Headache Institute of Texas
     
     
Symptoms & Problems | 4. Where is my problem coming from?
 
Symptoms & Problems
1. Do you have any of these symptoms?
2. Does this describe your life?
3. Quick headache test—do it now!
4. Where is my problem coming from?
5. What do I do now?
6. FAQ
 
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4. Where is my problem coming from?
The neurological literature confirms that various sources of NECK irritation create HEAD and FACE symptoms (see references). This occurs because irritated signals from damaged neck structures cascade up into the neck and face.
 
What structures in the neck? Discs, joints, muscles, or ligaments.
 
Disc Bulges
Disc bulges
  Adaptive Shortening of Upper Cervicals
Adaptive shortening of upper cervicals
 
Joint Inflammation
Joint inflammation
  Stress Overload
Stress overload
  Post-Traumatic Cervical Scarring
Post-traumatic cervical scarring
 
What does irritation of these neck structures have to do with head and face symptoms? If irritated, these neck structures feed pain signals into upper neck nerves (technically, C1, 2, 3 afferents). From there, the irritation feeds into the brainstem, which transmits those signals up into the head and face (through the trigeminal nerve). Illustration of trigeminocervical nucleus in the brainstemIllustration of trigeminocervical nucleus in the brainstem More specifically, research indicates that the pathway from the neck to the head and face is through the trigeminocervical nucleus in the brainstem. (See green structure in illustration to the right.) In addition, the vagus nerve (producing symptoms such as dizziness, nausea, ear pressure) appears to be activated through the same pathways by its connections with the trigeminocervical nucleus in the brainstem.
 
How can I fix that problem? We perform a meticulous evaluation of your neck (technically, an algorithm-driven mechanical evaluation of your cervical spine). This allows us to discover which neck movements and positions produce your head/face symptoms and which neck movements and positions shut your symptoms off. Once you’re armed with that information, you can then gain control of your problem, and get on the road to healing!
 
Summary: What patients learn at the Headache Institute of Texas is how to calm down the source of that neck-induced trigeminal and vagus nerve irritation that results in:
 
» Headaches/Migraine
» Dizziness/Vertigo
» Nausea
» Sinus Pressure
» Eye Pain/Dryness
» TMJD/Jaw Tightness
 
NEXT: Take action and START FIXING your root problem »
 
References
 
1. Biomed & Pharmaco (1995) 49, 435.445, Elsevier, Paris. Dossier “Headache and migraine” Anatomy and Physiology of Headache, N Bogduk, Faculty of Medicine and Health Sciences, University of Newcastle.
 
SUMMARY—Headache is a vast field with many different varieties of headaches and classifications. However, all headaches have a common anatomy and physiology. All headaches are mediated by the trigeminocervical nucleus, and are initiated by noxious stimulation of the endings of the nerves that synapse on this nucleus, by irritation of the nerves themselves, or by disinhibition of the nucleus. A mastery of the relevant anatomy and physiology of the trigeminocervical nociceptive system serves to predict and summarize the many varieties of headache systematically and with reference to their mechanisms.
 
2. Headache Currents, Vol. 2, No. 2 (March/April) 2005 pp. 42–48, 2005 American Headache Society and Blackwell Publishing. Anatomy and Physiology of Pain Referral Patterns in Primary and Cervicogenic Headache Disorders, T. Bartsch, M.D. and P. J. Goadsby, M.D., Ph.D., Department of Neurology, University of Kiel, Germany and Headache Group, Institute of Neurology, National Hospital for Neurology and Neurosurgery, Queen Square, London, UK.
 
SUMMARY—The clinical presentation of pain in primary headache disorders, such as migraine and cervicogenic headache, shows that the trigeminal and cervical innervation territories frequently are not respected during an attack. Here we review evidence that trigeminal afferents innervating the meninges, and cervical afferents in the greater occipital nerve (GON), have synaptic convergent input onto the same second-order neurons in the trigeminocervical complex. Furthermore, dynamic changes of excitability in terms of a sensitization to noxious input may occur on the central neuron level. The possible role of segmental mechanisms in the spinal cord and of inhibitory projections from brainstem structures such as the periaqueductal gray (PAG) in pain processing is discussed in view of data using neurostimulation of peripheral nerves in pain modulation. Recent experimental animal and human studies have facilitated our understanding of the role of these basic mechanisms in the spread, referral, and maintenance of pain in headache.
 
3. Cephalalgia 2007; 27:1050–1054. London. ISSN 0333-1024. Lower cervical disc prolapse may cause cervicogenic headache: prospective study in patients undergoing surgery. HC Diener, M Kaminski, G Stappert, D Stolke & B Schoch, Departments of Neurology and Neurosurgery, University Duisburg-Essen, Essen, Germany.
 
SUMMARY—In 1983 Sjaastad published for the first time diagnostic criteria for cervicogenic headache. Until now there have been no prospective studies investigating whether cervical disc prolapse can cause cervicogenic headache. Between July 2002 and July 2003 50 patients with cervical disc prolapse proven by computed tomography, myelography or magnetic resonance imaging were recruited and prospectively followed for 3 months. Patients were asked at different time points about headache and neck pain by questionnaires and structured interviews. These data were collected prior to and 7 and 90 days after surgery for the disc prolapse. Fifty patients with lumbar disc prolapse, matched for age and sex,undergoing surgery were recruited as controls. Headache and neck pain was diagnosed according to International Headache Society (IHS) criteria. Twelve of 50 patients with cervical disc prolapse reported new headache and neck pain. Seven patients (58%) fulfilled the 2004 IHS criteria for cervicogenic headache. Two of 50 patients with lumbar disc prolapse had new headaches. Their headaches did not fulfill the criteria for cervicogenic headache. One week after surgery, 8/12 patients with cervical disc prolapse and headache reported to be pain free. One patient was improved and three were unchanged. Three months after cervical prolapse surgery, seven patients were pain free, three improved and two unchanged. This prospective study shows an association of low cervical prolapse with cervicogenic headache: headache and neck pain improves or disappears in 80% of patients after surgery for the cervical disc prolapse. These results indicate that pain afferents from the lower cervical roots can converge on the cervical trigeminal nucleus and the nucleus caudalis.
 
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