By Eli Denham, DPT, FCAMPT, IFOMPT
Migraines currently represent one of the most common and poorly managed chronic conditions in the world. The Lancet’s Global Burden of Disease Survey 2016 describes migraines as the sixth most common neurologic condition and second in terms of years lived with disability.1 Historically, treatment strategies have primarily focused on pharmacological approaches and symptom management2,3. Physical therapy and management of migraines is a newer concept that is being explored in terms of utility and efficacy. However, the small amount of existing evidence finds that we as a profession really have not “hit the nail on the head.”4 Does Functional Dry Needling give us a previously unexplored avenue to affect migraines at their source rather than just managing symptoms? Perhaps… But first, let’s review a bit of background to set the scene and give us some context.
What Is A Migraine?
When patients report to our clinics with “migraine” as their chief complaint, it can be a bit overwhelming. The International Classification of Headache Disorder5 lists 29 types and complications of migraines! Fortunately, they have helped us out and adapted it into a very simple inclusion model which helps tremendously in clinical assessment and diagnosis.
If your patient’s head pain meets these rules you can begin to define it as a migraine:
A. At least five attacks1 fulfilling criteria B-D
B. Headache attacks lasting 4-72 hours (untreated or unsuccessfully treated)2,3
C. Headache has at least two of the following four characteristics:
- Unilateral location
- Pulsating quality
- Moderate or severe pain intensity
- Aggravation by or causing avoidance of routine physical activity (ie, walking or climbing stairs)
D. During headache at least one of the following occurs:
- Nausea and/or vomiting
- Photophobia and phonophobia
While these criteria help in the differential diagnosis of a migraine, practitioners with experience (read: frustration) in treating migraines will note that patients’ symptoms are rarely limited to the above criteria. Symptoms can range from the common — pain, fatigue and weakness — to the less common and more debilitating — visual auras, auditory hallucinations, partial paralysis, dysphagia, and the truly perplexing Alice in Wonderland syndrome (go ahead follow the link at right — I’ll wait).
These varied and confusing symptoms represent the chief frustration of migraine sufferers and those who treat them. However, there may be a common element in these symptoms and we, as physiotherapists, have a unique tool in Functional Dry Needling that could potentially address that tissue.
What’s the Common Element?
There is disagreement, of course, over the source of migraine symptoms with links being made to vascular pathologies, central nervous system dysfunction, immune system compromise, mental health conditions, and quite simply, the weather5-7. There is, however, an additional facet that has had little study in this pathology. It is the role of sensitization of the nervous system and how it may participate in migraine type symptoms.
What Is Sensitization and How Does It Work?
Sensitization, in its simplest terms, can be described as a hypersensitivity to stimuli as a result of chronic noxious input8. Pain Pressure Threshold (PPT) studies have been very useful in demonstrating this, as patients with chronic pain report pain with a lighter pressure than pain-free control groups9. Understanding central and peripheral sensitization is a field of study all its own, but for our purposes we can say that a sensitized segment would:
- Be hypersensitive to noxious, or potentially painful stimuli,
- Have an expanded field of perception (increased pain response evoked by stimuli outside the area of injury
- Demonstrate Allodynia, the sensation of pain in stimuli which is not normally painful.
Let’s use a few easy examples to understand this phenomenon. In terms of migraines, if we assume a sensitized nervous system, we may see these symptoms present as such:
|Nerve||Typical Role||Effects of Sensitization|
|Vestibulochlear Nerve (Sensory)||Hearing, Balance||Phonophobia5; Disequilibrium; Nystagmus; Motion Sickness; Nausea22|
|Oculomotor Nerve (Motor)||Eye movement and Pupillary Constriction||Painful Dysfunction eye movement5; Eye lid drooping; Painful movement at eye23; Painful pupillary constiction (photosensitivity)24|
Another feature of sensitization is referred pain with associated muscle weakness and motor control issues secondary to inhibition10,19. This is most easily represented by Multifidus and Gluteal Medius inhibition11,12 in people experiencing low back pain.
Sensitization In Migraines
There would appear to be a commonality between classic and reported migraine symptoms, and those we would expect from sensitization of the sensory and motor neurons of the brainstem. Hypersensitivity, allodynia and expanded field problems in the sensory nerves (i.e. phonosensitivity, photosensitivity), as well as motor weakness, referred pain, and trigger points in the motor nerves13 are all common presentations of those experiencing migraine headaches. Recognizing the commonality of these symptoms, while providing adequate explanation to the patient, is vital in beginning to help manage this condition. However, helping the patient understand their pathology is only half the battle14. Can we do anything to help desensitize the brainstem?
Can we Treat or Desensitize the Nervous System?
Several models exist in the treatment of central and peripheral sensitization, including patient education15, pharmacological16, manual therapy17, and exercise18. Although these are important tools to help address patients’ concerns with migraines, and no doubt valuable aspects of the treatment paradigm, they have not been able to provide a truly comprehensive approach to the condition.
Functional Dry Needling (FDN) may provide an important link between these treatment approaches as it can be used to modulate the peripheral and central nervous systems20. FDN may be helpful due to its effects at the local tissue, the inhibitory interneurons, and the central descending pain inhibition pathways. Firstly, Shah25,26 has shown us that FDN can positively alter the chemical environment in muscles with chronic pain reducing the chronic nociceptive input to the central nervous system which may be perpetuating sensitization and triggering symptoms in nearby nuclei. Secondly, by eliciting a twitch response in the muscle or by activating the muscle via electrical stimulation strong neural impulses are received by the inhibitory interneurons in the trigeminal nucleus and block transmission of pain signals to the higher processing centers that may be hypersensitive27. Lastly, studies have shown that FDN can activate the serotoninergic descending pain inhibitory pathways20 in the central nervous system resulting the in the release of serotonin in the trigeminal nucleus inhibiting upwards pain transmission and resetting the sensitivity of the peripheral neurons27. Activating this pathway by needling muscles innervated by the brainstem (i.e. Trapezius, SCM or Masseter) gives us a unique tool to help desensitize the sensory nerves and re-invigorate the motor nerves addressing many of the symptoms associated with migraines and chronic head and face pain.
Patient example: ‘Mae Headhertz’ is a 45-year-old woman who reports to physiotherapy for assessment and treatment of her migraines secondary to a whiplash injury she had 10 years ago. Her symptoms meet the ICHD criteria for migraine diagnosis (see above). She doesn’t currently have a migraine but gets migraines 2-3 times a month, which she relates to exposure to bright lights or loud noises. She is negative for other red flags and contraindications and is keen to try FDN because it helped her co-worker ‘Stif LoeBach.’
Management and Understandings
Through the lens of sensitization, we might think her migraines could be linked to the trauma she underwent with her whiplash injury. Sensitization, secondary to injury to the trapezius and SCM during whiplash, has gone untreated and now has made the whole brainstem more sensitive via the expanded field theory. Now normal input through the cranial nerves is allodynic, and output via those motor neurons is inhibited and dysfunctional.
In this case applying FDN to the trapezius, SCM and Masseter may have the effect of desensitizing the brainstem by reversing chronic local tissue trigger point noxious input, inhibiting upward transmission of pain signals and activating the descending pain inhibition pathways. These effects would address Mae’s complaints of head pain (muscular referral) and photo- and phonosensitivity (sensory allodynia) in the short term. To truly help Ms. Headhertz we would need a holistic approach using what we know from pain science literature.
Manual therapy may provide significant neurologic input to help desensitize the peripheral nervous system; local soft tissue techniques (ART, Graston) may address local tissue issues perpetuating chronic pain, and behavioural therapy and patient empowerment may help address central nervous system issues. Looking at migraines as a sensitization problem helps us use FDN to address components of this complicated pathology. However, migraines are multi-factorial. It is imperative we highlight the importance of therapeutic exercise, which further helps in the desensitization of chronic pain in all three of these mechanisms!
In summary, FDN is a tool we can use to address the neurophysiologic aspect of pain and dysfunction, but it isn’t the only tool we have. Using these principles, we can use our other physiotherapy tools to continue to help re-train the neuromuscular system at the brainstem to help patients manage and move forward with their pursuit of an active, healthy lifestyle!
- Lancet. Global, regional, and national incidence, prevalence, and years lived with disability for 328 diseases and injuries for 195 countries, 1990–2016: a systematic analysis for the Global Burden of Disease Study 2016. 2017; 390: 1211–59.
- Aminoff M, Greenberg D, Simon R. Clinical Neurology 6th ed. New York: Lange Medical Books/McGraw-Hill; 2005: 85-90.
- Božena J, Katić, S, Krause J. Adherence to Acute Migraine Medication: What Does It Mean, Why Does It Matter? Headache. 2010; 50(1):117.
- Chaibi A, Tuchin P, Bjørn M. Manual therapies for migraine: a systematic review. J Headache Pain. 2011; 12(2):127–133.
- Olesen J. International Classification of Headache Disorders, 3rd edition. Headache. 2013.
- Aminoff M, Greenberg D, Simon R. Clinical Neurology 6th ed. New York: Lange Medical Books/McGraw-Hill; 2005: 85-90.
- Beers M, Porter R, Jones T, et al. The Merck Manual of Diagnosis and Therapy 18th ed. Whitehouse Station: Merck Research Laboratories; 2006: 1847-1849.
- Nijs J, Torres-Cueco R, Van Wilgen P, et al. Applying modern pain neuroscience in clinical practice: criteria for the classification of central sensitization pain. Pain Physician. 2014; 17(5):447-457.
- Granges G, Littlejohn G. Pressure pain threshold in pain‐free subjects, in patients with chronic regional pain syndromes, and in patients with fibromyalgia syndrome. Arthritis & Rheumatology. 1993.
- Giamberardino M. Referred Muscle Pain/Hyperaldesia and central sensitisation. J Rehabil Med. 2003; Suppl. 41: 85–88.
- Cooper N, Scavo K, Strickland K. Prevalence of gluteus medius weakness in people with chronic low back pain compared to healthy controls. European Spine Journal. 2016; 25(4): 1258–1265.
- Falla D, Bilenkij G, Jull G. Patients with chronic neck pain demonstrate altered patterns of muscle activation during performance of a functional upper limb task. Spine. 2004; 29(13):1436-40.
- Fernández-de-las-Peñas C, Cuadrado M, Pareja J.Myofascial trigger points, neck mobility and forward head posture in unilateral migraine. Celphalagia. 2006;26(9):1061-70.
- Moseley G, Butler D. Fifteen years of explaining pain: the past, present, and future. Pain. 2015; 16(9):807-13.
- Nijs J, Van Wilgen C, Van Oosterwijck J, et al. How to explain central sensitization to patients with ‘unexplained’ chronic musculoskeletal pain: Practice guidelines. Man Ther. 2011;16(5):413-8.
- Moulin D, Clark A, Gilron I, et al. Pharmacological Management of Chronic Neuropathic Pain – Consensus Statement and Guidelines from the Canadian Pain Society. Pain Res Manag. 2014;19(6): 328–335.
- Voogt L, de Vries J, Meeus M, et al. Analgesic effects of manual therapy in patients with musculoskeletal pain: A systematic review. Man Ther. 2015;20(2):250-6.
- Nijs J, Kosek E, Van Oosterwijckn J, et al. Dysfunctional endogenous analgesia during exercise in patients with chronic pain: to exercise or not to exercise?. Pain Physician. 2012; 15(3S): ES205-ES213.
- Hides J, Stokes M, Saide M, et al. Evidence of lumbar multifidus muscle wasting ipsilateral to symptoms in patients with acute/subacute low back pain. Spine. 1994; 15;19(2):165-72.
- Li-Wei Chou, Mu-Jung Kao, and Jaung-Geng Lin. Probable Mechanisms of Needling Therapies for Myofascial Pain Control. Evidence-Based Complementary and Alternative Medicine. 2012: 11.
- Millan M. Descending control of pain. Progress in Neurobiology. 2002;66:355–474.
- Lempert T, Olesen J, Furman J, Waterston, J. Vestibular migraine: Diagnostic criteria. Journal of Vestibular Research: Equilibrium and Orientation. 2012: 22(4), 167-172.
- Savundra P, Carroll J, Davies R. Migraine-Associated Vertigo. Cephalalgia. 1997;17(4):505-510.
- Wieser T, Wolff R, Hoffmann K, et al. Persistent ocular motor disturbances in migraine without aura. Neurological Sciences. 2004;25(1):8–12.
- Shah J, Elizabeth, A. Gilliams. Uncovering the biochemical milieu of myofascial trigger points using in vivo microdialysis: An application of muscle pain concepts to myofascial pain syndrome. Journal of Bodywork and Movement Therapies. 2008;12(4):371-384
- Shah J, Danoff J, Desai M, et al. Biochemicals associated with pain and inflammation are elevated in sites near to and remote from active myofascial trigger points. Archives of Physical Medicine and Rehabilitation. 2008; 89(1):16-23.
- Cagnie B, Dewitte V, Barbe T, et al. Physiologic Effects of Dry Needling. Curr Pain Headache Rep. 2013;17:348