18/04/2025
The suboccipital muscle group plays a crucial role in the biomechanics and neural regulation of the head and neck. Studies indicate that approximately 68% of patients with chronic head and neck pain have myofascial trigger points (MTrPs) in the suboccipital muscles, with pathologies involving central sensitisation, fascial chain compensation, and neurovascular interactions. A deeper understanding of the characteristics of suboccipital muscle trigger points and acupuncture treatment plans is significant for enhancing the diagnosis and treatment of head and neck pain.
1. Anatomical Characteristics and Neural Connections
1.1 Muscle Composition and Location
The suboccipital muscle group consists of four pairs of short muscles: the re**us capitis major, the re**us capitis minor, the obliquus capitis superior, and the obliquus capitis inferior. The re**us capitis major originates from the spinous process of C2 and inserts at the lateral aspect of the inferior nuchal line; the re**us capitis minor originates from the posterior tubercle of C1 and inserts at the medial aspect of the inferior nuchal line; the obliquus capitis superior connects the transverse process of C1 with the lateral aspect of the occipital bone; and the obliquus capitis inferior spans between the transverse processes of C1 and C2. The re**us capitis minor forms a "brain-spine axis" structure with the spinal dura mater via the posterior atlanto-occipital membrane, and changes in its tension can affect cerebrospinal fluid dynamics. Additionally, this muscle group has a high density of muscle spindles, accounting for 40% of proprioceptive input in the neck, and participates in the vestibulo-ocular reflex and postural control.
1.2 Neural Innervation and Pathological Associations
The suboccipital muscle group is innervated by the posterior rami of C1-C3 and the auricular branch of the vagus nerve (Arnold's nerve). The former transmits nociceptive and proprioceptive signals, while the latter mediates autonomic responses. Continuous stimulation of trigger points can activate the trigeminal cervical nucleus complex (TCC), leading to headache sensitisation.
2. Biomechanical Mechanisms and Pathological Compensation
2.1 Posture-Related Dysfunction
Forward head posture increases the static load on the suboccipital muscle group; for every 2.5 cm of forward movement, the load increases by 4.6 kg, which can result in local ischaemia and ATP depletion. For individuals who use bifocal glasses for extended periods, compensatory head extension can lead to over 45° of rotation at C0-C1, activating trigger points within just 30 minutes. Children watching television with their chin resting on their hands may experience sustained contraction of the suboccipital muscles, leading to lactate accumulation, and due to immature muscle development, are more prone to fascial adhesions.
2.2 Traumatic Chain Reactions
Injury to the re**us capitis minor can alter the rhythm of cerebrospinal fluid pulsations, potentially inducing cortical spreading depression and related symptoms of migraine aura. Abnormal proprioceptive input can interfere with the vestibulo-ocular reflex; approximately 38% of patients with post-traumatic dizziness exhibit activation of suboccipital trigger points.
3. Characteristics of Trigger Points and Differential Diagnosis
3.1 Clinical Features
Primary MTrPs are concentrated in the deep part of the suboccipital triangle, requiring palpation depth of 3-4 cm. Satellite MTrPs often occur in the upper part of the sternocleidomastoid and temporalis muscles, forming a "cranio-cervical pain cycle." The first-order referred pain is a band-like pain from the occipital protuberance to the supraorbital ridge, while second-order radiation includes throbbing pain in the temporal region and a sense of pressure behind the eyes.
3.2 Diagnostic Criteria and Differential Testing
The four-tenderness sign (tight bands, tender points, referred pain, and local twitch response) serves as the diagnostic basis. The suboccipital inhibition test, where pressing for 30 seconds alleviates blurred vision, has a sensitivity of 79%. If the frequency of nystagmus decreases by over 40% after deactivation of trigger points, it is diagnostically significant. Ultrasound elastography and functional MRI can assist in diagnosis, with the former showing a Young's modulus value greater than 60 kPa in trigger point areas, and the latter finding a positive correlation between the activation level of the anterior cingulate gyrus and insula with pain intensity.
4. Mechanisms of Acupuncture Treatment and Practical Approaches
4.1 Mechanisms of Acupuncture
Acupuncture activates Aδ fibres, inhibiting the transmission of C fibres in the spinal dorsal horn and modulating the hypothalamic-pituitary-adrenal axis, thereby reducing pro-inflammatory factors. Dry needling induces local twitch responses, interrupting the myofascial pain-spasm cycle; floating needling helps release fascial adhesions and restores the sliding mechanism of the suboccipital triangle.
4.2 Classification of Acupuncture Techniques
Technique Type | Operational Points | Mechanism of Action | Clinical Evidence Level
Dry Needling | Vertical insertion into trigger points until local twitch response occurs | Disrupts calcium overload and restores ATP synthesis | Level Ia (RCT)
Skin Needle Therapy | Subcutaneous insertion into the fat layer to release superficial fascia and improve microcirculation | Level IIb
Electroacupuncture | Alternating stimulation at 2Hz/100Hz | Promotes endorphin release and inhibits NMDA receptors | Level Ib
Intramuscular Needling | Multi-directional puncture along the suboccipital muscle pathways | Regulates muscle spindle sensitivity | Level III
4.3 Treatment Plan Design
Main acupuncture points include Fengchi (GB20), Tianzhu (BL10), and Wangu (GB12), with supplementary points selected based on symptoms, such as Baihui (GV20) for dizziness or Taiyang (EX-HN5) for visual disturbances. Use 0.30×40 mm stainless steel filiform needles, insert to a depth of 25-35 mm, retain for 20-30 minutes, and perform intermittent needling. In the acute phase, treat three times a week for two weeks; in the chronic phase, treat twice a week for four weeks, achieving a total effective rate of 89%.
