Edward Lichten, M.D.,PC
555 S. Old Woodward Avenue Suite 700
Birmingham, MI 48009 

Email: drlichten



Lecturer #7:

Consultant: Paul J. Roubal, Ph.D., P.T., F.A.A.P.M.
Director, Physical Therapy Specialists, P.C., Troy, Michigan

Novi Headache Symposium 1994




In physical therapy, the most common complaint of all patients entering treatment is that of pain. Pain is nearly universal. At one time or another most people have experienced some level of pain, however, most mechanisms of pain have only recently beg un to be understood.

Pain has been defined as "an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage" (IASP Sub-Committee on Taxonomy, 1979).[1] Thus, essential components of any pain experience d would be a perception of possible or probable tissue damage, and general interpretation of this damage. When pain is perceived, the general nature of the response is to avoid activities or respond to stimulus that does not cause increased pain, and therefore this response may aid in tissue healing.

Pain is a very individual and subjective experience to certain stimuli. Many times, noxious stimulus, which may be perceived as pain in one individual may not be perceived as pain in the other. Without a psychological component, such as "unpleasant", t he noxious stimulus would not be considered painful. It is therefore difficult to evaluate the physiological aspects of pain and separate them from any psychological or other emotional aspects.[2-7] Pain perception also varies between individuals, and may also vary between sexes and with age.

Pain receptors are nociceptors generally described as unspecialized free nerve endings. They are highly branched and have large receptor fields. The overall sensitivity of tissue to noxious stimulation is generally influenced by the density of the nociceptors. Many times, with repeated stimulation of nociceptors, other sensations may start to develop, which one would consider a type of hyy been accepted that there is a convergence of nociceptive afferents in the dorsal horn of the spinal cord. When discussing referred pain, visceral referred pain is always in the direction from visceral to somatic structures. When discussing the areas innervated by the trigeminal or cervical nerves, referred pain can occur in either direction. Essentially, noxious cervical spine pain and inflammation may give rise to pain in the trigeminal area of innervation and likewise, noxious trigeminal input may be perceived as pain in the cervical spine.[8]

Referred pain is a recognized, but difficult, phenomenon to understand completely. Many times, the areas where pain is subjectively felt is not necessarily the area that is involved with the pain origination. Referred pain is primarily a central nervou s system phenomenon. Description and simple explanation for this is that of "phantom pain" of an amputated limb. In this example, the limb need not even be present, and the patient can present with severe and disabling pain referred to the lost limb. Therefore, pain is "recognized" within the central nervous system, although it is "perceived" by the patient to be in the tissue, such in these phantom limb pains. Following this central phenomenon model, the ability of both the cervical nucleus combined with the trigeminal nucleus in transmitting noxious stimulus in either direction explains many of the phenomenon occurring in head and neck pain and in our discussion of cervicogenic headaches. Referred pain from either the craniovertebral region, or the TMJ/head region can refer pain to either area. Thus, the craniovertebral region can give the sensation of pain in not only the suboccipital and occipital region, but also in the temporal and frontal area of the head, and the retro-orbital region. Conve rsely, TMJ dysfunction can refer pain in and around the ear, the craniovertebral region, may develop scalp soreness, and general or burning neck pain[9-10].


Most headaches are predominantly benign in nature. Headaches will strike 2/3 of the population at any one given time.[11-13] 15-20% are vascular, and the remaining 80-85% are placed under a multitude of diagnostic categories, and may be related to depression, fatigue, and structures in the cervical spine. Many structures in the cervical spine, especially in the craniovertebral region, may be a source of headache. However, there is controversy today as to the frequency and percentage that the cervical spine dysfunction would be the cause of the common nonvascular or benign headache. [14-15]

Maitland[16] performed a retrospective study of patient's referred for headache treatment and worked on delineating the associations of cervical spine pathology with the headache. During a one year period, 203 patients diagnosed as suffering with cervical spine dysfunctions were referred for treatment. In nearly half of the patients studied, there were reports of headaches as one of their symptoms. Variable medical diagnosis were presented, but the most common diagnosis was "neck pain with headache" o r "headache" alone, which accounted for greater than 50% of all of the patient's studied. Also, it appeared the age and sex distribution of headache subjects is greater than a 2 to 1 ratio of females to males. Also, history and clinical observation show ed that nearly 2/3 of the patients with cervical origin headaches have related tension, or sustained flexion during the activities of daily living. Pathology of the cervical spine may be the trigger for muscle contraction or conversely, tension may aggravate existing pathology to produce the headache.[17] Rees, studied more than 2,000 patients with chronic headache and believed that upper cervical spine joints consistently showed some degenerative changes, and therefore may be related to the cause of the headache.


Afferents from the spinal tract to the trigeminal nerve, as well as from nerve roots, C1, C2, and C3 terminate on the trigeminal- cervical nucleus. The spinal tract of the trigeminal nerve descends to the upper levels of the spinal cord, and reaches at least as far as C2 and sometimes as far as C4. Terminals of the trigeminal nerve and the upper 3 cervical nerves ramify in a continuous column of grey matter formed by the pars caudalis of the spinal nucleus of the trigeminal nerve, and also with the dorsal horns of the upper 3 cervical segments. In this area, the pars caudalis of the trigeminal nerve is not able to be differentiated from the spinal grey matter. Consequently, this region can ascends to the upper levels of the spinal cord, and reaches a t least as far as C2 and sometimes as far as C4. Terminals of the trigeminal nerve and the upper 3 cervical nerves ramify in a continuous column of grey matter formed by the pars caudalis of the spinal nucleus of the trigeminal nerve, and also with the d orsal horns of the upper 3 cervical segments. In this area, the pars caudalis of the trigeminal nerve is not able to be differentiated from the spinal grey matter. Consequently, this region can be seen as a single combined nucleus and therefore called t he trigeminal-cervical nucleus. This nucleus is involved primarily in the transmission of nociceptive information, and since it receives afferents from the trigeminal nerves, the trigeminal-cervical nucleus can be viewed as the nociceptive nucleus for th e entire head and upper back.[18-19]

The anatomical substrate for referred pain is the convergence of afferents of one region of the body onto neurons in the central nervous system that also receive afferents from topographically separate regions. For example, if units in the trigeminal-ce rvical nucleus that innervate the back of the head also receive afferents from the cervical vertebral column, the noxious vertebral stimuli could cause pain to be perceived as arising from the back of the head. Alternatively, if units that receive trigeminal afferents also receive vertebral afferents, then pain in the forehead or face could be generated by noxious stimuli from the upper cervical spine. The trigeminal nerve contains sensory roots which carry afferents from much of the head and face region. There is also a small motor root which innervates the muscles of mastication.[20]

The major sensory divisions of the trigeminal nerve carry primarily light touch, pain, and temperature pathways to the thalmus by way of the tract of trigeminal cervical nucleus. Again, there is a significant relationship between sensation and dysfunction in the face and head region, and their relationship to craniovertebral region dysfunction and hence referred pain in either direction.

Sensory information is transmitted to the dorsal rami, and exits the spinal cord opposite each cervical articulation. At each cervical level, two branches will penetrate the joint capsule and deliver sensory input back to the trigeminal-cervical nucleus through these innervations. Not only do these branches supply the joint capsule and surrounding soft tissues, but also the musculature in the region. Along with supplying the articular capsule of the joints and some deep muscles in the cervical spine, communications are also seen with the spinal ganglion, dorsal and ventral rami, as well as the sympathetic trunk.[21]

There is overwhelming agreement that craniovertebral dysfunction can, and very often does, cause cervical origin headache or benign headache. In an overview of the neuroanatomy of this region, we find that there is significant influence of the cervical spine dysfunction into the nature of head and facial pain. If we were to assume that at least half of the people that have cervical spine dysfunction or derangement in the craniovertebral region also have complaints of headache, we would also have to assume that treatment of these regions should reduce the afferent/sensory input to the trigeminal cervical nucleus and reduce or eliminate the headache. In much of the literature, this is the case. In order to appropriately treat the cervical spine, one mu st understand the structures associated with the cervical spine including, but not limited to possible lesions in ligaments, joint capsule, disc musculotendinous structures, and how they function biomechanically. If there is an inherent biomechanical dysfunction biomechanically in these structures, these dysfunctions might be related to the head and facial pain or headache. Treatment of these structures to more normalize their function should then reduce the headache.


In order to understand the nature of cervical spine dysfunction in structures that may be involved, it is necessary to understand the general biomechanics of the craniovertebral region.

There is first a general interrelationship of weight and gravitational forces on the head and neck. The head is positioned in an anterior location, with gravity pulling the head forward in front of the cervical spine. There is a subsequent opposite force produced by posterior muscles of the neck, which constantly counterbalance the weight of the head which tends to tilt forward. With significant changes in posture, such as a forward head posture, it is obvious that not only specific muscle changes wil l occur with regard to strain and increased abnormal contraction of these balancing forces, but also, the biomechanics of the cervical spine will change. These biomechanics may cause the cervical spine to develop abnormal joint capsule function and other soft tissue lesions in the craniovertebral region from hyperextension at that area, and the constant muscle contraction.

Biomechanical ranges of motion in the OA (occipital-atlanto) (C-01) joint are primarily flexion and extension. There is minimal lateral flexion and side bending in a coronal plane, with relatively little or no rotation. This rotation is limited primarily through the atlanto-occipital ligament. Flexion and extension ranges are approx. 15 degrees, lateral flexion is generally less than 3 degrees. AA (atlanto-axial) (C-1-2) joint range of motion is generally considered to be rotatory motion. This rotat ion range of motion is in the 45-50 degree range and there is also some flexion extension available and very little side bending. Also, there are coupled motions between OA and AA that must be evaluated. On right side bending, C1 will slip towards the s ide of side bending, and a rotation of C2 occurs in the opposite direction. Also, the occipital condyles will rotate in the same direction. The cervical intervertebral joints, as well as the intervertebral disc segment, will also undergo some significant biomechanical changes during motion. During extension, the overlying vertebral body tilts and slides posteriorly. During flexion, we find that the upper vertebral body tilts and slides and anteriorly. In both of these motions, the nucleus is driven i n the opposite direction of the superior vertebral body motion. In the cervical spine, along with discs and facet joints, there are also U-joints (joints of Luschka). During flexion and extension, these U-joints also slide relative to each other. They are cartilage lined articular joints and are closed within a capsule. These joints may also impinge, and may also be a secondary source not only of cervical pain, but also, referred pain through the trigeminal-cervical nucleus.

Another important consideration of any evaluation in the cervical spine by manual therapist is the evaluation of possible compromise of the vertebral artery. The vertebral artery passes in the foramen transversarium, and may be compromised by degenerative joint disease particularly in the facet joints. Specific vertebral artery tests should be performed before any form of mobilization or manual therapy is initiated.[21-22]


When evaluating the craniovertebral region for dysfunction, not only must the biomechanics of the cervical spine be evaluated, but the structures that may be causing biomechanical dysfunction must also be evaluated closely. There are strict relationship s between muscular support, soft tissue blockages, and possible inherent joint dysfunctions that must be distinguished. These are all treated differentially. However, one or more of these structures may be involved in a general dysfunction and may creat e cervical origin headache.

Craniovertebral ligaments are quite complex and crucial to the function of the craniovertebral region. Stability between the first and second cervical vertebrae is provided primarily by the transverse ligament, alar ligament, and atlantoaxial ligaments. The transverse ligament stabilizes the odontoid and keeps it from impinging on the spinal cord. The alar and atlantoaxial ligaments are important structures which primarily check rotation of the head with the atlas on axis becoming taut at approx. 30-4 0 degrees of rotation. These ligaments also restrict lateral flexion. All of these ligaments should be tested for their integrity before any specific treatment is performed, such as manipulation and mobilization. Along with the major support of muscula ture, such as the upper trapezius, levator scapulae, rhomboids, middle trapezius, and paraspinal musculature, there are also eight small suboccipital muscles. These include the obliquus capitis superior and inferior, as well as rectus capitis posterior minor and major bilaterally.[22]

Along with gross evaluations of particularly the upper trapezius, levator scapulae, and other large accessory muscles in the cervical spine that may support the upper cervical spine and head, the small suboccipital muscles of the craniovertebral region are important in a number of ways. Most important is that they have a high innervation ratio and potential rate of contraction approaches that of the extrinsic eye muscles. They are also able to control head posture and produce rapid movements with a fin e degree of precision. These muscles functionally align with the major influence of the head position on body posture, and the correct orientation of the head in space with the requirements of the visual system. Joint stiffness, and therefore muscle shortening or weakness in the craniovertebral region has a more extensive effect than muscle shortening or weakness in other regions of the body and must be evaluated closely. These small muscles of fine tuning are vital in determining the position of the h ead by reinforcing wanted or eliminating unwanted components of the triple movement of the cervical column: mainly rotation, lateral flexion, and flexion- extension patterns. These muscles are innervated by dorsal rami, primarily C1 the suboccipital nerve. Again, we see the possible communication between this region in the trigeminal-cervical nucleus pain, possible neck, and fascial pain and headache.

The interrelationship and specific relationships of each of these soft tissue structures, as related to the biomechanics in the cervical spine, must be evaluated. If proper evaluations are performed and the involved dysfunctional structures are identifi ed, the practitioner then has the ability to treat these structures, as well as dynamically improve the function of the craniovertebral region. This, in turn, should reduce craniovertebral dysfunction that may be causing cervical origin headache.

Along with the craniovertebral region, and the structures causing head and neck pain, there are also myofascial trigger points that may be referring pain to other areas of the head and neck. These are described well by Travell and Simons10. Myofascial trigger points can be classified as active (more acute), or latent type trigger points. More acute trigger points are generally a reactive trigger point to an acute injury in which muscles go into spasm to protect an injured area. Latent trigger points may be present from old injuries in which a muscle is somewhat shortened and hypomobile. This may be from an older injury that may never have been completely healed or brought back to normal physiological function. In these cases, slight stretching or a ttempts at normal range of motion through these soft tissue structures/muscles could aggravate the soft tissue and subsequently, develop trigger point dysfunction and referred pain. These include many muscles such as the muscles of mastication, sternocleidomastoid, cervical paraspinals, suboccipital, and levator scapulae. In all these cases, evaluation for appropriate range of motion in these muscles should be made. If trigger points are suspected, and the referred pain pattern is present, appropriate treatment with exercises, stretching, modalities, or possibly trigger point injections or these modalities in combination can be very successful. Again, these are areas of soft tissue dysfunction related to the neck and upper trunk area that may be a cau sative factor in head and face pain.

In most cases, the treatment of headache is a multi-disciplinary process. Appropriate evaluation tools in all areas must be utilized, including diagnostics for vascular dysfunction, tumors, temporomandibular dysfunction, and craniovertebral dysfunction, as well as other soft tissue abnormalities. Once an appropriate differential diagnosis is made, treatment programs can be developed and the appropriate practitioners may work together in order to most effectively deal with the dysfunctions and relief of this patient's pain and headache.


  1. IASP Subcommittee on Taxonomy. Pain Terms: A list with definitions and notes on usage. Pain 1979; 6: 249-252.
  2. Melzack, R. The McGill pain questionnaire: Major properties and scoring methods. Pain 1976;10:1-17.
  3. Willer, J.C. Boureau F. Berny, J. Nociceptive flexion reflexes elicited by noxious laser radiant heat in man. Pain 1979;7: 15-20.
  4. McGrath, P.A. Sharav, Y. Dubner, R. Gracley, R.H. Masseter inhibitory periods and sensations evoked by electrical tooth pulp stimulation. Pain 1981;10: 1-17.
  5. Bromm B. Treede R.D. Withdrawal reflex skin resistance reaction and pain ratings due to electrical stimulation in man. Pain 1980;9: 339-354.
  6. Kosterlitz, H.W.; Terenuis, L.Y. (eds) Pain and Society. Dahlem Kongerenzen Weinheim, Verlag Chemie Gmb H. 1980.
  7. Reading, A.E. A comparison of pain rating scale. Journal of Psychosomatic Research 1980;24: 119-124.
  8. Greive, Gregory P. Modern Manual Therapy New York, NY: Longman Group Limited, 1986; 228, 248, 388.
  9. Miller, J. How Do You Feel? The Listener 1978;100: 665-666.
  10. Travell, Janet G.; Simons, David G. Myofascial Pain and Dysfunction (The Trigger Point Manual) Baltimore, MD: Williams and Wilkins, 1983.
  11. Lederer, F.L. Tenta, L.T. Tardy, M.E. Otorhinolaryngologic aspects of headache and head pains. Headache 1971;11: 19-30.
  12. Nikiforow, R. Hodgen, E. 1An epidemiological study of headache in an urban and rural population in Northern Finland. Headache 1978; 18: 137-145.
  13. Turner, D.B. Stone, A.J. Headache and its treatment: A random sample survey. Headache 1979; 19: 74-77.
  14. Edmeads, J. Headaches and head pains associated with diseases of the cervical spine. Medical Clinics of North America 1978; 62: 533-544.
  15. Peterson, D.I. Austin, G.M. Dayles, L.A. Headache associated with discogenic disease of the cervical spine. Bulletin of the Los Angeles Neurological Society 1975; 40: 96-100.
  16. Maitland, G.D. Vertebral Manipulation, 4th ed. Butterworths, London. 1977.
  17. Rees, S. Relaxation therapy in migraine and chronic tension headaches. Medical Journal Australia 1975; 2: 70.
  18. Rothman, Richard H.; Simeone, Frederick, A. The Spine _ Volume I Philadelphia, PA: WB Saunders Company.
  19. Rothman, Richard H.; Simeone, Frederick, A. The Spine Volume II Philadelphia, PA: WB Saunders Company.
  20. deGroot, Jack; Chusid, Joseph G. 1985 Correlative Neuroanatomy New York, NY: Appleton and Lange.
  21. Greive, Gregory P. Common Vertebral Joint Problems New York, NY: Churchill Livingston. 1978.
  22. Kapandji, I.A.; Hanore', L.H.; D'Aubigne, R. Merle The Physiology of the Joints New York, NY: Longman Group Limited. 1974.
    Selected Reading
  23. Melzack, R.; Wall, P.D. The Challenge of Pain, Penguin, Harmondsworth, Ch3, Ch5. 1982.
  24. White III, Augustus A.; Panjabi; Manohar, M. Clinical Biomechanics of The Spine Philadelphia, PA: JB Lippencott Company.1985.

Revised: January 1, 2011