Headaches and migraines can be attributed to and complicated by many different conditions. The cervical spine is just one of the areas to be examined. Peculiarities of the neuro- and myofascial anatomy of this area throw potential light on areas not just associated with the neck but many structures around the face.
Outlined in this article are specific myofascial, articular and neurological structures. Through either mechanical impingement or nociceptive and proprioceptive reflex action these structures cause pain and an array of autonomic phenomena.
(1) C2 dorsal root ganglia and its ventral ramus (lateral branch: lesser occipital nerve) and dorsal ramus (medial branch: greater occipital nerve)
(3) Meningeal traction and inflammation
(4) Spinal trigeminal nucleus
(5) Trigeminal mechanoreceptors
(6) Temperomandibular disorders (TMD)
(7) Eye strain
C2 dorsal root ganglia and the ventral ramus (lesser occipital nerve) and dorsal ramus (greater occipital nerve)
The nerve roots of C2 unite to form a very short spinal nerve which divides into dorsal and ventral rami. The spinal nerve and its dorsal and ventral rami are intimately connected to the posterior atlanto-axial membrane (Lucas et al 1994).
C2 dorsal root ganglion
- Prone to torsions as encased in connective tissue
- Proximity to facet joint renders it prone to compression from hypertrophy
The C2 dorsal root ganglion has been associated with chronic headaches (Hamer & Purath 2014). Its anatomical position of being extradural is a unique characteristic as it occupies the dorsal aspect of the C1-2 facet joint. For this reason it is prone to compression from (1) hypertrophy of the lamina or C1–C2 articulation, (2) osteoarthritis and spondylosis, (3) hypertrophy of the atlantoepistrophic ligament, and (4) the movement (rotation and extension) between the posterior arches and articular facets of the atlas and axis (Zhang et a 2011).
Although it is widely documented as being encased in the atlantoepistrophic ligament Bogduk (1981) describes the nerves and veins as being invested by fascia which holds the C2 roots, ganglion and spinal nerve against the capsule of the lateral atlanto-axial joint. To illustrate the effects of torsion on this ganglion he attributes it to neck-tongue syndrome where rotation of the neck can give suboccipital pain and anaesthesia to the tongue.
Lesser occipital nerve (LON)
- Prone to entrapment from myofascial structures and blood vessels.
The LON originates from the lateral branch of the ventral ramus of spinal nerve C2 (sometimes C3). Lucas et al (1994) found the ventral ramus of C2 initimately connected to the posterior antlo-axial membrane. It ascends to supply the skin behind the auricle and part of the auricle.
Lucas et al (1994) found the C2 ventral ramus (lateral branch forming the LON) adherent to:
- Fascia of the obliquus capitis inferior muscle, which is also adherent to the atlanto-axial membrane (refer to 'Meningeal traction and inflammation', myodural bridges).
- Posterolateral surface of the vertebral artery.
- Surface of the scalene medius or levator scapula depending on what muscle is inserted into the posterolateral surface of the C1 TP.
Peled et al (2016) found three zones of entrapment from compressile connective tissue/fascial bands, muscle insertions and blood vessels. These three zones were:
(1) Emergence of the LON from behind/deep to the sternocleidomastoid.
(2) Ascent of the LON along the posterior boundary or posterior to the sternocleidomastoid.
(3) Where the LON crosses the nuchal line.There was a constant fascial band noted at this level.
Greater occipital nerve (GON)
- Prone to entrapment neuropathy as it passes through myofascial structures
The GON originates from the medial branch of the dorsal ramus of spinal nerve C2. After coursing backwards between the first and second vertebrae, the GON ascends upwards and then subcutaneously over the vertex of the skull.
Like all nerves anatomical variations in its course exist. Potential sites of myofascial entrapments include (Tubbs et al 2014):
- Obliquus capitis inferior muscle: Scherer et al (2019) found the obliquus capitis inferior remains relatively immobile during traumatic events, like whiplash injuries, placing strain as a tethering point on the greater occipital nerve.
- Semispinalis muscle near its attachment on to the occiput or a horizontally positioned tendinous band (intersection) of the semispinalis capitis.
- Trapezius or its aponeurosis around the external occipital protuberance.
- Through an aperture above the aponeurotic sling between the trapezius and the sternocleidomastoid.
- Hypertrophied atlantoepistrophic (C1-C2) ligaments (Son et al 2013).
Meningeal traction and inflammation
- Soft tissue tightness can transmit through connective tissue bands to the spinal dura
- These tightness's can stimulate the recurrent meningeal nerve and cause headaches
The meninges are a pain sensitive structure being supplied by the recurrent meningeal nerve. Traction and inflammation to the dura can be caused by two potential structures in the cervical spine. Both these structures function to anchor and control movement of the spinal cord during cervical spine movement. There is some debate as to whether at some levels these are the same structures (Shi et al 2014).
- Myodural bridges (Scali et al 2013): bands of fascia crossing the epidural space linking the suboccipital muscles and the dura. This suboccipital fascia is continuous with the galea aponeurotica (Dacey et all 2018). Myodural bridges exist in the Rectus Capitis Posterior Major, Rectus Capitis Posterior Minor, Obliquus Capitis Inferior and the Ligamentus Nuchae.
- Meningodural ligaments (Shi et al 2014): connective tissue bands running mainly from the ligamentum nuchae but also the laminae to the dura. Most commonly from C5 up with the strongest attachments being at C2
Soft tissue tightness in the muscles associated with the myodural bridge and those associated with the ligamentum nuchae (upper trapezius, rhomboideus minor, serratus posterior superior, and splenius capitis (Nan Zhen et al 2014)) has been linked to headaches. Also changes to the suboccipital muscle fiber type post whiplash can alter these muscles proprioceptive function and so alter their neuromuscular control and tone exerting a direct traction through their attachments to the dura (Enix et al 2014).
Superior attachments of the suboocipital fascia comes from the galea aponeurotica. Dacey et al (2018) found the galea aponeurotica transitions to the suboccipital fascia by dense fibrous attachments. Can myofascial continuity from Tenon's capsule running posteriorly via the occipitofrontalis to the galea aponeurotica/suboccipital fascia terminating in the myodural bridges play a role in headaches and migraines? This myofascial continuity is outlined in more detail in 'Trigeminal mechanoreceptors'.
Spinal Trigeminal Nucleus
- Cervical nociceptive afferents synapse in the spinal trigeminal nucleus
- Vascular and meningeal afferents synapse in the spinal trigeminal nucleus
- Projections from the spinal trigeminal nucleus go the hypothalamus associated with nociceptive and autonomic pathways
Cervical afferents terminate in the spinal trigeminal nucleus that extends down to C2/3. However because the spinal trigeminal nucleus is an extension of Lissauer’s tract afferent information from lower down in the cervical spine can travel up to the spinal trigeminal nucleus. This relation between the trigeminal spinal nucleus and cervical spine is called the 'trigeminocervical complex'.
It’s not just cervical afferents that terminate in the spinal trigeminal nucleus but afferent neurones from the pain sensitive intracranial blood vessels and meninges. This is called the trigeminovascular system. These nerves originate in the ophthalmic branch of the trigeminal nerve (V1) and to a lesser extent through the maxillary (V2) and mandibular (V3) divisions. Additional innervation of the dura is provided by neurons in the upper cervical dorsal root ganglia. From here they enter the brainstem via the trigeminal tract giving off collaterals that terminate in the spinal trigeminal nucleus and upper cervical spinal cord (C1-3) (Noseda & Burnstein 2013).
Although typically activation of the trigeminovascular pathway has been associated with depolarisation of the cortex (cortical spreading depression, Zhao & Levy 2015) and its associated metabolic/vascular changes Noseda & Burnstein (2013) claimed this activation can also occur by pain signals that originate in peripheral nociceptors. This throws open the potential to modulate the trigeminovasular reflex through work to the cervical spine. Allied to this Zhao et al (2017) found electroacpuncture at the top of the neck (G-20), in a rat model, regulated the trigeminovascular system.
From the spinal trigeminal nucleus nociceptive pathways project to higher centres including the hypothalamus. From here a reflex activation provides the efferent loop for an array of nociceptive and autonomic pathways associated with Trigeminal Autonomic Cephalagias (Goadsby) and migraines such as sleep-wake cycle disturbances, changes in mood, appetite, thirst and urination (Noseda & Burstein 2013)
- Trigeminal nerve supplies proprioceptive afferents to the Muller’s (supratarsal) muscle
- Stimulation of the Muller’s (supratarsal) muscle stimulates locus coeruleus associated with vigilance, chronic pain and elevated sympathetic responses
- Anatomical links exist between the cervical fascia, superior tarsus and Tenon’s capsule. This provides a potential link with cervical tension, stimulation of Muller’s (supratarsal) muscle and eye strain
Mechanoreceptors in Muller’s (supratarsal) muscle is innervated by the trigeminal nerve that terminates in the mesencephalon. Eyelid opening stretches mechanoreceptors in the Müller (supratarsal) muscle to activate the proprioceptive fibers supplied by the trigeminal mesencephalic nucleus. This proprioception induces reflex contractions of the levator palpebrae superioris and frontalis muscles to sustain eyelid and eyebrow positions against gravity (Matsuo et al 2015) and the occipitofrontalis (Bordoni & Zanier, 2014).
There is a direct myofascial link whereby tension in the posterior superficial cervical fascia pulls on and stimulates mechanoreceptors in Muller’s muscle via the occipitofontalis and levator palpebrae (Bordoni & Zanier, 2014). Dacey et al (2018) outlined this myofascial continuity further by identifying the continuity of the galea aponeurotica with the suboccipital fascia and myodural bridges that terminates in the cervical dura.
This stimulation of mechanoreceptors in Muller’s muscle not only exerts a somatic neurological reflex in tightening muscles in the head but also an autonomic reflexs via the locus coeruleus.
Based on these neural connections day to day activities of the eyes creates varying states of arousal and vigilance to facilitate our everyday activities.
Stimulating the mechanoreceptors in Mullers (supratarsal) muscle stimulates the locus coeruleus creating arousal just as not stimulating them can create sedation. For example opening and rubbing the eyes will stimulate mechanoreceptors in Mullers muscles to evoke vigilance such as when opening our eyes on waking, rubbing our eyes to stay awake or evoking memory retrieval by an upward gaze. Closing our eyes or evoking a downward gaze can decrease stimulation in the mechanoreceptors in Muller’s muscle to help with sedation of the locus coeruleus such as when meditating or sleeping (Matsuo et al 2015).
The Locus coeruleus is not just associated with day to day vigalence but in pain modulation via locus coeruleus-noradrenergic neuromodulatory system. When dysfunctional it has been associated with a range of chronic pain conditions such as temperomadibular dysfunction (TMD) associated with dysfunction of the noradrendergic arousal system (Monaco et al 2015).
The potential for stimulation of the locus coeruleus via trigeminal afferents is reflected in the sympathetically mediated sweat response in response to prolonged upward gaze (Matsuo et al 2015) a phenomena also associated with trigeminal autonomic cephalagia (Costa et al 2015).
To extend the myofascial chain from the cervical dura/suboccipital fascia via the occipitofrontalis to the Levator Palpebrae further; the Levator Palpebrae and rectus superior muscle is connected with Tenon’s capsule, where the eyeball is located. Particularly, they share extraocular muscles; Tenon’s capsule surrounds the optic nerve where it terminates in the eye, blending with the meningeal tissue. Could it be that tension in the fascial area in the upper cervical spine affects the movement of the eyeball, altering the visual field and posture, or causing dysfunction related to the fascial traction on the optic nerve, with resultant alteration in the ocular reflexes? (Bordoni & Zanier 2014).
Temperomandibular disorder (TMD)
A direct correlation exists with TMD and migraines which has been associated with central sensitisation (Florencio et al 2017). The influence of cervical spine movement and TMD has been well documented by Greenbaum et al (2017). Be it through a neurological or myofascial link TMD and cervical spine disorders tend to be correlated.
The anatomy of the Zygomaticotemporal nerve (ZTN): Trigeminal nerve --> maxillary nerve --> zygomatic nerve --> zygomaticotemporal nerve.
Direct compression of the ZTN can occur in the anterior fibers of the temporalis (Hagan et al 2016) and between the deep layer and superficial layer of the deep temporalis fascia (Hwang et al 2004). The temporalis muscle orginates in part from the deep temporalis fascia.
The two nerves associated with eye strain headache are the:
- Supraorbital nerve (SON).
- Supratrochlear nerve (STN).
Hagan et al (2016) describes the anatomy of the supraorbital nerve (SON) and supratrochlear nerve (STN) as: Trigeminal nerve --> opthalamic nerve --> frontal nerve (runs between the levator palpebrae superioris and the periosteum) --> branches into the SON and STN.
The SON exits the skull at the supraorbital foramen although the nerve may branch into the superficial (medial) and deep (lateral) division either proximal or distal to the supraorbital foramen.
The STN exits the skull on to the supraorbital rim below a dense broad periosteal or fascial band. Less commonly the nerve exits the skull on to the supraorbital rim via a bony foramen.
Supraorbital nerve entrapment (Janis et al 2013 & Fallucco et al 2012):
- Supraorbital notch/foramen (including the fascial band of the notch).
- Glabellar myofascial complex (including the corrugator muscle).
Supratrochlear nerve entrapment:
- Corrugator muscle (Janis et al 2013).
- Periosteal or fascial band along the supraorbital rim (Hagan et al 2016).
There is some debate as to whether the fascial band compressing the SON at the supraorbital notch or the STN along the supraorbital rims comes from the arcus marginalis (Hagan et al 2016).
The two muscles associated with eye strain induced headaches and migraines are:
- Corrugator muscle.
- Orbicularis Oculi.
The Corrugator muscle extends from the medial end of the eyebrow (deep to the occipitofrontalis and orbicularis oculi) to pass laterally and superiorly to the skin above the middle of the supraorbital region. Contraction of the muscle creates a frown.
Janis et al (2013) found the supratrochlear nerve to pierce, and be compressed, by the corrugator muscle causing migraine headaches.
The Orbicularis Oculi occupies the eyelid spreading onto the temporal region and cheek. It attaches to the nasal part of the frontal bone, frontal process of the maxilla and lacrimal bone. It blends with the occipiofrontalis and corrugator muscle. It also blends with the medial palpebral ligament and forms the lateral palpebral raphe.
The orbicularis oculi acts as a sphincter of the eyelids (and draws them slightly medially), draws the skin of the forehead, temporal region and cheek towards the medial end of the orbit (causing crow's feet), creates a vertical furrowing above the bridge of the nose and can cause lacrimation.
Not only can myofascial trigger points create head pain but orbicularis oculi twitching has been associated with cluster headaches (Bagheri et al 2017) and abnormal blink reflexes have been associated with migraine sufferers (Unal et al 2016).
Metha and Sheshia (1976) found electrical stimulation of the SON evoked contraction of the orbicularis oculi. Could entrapment of the SON in the corrugator muscle and the fascia of the supraorbital notch cause trigger points in the orbicularis oculi?
There seems to be a direct mechanical and neurological link between cervical spine disorders and headaches and migraines. What has been neglected here, although briefly mentioned with regards to the locus coeruleus, is the influence of central sensitisation. Differences in neurological excitability in response to mechanical stress explains why some patients get suboccipital pain and others suboccipital pain with a headache or migraine.
Areas to be researched more could be the effects of lymphatic drainage of the central nervous system on CSF flow. As yet no studies have been done on the effects of manual lymphatic drainage on this although Zheng et al (2014) postulated as to the effects of movement in myodural bridges on CSF flow.
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