptoms by intervention along the arrangement.

Conclusion

This article described the importance of evaluation and treatment with FM^® from a musculofascial viewpoint for a patient who developed trigger finger after she repeated cervical sprain several times.

It has been believed that the occurrence of trigger finger is idiopathic. The symptoms appear spontaneously and have correlation with occupational or repetitive activities. The condition shows compensatory movements due to fascial dysfunction very frequently. Not only palliative treatment of the present symptoms but also specification of the causative sites and tissue by physical therapeutic evaluation may make an appropriate approach possible to resolve problems with the high-density site of pain and force transmission by addition of movement test and precise palpation test for fascia in view of a past history and the timeline. It is further important for trigger finger patient to do exercise for correction of compensatory movements after improvement in fascial sliding and the high-density site and to advance the movement to functional movement and to ADL movement.

References

1. ……………………………
2. Atsushi Yoshida (2019) The interaction between muscle and fascia (myofascial chain).  Spine & Spinal Cord. 32: 301–306.
3. …………….
4. Stecco C (2018) Atlas of Functional Anatomy of Fascial System.  Hitoshi Takei (Tr.). Ishiyaku Publishers, Inc. : 234–291.
5. Hitoshi Takei (2014) Expansion of Systemic and Therapeutic Technique.  H. Takei, et al. (Ed.). KYODO ISHO SHUPPAN CO., LTD., Tokyo.
6. Atsushi Yoshida (2015) Practical approach to muscle and fascia (Special Issue: Manipulative physical therapy for sports injury). The Journal of Clinical Sports Medicine. 32: 1000–1004.
7. Stecco L et al (2011) Fascial Manipulation—Theory Edition. H. Takei (Tr.) Ishiyaku Publishers, Inc., Tokyo.
8. Schleip et al (2015) Membrane and Fascia. Up-to-date knowledges and therapeutical approach. H. Takei (Tr.), Ishiyaku Publishers, Inc., Tokyo, 343–349.
9. Misako Nishimori: Pathological characteristics of tenosynovitis of the flexor tendon (trigger finger) on ultrasonic images of the joint.  Japanese Journal of Medical Ultrasound Technology. 38: 2013.
10. ……………….
11. ………………..

Introduction

Fascial Manipulation^® (FM^®), a modality of manipulative physical therapy originated with an Italian physical therapist, Luigi Stecco, is classified roughly into two types, i.e., FM^® for musculoskeletal dysfunction and FM^® for internal dysfunction.  In the FM^® for musculoskeletal dysfunction, a route to fascial compensation is revealed from results of inquiries, exercise test, and palpation test, and then points of Center of Coordination (CC) and Center of Fusion (CF), which are associated with the compensation, are treated.  In general, FM^® is therapeutically designed to recover the feature of sliding of the deep fascia and to improve patient’s pain, Range of Motion (ROM), and muscle strength [1,2]. Focusing on low back pain, which physical therapists and physicians frequently encounter and treat in clinical settings, practical cases of FM^® for musculoskeletal dysfunction are mentioned through 2 case reports in this article.

Practical cases of FM^®

Case 1 – Ascending Fascial Compensation

General information

A 32-year-old woman, a care worker, has started playing badminton since her age of 10 years.  At present she plays badminton about once a month.  The physician who examined the patient made a diagnosis of myofascial low back pain, as any distinct finding on X-ray or MRI image was observed, and treated the patient by physical therapy.

Inquiries

The chief complaint of the patient was left low back pain (at the level of the 4th-5th lumbar vertebrae).  She had the pain 6 months ago without manifestation by any overt symptom.  It was caused by the long-time standing position and assistance for transfer activities during the work.  She had no pain in her sitting or lying position.  The most severe pain showed score 7 based on the Numerical Rating Scale (NRS). The patient has always been feeling physical disorder at her medial left scapula since 3 months ago (NRS: 1-2).

Inquiries about past histories revealed that the patient had fracture of the distal end of the right radius one year ago and received the 4-week treatment by plaster fixation.  She had pain in the lateral region of the left elbow joint 10 years ago.  The longest past history was left ankle joint inversion sprain 17 years ago.  It was treated by plaster fixation for 3 weeks, and it needed 4 months to have fully recovered. The patient had no dysesthesia at any terminal point (head, fingers, or toes), surgical history, or non-contributory internal past history.

Hypothesis

In FM^® a hypothesis is built up regarding a route to fascial compensation from temporal/spatial viewpoints on the basis of the results of inquiries [1]. Figure 1 shows a timeline of information, which was collected on inquiries about the chief complaint (the most severe pain at present), its associated pain, and past histories of he patient.  Figure 2 shows a body chart including the same information as that in Figure 1.

Figure 1. A timeline (case 1).

Figure 2. A body chart (case 1).

Several hypotheses can be built up about the route to fascial compensation from Figures 1 and 2.  When the occurrence of low back pain as chief complaint in a standing position is taken into consideration, however, insufficient sliding of the deep fascia may have been induced by long-term plaster fixation of the left ankle during the treatment of ankle inversion sprain [1], probably leading to the ascending fascial compensation and left low back pain in the patient.

Evaluation by the therapist

(1) Exercise test

On the basis of the above-mentioned hypothesis, two segments, i.e., pelvic girdle (PV) and ankle joint (TA), were selected for exercise test.  As a result, the same type of pain (NRS: 6) as the chief complaint, was induced to PV by pelvic anterior tilt movement in a standing position, while no marked finding was observed in TA.

(2) Palpation test

The segments selected first for palpation test were PV, i.e., segment of the chief complaint, TA, i.e., the origin of the fascial compensation, and the hip joint (CX) localized between the PV and TA segments.  As for these segments, all CC points (anterior, rearward, inward, outward, internal rotation, and external rotation) were palpated. As a result of palpation test for CC, there was no difference in the number of the points at which findings of high density were observed, or the degree of high density among sagittal planes (anterior/rearward), frontal planes (inward/outward), and horizontal planes (internal rotation/external rotation), suggesting that fascial diagonal or fascial spiral, rather than fascial arrangement, is involved with fascial compensation.  Therefore, palpation test for CF points of the above-mentioned three segments was conducted, revealing that CF of left RE-LA-PV1 (Figure 3) showed a large area of high density and had remarkable pain associated with irradiating pain.  As other findings, left RE-LA-TA2 and left Re-LA-CX showed moderately high density.

Figure 3. Palpation and treatment for RE-LA-PV1 CF.

It was considered from the results of palpation test for the PV, TA, and CX that a left RE-LA diagonal or a left AN-ME spiral was involved with the patient’s chief complaint.  Faced with this situation, CF points were palpated at RE-LA and AN-ME of segments of toes (PE) and knee joint (GE) on the left side and low back (LU), and thorax (TH) on both sides.  As a result, left RE-LA-TH showed findings of a large area of high density, and left RE-LA-PE3 and RE-LA-LU on both sides showed findings of moderately high density.  It was judged from these findings that a left RE-LA diagonal was mostly involved with the patient’s chief complaint.  Then, the patient was treated based on the evaluation.

Treatment

In FM^® the CC/CF points treated are selected, and routes to fascial compensation are taken into consideration even on determining the treatment order [1, 2].  In general, since CC/CF points of segments with the chief complaint frequently show serious pain, the treatment rarely starts with the segments. In this patient the treatment started with RE-LA-PE3 (Figure 4) and RE-LA-TA2 (Figure 5), which were localized at the left ankle joint, i.e., the estimated origin of fascial compensation.  As a result of the judgment of the efficacy of the treatment of these CF points from the exercise test results, pain on the pelvic anterior tilt movement was reduced to 50% of that before the treatment.  Consequently, the hypothesis built up was judged to be valid, and the treatment of the RE-LA diagonal was advanced.

Figure 4. Palpation and treatment for RE-LA-PE3 CF.

Figure 5. Palpation and treatment for RE-LA-TA2 CF.

CF points of the left RE-LA-PE3 were treated first, followed by those of the left RE-LA-TA2, left RE-LA-TH, left RE-LA-LU, left RE-LA-CX, left RE-LA-PV, and right RE-LA-LU, in that order.  After all these CF points were treated, exercise test was conducted again.  As a result, the left low back pain on pelvic anterior tilt movement was fully resolved, and the patient had no pain on any other low back movement.

Case 2 – Descending Fascial Compensation

General information

A 54-year-old man, a viola player, has been practicing the viola for 4-8 hours almost every day since he was a child.  According to his reminiscence, he has taken the same posture, i.e., putting the viola on his left shoulder and settling it with his neck, for a long time.  The physician who examined him recognized the narrow intervertebral space of L3/4 and L4/5 on X-ray images, made a diagnosis of lumbar disc disease, and treated the patient by physical therapy.

Inquiries

The chief complaint of the patient was left low back pain (at the level of the 1st-3rd lumbar vertebrae).  He had the pain 6 years ago without manifestation by any overt symptom.  He had the pain particularly during getting up at the time of rising from his bed and in a long-time sitting position.  The most severe pain showed score 5 based on NRS.

The patient has been suffering from left shoulder pain (NRS: 4) since 7 years ago, as well as the left low back pain. Inquiries about past histories revealed that the patient had left elbow joint pain 10 years ago, right elbow joint pain 12 years ago, and neck pain 20 years ago.  He had no past history of either lower extremity. He had no headache or numbness in any finger/toe.  He had no surgical history or noncontributory internal past history.

Hypothesis

Figure 6 shows a timeline of information, which was collected on inquiries about the chief complaint, its associated pain, and past histories of the patient.  Figure 7 shows a body chart including the same information as that in Figure 6. In this patient, his past histories were restricted to his upper body, and he had low back pain as the chief complaint in such an occasion as that without body weight bearing on lower extremities; it occurred during getting up and taking a sitting position for a long time.  Based on these situations, it was considered that the patient took a specific posture because of playing a viola and the overuse of the neck and upper extremities led to insufficient sliding of the deep fascia [1], which was responsible for the descending fascial compensation.

Figure 6. A timeline (case 2).

Figure 7. A body chart (case 2).

Evaluation by the therapist

(1) Exercise test

On the basis of the above-mentioned hypothesis, two segments, i.e., low back region (LU) and shoulder joint (HU), were selected for exercise test.  Consequently, low back pain was induced as a chief complaint by extension movement and right flexion movement of the low back region.  On the other hand, shoulder pain was induced to the same site as that where the patient felt pain during abduction movement of the left shoulder.  ROM on active movement was 120°.

(2) Palpation test

The segments selected first for palpation test were LU, i.e., the segment of chief complaint, the cervical vertebra (CL) involved with the longest past history, and HU, i.e., the segment of its associated pain.  As for these segments, all 6 CC points were palpated. As a result of palpation test, RE-CL on both sides (Figure 8) and left RE-LU (Figure 9) showed high-density areas, and had remarkable pain associated with irradiating pain.  As other findings, RE-HU and AN-LU on the left side and right RE-LU showed moderately high density.  When the frequency of high density was compared among the sagittal, frontal, and horizontal planes, it was highest on the sagittal planes.

Figure 8. Palpation and treatment for RE-CL CC.

Figure 9. Palpation and treatment for RE-LU CC.

From the results of palpation test for LU, CL, and HU, it was judged that left fascial arrangement on the sagittal plane was most involved with the patient’s chief complaint.  To find latent CC points, anterior (AN) and rearward (RE) CC points of segments of the shoulder girdle (SC), thorax (TH), and pelvis (PV) on both sides were palpated.  As a result, RE-TH, RE-SC, and AN-PV on the left side showed findings of moderately high density.

Treatment

The treatment started with the CC points of the RE-TH of the adjacent TH segment (Figure 10) because of remarkable tenderness in CC points of CL (RE-CL on both sides), i.e., the estimated origin of fascial compensation.  The exercise test following the treatment of the CC points revealed that the pain on low back extension and right low back flexion decreased to 50% of that before treatment.  Furthermore, the pain during shoulder abduction movement was reduced to 20% of that before treatment, and the restricted ROM was almost resolved.  From the results, the built-up hypothesis was judged to be valid, and treatment of the points on the sagittal planes was advanced. CC points of the left RE-TH were treated first, followed by those of the left RE-SC, RE-CL on both sides, left RE-HU, RE-LU on both sides, and left AN-LU, in that order.  When RE-CL points were palpated again after the treatment of the RE-SC, tenderness was reduced.  Therefore, they were included in the subjects of treatment. After all the above-mentioned CC points were treated, exercise test was implemented again.  As a result, the patient had no pain in his low back or shoulder during any movement.

Figure 10. Palpation and treatment for RE-TH CC.

Conclusion

In this article the treatment using FM^® for 2 patients with low back pain was surveyed.  They had left low back pain in common.  Particularly noteworthy is the fact that they were different from each other regarding the segments evaluated and the CC/CF points treated despite the feature common to them.  It is important for implementation of the treatment appropriate for the individual patient to collect information about pain at present and in the past as accurately as possible on inquiries.  On the occasion of information collection, specific attention should be paid to trauma, immobilization, and overuse, because they may lead to increased mucosity associated with aggregation (high density) of hyaluronic acid in the deep fascia ad to adversely influence the sliding system of the deep fascia [1].  It should also be mentioned that setting-up of the hypotheses about routes to fascial compensation on the basis of information collected on inquiries before the start of exercise test and palpation test was important for evaluation and treatment to proceed smoothly. This article did not describe any concrete method of exercise or palpation test or position of each point of CC/CF as space is limited.  The author would be obliged if the readers would be confirmed in FM^®-related publications.

References

1. Luigi Stecco, Antonio Stecco (2018) Fascial Manipulation Practical Part – First Level. Padova: Piccin Nuova Libraria S.p.A.
2. Luigi Stecco, Carla Stecco (2019) Fascial Manipulation Practical Part – Second Level. Padova: Piccin Nuova Libraria S.p.A.

Fascial Dysfunction

Fascial degeneration can be caused by various factors (Table 1). Injury, disuse, lack of exercise due to circulatory failure, repetitive movement, and persistent poor posture can cause twisting of collagen fiber bundles and densification of the fascia, eventually leading to dehydration, hardening, and gelation of the fascial matrix. Aggregation of hyaluronic acid due to overuse and sustained muscle contraction can also limit myofascial gliding [1–3]. Generally, fascial dysfunction is caused by 1) densification of the fascia, 2) gelation of the fascial matrix, and 3) aggregation of hyaluronic acid. Fascial dysfunction reduces the gliding property and mobility of the fascia and all underlying tissues such as muscles, thereby limiting the maintenance of antigravity posture as well as smooth, functional, and efficient movements. Fascia is composed of the superficial fascia, deep fascia (aponeurotic fascia), epimysium, perimysium, and endomysium (Figure 1). The superficial fascia is in the subcutaneous tissue while the deep fascia covers muscles and connects the whole body in 14 different arrangements. The epimysium is a thin membrane that covers muscles; it connects to the perimysium to cover muscle bundles and to the endomysium to cover muscle fibers. Muscle fibers enter from the epimysium into the deep fascia and connect muscles across joints along 14 different arrangements (Figure 2). Because the epimysium, perimysium, and endomysium are connected to each other, muscle spindles attached to the endomysium are over activated, resulting in increased alpha-motor neuron excitability. Moreover, poor gliding of muscle fiber results in reduced muscular flexibility and output.

Table 1. Causes of fascial degeneration.

Figure 1. Superficial fascia, deep fascia, epimysium, perimysium, endomysium

Figure 2. Muscle fibers enter from epimysium into the deep fascia

All traction forces exerted by muscle spindles on the endomysium converge simultaneously on the epimysium. In the simplest fascial unit, traction forces are transmitted along the same muscle and converge on the midpoint. Even in a more complex fascial unit formed by many different muscle motor units, these forces converge on a single point. This exact point on the epimysium where muscle force vectors converge is referred to as the Center of Coordination (CC). The point where vectors from two adjacent fascial units converge in a multiplanar, diagonal, composite motion method (anterior-lateral, anterior-medial, and rear-lateral, rear-medial) is referred to as the Center of Fusion (CF). The human body can be divided into 14 segments: scapula (sc), humerus (hu), elbow (cu), carpus (ca), and fingers (di), which constitute the upper limbs; head (cp), neck (cl), thorax (th), lumbar (lu), and pelvis (pv), which constitute the trunk; and hip (cx), knee (ge), talus (ta), and toes (pe), which constitute the lower limbs. Abbreviations for body segments are written in Latin [1,2] (Table 2).

Table 2. Body segments and terms used to represent their abbreviations.

There are 6 arrangements of CCs and 8 arrangements of CFs connecting these segments; thus, at least one of these 14 arrangements is affected in fascial dysfunction. The wavy collagen fibers of the epimysium and perimysium/endomysium connect to the tendon. When the tendon stimulates mechanoreceptors and nociceptors in a joint, the patient feels pain around the joint. The area where the patient feels or perceives pain is referred to as the Center of Perception (CP). Thus, therapists should be aware that the problem is not in the joint, but in the fascia. Successful treatment of fascial dysfunction relieves muscle/fascial pain and improves muscular output/flexibility and motor paralysis, resulting in improved exercise performance and activities of daily living.

Treatment of Fascial Dysfunction

Treatment for fascial dysfunction includes muscle pain relief as an indirect approach, and myofascial release and Fascial Manipulation® (FM) as direct approaches (Table 3). General assessments include current history of pain and concomitant pain, detailed history taking, alignment, Range of Motion (ROM) during exercise, muscle strength, abnormal sensation, and determination of the site of pain by palpation. Motion assessment (active/passive motion, stretching, resistance exercise) is then performed to determine whether there is any pain, ROM restriction, and/or muscle weakness. These assessments are combined with assessment of CCs and CFs by palpation to assess each segment and arrangement. Balance between agonist and antagonist muscles should also be considered when performing treatment.

Table 3. Therapeutic techniques for fascial dysfunction.

Muscle Pain Relief

Muscle Pain Relief (MPR) is a technique based on the therapeutic principle of Strain-Counterstrain (S-CS) with some original modifications. The technique was developed by Takei as a treatment for muscle/fascial pain, taking into account the fascial arrangement. S-CS, also referred to as ‘positional release,’ is a technique used to relieve pain by moving a body part affected by somatic dysfunction to an easy, less painful position to reduce or suppress the inappropriate proprioceptive activity responsible for the somatic dysfunction [4–12]. However, this technique does not involve whole-segment assessment/treatment along the anatomical fascial arrangement and focuses on treating muscle pain at each part. Moreover, in S-CS, “tender points” are considered to indicate somatic dysfunction, whereas the therapeutic targets of MPR are CCs on the epimysium where muscle force vectors converge. CCs are scientifically defined points based on the anatomical fascial arrangement [1,2].

Therapeutic Principle

A muscle spindle is located in parallel with the course of muscle fibers and senses the length of a muscle and the degree of change thereof [13,14]. In the middle and adjacent parts of the muscle spindle are sensory receptors known as the primary and secondary endings, which are innervated by group Ia and II sensory nerve fibers, respectively. The middle part of the muscle spindle is non-contractile and contains a receptor formed by annulo-spiral endings while both its ends form a contractile intrafusal muscle fiber that connects to an extrafusal muscle fiber. The intrafusal muscle fiber at both ends is innervated by gamma-motor neurons, which only innervate intrafusal muscle fibers, and beta-motor neurons that innervate both the extra- and intrafusal muscle fibers via a single axonal branch. Activation of these neurons causes both ends of the spindle to contract. This force is too weak to cause muscle tension but does increase the tension of the muscle spindle, thereby enhancing its sensitivity as a receptor. Excitation of the muscle spindle or gamma efferent fibers and subsequent muscle contraction results in increased impulse from the primary endings (group Ia fibers). Taking a joint position that allows this strained and activated muscle spindle to be shortened passively leads to decreased afferent firing from the primary endings and decreased alpha- and gamma-motor neuron firing in the central nervous system, resulting in relaxation of the extrafusal muscle fibers [4–8, 15–17].

General principles of treatment

Therapists with minimal experience should try various postures and identify those which are comfortable and uncomfortable based on feedback from the patient. The optimal posture should relieve pain. If pain/tenderness is successfully relieved, the patient will perceive it distinctly. As more experience is gained, it will be easier to feel changes with the fingertips and find an ideal posture. Therapists with more experience can tell that the ideal posture has been achieved even when the patient is still in pain. Even such patients are likely to have pain relief in about 30 seconds.

Actual treatment procedure

The MPR techniques are applied to CCs all over the body. In MPR, tender points in specific areas of the musculoskeletal system are identified and used for both diagnostic and therapeutic monitoring purposes. Once a CC is identified, it is necessary to find a position that can reduce both tenderness and the sensitivity of the tissue felt by the therapist. What is important here is to understand the action of each muscle three-dimensionally. It is important to find a position that can reduce pain three-dimensionally, taking into account composite factors such as flexion/extension, adduction/abduction, and external/internal rotation, rather than a position that simply shortens the muscle to the maximum extent. During treatment, keep the finger on the CC, but with a lighter touch than during diagnosis, to feel changes in the tissue. Feel with the fingertips that tension is released and ask the patient if pain/tenderness is released while pressing the point intermittently. Hold this posture for about 90–120 seconds. Then, slowly return the patient to the normal posture and perform reassessment. The following part of the section describes example treatment procedures for Antemotion (AN) of the upper limbs.

Example treatment cases

AN-SC: Pectoralis minor (Figure 3)

Figure 3. MPR for AN-SC (pectoralis minor)

CC: Located inferior to the coracoid process and on the belly of the pectoralis minor and the coracoclavipectoral fascia.

CP: Pain in the shoulder, clavipectoral fascia, and acromioclavicular joint (CC and CP are close).

Treatment position: Supine position. The CC-side upper limb is placed across the front of the body. Scapula: Tilted anteriorly, rotated inferiorly, and depressed.

AN-CU: Biceps brachii (Figure 4)

Figure 4. MPR for AN-CU (biceps brachii)

CC: Located just below the deltoid attachment and lateral to the belly of the biceps brachii.

CP: Pain at the anterior elbow, often at the epicondyle or distal biceps brachii tendon.

Treatment position: Supine position. Shoulder joint: Flexed to 90°, slightly to moderately abducted (or slightly to moderately adducted for the short head). Elbow: Moderately flexed. Forearm: Supinated.

Myofascial Release (MFR)

The purpose of MFR is to restore the normal function of muscles and other structures by reversing fascial twisting and to improve the mobility and stretchability between muscles or between muscles and other structures. The deepest fascial tissue forms a dural tube that wraps and supports the central nervous system and impaired dural mobility may limit the physiological movement of the skull and sacrum, causing various forms of dysfunction [18–21]. Because the fascial tissue forms a systemic network, MFR is often combined with cranio-sacral therapy [18]. Although similar therapeutic techniques have traditionally been applied in osteopathy, the MFR technique described here was systematically established by John F. Barnes et al. and is intended to release and unravel fascial twisting, rather than simply stretching the fascia [18,22–25]. Based on this technique, Takei et al. incorporated the concepts of CCs and fascial arrangement to establish their original therapeutic principles and techniques (Takei’s concept). This modification has made MFR a more effective technique.

What is “release”?

The objective of MFR, in particular, deep myofascial release, is to release densified and cross-linked collagen and elastin fibers and change the viscosity of the fascial matrix (intercellular material) from gel to sol. Barriers formed by the collagenous component cannot be corrected forcibly. Instead, applying gentle and sustained stretching and pressure can change the viscosity or density of the matrix and release the restriction caused by collagen fibers, resulting in a change in tissue length. First, apply pressure down to the deep fascia. Then, while keeping the pressure, apply gentle stretching motions to the site of fascial restriction, causing the elastic component to be stretched by the initial stretch applied to the fiber complex. The elastic element is slowly pulled like an elastic or spring coil until the hand applying the stretch stops at a tough barrier formed by the collagenous component. It should be kept in mind that elastin fibers have shape-memory properties and if stretching stops here, they return to their original length due to elasticity. Although barriers formed by the collagenous component cannot be corrected forcibly, applying sustained stretch can cause gradual stretching of collagen fibers due to the viscoelasticity of elastin fibers [26]. The stretched elastin fibers allow the tissue to regain its original shape and flexibility, resulting in restoration of the proper biomechanical alignment of the skeleton. Barriers formed by the collagenous fibers cannot be corrected forcibly. Lower load (gentle pressure) is more effective than higher load (fast, pressure applied) in changing the viscosity of the matrix [18]. Applying gentle and sustained stretching and pressure over 90 seconds to 3 minutes (5 minutes maximum) can change the viscosity or density of the matrix and release the restriction caused by collagen fibers, resulting in a change in the tissue length.

Precautions during release

After successful myofascial release, many patients experience an emotional change known as “somatoemotional release.” Just as emotional stress causes physical tension, physical stress causes emotional tension. Thus, releasing the fascial tissue from physical stress also results in emotional release [18,19,21].

Goal of myofascial release

The goal of myofascial release is to release fascial restriction and restore the overall musculoskeletal balance leading to a balanced posture. Acquisition of a structurally balanced posture will permit normalization of the center-of-gravity line and the symmetrical functioning of the entire musculoskeletal system. Applying gentle stretching to the fascial restriction elicits heat, which is a vasomotor response that increases blood flow in the affected area, improves lymph drainage, reorganizes the fascial tissue, and most importantly resets the sensory mechanism of soft-tissue proprioception [18,19–21]. This activity will reprogram the central nervous system, allowing a normal functional range of motion without eliciting old pain patterns [27]. The final goal is to achieve optimal function and performance with the least amount of energy. Because this technique is mild, MFR is applicable to various signs and symptoms. Systemic contraindications include malignant tumors/cancer, aneurysms, acute rheumatoid arthritis, and systemic/local infection; local contraindications include hematomas, open wounds, sutured wounds, and fracture sites during the healing process.

Actual treatment procedure

The three basic MFR techniques are 1) longitudinal release, 2) transverse release, and 3) pulling or traction (Fig. 5). Longitudinal release is a technique used to stretch the fascia while gently applying pressure so as to sandwich the CC, taking into account the fascial arrangement, and to keep stretching after feeling the restriction of elastin fibers until the restriction of collagen fibers is released and myofascial release is achieved. Transverse release is a technique used to release the fascia on the transverse plane while simultaneously feeling the ventral and dorsal connections of the deep fascia. Pulling is a technique that is used to easily move the upper or lower limbs in various directions while releasing the fascia distally. While performing release, the therapist should be relaxed and feel as if their palm or finger pulps were fused with the patient’s skin. While applying pressure down to the deep fascia while stretching the skin, the deep fascia is also stretched. In the initial phase of release, the elastic component is slowly pulled like a spring coil. Then, maintain the pressure for 90 seconds to 3 minutes (5 minutes maximum) to release the collagen component, causing the tissue to soften like melting butter. Pressure reaches the deeper layers gradually. The time required to complete the procedure will decrease with improved technique. Successful release will allow elastin, a constituent of elastin fiber, to help restore the original shape and flexibility of the tissue. The following part of this section describes representative treatment procedures for Lateromotion (LA) of the upper limbs.

Figure 5. Three basic techniques for myofascial release

Representative treatment cases

LA-CX: Tensor Fascia Lata (Figure 6)

Figure 6. Release of LA-CX (tensor fascia lata)

CC: Located inferior to the anterior superior iliac spine and on the tensor fascia lata.

CP: Pain in the lateral thigh around the tensor fascia lata. Numbness at a lower part of the lateral thigh.

Treatment position: Lateral position, with the lower leg placed forward and the upper leg placed slightly backward. Place your hands crossed over the CC (cross-hand technique) to apply pressure and stretch.

LA-TA: Extensor Digitorum Longus (EDL) (Figure 7)

CC: Located between the proximal one-third and middle one-third of the lower leg, anterior to the fibula and on the EDL. Another located on the peroneus tertius.

CP: Pain in the lateral ankle. Pain secondary to ankle sprain.

Treatment position: Lateral position. Apply pressure and stretch to the EDL at the middle one-third of the lower leg (slightly above the mid-point) and anterior to the fibula.

Figure 7. Release of LA-TA (extensor digitorum longus)

Fascial Manipulation®

The therapeutic principle of FM consists of mechanical (movement – friction), physical (heat – inflammation) and chemical (metabolism – repair) elements. The therapeutic targets are CCs and CFs. CCs are located in the 6 fascial units that move various body segments in 3 spatial planes (anterior and rearward movements in sagittal plane, medial and lateral movements in frontal plane, and internal and external rotation in horizontal plane). CFs are involved in multiplanar composite movements on diagonal lines and spirals (anterior-lateral [AN-LA], anterior-medial [AN-ME], rear-lateral [RE-LA], and rear-medial [RE-ME]). Differences between CC and CF are shown in
table 4. FM is also effective in evaluating and treating the musculoskeletal system affecting internal dysfunction, including visceral, vascular, and glandular dysfunction; in treating sensory organs in the head, including the face; and in treating the superficial fascia for lymphatic/immunological, dermatological/thermoregulatory, fat/metabolism, and neurogenic/psychogenic disorders [28]. An alternative treatment approach for lymphatic/immunological, dermatological/thermoregulatory, fat/metabolism and neurogenic/psychogenic disorders is to divide each of the trunk, upper, and lower limbs into 4 areas (AN-LA, AN-ME, RE-LA, and RE-ME) and treat the superficial fascia in each area.

Table 4. Differences between center of coordination (CC) and center of fusion (CF)

Actual assessment procedure

Fascial dysfunction may occur on the fascial arrangements where fascial units in each segment involved in local pain are arranged on the frontal, sagittal, and horizontal planes (Figure 8); the fascial diagonal lines on these planes (Figure 9); and the fascial spirals involved in extensive pain (Figure 10). Motion assessment is performed to assess the entire bone-nerve-myofascial complex or individual fascial units instead of individual muscles, by moving each segment in a specific direction. Each CC is located slightly away from their corresponding CPs and pain is only detectable on assessment by palpation. Based on the results of motion and assessment by palpation, it is necessary to identify densified and degenerated fasciae, treat the fasciae to reverse fascial degeneration, and continue verifying hypotheses and results.

Figure 8. Example fascial arrangement: Sagittal view of the fascial arrangement involved in backward movement of the lower limb (adapted from reference 1 with some modifications)

Center of coordination:  Center of perception (site of pain):

Figure 9. Example diagonal lines: Centers of fusion (CFs) on rear-lateral diagonal lines²⁾

Figure 10. Example fascial spiral: A RE-LA (rear-lateral) spiral originating from the rear lateral aspect of the hand and foot.

Actual treatment procedure

FM should be performed on a densified area that needs to be treated by applying deep pressure to the area (CC or CF) while applying friction for a sufficient length of time to generate heat. This heat helps correct the viscosity of the matrix and initiates inflammatory processes required for healing. This technique should be continued until fascial correction is achieved and pain resolves. Increased temperature promotes the gel-to-sol transition and results in a corrected fascial matrix. In general, the viscosity transition of a densified fascia can be achieved in several minutes. Sudden release of free nerve endings results in reduced densified loci, leading to improved motor coordination, normalized joint motion trajectory, and subsequent reduction of associated pain. This results in elimination of a fibronectin network that interferes with the functionality of CCs. Immediately after treatment, patients may perceive improvement in symptoms and local warmth around the treated area. With no swelling, they feel even better than before treatment. A small depression due to change in loose connective tissue may occur in this area. After 10 minutes, some patients may notice worsening of symptoms and local pain. This is due to increased blood flow to the area and swelling formed as a consequence of the exudation phase. FM prevents matrix binding to allow for a new orientation of fibroblasts. During several hours after the fascial inflammation phase, neutrophils appear following macrophages and are removed simultaneously with newly formed necrotic material. Myofibroblasts are activated and produce new type-III collagen fibers.

During the following 3 days, a small hematoma may appear at the treated area, which may worsen symptoms temporarily depending on predisposing factors. At this time, the use of anti-inflammatory compresses or medications should be avoided because they inhibit normal inflammatory reaction. Patients in good condition should also refrain from walking longer than usual or going shopping or to a fitness gym. By 5 days after treatment, reduced local pain, improved fascial tension balance, and resolution of symptoms and swelling should be observed. During the next 20 days, the initial type-III collagen fibers are gradually arranged along the traction line and are replaced by more stable type-I collagen fibers. It is important to inform patients in advance of the possibility of these reactions.

Example treatment cases

AN-GE: Lateral aspect of rectus femoris (Figure 11)

Figure 11. Fascial manipulation on AN-GE (lateral aspect of rectus femoris)

CC: Located at half of the length of the thigh and on the vastus intermedius between the rectus femoris and vastus lateralis.

CP: Pain in the inguinal region and the medial thigh. Pain in the muscles attached to the pubic bone.

Treatment position: Supine. Apply pressure and friction with a knuckle or elbow placed on the fascia lata in the lateral aspect of the rectus femoris between the patella and the inguinal ligament.

RE-PV: Iliocostalis lumborum (Figure 12)

Figure 12. Fascial manipulation on RE-PV (iliocostalis lumborum)

CC: Located at the L5 level and medial to the posterior superior iliac spine on the quadratus lumborum muscle originating from the iliolumbar ligament.

CP: Pain at a site medial to the sacrum, piercing in nature, may diffuse along the posterior thigh/lower leg.

Treatment position: Prone. Apply pressure and friction with the elbow placed between the fifth lumbar spine and the anterior superior iliac spine.

RE-LA-LU: Latissimus dorsi (Figure 13)

Figure 13. Fascial mobilization on RE-LA-LU (latissimus dorsi)

CF: Located at the center of the latissimus dorsi at the costal attachment of the upper margin of the serratus posterior inferior and the iliocostalis.

CP: Back pain occurs on torsion, lateral bending, or extension.

Treatment position: Prone. Apply a lower pressure and a slightly broader friction than for CC treatment (fascial mobilization) to the center of the latissimus dorsi at the costal attachment of the upper margin of the serratus posterior inferior and the iliocostalis.

Three treatment techniques for fascial dysfunction were described. Of these, muscle pain relief is an indirect treatment technique and is less effective than others for physical improvement of fascial dysfunction. Still, causing no inflammatory reaction, this technique is effective for persons with low pain threshold, children, the elderly, and athletes scheduled to participate in an event on the same or following day. Myofascial release and FM are both direct treatment techniques, although the former is more effective for those people sensitive to pain and those athletes scheduled to participate in an event on the following day. FM is most likely to cause inflammatory reaction among these techniques, and therefore requires sufficient patient orientation and accurate assessment. Therapists should also be able to select the most suitable technique for each patient.

References

1. Takei H (2011) Fascial Manipulation, Theoretical. Ishiyaku Publishers Tokyo.
2. Takei H (2011) Fascial Manipulation, Practical. Ishiyaku Publishers Tokyo.
3. Takei H (2013) Fascial manipulation. In: Shimada T, Arima Y and Saito H (eds.) Physiotherapy practice based on clinical thinking: Guidance for Clinical Application of Recent Findings for Unexperienced and Young Physical Therapists – Musculoskeletal physiotherapy, Bunkodo, Tokyo, 46–60.
4. Jones LH, Kusunose RS (1995) Strain and Counterstrain. Course taken in San Francisco, Jones Institute, INC.
5. Kusunose RS (2003) Strain and Counterstrain. Advanced and cranials syllabus. Course taken in Seattle, Jones Institute, INC.
6. Jones LH (1995) Jones Strain and Counterstrain. Jones Strain-CounterStrain, Inc., Boise, ID.
7. Jones LH: Strain and counterstrain. The American Academy of Osteopathy, Indianapolis, IN, 1981.
8. Kusunose RS (1993) Strain and counter strain. In: Basmajian JV, Nyberg R (eds.), Rational manual therapies. Williams & Wilkins,Baltimore 323–333.
9. Jones LH (1964) Spontaneous release by positioning. DO 1:109–116.
10. Jones LH (1973) Foot treatment without hand trauma. Journal of the American Osteopathic Association 72: 481–489.
11. Mitchell FL, Moran PS, Pruzzo NA (1979) An evaluation and treatment mannual of osteopathic muscle energy procedures. Mitchell, Moran and Pruzzo,Valley Park, Pg-no: 1–3.
12. Korr IM (1975) Proprioceptors and Somatic Dysfunction. Journal of the American Osteopathic Association 74: 638–650.
13. Takei H (2004) Structure of Locomotor System. Kinematics (Edited by Maruyama H). Chugai-Igakusha, Tokyo, Pg-no: 5–54
14. Takei H (2008) Color Atlas of Palpation and Functional Anatomy. Vol.2. Bunkodo, Tokyo.
15. Lee DG Principles and practice of muscle energy and functional techniques. In: boyling JD & Palastanga N (eds.), Grieve’s modern manual therapy(2nd ed), Churchill.
16. Sydenham RW (1994) Manual therapy techniques for the thoracolumbar spine. In: Donatelli RA, Wooden MJ (eds.), Orthopaedic Physical therapy(2nd ed), Churchill Livingstone, New York, Pg no: 421–465.
17. Nakamura Y (1996) Reflexes. Edited by Hoshi T et al., Review of Medical Physiology, Maruzen Publishing, Tokyo, Pg no: 123–132.
18. Barnes JF (1990) Myofascial release. John F.barnes,P.T. and Rehabilitation Services, Inc., Pennsylvania.
19. Swenson C (1995) Craniosacral therapy. Course taken in Mineapollis,The upledger institute, INC.
20. Upledger JE, Vredevoogd JD (1983) Craniosacral therapy. Eastland Press Seattle.
21. Upledger JE (1987) Craniosacral therapy. Eastland Press Seattle.
22. Takei H (2007) Myofascial Release In: Development of Therapeutic Techniques of Different Categories, 2nd Edition, Edited by Nara I et al., Kyodo Isho Shuppan, Toyo, Pg no: 95–128.
23. Takei H (2005) Myofascial Release. In: Advanced Illustrated Physiotherapy Technical Guide, Edited by Hosoda K et al., Bunkodo, Tokyo, Pg no: 709–729.
24. Takei H (2000) Overview of myofascial release approaches. Manipulation 15: 14–20.
25. Ward RC (1993) Myofascial release concepts. In: by Basmajian JV & Nyberg R (eds.), Rational manual therapies, Williams & Wilkins, Baltimore, Pg no: 223­241.
26. Twomley L, Taylor J (1982) Flexion,creep,dysfunction and hysteresis in the lumbar vertebral column. Spine 7: 116­122.
27. Barnes JF, Smith G (1987) The body is a self­correcting mechanism.Physical Therapy Forum, 8: 8­9.
28. Takei H (2017) Fascial Manipulation for Internal Dysfunctions (Theoretical). Ishiyaku Publishers, Tokyo.