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Proprioception Part II - It's More Complex Than You Thought
May 22, 2010 by Dr Matthew D. Long
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Proprioception Part II - It's More Complex Than You Thought
May 22, 2010 by Dr Matthew D. Long
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Proprioception Part II - It's More Complex Than You Thought
May 22, 2010 by Dr Matthew D. Long
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In our last Clinical Clarity Blog entry (found here) we looked at the accruing evidence that chronic and recurrent spinal disorders are frequently accompanied by proprioceptive deficits. We also took the view that these deficits might actually be the 'weakness' that precedes an acute episode of pain.
So far it has been suggested that this lack of sensory feedback might exist somewhere in the peripheral structures, such as in the multifidus muscle groups, or in the muscle spindles themselves. Brumagne and colleagues (1) suggested that, "it is possible that reduced proprioceptive acuity in the lumbosacral spine is a precursor to back injuries and their sequelae. Poor perception of spine orientation may lead to more frequent excursions beyond the range of mechanical stability, thereby risking mechanical injury to spinal tissues."
But could the problem be central - in the brain itself?
A new paper by Wand et al (2) takes this view and makes the case that chronic lower back pain might be the result of perceptual abnormalities in the cortex. They examined the possibility that a disruption in the way the cortex represents a painful back might underpin the chronic nature of the condition (not unlike phantom limb pain). By cleverly assessing a subject's performance of two-point discrimination and graphaesthesia over the skin of the lumbar spine the authors' showed that:
(a) while there was no loss of touch sensitivity (meaning that the peripheral receptors in the skin worked just fine),
(b) there was a marked loss of ability to integrate this sensory data into meaningful information.
In other words, a chronic back pain patient could detect the sensory inputs from their back, they just couldn't assemble it correctly in their cortex to make useable perceptual information.
The authors concluded by saying that, "These results are supportive of the notion that chronic non-specific low back pain is characterised by dysfunction of sensory processing of information from the painful area."
Such claims of cortical maladaptation are further supported by the work of Apkarian et al (3) who found that patients with chronic lower back pain demonstrated 5-11% less neocortical gray matter volume than control subjects - a feature that was directly related to the longevity of the pain (a 1.3 cubic cm loss for every year of chronic pain!). Schmidt-Wilcke (4) also documented functional reorganisation in the somatosensory cortex and brainstem of chronic back pain patients.
So could it be that the tendency to chronic spinal dysfunction resides not only in the damaged or wasted tissues of the spine itself, but in the higher processing centres of the brain?
Could it be that our chronic patients simply cannot assemble the barrage of sensory feedback from their spines into a realistic cortical representation sufficient to guide normal movement or protective behaviours?
It appears that this might be the case.
The question is, what are we, as chiropractors, doing about these central defects?
Well that is the subject of a future blog entry...
Matthew D. Long
BSc (Syd) M.Chiro (Macq)
So far it has been suggested that this lack of sensory feedback might exist somewhere in the peripheral structures, such as in the multifidus muscle groups, or in the muscle spindles themselves. Brumagne and colleagues (1) suggested that, "it is possible that reduced proprioceptive acuity in the lumbosacral spine is a precursor to back injuries and their sequelae. Poor perception of spine orientation may lead to more frequent excursions beyond the range of mechanical stability, thereby risking mechanical injury to spinal tissues."
But could the problem be central - in the brain itself?
A new paper by Wand et al (2) takes this view and makes the case that chronic lower back pain might be the result of perceptual abnormalities in the cortex. They examined the possibility that a disruption in the way the cortex represents a painful back might underpin the chronic nature of the condition (not unlike phantom limb pain). By cleverly assessing a subject's performance of two-point discrimination and graphaesthesia over the skin of the lumbar spine the authors' showed that:
(a) while there was no loss of touch sensitivity (meaning that the peripheral receptors in the skin worked just fine),
(b) there was a marked loss of ability to integrate this sensory data into meaningful information.
In other words, a chronic back pain patient could detect the sensory inputs from their back, they just couldn't assemble it correctly in their cortex to make useable perceptual information.
The authors concluded by saying that, "These results are supportive of the notion that chronic non-specific low back pain is characterised by dysfunction of sensory processing of information from the painful area."
Such claims of cortical maladaptation are further supported by the work of Apkarian et al (3) who found that patients with chronic lower back pain demonstrated 5-11% less neocortical gray matter volume than control subjects - a feature that was directly related to the longevity of the pain (a 1.3 cubic cm loss for every year of chronic pain!). Schmidt-Wilcke (4) also documented functional reorganisation in the somatosensory cortex and brainstem of chronic back pain patients.
So could it be that the tendency to chronic spinal dysfunction resides not only in the damaged or wasted tissues of the spine itself, but in the higher processing centres of the brain?
Could it be that our chronic patients simply cannot assemble the barrage of sensory feedback from their spines into a realistic cortical representation sufficient to guide normal movement or protective behaviours?
It appears that this might be the case.
The question is, what are we, as chiropractors, doing about these central defects?
Well that is the subject of a future blog entry...
Matthew D. Long
BSc (Syd) M.Chiro (Macq)
References:
1. Brumagne S, Cordo P, Lysens R, Verschueren S, Swinnen S. The role of paraspinal muscle spindles in lumbosacral position sense in individuals with and without low back pain. Spine 2000. 25 (8) 989-94
2. Wand BM, Di Pietro F, George P, O'Connell NE. Tactile thresholds are preserved yet complex sensory function is impaired over the lumbar spine of chronic non-specific low back pain patients: a preliminary investigation. Physiotherapy 2010. doi:10.1016/j.physio.2010.02.005
3. Apkarian AV, Sosa Y, Sonty S, Levy RM, Harden RN, Parrish TB, Gitelman DR. Chronic Back Pain Is Associated with Decreased Prefrontal and Thalamic Gray Matter Density. J Neurosci 2004. 24 (46) 10410-5
4. Schmidt-Wilcke T, Leinisch E, Gänssbauer S, Draganski B, Bogdahn U, Altmeppen J, May A. Affective components and intensity of pain correlate with structural differences in gray matter in chronic back pain patients. Pain 2006. 125 (1-2) 89-97
1. Brumagne S, Cordo P, Lysens R, Verschueren S, Swinnen S. The role of paraspinal muscle spindles in lumbosacral position sense in individuals with and without low back pain. Spine 2000. 25 (8) 989-94
2. Wand BM, Di Pietro F, George P, O'Connell NE. Tactile thresholds are preserved yet complex sensory function is impaired over the lumbar spine of chronic non-specific low back pain patients: a preliminary investigation. Physiotherapy 2010. doi:10.1016/j.physio.2010.02.005
3. Apkarian AV, Sosa Y, Sonty S, Levy RM, Harden RN, Parrish TB, Gitelman DR. Chronic Back Pain Is Associated with Decreased Prefrontal and Thalamic Gray Matter Density. J Neurosci 2004. 24 (46) 10410-5
4. Schmidt-Wilcke T, Leinisch E, Gänssbauer S, Draganski B, Bogdahn U, Altmeppen J, May A. Affective components and intensity of pain correlate with structural differences in gray matter in chronic back pain patients. Pain 2006. 125 (1-2) 89-97