Introduction

Osteopathic manipulative techniques are classified as direct or indirect. Direct techniques require positioning the patient against a restrictive barrier. Indirect techniques involve placing the patient in a position of ease.[1] Strain-counterstrain (SCS), also called "counterstrain," and facilitated positional release (FPR) represent commonly used indirect osteopathic manipulative techniques. SCS constitutes a soft tissue approach that passively addresses musculoskeletal pain, impaired range of motion (ROM), and somatic dysfunction by modulating cellular function within the targeted tissues.[2][3]

Dr. Lawrence Jones developed SCS in 1955 after encountering a challenging back pain case. The patient's symptoms improved after assuming a physician-directed position of ease. Repetition of this method in other patients produced consistent results. These experiences led to the identification of "tenderpoints," defined as areas with maximal pain within a muscle group. Tenderpoints demonstrate concomitant soft tissue texture changes at locations not typically associated with pain. Effective management requires precise identification of these regions.

SCS employs palpation and physician-guided manipulation to place soft tissues or joints into a position of ease, away from the restrictive barrier. Compression or shortening of the dysfunctional region facilitates relaxation of hypertonic muscles.[4] FPR shares similarities with SCS, as positioning in a state of comfort follows identification of the tender area. Application of an additional activating force accelerates the relaxation of the affected muscle. Stanley Schiowitz developed this technique in 1990.[5]

Issues of Concern

Clinical research investigating the physiologic basis of SCS and FPR remains limited.[6] Most evidence derives from animal models and in vitro studies.[7] Questions regarding the effectiveness of these techniques persist. Several studies evaluating SCS and FPR for specific dysfunctions report promising results, indicating potential beneficial effects on clinical practice.[8][9][10]

Cellular Level

SCS and FPR exert effects at the cellular level to alleviate pain, somatic dysfunction, and ROM limitations. Both techniques influence muscle spindles, Golgi tendon organs (GTOs), and inflammatory pathways.

Proprioceptors constitute end organs that detect physical changes in musculoskeletal tissues, muscle length, joint position, and tendon tension.[11] These receptors contribute substantially to somatic dysfunction, mobility restriction, and the formation of tenderpoints.

Aberrant activity of spindle fibers and nociceptors contributes to the development of tenderpoints and muscle pain.[12] Muscle spindles function as mechanosensors, transmitting information regarding muscle contraction to the central nervous system.[13][14] Each spindle contains multiple intrafusal fibers, predominantly type Ia and type II sensory fibers. Fusimotor neurons, consisting of γ- and β-motor neurons, also reside within muscle spindles. The mechanosensor is encapsulated within a connective tissue sheath and aligned parallel to extrafusal muscle fibers.[15]

The stretch reflex originates at the sensory fibers of muscle spindles. Type Ia sensory fibers convey velocity information to nerve afferents, while type II sensory fibers transmit information regarding muscle length.[16] These fibers fire rapidly during muscle stretch. Signals reach the dorsal root ganglion of the spinal cord and then travel monosynaptically to α-motor neurons within the same muscle spindle as the sensory fibers.[17][18] Muscle spindle firing decreases during muscle contraction and diminishes further as reflexive input to α-motor neurons declines.

Contracted intrafusal fibers amplify afferent signals from stretched muscles. The CNS modulates intrafusal fiber tonicity and adjusts the stretch reflex, thereby modifying muscle contraction intensity at a given length. “Automatic gain control” occurs when γ-motor neurons continuously alter intrafusal fiber length. A γ-motor neuron is a lower motor neuron that regulates intrafusal fiber contraction and tonicity, influencing the stretch reflex.

GTOs function as proprioceptors located in tendons and joint capsules. These sensory structures convey information to the CNS regarding tension generated by muscle contraction. Fast-conducting type Ib afferent fibers innervate GTOs. These fibers transmit signals to the dorsal horn and synapse with interneurons that relay inhibitory signals to the muscle-tendon complex.[19] This pathway, initiated by GTOs, constitutes the Golgi-tendon reflex, also known as autogenic inhibition or the inverse stretch reflex.[20]

Muscle stress or strain induces fibroblasts to release interleukins 1α, 1β, 2, 3, 6, and 16. These proinflammatory cytokines activate the immune system by recruiting and stimulating neutrophils, macrophages, and eosinophils. The cytokines also promote increased tissue perfusion, swelling, and local temperature.[21][22] Muscle injury results in leakage of cellular adenosine triphosphate. Extracellular pH decreases, whereas bradykinin, prostaglandin E2, and endogenous neuropeptides accumulate at the injury site. These events initiate an inflammatory cascade that activates nociceptors and triggers the release of the neuropeptides substance P and calcitonin gene-related peptide.

Substance P and calcitonin gene-related peptide dilate blood vessels and increase vascular permeability. The proposed cellular pathophysiology of tenderpoints begins with musculoskeletal alterations and culminates in the inflammatory cascade.

Development

Skeletal muscle fibers and myofibers originate from mesenchymal stem cells during primary (weeks 8–10) and secondary (weeks 16–18) myogenesis.[23][24] Muscle spindles begin developing from flat mesenchymal cells adjacent to nervous tissue fibers around week 11.[25][26] Muscle spindles attain definitive structure by week 20 and continue to mature after birth. Postnatal muscle growth predominantly occurs through increases in muscle fiber size. Muscle satellite cells facilitate repair following injury.[27] GTOs form during the late fetal stage, as thin collagen bundles establish myotendinous junctions at the tips of myotubules. GTO development continues for several weeks after birth, during which the subcapsular space divides and type Ib fibers undergo myelination.[28]

Organ Systems Involved

The musculoskeletal and nervous systems constitute the primary organ systems engaged in SCS and FPR. Tenderpoints originate from musculoskeletal injury and inflammation. Receptors and neural pathways mediate the physiological response and are critical for the accurate execution of SCS and FPR techniques.

Function

SCS alleviates somatic dysfunction, pain, and tissue texture abnormalities that generate tenderpoints. This indirect technique is indicated for patients who require a gentler osteopathic approach or have not responded to other manipulative techniques. FPR addresses tender areas more rapidly than SCS by applying an additional compressive force that accelerates the cellular response.

Mechanism

SCS begins with the identification of tenderpoints, which are monitored during and after treatment. No standardized pain scale reliably identifies tenderpoints. However, assessment may include the use of a visual analog scale, a dichotomous determination of the presence or absence of pain, and observation of the "jump sign," defined as sudden physical withdrawal from palpation. Establishing somatic dysfunction requires evaluation of the ROM, joint mobility, and muscle strength.

Following tenderpoint identification, the patient is positioned into a state of comfort such that tenderness at the site decreases by at least 70%. The optimal position exhibits minimal tenderness and relaxation of the surrounding fascia. This position is determined by sequential joint manipulation around the tenderpoint, which contracts the affected muscle. The patient is maintained in this position for approximately 90 seconds while the practitioner monitors the muscle and fascia for changes in tenderness and tightness through palpation. The patient returns to a neutral resting position and undergoes reassessment upon achieving improvement.

In FPR, a compressive or distracting force is applied to the affected tissues while the patient occupies a position of ease. This approach reduces the treatment interval from approximately 90 seconds to about 5 seconds. FPR relies on a 3-plane diagnosis rather than tenderpoint identification.

The patient is first positioned neutrally to unload pressure on the affected joint. Compression, torsion, or traction is then applied to activate the dysfunctional area. Soft tissue relaxation may be detected during this phase. The patient remains in the position of ease for approximately 5 seconds while the activating force is maintained on the dysfunctional segment. Dr. Schiowitz often concluded treatment by setting the segment against a barrier, although this step is not mandatory.[29][30]

Related Testing

Up to 200 tenderpoints have been identified since the time of Dr. Jones. No definitive imaging modality exists for tenderpoints. However, these regions may be visualized using ultrasonography and sonomyoelastography, in contrast to fibromyalgia.[31] Tender areas in fibromyalgia typically localize to tendinous junctions where muscles attach to bones. Patients with this condition exhibit reduced pain thresholds, such that normal tension between muscle and bone can elicit pain.[32]

SCS tenderpoints differ from Travell triggerpoints despite overlap in affected spinal segments. Triggerpoints generally produce radiating pain, whereas tenderpoints remain localized. Triggerpoints respond to interventions such as injections, soft tissue manipulation, and the spray-and-stretch technique.

Pathophysiology

The formation of tenderpoints and their responsiveness to SCS can be explained by 3 theories: the proprioceptive theory, local inflammatory circulatory effects, and the ligamento-muscular reflex. These concepts are explained below.

Proprioceptive Theory

The proprioceptive theory provides the most widely accepted explanation for the effectiveness of SCS. According to this theory, antagonist muscle spindles initiate a counter-contraction in response to the stretch reflex. This response produces a sustained muscle spasm, resulting in neuromuscular imbalance, hypertonicity, and referred pain, which are hallmarks of tenderpoints. The neuromuscular imbalance may contribute to the ropelike quality observed in some tenderpoints. Tenderpoints represent active injuries that persist as long as the affected muscle maintains a shortened state.

Muscle shortening can restrict joint mobility. SCS modulates γ-motor neuron output, reducing the disparity between intrafusal and extrafusal fibers. This modulation inhibits the stretch reflex and restores the muscle to its resting length.

Clinical studies demonstrate that individuals with tenderpoints exhibit measurable changes following SCS, including tenderness at lower electrical thresholds, reduced stretch reflex amplitudes, and decreased pain with improved ROM. However, direct experimental tests of the proprioceptive theory have produced conflicting results.[33][34]

Local Inflammatory Circulatory Effects

Local inflammatory and circulatory mechanisms may contribute to the efficacy of SCS and FPR. Repositioning the patient can increase blood flow to tenderpoints. Enhanced circulation improves nutrient delivery, facilitates waste removal, reduces swelling, and alleviates ischemic pain.

A study measuring cytokine release from fibroblasts during treatment demonstrated that a minute of SCS reduced interleukin 6 production at the tenderpoint, supporting a role for local circulatory effects.[35]

Ligamento-Muscular Reflex

The ligamento-muscular reflex serves to protect ligaments by contracting selected muscles while relaxing others, thereby limiting ligament mobility following injury.[36] SCS and FPR exploit inhibitory responses generated by the ligamento-muscular and GTO reflexes to relax the affected muscle. This theory is less widely cited than the proprioceptive and local circulatory mechanisms.

In SCS, tenderpoints originate from the body’s attempt to contract and protect an injured muscle, causing reflexive stretching of the antagonist muscle. Palpable hypertonic myofascial tissue subsequently develops in the antagonistic muscle. SCS shortens the antagonist muscle to reduce aberrant proprioceptive signals and relieve persistent muscle strain.

In FPR, stimulation of γ-motor neurons increases muscle spindle sensitivity to stretch. Stretch fibers of the affected muscle continue to transmit signals to the spinal cord at rest, maintaining α-motor neuron activation. The muscle remains hypertonic even in a neutral position. Application of an activating force while the muscle occupies a position of ease allows γ-motor neurons to reset, terminating persistent contraction signals.

Clinical Significance

SCS and FPR are particularly effective for chronic pain that requires gentle osteopathic techniques or has not responded to other interventions.[37] Contraindications are limited and include fractures, significant ligamentous tears in the affected region, and the patient's inability to achieve muscular relaxation. Evidence supports the use of SCS for the following conditions:

• Hip tenderpoints
• Trapezius pain
• Mechanical neck pain
• Chronic ankle instability and sprains
• Plantar fasciitis pain
• Shoulder pain
• Sacral torsion
• Lower back pain
• Cervical hysteresis
• Iliotibial band friction syndrome
• Headache
• Tendonitis
• Epicondylalgia
• Knee pain
• Rotator cuff syndrome
• Fibromyalgia
• Osteoarthritis [38][39][40][41][42][43][44][45]

Identification of a tenderpoint permits treatment with SCS. The osteopathic principle of “fold and hold” describes the technique, in which the affected segment is positioned to shorten the muscle and maintained in that posture for a minimum of 90 seconds.

Clinical evidence supporting FPR for the treatment of pain and somatic dysfunction remains limited.[46] Despite this lack of data, the similarity of FPR to SCS permits its application for comparable indications and provides benefit in certain patient populations as an adjunctive therapy.

The roles of SCS and FPR in managing piriformis syndrome, iliacus dysfunction, and psoas dysfunction have not been fully established. Nonetheless, these indirect manipulative techniques are incorporated into osteopathic curricula and clinical practice. These modalities are contraindicated when tenderpoints occur in regions of active inflammation, pain arises from alternative causes such as infection, or the patient either cannot provide feedback regarding tenderness or tolerate manual therapy.

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Disclosure: Kristina Fritz declares no relevant financial relationships with ineligible companies.

Disclosure: Kristina Krupa declares no relevant financial relationships with ineligible companies.

Disclosure: Reddog Sina declares no relevant financial relationships with ineligible companies.

Disclosure: Charles Carr Jr declares no relevant financial relationships with ineligible companies.