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Migraine, Colic and Complexity
March 13, 2012 by Dr Matthew D. Long
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Migraine, Colic and Complexity
March 13, 2012 by Dr Matthew D. Long
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Migraine, Colic and Complexity
March 13, 2012 by Dr Matthew D. Long
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The results of a recent study to be presented next month at the American Academy of Neurology (AAN) 64th Annual Meeting has focused attention yet again upon the complexity of migraine. Dr Amy Gelfand will discuss the findings of an investigation into the relationship between mothers with migraine and the tendency for their children to suffer infantile colic. In summary, maternal migraine is associated with a greater-than two-fold increase in the chance of having a colicky baby.
But what underlies this relationship?
Migraine is a genetic neurological disease that is frequently misunderstood. While the condition certainly can cause headache, it should not be defined by headache symptoms nor restricted to a category of headache pain. In essence, migraine represents a fundamentally flawed brain that struggles to regulate neuronal activity and maintain equilibrium. One could describe the migrainous brain as a genetically predisposed, serotonin depleted, nor-adrenaline deficient, dopamine sensitive, calcium channel deformed, ATP constrained, magnesium compromised, bundle of hyper-excitable circuitry in a state of precarious membrane stability. The end result - a highly reactive brain that is unduly sensitive to both internal and external stimuli. Furthermore, the way in which this instability manifests is not limited to 'bad headaches' or even the more complex aura symptoms.
Many migraineurs go through life experiencing signs and symptoms of their disease that are never attributed as such. It now appears that these symptoms may well manifest in infants as colicky behaviour. The concept of 'abdominal migraine' in children has gained greater acceptance in recent years (2), with Carson et al suggesting that it accounts for 4-15% of recurrent idiopathic abdominal pain. Furthermore, as childhood progresses even more complex 'migraine equivalents' start to appear and challenge our notions of what exactly constitutes a migraine. Such migraine equivalents include abdominal migraine and cyclical vomiting syndrome, acephalgic migraine (visual), acute confusional migraine, migrainous vertigo and torticollis (3). The trouble is, these episodes are often unrecognised as an expression of the underlying disease that lies at its core.
To return to the subject of colic, we must ask ourselves what this new insight might do for colic management? Chiropractors have long claimed efficacy for treating infantile colic, but the evidence is definitely patchy (4,5). However, we must also understand that the diagnosis of colic is subjective and there is no firm agreement on an underlying pathophysiology. With so much confusion and uncertainty it is of no surprise that controversy reigns. But what if we included migraine as a possible aetiology for 'colicky behaviour'? How would this change our approach? If colic was now viewed as a brain disorder what would this mean for contemporary chiropractic and medical theories about treating the condition?
Migraine illness represents a condition of undue sensitivity to both internal and external stimuli. Whether the stimulus is a flashing light, a loud noise or the distension of an internal organ such as the bowel, a migraineur's brain responds with increasing intensity. Many studies have catalogued the broad-spectrum sensitivities of migraine. But irritable bowel syndrome (IBS) is probably one of the better studied examples, and the most relevant to infant colic. Indeed, one could easily propose that IBS sits on the migraine disorder spectrum. Sufferers of IBS also exhibit a generalised sensitivity to non-bowel stimuli (6), "including back pain, migraine headaches, heartburn, dyspareunia, and muscle pain in body regions somatotopically distinct from the gut. Collectively, these somatic symptoms suggest that IBS patients may also suffer from central hyperalgesic dysfunction" (7). This has been described as a failure of a central analgesic mechanism known as diffuse noxious inhibitory controls (DNIC) (8). As such, irritable bowel syndrome has been conceived as a problem of how the brain perceives the gut, rather than an intrinsic gut disorder itself. In just the same way, infant colic might represent an unduly sensitive brain that allows normal levels of gut distension to register as pain.
So what does this mean for chiropractors?
If migraine and colic exist on a continuum of brain disorders in which descending pain modulation is compromised, can we claim that spinal dysfunction somehow 'causes' colic or migraine headache?
Probably not.
However, spinal dysfunction may well act as a 'trigger' for acute episodes in just the same way that flashing lights, loud sounds or gut distension might. If this is the case, it would make sense that adjustments to the spine may reduce the burden of irritation flooding the sensory system that allow other noxious pathways from the gut to reach threshold. We could also conceive of a manipulation as a 'sensory lever' that alters modulation of the pain pathways and facilitates greater inhibition of pain from other sources - including the gut.
Something to think about...
Dr Matthew D. Long
BSc (Syd) M.Chiro (Macq)
But what underlies this relationship?
Migraine is a genetic neurological disease that is frequently misunderstood. While the condition certainly can cause headache, it should not be defined by headache symptoms nor restricted to a category of headache pain. In essence, migraine represents a fundamentally flawed brain that struggles to regulate neuronal activity and maintain equilibrium. One could describe the migrainous brain as a genetically predisposed, serotonin depleted, nor-adrenaline deficient, dopamine sensitive, calcium channel deformed, ATP constrained, magnesium compromised, bundle of hyper-excitable circuitry in a state of precarious membrane stability. The end result - a highly reactive brain that is unduly sensitive to both internal and external stimuli. Furthermore, the way in which this instability manifests is not limited to 'bad headaches' or even the more complex aura symptoms.
Many migraineurs go through life experiencing signs and symptoms of their disease that are never attributed as such. It now appears that these symptoms may well manifest in infants as colicky behaviour. The concept of 'abdominal migraine' in children has gained greater acceptance in recent years (2), with Carson et al suggesting that it accounts for 4-15% of recurrent idiopathic abdominal pain. Furthermore, as childhood progresses even more complex 'migraine equivalents' start to appear and challenge our notions of what exactly constitutes a migraine. Such migraine equivalents include abdominal migraine and cyclical vomiting syndrome, acephalgic migraine (visual), acute confusional migraine, migrainous vertigo and torticollis (3). The trouble is, these episodes are often unrecognised as an expression of the underlying disease that lies at its core.
To return to the subject of colic, we must ask ourselves what this new insight might do for colic management? Chiropractors have long claimed efficacy for treating infantile colic, but the evidence is definitely patchy (4,5). However, we must also understand that the diagnosis of colic is subjective and there is no firm agreement on an underlying pathophysiology. With so much confusion and uncertainty it is of no surprise that controversy reigns. But what if we included migraine as a possible aetiology for 'colicky behaviour'? How would this change our approach? If colic was now viewed as a brain disorder what would this mean for contemporary chiropractic and medical theories about treating the condition?
Migraine illness represents a condition of undue sensitivity to both internal and external stimuli. Whether the stimulus is a flashing light, a loud noise or the distension of an internal organ such as the bowel, a migraineur's brain responds with increasing intensity. Many studies have catalogued the broad-spectrum sensitivities of migraine. But irritable bowel syndrome (IBS) is probably one of the better studied examples, and the most relevant to infant colic. Indeed, one could easily propose that IBS sits on the migraine disorder spectrum. Sufferers of IBS also exhibit a generalised sensitivity to non-bowel stimuli (6), "including back pain, migraine headaches, heartburn, dyspareunia, and muscle pain in body regions somatotopically distinct from the gut. Collectively, these somatic symptoms suggest that IBS patients may also suffer from central hyperalgesic dysfunction" (7). This has been described as a failure of a central analgesic mechanism known as diffuse noxious inhibitory controls (DNIC) (8). As such, irritable bowel syndrome has been conceived as a problem of how the brain perceives the gut, rather than an intrinsic gut disorder itself. In just the same way, infant colic might represent an unduly sensitive brain that allows normal levels of gut distension to register as pain.
So what does this mean for chiropractors?
If migraine and colic exist on a continuum of brain disorders in which descending pain modulation is compromised, can we claim that spinal dysfunction somehow 'causes' colic or migraine headache?
Probably not.
However, spinal dysfunction may well act as a 'trigger' for acute episodes in just the same way that flashing lights, loud sounds or gut distension might. If this is the case, it would make sense that adjustments to the spine may reduce the burden of irritation flooding the sensory system that allow other noxious pathways from the gut to reach threshold. We could also conceive of a manipulation as a 'sensory lever' that alters modulation of the pain pathways and facilitates greater inhibition of pain from other sources - including the gut.
Something to think about...
Dr Matthew D. Long
BSc (Syd) M.Chiro (Macq)
References:
1. Gelfand, A. American Academy of Neurology (AAN) 64th Annual Meeting. Abstract 113. April 21 - 28, 2012. First results released February 20, 2012.
2. Carson, L., Lewis, D., Tsou, M., McGuire, E., Surran, B., Miller, C., & Vu, T.-A. (2011). Abdominal migraine: an under-diagnosed cause of recurrent abdominal pain in children. Headache, 51(5), 707–712. doi:10.1111/j.1526-4610.2011.01855.x
3. Al-Twaijri, W. A., & Shevell, M. I. (2002). Pediatric migraine equivalents: occurrence and clinical features in practice. Pediatric neurology, 26(5), 365–368.
4. Wiberg, J. M., Nordsteen, J., & Nilsson, N. (1999). The short-term effect of spinal manipulation in the treatment of infantile colic: a randomized controlled clinical trial with a blinded observer. Journal of manipulative and physiological therapeutics, 22(8), 517–522.
5. Wiberg, K. R., & Wiberg, J. M. M. (2010). A retrospective study of chiropractic treatment of 276 danish infants with infantile colic. Journal of manipulative and physiological therapeutics, 33(7), 536–541. doi:10.1016/j.jmpt.2010.08.004
6. Piché, M., Arsenault, M., Poitras, P., Rainville, P., & Bouin, M. (2010). Widespread hypersensitivity is related to altered pain inhibition processes in irritable bowel syndrome. Pain, 148(1), 49–58. doi:10.1016/j.pain.2009.10.005
7. Zhou, Q., Fillingim, R. B., Riley, J. L., Malarkey, W. B., & Nicholas Verne, G. (2010). Central and peripheral hypersensitivity in the irritable bowel syndrome. Pain, 148(3), 454–461. doi:10.1016/j.pain.2009.12.005
8. Heymen, S., Maixner, W., Whitehead, W. E., Klatzkin, R. R., Mechlin, B., & Light, K. C. (2010). Central processing of noxious somatic stimuli in patients with irritable bowel syndrome compared with healthy controls. The Clinical journal of pain, 26(2), 104–109. doi:10.1097/AJP.0b013e3181bff800
1. Gelfand, A. American Academy of Neurology (AAN) 64th Annual Meeting. Abstract 113. April 21 - 28, 2012. First results released February 20, 2012.
2. Carson, L., Lewis, D., Tsou, M., McGuire, E., Surran, B., Miller, C., & Vu, T.-A. (2011). Abdominal migraine: an under-diagnosed cause of recurrent abdominal pain in children. Headache, 51(5), 707–712. doi:10.1111/j.1526-4610.2011.01855.x
3. Al-Twaijri, W. A., & Shevell, M. I. (2002). Pediatric migraine equivalents: occurrence and clinical features in practice. Pediatric neurology, 26(5), 365–368.
4. Wiberg, J. M., Nordsteen, J., & Nilsson, N. (1999). The short-term effect of spinal manipulation in the treatment of infantile colic: a randomized controlled clinical trial with a blinded observer. Journal of manipulative and physiological therapeutics, 22(8), 517–522.
5. Wiberg, K. R., & Wiberg, J. M. M. (2010). A retrospective study of chiropractic treatment of 276 danish infants with infantile colic. Journal of manipulative and physiological therapeutics, 33(7), 536–541. doi:10.1016/j.jmpt.2010.08.004
6. Piché, M., Arsenault, M., Poitras, P., Rainville, P., & Bouin, M. (2010). Widespread hypersensitivity is related to altered pain inhibition processes in irritable bowel syndrome. Pain, 148(1), 49–58. doi:10.1016/j.pain.2009.10.005
7. Zhou, Q., Fillingim, R. B., Riley, J. L., Malarkey, W. B., & Nicholas Verne, G. (2010). Central and peripheral hypersensitivity in the irritable bowel syndrome. Pain, 148(3), 454–461. doi:10.1016/j.pain.2009.12.005
8. Heymen, S., Maixner, W., Whitehead, W. E., Klatzkin, R. R., Mechlin, B., & Light, K. C. (2010). Central processing of noxious somatic stimuli in patients with irritable bowel syndrome compared with healthy controls. The Clinical journal of pain, 26(2), 104–109. doi:10.1097/AJP.0b013e3181bff800