Reaching everyone through a blog isn't easy. So for about 6 months now I've been writing a monthly newsletter along with my noigroup team which discusses lots of different topics - making them relevant to both the patient and clinician.
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Wednesday, July 23, 2008
Tuesday, December 18, 2007
'Neurogenic' iliotibial band syndrome
One of the most fascinating things about neurodynamic testing is the continual challenges it creates about the basis of certain syndromes. In earlier blogs, we have suggested that plantar fasciitis may not all be in the fascia, but another syndrome worthy of more careful analysis is ITB band syndrome.
I have noted that sometimes in the slump knee bend test (see figure), that cervical flexion and extension will alter evoked lateral thigh symptoms, the kind that may get labeled as ITB band syndrome.
It is quite interesting when the ITB symptoms and even tightness, evaporate before your eyes and in your hands. It does suggest that in some cases there is a neurogenic component to ITB syndrome, maybe in the fascia but more likely spinal or even thoracic. From the clinical angle, the test is certainly worth performing.
Fig 11.3A From Butler DS 2000 The Sensitive Nervous System, Noigroup, Adelaide
I have noted that sometimes in the slump knee bend test (see figure), that cervical flexion and extension will alter evoked lateral thigh symptoms, the kind that may get labeled as ITB band syndrome.
It is quite interesting when the ITB symptoms and even tightness, evaporate before your eyes and in your hands. It does suggest that in some cases there is a neurogenic component to ITB syndrome, maybe in the fascia but more likely spinal or even thoracic. From the clinical angle, the test is certainly worth performing.
Fig 11.3A From Butler DS 2000 The Sensitive Nervous System, Noigroup, Adelaide
Monday, December 10, 2007
What about neurapraxia, axonotmesis and neurotmesis?
Many clinicians would have learnt the classification system of peripheral nerve injury listed in the title. It comes from Seddon in 1943. Others may be familiar with the similar Sunderland (1951) system where nerve injury it is graded from 1-5, with 1 being neurapraxia, a conduction block.
However, most clinicians would never use these classifications unless they are working in specialist areas such as peripheral nerve surgery.
What has become apparent, is that there are many nerve injuries which can be painful, and debilitating, yet they may never rate a classification of neurapraxia and rarely show up on nerve conduction studies. Sunderland was aware of this and referred to it as “perversions of function” of nerves and other researchers such as Lundborg (1988) have referred to “pre category 1 classifications”.
It is these “preneurapraxias” which we are likely to find with skilled neurodynamic testing. The neurobiology of the preneurapraxias is related to mid axon abnormal impulse generation, i.e. ion channel accumulation at injured sites along the peripheral nerve. The cardinal sign of these nerve injuries will usually be mechanosensitivity, not failing conduction. They are a possible contribution to a range of syndromes including tennis elbow, de Quervain’s tenosynovitis, plantar fasciitis and hamstring pain. With good handling, clinicians will ‘find’ these pathologies.
Contact us anytime for discussion
However, most clinicians would never use these classifications unless they are working in specialist areas such as peripheral nerve surgery.
What has become apparent, is that there are many nerve injuries which can be painful, and debilitating, yet they may never rate a classification of neurapraxia and rarely show up on nerve conduction studies. Sunderland was aware of this and referred to it as “perversions of function” of nerves and other researchers such as Lundborg (1988) have referred to “pre category 1 classifications”.
It is these “preneurapraxias” which we are likely to find with skilled neurodynamic testing. The neurobiology of the preneurapraxias is related to mid axon abnormal impulse generation, i.e. ion channel accumulation at injured sites along the peripheral nerve. The cardinal sign of these nerve injuries will usually be mechanosensitivity, not failing conduction. They are a possible contribution to a range of syndromes including tennis elbow, de Quervain’s tenosynovitis, plantar fasciitis and hamstring pain. With good handling, clinicians will ‘find’ these pathologies.
Contact us anytime for discussion
Friday, November 16, 2007
Adrenaline sensitive peripheral nerves and the amazing ion channel turnover
About 20 or more years ago, some juicy basic research demonstrated what most aware clinicians and many patients already knew – that injured peripheral neurones were sensitive to adrenaline, or simply, – stress can make a peripheral nerve fire. More recent research in the last 10 years has shown that in the dorsal root ganglia, injured neurones will express more adrenaline sensitive channels and sympathetic fibres will actually sprout allowing more adrenaline to dribble onto the channels (For a reviews see Ramer et al 1999 and/or Pertovaara 2006).
If you combine this with two facts, (a) ion channels are produced in response to need, thus adrenaline sensitivity is the brain’s response to stress and (b) the ion channels will only be in situ for a day or two before they die and are replaced, the simple follow on is that reduction of stress can have a very rapid influence on the sensitivity of peripheral nerves.
Most clinicians will know of the patient who returns for their second visit feeling much better, although little ‘therapy’ might have been carried out or had time to really influence the problems. The probable basis of the improvement was that the clinical intervention was helpful and threat reducing (call it placebo if you wish) resulting in a powerful alteration in billions of ion channels as neural tissue returned to pre-stress ion channel numbers and kind. And of course nerves will move and slide better if the adrenaline reactivity is reduced.
Ramer MS et al (1999) Pain Suppl 6 S111-S120
Pertovaara A (2006) Progress in Neurobiology 80 (2) 53-83
If you combine this with two facts, (a) ion channels are produced in response to need, thus adrenaline sensitivity is the brain’s response to stress and (b) the ion channels will only be in situ for a day or two before they die and are replaced, the simple follow on is that reduction of stress can have a very rapid influence on the sensitivity of peripheral nerves.
Most clinicians will know of the patient who returns for their second visit feeling much better, although little ‘therapy’ might have been carried out or had time to really influence the problems. The probable basis of the improvement was that the clinical intervention was helpful and threat reducing (call it placebo if you wish) resulting in a powerful alteration in billions of ion channels as neural tissue returned to pre-stress ion channel numbers and kind. And of course nerves will move and slide better if the adrenaline reactivity is reduced.
Ramer MS et al (1999) Pain Suppl 6 S111-S120
Pertovaara A (2006) Progress in Neurobiology 80 (2) 53-83
Friday, November 9, 2007
Pinched nerves
In neurodynamic theory, much emphasis is placed upon testing nerves via elongation. The vascular, mechanical and emotional challenges of a neurodynamic test are likely to reproduce symptoms from active impulse generating sites in peripheral nerves. However, perhaps forgotten, is the effect of a pinch on nerves. For example, sometimes cervical extension and lateral flexion can pinch nerve roots (Spurling’s test), and wrist flexion can pinch the median nerve (Phalen’s test). Hip flexion pinching the femoral nerve is another example.
If you note pinch based symptoms in your patients, which can be reasoned to be peripheral neurogenic in origin, then it is logical that the structure around the neural structure may be unhealthy. This could be facet joint arthritic changes in the case of nerve roots, or swollen carpal canal contents in the case of median nerve changes in the carpal tunnel. The surrounding tissues would be logical targets of therapy.
'Pinch pains' are often very sudden, even shocking, and if repeated may lead to fearful avoidance of the pinching movement. Secondary changes in other tissues and brain representations may follow.
The public often talks about 'pinched nerves' and the notion may be worth a rethink by clinicians.
If you note pinch based symptoms in your patients, which can be reasoned to be peripheral neurogenic in origin, then it is logical that the structure around the neural structure may be unhealthy. This could be facet joint arthritic changes in the case of nerve roots, or swollen carpal canal contents in the case of median nerve changes in the carpal tunnel. The surrounding tissues would be logical targets of therapy.
'Pinch pains' are often very sudden, even shocking, and if repeated may lead to fearful avoidance of the pinching movement. Secondary changes in other tissues and brain representations may follow.
The public often talks about 'pinched nerves' and the notion may be worth a rethink by clinicians.
Wednesday, October 24, 2007
Structural differentiation
A key element of examination of the physical health and sensitivity of the nervous system (neurodynamics) is structural differentiation (SD). Based on the fact that the nervous system is a continuum, the aim of SD is to provide a clinical diagnosis of whether or not the nervous system is physically compromised in a pain state.
Two examples are below. If spinal flexion hurts in the lumbar spine and neck extension relieves evoked responses, then the inference is that the nervous system is physically compromised, although further clinical data will be need to ascertain where the compromise is. Note that the lumbar and thoracic spines have not been moved only the neck. In the second example, stretch of the upper trapezius muscle could be mechanically loading neural and muscle tissue. If the response is enhanced with the elbow extended, the inference is that neural tissues may be physically compromised.
Fig 10.4 From Butler DS 2000 The Sensitive Nervous System, Noigroup, Adelaide
Michel Coppieters (2006) and colleagues at the University of Queensland carried out a nice piece of cadaveric research on structural differentiation at the ankle. They demonstrated that hip flexion will increase the strain in the tibial nerve at the ankle without altering the strain on the plantar fascia – can you see the diagnostic possibilities here with plantar fasciitis? Clinicians who use the slump test to assist in analysis of plantar fasciitis may have noted that neck movement can alter “plantar fasciitis” symptoms.
It would be nice if it was all that easy! Remember – SD is crude, it calls for skilled manual handling and results need to be taken with other clinical data. And while clear cut responses may occur in pain states involving peripheral neural tissues, it will be a bit more complex and a clinical headache where central sensitisation is a clinical feature. For example, traditional SD teaching is that if ankle dorsiflexion increases lumbar or pelvic responses evoked by a SLR, then “its neural – something is tight or stuck” . However, with central sensitisation, the addition of ankle dorsiflexion could just provide more normal movement input adding to an exiting barrage into the CNS. In future blogs, I will discuss central sensitisation and physical examination of neural tissues.
Talk to me anytime…b1@noigroup.info
Coppieters, M. W., A. M. Alshami, et al. (2006). "Strain and excursion of the sciatic, tibial and plantar nerves during a modified straight leg raise test." J Orthop Res 24: 1883-1889.
Two examples are below. If spinal flexion hurts in the lumbar spine and neck extension relieves evoked responses, then the inference is that the nervous system is physically compromised, although further clinical data will be need to ascertain where the compromise is. Note that the lumbar and thoracic spines have not been moved only the neck. In the second example, stretch of the upper trapezius muscle could be mechanically loading neural and muscle tissue. If the response is enhanced with the elbow extended, the inference is that neural tissues may be physically compromised.
Fig 10.4 From Butler DS 2000 The Sensitive Nervous System, Noigroup, Adelaide
Michel Coppieters (2006) and colleagues at the University of Queensland carried out a nice piece of cadaveric research on structural differentiation at the ankle. They demonstrated that hip flexion will increase the strain in the tibial nerve at the ankle without altering the strain on the plantar fascia – can you see the diagnostic possibilities here with plantar fasciitis? Clinicians who use the slump test to assist in analysis of plantar fasciitis may have noted that neck movement can alter “plantar fasciitis” symptoms.
It would be nice if it was all that easy! Remember – SD is crude, it calls for skilled manual handling and results need to be taken with other clinical data. And while clear cut responses may occur in pain states involving peripheral neural tissues, it will be a bit more complex and a clinical headache where central sensitisation is a clinical feature. For example, traditional SD teaching is that if ankle dorsiflexion increases lumbar or pelvic responses evoked by a SLR, then “its neural – something is tight or stuck” . However, with central sensitisation, the addition of ankle dorsiflexion could just provide more normal movement input adding to an exiting barrage into the CNS. In future blogs, I will discuss central sensitisation and physical examination of neural tissues.
Talk to me anytime…b1@noigroup.info
Coppieters, M. W., A. M. Alshami, et al. (2006). "Strain and excursion of the sciatic, tibial and plantar nerves during a modified straight leg raise test." J Orthop Res 24: 1883-1889.
Wednesday, October 17, 2007
Reflections on the Upper Limb Neurodynamic Test (ULNT)
It is worth reflecting on a test now widely used in clinical diagnosis and therapy within physical therapy, yet still with little attention outside the world of physical therapy.
Taken from Figs 12.2D, 12.2E, 12.2F, 12.2G From Butler DS 2000 The Sensitive Nervous System, Noigroup, Adelaide
The Perth based physiotherapist, Bob Elvey, via research and teaching was instrumental in getting the test integrated into manual therapy management in the late 1970s and 80s. Bob always had an emphasis on skilled handling, and perhaps a reason for slow integration outside physiotherapy is that it can be difficult for unpracticed hands. I always liked a description of the test as the “straight leg raise of the arm” (Kenneally et al., 1988) and hoped that this would enhance clinical integration.
In early writings (Butler, 1991), a fairly peripheral and mechanistic approach to the test was taken; the neuroscience revolution in knowledge was yet to unfold. These days we realize that the responses to the test (and also the performance of the test) will be dictated by the underlying pathobiological mechanisms. Simply said, if a person has peripheral neurogenic mechanisms related to scarring, pinching, blood around a nerve, or ” mechanosensitive hot spots” etc in the peripheral nervous system, then the test is very likely to reproduce these problems and identify a neural tissue health issue. However in other pain states where central mechanisms are dominating (eg fibromyalgia), the test needs to be seen as a test of movement rather than a test of damaged tissues.
In summary, the ULNT is a test of all tissues in the upper limb with a preferential focus on the median nerve and its associated plexus and roots. It is also a test of the neural representational stability of the ULNT movement and the meaning of the movement to that person.
For optimal test performance and analysis see “The Sensitive Nervous System” or the neurodynamics DVD. For up to date research on aspects of the test and neurodynamics, Pubmed Coppieters MW.
Butler, D. S. (1991). Mobilisation of the nervous system. Melbourne: Churchill Livingstone.
Kenneally, M., Rubenach, H., & Elvey, R. (1988). The upper limb tension test: The slr of the arm. In R. Grant (Ed.), Physical therapy of the cervical and thoracic spine. New York: Churchill Livingstone.
Taken from Figs 12.2D, 12.2E, 12.2F, 12.2G From Butler DS 2000 The Sensitive Nervous System, Noigroup, Adelaide
The Perth based physiotherapist, Bob Elvey, via research and teaching was instrumental in getting the test integrated into manual therapy management in the late 1970s and 80s. Bob always had an emphasis on skilled handling, and perhaps a reason for slow integration outside physiotherapy is that it can be difficult for unpracticed hands. I always liked a description of the test as the “straight leg raise of the arm” (Kenneally et al., 1988) and hoped that this would enhance clinical integration.
In early writings (Butler, 1991), a fairly peripheral and mechanistic approach to the test was taken; the neuroscience revolution in knowledge was yet to unfold. These days we realize that the responses to the test (and also the performance of the test) will be dictated by the underlying pathobiological mechanisms. Simply said, if a person has peripheral neurogenic mechanisms related to scarring, pinching, blood around a nerve, or ” mechanosensitive hot spots” etc in the peripheral nervous system, then the test is very likely to reproduce these problems and identify a neural tissue health issue. However in other pain states where central mechanisms are dominating (eg fibromyalgia), the test needs to be seen as a test of movement rather than a test of damaged tissues.
In summary, the ULNT is a test of all tissues in the upper limb with a preferential focus on the median nerve and its associated plexus and roots. It is also a test of the neural representational stability of the ULNT movement and the meaning of the movement to that person.
For optimal test performance and analysis see “The Sensitive Nervous System” or the neurodynamics DVD. For up to date research on aspects of the test and neurodynamics, Pubmed Coppieters MW.
Butler, D. S. (1991). Mobilisation of the nervous system. Melbourne: Churchill Livingstone.
Kenneally, M., Rubenach, H., & Elvey, R. (1988). The upper limb tension test: The slr of the arm. In R. Grant (Ed.), Physical therapy of the cervical and thoracic spine. New York: Churchill Livingstone.
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