TENSION HEADACHE

Tension headaches are the most common type of headache. Stress and muscle tension are often factors in these headaches. Tension headaches typically don't cause nausea, vomiting, or sensitivity to light. They do cause a steady ache, rather than a throbbing one, and tend to affect both sides of the head. Tension headaches may be chronic, occurring often, or every day (1). 

​Evidence suggests that chiropractic care, including spinal manipulation, improves migraine and cervicogenic headaches. The type, frequency, dosage, and duration of treatment(s) should be based on guideline recommendations, clinical experience, and findings. Evidence for the use of spinal manipulation as an isolated intervention for patients with tension-type headache remains equivocal (2). 

By evaluating the brain, spine and nervous system in its entirety, specifically within the cervical spine, occipital region, trigeminal nuclear complex, and thoracic/rib regions, we can localize regions that are dysfunctional and misrepresenting sensory information to the brain. Autonomic dysregulation may be involved and we perform careful evaluation of this potential involvement.
(1) https://www.hopkinsmedicine.org/health/conditions-and-diseases/headache/tension-headaches(2) Bryans et al. Evidence-Based Guidelines for the Chiropratic Treatment of Adults With Headache. Journal of Man and Physol therapy. Vol 35, issue 5. 274-289. (3) Scheider KJ, et al. Cervicovestibular rehabilitation in sport-related concussion: a randomized controlled trial. Br J Sports Med 2014; 48:1294-1298

CERVICOGENIC HEADACHE

CERVICOGENIC HEADACHE

Although cervicogenic headache (CGH) has been described as a “final common pathway” of cervical spine dysfunction (7), its true prevalence is difficult to determine due to inconsistent use of diagnostic criteria in the literature. Incidence of cervicogenic headache has been reported to range from 0.7% to as high as 13.8% in populations of patients suffering from headache disorders (8). Others have reported cervicogenic origins of higher values (14% to 18%) in all chronic headaches (9).

The anatomical basis for CGH is the convergence of the afferent input of the upper cervical spine nerve roots (C1-C3) with the afferent tracts of the trigeminal nerve in the trigeminocervical nucleus. This convergence results in cervical spine nociceptive input being expressed in the sensory distribution of the trigeminal nerve, most commonly the ophthalmic branch of the trigeminal nerve, which innervates the forehead, temple, and orbit and has its greatest topographic representation near the dorsal horns of spinal nerves C1-C3 (4-5). Therefore, any structure innervated by C1, C2, or C3 spinal nerves can be implicated in the etiology of CGH. This includes the atlanto-occipital, median atlanto-axial, lateral atlanto-axial, and C2-3 zygapophyseal joints as well as the C2-3 intervertebral disc, suboccipital, upper posterior cervical, and upper paravertebral musculature, the trapezius and sternocleidomastoid muscles, upper cervical spinal dura mater, and the vertebral arteries (4-6). Because of the ability of afferent nerves to travel up to three segments cephalically or caudally in the cervical spinal cord, bony and soft tissue structures of the middle and lower cervical spine cannot be excluded from contributing to CGH (4-5)
​
(1) https://www.hopkinsmedicine.org/health/conditions-and-diseases/headache/tension-headaches(2) Bryans et al. Evidence-Based Guidelines for the Chiropratic Treatment of Adults With Headache. Journal of Man and Physol therapy. Vol 35, issue 5. 274-289. (3) Scheider KJ, et al. Cervicovestibular rehabilitation in sport-related concussion: a randomized controlled trial. Br J Sports Med 2014; 48:1294-1298(4) Biondi DM. Cervicogenic headache: Mechanisms, evaluation, and treatment strategies. J Am Osteopathic Assoc. 2000;100(9Suppl):S7–S14. [PubMed] [Google Scholar](5) Bogduk N. The neck and headaches. Neurologic Clinics. 2004;22(1):151–171. [PubMed] [Google Scholar](6) Sizer PS, Phelps V, Brismee J. Diagnosis and management of cervicogenic headache and local cervical syndrome with multiple pain generators. J Man Manipulative Ther. 2002;10:136–152. [Google Scholar]

MIGRAINE

It's all about the Trigeminovascular pathway

The World Health Organization lists Migraine as the sixth most disabling disorder globally, and the most disabling of all neurological disorders (1). Migraine affects females 3:1 (2). Migraines are described as a disorder of brain sensory processing that itself likely cycles, influenced by genetics and the environment (3). It's a complex and multifaceted disorder of the brain which in its entirety may last over several days (3). It is widely accepted that Migraine involves activation and sensitization of the trigeminovascular pathways, as well as brain stem and diencephalic nuclei (4,5). A primary dysregulation of sensory processing is likely to result in a constellation of neurological symptoms that affect our senses. It has been suggested that migraine may be considered a brain state of altered excitability (6-10). 

In real terms, it means that a Migraine is a disruption in normal signaling within a specific pathway in your brain that alters the function of the entire brain. Along this pathway are many areas that may be involved in the brain stem, Mesencephalon, Pons, Medulla and Diencephalon- Specifically the SuS, TCC, RVM, LC, PAG, Hypothalamus, Thalamus, Cortex (ACC, S1, S2, PFC). If you want to know more, reference article (3). It specifically affects the Trigeminal Cervical Complex (TCC), which is your fifth cranial nerve and C1-2 regions. The reason the TCC is so important to your Migraine experience is that it's the one that carries sensory information from your face and head, or PAIN. The "hyperexcitability" refers to the excessive signaling of the trigeminal nerve complex and other regions of the brain that make a person extremely sensitive to sensory input, whether sounds, light, irritability, pain, movement, etc. It is basically an inability to gait sensory information entering the brain so that we can't weight it appropriately and a small amount of movement or stimulation to the face/head/eyes/ears is experienced as an exaggerated pain, light or sound response, resulting in headache pain. The Thalamus is a part of our brain that gates all sensory information, except smell to the rest of our cortex and is thought to be a major component of Migraine. It is believed to be at the heart of the central processing and integration of nociceptive (pain) information and is regarded as a relay center for handling all incoming sensory information, and even modulating it (3). 

The path that regulates pain is skewed and exaggerating the signal within the brain, resulting in Migraine. This path can be treated once we locate the culprit(s) along the pathway. 

We used to think Migraines were a vascular disorder, but it is much different than that. The brain is largely insensate, but a rich plexus of nociceptive nerve fibers that originate in the trigeminal ganglion innervate the pial, arachnoid, and dural blood vessels, including the superior sagittal sinus and middle meningeal artery, as well as large cerebral arteries. Activation of these structures, particularly the dura mater, with mechanical, chemical, or electrical stimulation results in headache pain very similar to the pain in migraine, as well as other symptoms associated with migraine, including nausea and photophobia. The normal throbbing of blood vessels leads to head pain because of an error(s) within the Trigeminovascular pathway that includes the PAG, RVM, Locus Coeruleus, Sus, and Diencephalic nuclei, including the Hypothalamus, Thalamus, and Cortex (3). 
​

Why do I have throbbing pain in my head? 

The pain can be terrible with Migraines, although some people do not experience pain during their cycle, which is known as a silent migraine. Migraine is defined by 4 Phases- Premonitory, Aura, Pain and Postdrome. The most important phase is the premonitory phase as you can either take your medication as early as possible to mitigate the Migraine response, or receive other treatments to restore the trigeminovascular pathway input to a normal functional level (16-18). This where the throbbing head pain comes in, normal activity of dilation and constriction within the blood vessels that supply the meninges that usually does not elicit painful information now becomes painful due to the heightened sensitivity within the trigeminovascular pathway. Somewhere along this pathway, particularly the Thalamus skews the sensory information to the brain and we perceive pain during normal vascular activity instead of normal, painless proprioception. Many medication such as the CGRP monoclonal antibodies aim to block this pain pathway from sending painful information to the brainstem and cortex. ​

Migraine Phases

However, there may be a better way to get to the source by reducing the hypersensitivity and restoring normal neuronal function along the trigeminovascular pathway by reconnecting the brain's normal signaling network utilizing a combination of neuroplasticity retraining, vestibular rehabilitation, visuomotor rehab, chiropractic, physical therapy and oxygenation. 
Phases of Migraine
Phase 1- Premonitory, which may precede the actual headache, or pain phase, by 72 hours (11). Include changes in mood and activity, irritability, fatigue, food cravings, repetitive yawning, stiff neck, and phonophobia (irritation of sounds). These symptoms may endure well into the aura, headache and even podrome phases. This dysfunction is shown to be as a result of the Hypothalamus (3).
Phase 2- Aura, about one third of migraines experience transient neurological deficits, the migraine aura (12). A transient wave of neuronal depolarization of the cortex, the cortical spreading depression (CSD), is believed to be the pathophysiological brain mechanism underlying the clinical phenomena of migraine aura (3). The ICHD-3 defines the migraine aura as one or more transient, fully reversible neurological deficits. of which at least one has to have a unilateral localization, that develops over 5 min or more and of which each deficit lasts between 5 and 60 min, 26% of patients have at least one of three auras that lasts longer than an hour. Five percent of auras are over 4 h (13). Visual aura is found in over 90% of the cases, and the most common deficit, however sensory, motor, speech, brainstem and retinal aura symptoms may also occur. Aura symptoms may precede the headache phase but may last well into the headache phase or even initiate during the headache phase. An example of motor aura would be hemiplegic migraine and may last up to 72 hours (14). 
Phase 3- Headache, ICHD-3 defines migraine as a headache attack lasting 4-72 h that is accompanied by nausea, photophobia (light sensitivity) and phonophobia (sound sensitivity), or both. The headache is characterized as unilateral, pulsating, of moderate or severe intensity and aggravated by physical activity; two of these characteristics uffice to fulfill the diagnostic criteria. Chronic migraine is defined as a migraine that occurs on 15 or more days per month as compared to episodic, which is less than 15 days per month (15).
Phase 4- Postdrome, this is often referred to as the Migraine hangover and it does reflect some of the symptoms experienced in the premonitory phase.
Migraines due to improper breathing mechanics (Respiration), creating a global hyperexcitability of the brain, increasing that inividual's symptoms, especially pain. Respiration can greatly affect Migraine sufferers. When Hyperventilation occurs, which often happens if we are lacking proper lumbar lordosis, rib expansion, abdominal strength, sacral flexibility (nutation), we do not fill our lower lobes where most gas exchange occurs and progress into a state of Respiratory Alkalosis. This causes increased binding of Calcium in our blood by a protein known as Albumin. Since Calcium and Sodium compete with one another for neuronal activation, when Ca2+ levels drop, Na+ rises and they now freely enter our brain cells and cause a level of hyperexcitability within those neurons, similar to what we're discussing in regards to Migraine, causing increased activation to the pain pathways on top of an already hypersensitive and dysregulated system. This can be due to abnormal rib activity, posture, spinal misalignment/dysfunction, weakness in abdominal and spinal extensor musculature and responds very well to Chiropractic Neurological Treatment and Physical Therapy. ​

Technical Migraine Overview

From a genetic predisposition, to brain hyperexcitability, to peripheral and central sensitisation, and brain stem and hypothalamus dysfunction. They all contribute to the phenotype of the migraineur. Migraine is a complex, basically inherited variable disorder of brain function. Its afferent pathway arises in the nociceptive durovascular afferents that seemed design to warn not localise. Their projection to the thalamus and cortex, and the regulation of this pathway, importantly at each level, and by multiple systems offers the possibility to understand the complex symptoms and target therapies. Rather than a sequential activation of different brain regions, migraine is a disorder of brain and therefore considered a "brain state," and is a consequence of changes, or dysfunction, in brain stem and hypothalamic regions which contribute to changes in cellular and vascular function in many regions of the brain. Migraine is best described as a consequence of dysfunction in the brain stem and hypothalamic nuclei that normally modulate or gate sensory inputs, including touch, light, sounds, and smells. These brain stem and hypothalamic nuclei can be considered "migraine mediators," and their dysfunction can lead to the failure of the brain integration and filtering mechanisms. The complex network of connections between regions of the brain stem, which include the PAG, RVM, locus coeruleus, and SuS, and diencephalic nuclei including hypothalamus, thalamus, and cortex can lead to the generation of symptoms through the same core of dysfunction. Dysfunction in these regions, though descending control of trigeminovascular nociceptive traffic, can lead to the perception of head pain through normal vessels throbbing, and continued dysfunction can lead to central sensitization of trigeminovascular neurons and the exacerbation of pain to normal physical activity as well as cutaneous cephalic and extracephalic allodynia. Convergence of sensory inputs to the thalamus that project to the cortex can explain the hypersensitivity to light, sounds and smells. The same dysfunction can lead to homeostatic changes, controlled by Hypothalamus related to sleep, feeding and activity. The general alteration of cortical and subcortical function can trigger events such as migraine aura, and extend to general inability to function properly. Inherited genetic factors clearly play a role in predisposing migraine susceptibility, as do the role of potential migraine triggers, whose common link seems to play at the heart of brain homeostasis in the hypothalamus and brainstem (3). 

(1) Global Burden of Disease Study. Global, regional, and national incidence, prevalance and years lived with disaiblity for 301 acute and chronic diseases and injuries in 188 coutnires, 1990-2013; a systematic analysis for the Global Burden of Disease Study 2013. Lancet 386: 743-800, 2015(2) Buse DC, et al. Sociodemographic and comorbidity profiles of chronic migraine and episodic migraine suffers. J Neurol Neurosurg Psychiatry 81: 428-432, 2010. (3) Goadsby Peter J., et al. Pathophysiology of Migraine: A Disorder of Sensory Processing. Physiol Rev 97 553-622, 2017. (4) Akerman S, Holland P, Goadsby PJ. Diencephalic and brainstem mechanisms in migraine. Nature Rev Neurosci 12: 570-584, 2011. (5) Bernstein C, Burstein R. Sensitization of the trigeminovascular pathway: perspective and implications to migraine pathophysiology. J Clin Neurol 8: 89-99, 2012. (6) Charles A. Migraine: a brain state. Curr Opin Neurol 26: 235-239, 2013. (7) Coppola G, et al. Is the cerebral cortex hyperxcitable or hyperresponsive in migraine? Cephalgia 27: 1427-1439, 2007.(8) Coppola G, et al. Reply to the topical review entitled "the phenomenon of changes in cortical exctiabiltiy in migraine is not migraine-specific-unifying thesis" by Anne Stankewitz adn Arne May published in Pain 2009; 145:1407. Pain 149: 407-409, 2010.(9) De Tommaso M, et al. Altered processing of sensory stimuli in patients with migraine. Nat Rev Neurol 10:144-155, 2014. (10) Stankewitz A, et al. The phenomenon of changes in cortical excitability in migraine is not migraine-specific-a unifying thesis. Pain 145: 14-17, 2009.(11) Gifffin NJ, et al. Premonitory symptoms in migraine: an electronic diary study. Neurology 60: 935-940, 2003. (12) Rasmussen BK, et al. Migarine with aura and migraine without aura: an epidemiological study. Cephalgia 12: 221-228, 1992. (13) Viana M, et al. Migraine aura symptoms: duration, succession and temporal relationship to headache. Cephalgia 36: 413-421, 2016. (14) Hansen JM, et al. Migraine headache is present in the aura phase: a prospective study. Neurology 79: 2044-2049, 2012. (15) Olesen J, et al. New appendix criteria open for a broader concept of chronic migraine. Cephalgia 26: 742-746, 2006. (16) McNaughton FL, et al. Innervation of intracranial structures: a reappraisal. In:Physiological Aspects of Clincal Neurology, edited by Rose FC. Oxford: Blackwell Scientific, 1977, p. 279-293(17) Penfield W, et al. Dural headache and the innervatin of hte dura mater. Arch Neurol Psychiatry 44:43-75(18) Ray BS, et al. Experimental studies on headache. Pain sensitive structures of the head and their significance in headache. Arch Surg 41:813-856, 1940. (19) Headache Classification Committe of the International Headache Society. The international classification of headache disorders, 3rd edition. Cephalgia 33: 629-808, 2013. (20). https://www.hopkinsmedicineorg/health/conditions-and-diseases/vestibular-migraine