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Adhesions Revisited
December 16, 2010 by Dr Matthew D. Long
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December 16, 2010 by Dr Matthew D. Long
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Adhesions Revisited
December 16, 2010 by Dr Matthew D. Long
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Spinal pain syndromes, and the functional disorders that underpin these conditions, are clearly complex. And as successful clinicians we need to be able to define the extent and boundaries of the problem - and understand the nature of the variables present. In previous blog entries we have focussed upon some of the functional neurological deficits that seem to lie beneath recurrent spinal pain. These include lack of joint proprioception, inappropriate muscular recruitment and coordination, and even changes to cortical architecture and control. But what about some of the other mechanical or tissue-based aspects of spinal disorders? What else can go wrong 'in there'?
In our last Blog entry (found here) we looked at the prospect of adhesions playing a role in the mechanism of facet joint pain - or at least in the production of joint stiffness and subsequent degeneration. So where else might adhesions have their influence upon the spinal pain patient?
A recent study by Kobayahsi et al (1) identified periradicular adhesions as a possible culprit in the perpetuation of nerve root compression and sciatica. While other sources of root deformation have been identified (such as the classic disc herniation, or due to degenerative hypertrophy of the facets, ligamentum flavum or pedicles) it is also known that compression per se is not the instigator of radicular pain. Rather, it is the inflammatory chemical soup that bathes neural tissue that is the main factor, particularly noxious substances such as TNF-alpha. But what happens when the inflammation subsides and the patient still has pain? After all, radiation of pain into the leg is a significant and reliable predictor of future chronicity (2).
Kobayashi's paper looked at the question of adhesions between herniated disc material and the neighbouring nerve root. It seems that the sudden appearance of nucleus pulposus in the epidural space is not looked upon kindly by the immune system. An immune response is mounted, complete with migration of macrophages, mast cells and neovascularisation. Ultimately granulation tissue is deposited, forming a connective tissue matrix that may enmesh the nerve root and tether it to the protruding disc material. The net result of this?
According to Kobayashi, "The presence of periradicular fibrosis will compound the nerve root pain by fixing the nerve in one position and thus increasing the susceptibility of the nerve root to tension or compression...
These adhesions led to severe tension or compression on the nerve root, thus causing disturbance of intraradicular blood flow and breakdown of the blood-nerve barrier, resulting in intraradicular inflammatory changes such as edema and demyelination."
Furthermore, in another paper Kobayashi and colleagues (3) also noted that root compression produces significant and often irreversible damage to the synapses in the dorsal horn - thereby producing central sensitisation and further tipping the patient towards a chronic pain state.
So what can we do about this?
Ellis and Hing have written about neural mobilisation techniques and analysed the success of various approaches. They suggested that, "When neural mobilization is used for treatment of adverse neurodynamics, the primary theoretical objective is to attempt to restore the dynamic balance between the relative movement of neural tissues and surrounding mechanical interfaces, thereby allowing reduced intrinsic pressures on the neural tissue and thus promoting optimum physiologic function. The hypothesized benefits from such techniques include facilitation of nerve gliding, reduction of nerve adherence, dispersion of noxious fluids, increased neural vascularity, and improvement of axoplasmic flow."
While Ellis and Hing did find evidence of efficacy for such treatment in the cervical region, they were less confident about the benefits in the case of sciatica. However, Cleland and colleagues showed that slump stretching (a form of neural mobilisation) was certainly helpful in patients with lower back pain only and a negative straight-leg raise test. The problem with assessing the benefits of neural stretching in the presence of sciatica is that there is more than one distinct sub-type of the condition. And wherever there is a different underlying mechanism, there will be a different prognosis. So this means that we need a better way to diagnose the different sub-types of sciatica.
To try to improve patient selection, and therefore the predictability of treatment, there has been a move in recent years towards subgrouping patients with lower back pain and sciatica. The thinking is, if we can identify those who will respond best prior to initiating treatment, we have the best chance of a successful outcome and can triage patients more effectively. To this end, Schafer et al classified patients according to the following criteria:
"Patients were classified according to the findings of simple clinical tests into four distinct categories:
(1) neuropathic sensitization (NS) comprising major features of neuropathic pain with sensory sensitization such as allodynia, hyperalgesia and paroxysmal pain;
(2) denervation (D) arising from significant axonal compromise with marked sensory and motor deficits;
(3) peripheral nerve sensitization (PNS) arising from nerve trunk inflammation with marked nerve mechanosensitivity; and
(4) musculoskeletal (M) with pain referred from non-neural structures such as the disc or facet joints."
Interestingly, they found very different results from each patient group. Only 15% of the 'D' patients responded favourably to neural mobilisation. Similarly, only 11% of the 'NS' patients were helped convincingly, with the 'M' individuals also coming in at 11%. However, 56% of the 'PNS" subjects responded well, which means that successful subgrouping of patients can help us to select those with the greatest chance of success.
In our last Blog entry (found here) we looked at the prospect of adhesions playing a role in the mechanism of facet joint pain - or at least in the production of joint stiffness and subsequent degeneration. So where else might adhesions have their influence upon the spinal pain patient?
A recent study by Kobayahsi et al (1) identified periradicular adhesions as a possible culprit in the perpetuation of nerve root compression and sciatica. While other sources of root deformation have been identified (such as the classic disc herniation, or due to degenerative hypertrophy of the facets, ligamentum flavum or pedicles) it is also known that compression per se is not the instigator of radicular pain. Rather, it is the inflammatory chemical soup that bathes neural tissue that is the main factor, particularly noxious substances such as TNF-alpha. But what happens when the inflammation subsides and the patient still has pain? After all, radiation of pain into the leg is a significant and reliable predictor of future chronicity (2).
Kobayashi's paper looked at the question of adhesions between herniated disc material and the neighbouring nerve root. It seems that the sudden appearance of nucleus pulposus in the epidural space is not looked upon kindly by the immune system. An immune response is mounted, complete with migration of macrophages, mast cells and neovascularisation. Ultimately granulation tissue is deposited, forming a connective tissue matrix that may enmesh the nerve root and tether it to the protruding disc material. The net result of this?
According to Kobayashi, "The presence of periradicular fibrosis will compound the nerve root pain by fixing the nerve in one position and thus increasing the susceptibility of the nerve root to tension or compression...
These adhesions led to severe tension or compression on the nerve root, thus causing disturbance of intraradicular blood flow and breakdown of the blood-nerve barrier, resulting in intraradicular inflammatory changes such as edema and demyelination."
Furthermore, in another paper Kobayashi and colleagues (3) also noted that root compression produces significant and often irreversible damage to the synapses in the dorsal horn - thereby producing central sensitisation and further tipping the patient towards a chronic pain state.
So what can we do about this?
Ellis and Hing have written about neural mobilisation techniques and analysed the success of various approaches. They suggested that, "When neural mobilization is used for treatment of adverse neurodynamics, the primary theoretical objective is to attempt to restore the dynamic balance between the relative movement of neural tissues and surrounding mechanical interfaces, thereby allowing reduced intrinsic pressures on the neural tissue and thus promoting optimum physiologic function. The hypothesized benefits from such techniques include facilitation of nerve gliding, reduction of nerve adherence, dispersion of noxious fluids, increased neural vascularity, and improvement of axoplasmic flow."
While Ellis and Hing did find evidence of efficacy for such treatment in the cervical region, they were less confident about the benefits in the case of sciatica. However, Cleland and colleagues showed that slump stretching (a form of neural mobilisation) was certainly helpful in patients with lower back pain only and a negative straight-leg raise test. The problem with assessing the benefits of neural stretching in the presence of sciatica is that there is more than one distinct sub-type of the condition. And wherever there is a different underlying mechanism, there will be a different prognosis. So this means that we need a better way to diagnose the different sub-types of sciatica.
To try to improve patient selection, and therefore the predictability of treatment, there has been a move in recent years towards subgrouping patients with lower back pain and sciatica. The thinking is, if we can identify those who will respond best prior to initiating treatment, we have the best chance of a successful outcome and can triage patients more effectively. To this end, Schafer et al classified patients according to the following criteria:
"Patients were classified according to the findings of simple clinical tests into four distinct categories:
(1) neuropathic sensitization (NS) comprising major features of neuropathic pain with sensory sensitization such as allodynia, hyperalgesia and paroxysmal pain;
(2) denervation (D) arising from significant axonal compromise with marked sensory and motor deficits;
(3) peripheral nerve sensitization (PNS) arising from nerve trunk inflammation with marked nerve mechanosensitivity; and
(4) musculoskeletal (M) with pain referred from non-neural structures such as the disc or facet joints."
Interestingly, they found very different results from each patient group. Only 15% of the 'D' patients responded favourably to neural mobilisation. Similarly, only 11% of the 'NS' patients were helped convincingly, with the 'M' individuals also coming in at 11%. However, 56% of the 'PNS" subjects responded well, which means that successful subgrouping of patients can help us to select those with the greatest chance of success.
Image from Schafer et al. Courtesy Springer.
I suppose that one of the important lessons to draw from such research is that there is no singular spinal lesion. There are many different things that can go wrong within the spine and that we must be as adept as possible at defining the extent of the problem that we are presented with and adapt our management accordingly. What's more, you might consider adding some neural mobilisation techniques to your armamentarium for those tricky sciatica cases.
Dr Matthew D. Long
BSc (Syd) M.Chiro (Macq)
Dr Matthew D. Long
BSc (Syd) M.Chiro (Macq)
References:
1. Kobayashi S, Takeno K, Yayama T, Awara K, Miyazaki T, Guerrero A, Baba H. Pathomechanisms of sciatica in lumbar disc herniation: effect of periradicular adhesive tissue on electrophysiological values by an intraoperative straight leg raising test. Spine (2010) vol. 35 (22) pp. 2004-14
2. Grotle M, Brox JI, Glomsrod B, Lonn JH, Vollestad NK (2007). Prognostic factors in first-time care seekers due to acute low back pain. Eur J Pain 11:290–298
3. Kobayashi S, Uchida K, Kokubo Y, Takeno K, Yayama T, Miyazaki T, Nakajima H, Nomura E, Mwaka E, Baba H. Synapse involvement of the dorsal horn in experimental lumbar nerve root compression: a light and electron microscopic study. Spine (2008) vol. 33 (7) pp. 716-23
4. Ellis RF, Hing WA. Neural mobilization: a systematic review of randomized controlled trials with an analysis of therapeutic efficacy. The Journal of Manual & Manipulative Therapy (2008) vol. 16 (1) pp. 8-22
5. Cleland JA, Childs JD, Palmer JA, Eberhart S. Slump stretching in the management of non-radicular low back pain: a pilot clinical trial. Manual therapy (2006) vol. 11 (4) pp. 279-86
6. Schafer A, Hall T, Muller G, Briffa K. Outcomes differ between subgroups of patients with low back and leg pain following neural manual therapy: a prospective cohort study. Eur Spine J. DOI 10.1007/s00586-010-1632-2
1. Kobayashi S, Takeno K, Yayama T, Awara K, Miyazaki T, Guerrero A, Baba H. Pathomechanisms of sciatica in lumbar disc herniation: effect of periradicular adhesive tissue on electrophysiological values by an intraoperative straight leg raising test. Spine (2010) vol. 35 (22) pp. 2004-14
2. Grotle M, Brox JI, Glomsrod B, Lonn JH, Vollestad NK (2007). Prognostic factors in first-time care seekers due to acute low back pain. Eur J Pain 11:290–298
3. Kobayashi S, Uchida K, Kokubo Y, Takeno K, Yayama T, Miyazaki T, Nakajima H, Nomura E, Mwaka E, Baba H. Synapse involvement of the dorsal horn in experimental lumbar nerve root compression: a light and electron microscopic study. Spine (2008) vol. 33 (7) pp. 716-23
4. Ellis RF, Hing WA. Neural mobilization: a systematic review of randomized controlled trials with an analysis of therapeutic efficacy. The Journal of Manual & Manipulative Therapy (2008) vol. 16 (1) pp. 8-22
5. Cleland JA, Childs JD, Palmer JA, Eberhart S. Slump stretching in the management of non-radicular low back pain: a pilot clinical trial. Manual therapy (2006) vol. 11 (4) pp. 279-86
6. Schafer A, Hall T, Muller G, Briffa K. Outcomes differ between subgroups of patients with low back and leg pain following neural manual therapy: a prospective cohort study. Eur Spine J. DOI 10.1007/s00586-010-1632-2