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Clinical instability of the lumbar spine

Clinical Instability of the Lumbar Spine

by Martin Krause

Pathological basis, diagnosis, and conservative management

Contemporary approaches to viewing stability create a belief that all control occurs around the neutral zone and hence exercise must be prescribed which maintain the neutral spine. Although this is plausible and potentially true for a structurally unstable spine, and is a useful approach during an acute inflammatory, or seriously splinted by muscle spasm pathology, it is probably a misdirected concept in subacute and chronic pathology. Our rational in the past is to correct what we believe to be incorrect. However, what if the person has a directional preference for recovery? A direction which encourages movement away from the painful pattern rather than towards it. Should this be encouraged to promote blood flow, reduce movement anxiety and engage the dynamic stabilising biomechanics? Afterall, the multifidus has been considered the 'sensor of the spine', yet logic would dictate that it cannot sense any movement, if the spine doesn't move out of it's neutral zone.

Introduction to the stabilizing system

• Passive system comprising the vertebrae, intervertebral discs, zygapophysial joints and ligaments
• The active system comprising the muscles and tendons surrounding and acting on the spinal column
• The neural system comprising the peripheral nerves and central nervous system which direct and control the active system in providing dynamic stability (Panjabi 1992).

Bergmark (1989) hypothesized the presence of two muscle systems that act in the maintenance of spinal stability
• The global system consisting of large torque producing muscles that act on the trunk and spine without directly attaching to it. Tendon to be direction-specific in their stabilising role and therefore produce stability through compression of the vertebrae
• The segmental ‘local’ muscle system consisting of muscles attaching directly to the lumbar vertebrae and are responsible for providing segmental stability and directly controlling the lumbar segments. Tend to be tonically active at low loads and tend to have a multi-directional stabilizing function

Co-ordinated patterns of muscle recruitment are essential between the global and local muscle systems to ensure dynamic stability during activities of daily living (Cholewicki & McGill 1996)

Stabilizing system

• The neuromuscular system must provide the necessary compressive forces whilst maintaining the arch like structure of the spine (Aspden 1992)
– The erector spinae and the psoas major are known to significantly increase the compressive load on the lumbar spine (Bogduk 1992) which enhances spinal stiffness and hence stability of the lumbar spine
– The segmental stabilizing role of the multifidus, with separate segmental innervation, acts to maintain the lumbar lordosis and ensure control of individual vertebral segments particularly within the neutral zone (Panjabi et al 1989, Wilke et al 1995). Multifidus also provides proprioceptive information vital for safe functioning of the lumbar spine (Brumagne et al 2000)
– The transverse abdominis and transverse fibres of internal oblique whilst applying some compressive forces to the lumbar spine (McGill & Norman 1987) and pelvis (Richardson et al 2002) are primarily active in providing rotational and lateral stability to the spine via the thoracolumbar fascia while maintaining levels of intra-abdominal pressure (IAP) (Cresswell et al 1992)
– The intra-abdominal pressure mechanism, primarily controlled by the diaphragm, transverse abdominis and pelvic diaphragm also provide an important role in stabilizing the lumbar spine (Aspden 1992, McGill & Norman 1987)
– Pre-activation of the stabilizing muscles provides a base upon which the torque-producing muscles can act safely (Cresswell et al 1994, Hodges & Richardson 1996)
– Inappropriate timing or altered control of these complex mechanisms can result in tissue damage rather than stability to the motion segment (Gardner-Morse et al 1995, McGill & Sharratt 1990)
– Lumbar spine is more vulnerable to instability at low loads (Cholewicki & McGill 1996) and under such conditions only 1-3% MVC may be sufficient to ensure dynamic stability
– During power lifting maintenance of the neutral zone prevents end of range loading tissue strain (McGill & Cholewicki 1992, 2001) through the maintenance of intra abdominal pressure through the co-contraction of loacl and global muscles


Dysfunction of the neuromuscular system

• Disruption in the patterns of co-recruitment within and between different muscle synergies (O’Sullivan et al 1997)
• Multifidus and transverse abdominis adversely affected during low back pain (Hides et al 1996), chronic low back pain (Daneels et al 2000) and lumbar instability (Lindgren et al 1993, Sihvonen & Partanen 1990)
• The manner of multifidus dysfunction may vary with different lumbar pathology (Daneels et al 2000; Stokes et al 1992)
• Compensatory substitution strategy to adopt global muscles systems for stabilization with high levels of intra-abdominal pressure (O’Sullivan 2002)
• Changes in the neural control strategy affecting timing of patterns of co-contraction, balance, reflex and righting responses (O’Sullivan et al 1997)
• Generalised changes to trunk musculature such as loss of strength, endurance and muscle atrophy are likely the result of disuse and inactivity, whereas the localised muscle atrophy may be the result of either motor or sensory nerve damage, reflexogenic excitation or inhibition of the muscles proximal to the site of pathology (Stokes et al 1992) and inappropriate mechanoceptive and proprioceptive input, leaving the subject biomechanically vulnerable (O’Sullivan 2005)

Movement based classification of pain disorders

• Mobility of spinal segments in isolation is not predictive or diagnostic in classifying pain disorders
• “It is the association between the mobility and control of the spinal segment, and its relationship to the pain disorder, which appears to be critical” (O’Sullivan 2005)

Peter O'Sullivan has put forward 3 sub-categories
• "Pain disorders associated with movement impairments are associated with a loss of normal physiological movement of lumbo-pelvic mobility, and abnormally high levels of muscle guarding and co-contraction of lumbopelvic muscles with generation of intra-abdominal pressure....[resulting in].....excessive force closure"
• "Pain disorders associated with control impairment are associated with no impairment to the mobility of the symptomatic spinal segment, but rather present with impairments or deficits in control of the symptomatic spinal
segment pressure...[resulting in]....reduced force closure"
• "......mal-adaptive movement and motor patterns result in chronic abnormal tissue loading and ongoing pain and distress......These disorders are also invariably associated with non-organic factors but these factors do not dominate the disorder, leaving them more amenable to physiotherapy intervention based on a cognitive behavioural motor learning model" (5th Interdisciplinary World Congress on Low Back and Pelvic Pain, Melbourne, 2004, Australia p132)

Clinical instability

“Clinical instability of a spinal segment represents a loss of functional competence of a spinal segment within its neutral zone of motion with a resulting loading and movement based pain disorder associated with a loss of control” (O’Sullivan 2005)

Pain associated with a functional loss of neutral zone control may manifest in
1. Through range movement pain due to non-physiological motion of the spinal segment
2. Loading based pain due to non-physiological loading of the spinal segment
3. End of range pain or overstrain due to repetitive strain of the spinal motion segment at the end of range (O’Sullivan et al 2003)
One of the problems in the diagnosis of clinical instability lies in the difficulty measuring accurately the functional control of the spinal segment within its neutral zone
Radiological findings only become significant when they can be correlated with clinical findings
50% of people with clinical instability report this to have occurred after a single episode of back pain, whereas the other 50% reported a gradual onset in relation to multiple minor events (O’Sullivan 1997)

Clinical Instability – physical presentation

• Active range of movement reveals good spinal mobility but with aberrant spinal motion associated with a painful arc with or without end range pain (O’Sullivan 1997)
• The aberrant movement is associated with sudden acceleration, hesitation or lateral movement within the mid range of spinal motion
• Segmental hinging of the symptomatic segment is a common feature
• Assistance of movement with the hands is another common feature
• Abolition or significant reduction in pain with the contraction of the transverse abdominis
• Absence of abnormal neurological features (O’Sullivan 1997)
• Confirmation of the abnormality is essential through passive physiological motion testing where flexion/extension and rotation were reported to be most sensitive to detect excessive intersegmental motion.
• For spondylolisthesis and spondylosis excessive motion was detected at the level above the pars defects (O’Sullivan 1997)
• All the physical examination findings have also been reported by Nachemson (1985) and Kirkaldy-Willis 1983), however the sensitivity and specificity and predictive value of these signs are largely unproven (Nachemson 1991; O’Sullivan 2005)

Clinical Instability – neuromuscular examination

• Neuromuscular examination determines the relationship between the motor control of the spinal segment and the pain disorder
• Posture and movement analysis
1. Analysis of aggravating and easing postures and functional movements of the lumbo-pelvic region. Need to determine if there is a strategy of dynamic postural stabilisation and secondly identify whether there is a directional emphasis to the pain disorder
2. Specific movement and postural loading tests dependent upon step 1 and involve tests of spinal proprioception and thoracolumbar control. Here the therapist attempts to correct the posture, movement pattern or specific activation of stabilising muscles then this confirms or negates the notion that motion control affects the pain disorder (O’Sullivan 2005)
3. Specific muscle tests – non functional cognitive tests and therefore lack specificity
– Pelvic floor and transverse abdominal wall (supine, side-lying, sitting)
– Lumbar multifidus with co-contraction of transverse abdominal wall muscles in neutral lordosis (prone, side-lying, four point kneeling, sitting)
– Gluteus maximus (prone)
– Iliopsoas (hip flexion sitting, anterior pelvic rotation in supine and sitting)
– Hip flexor test (Thomas position)

Directional patterns of clinical instability (Peter O'Sullivan)

1. Flexion pattern
– Most common pattern
– Loss of segmental lumbar lordosis at the level of the unstable motion segment. Sometimes noticeable in standing , accentuated in sitting postures with a tendency to hold pelvis in a degree of posterior pelvic tilt.
– Loss of segmental lordosis is accentuated in flexed postures and is usually associated with increased erector spinae tone in the upper lumbar/low thoracic spine with an associated increase in lordosis in the thoracic spine
– Movement into forward bending tends to be initiated at and flex more at the segmental level than at the adjacent levels where there is a tendency to hold the upper lumbar/low thoracic in lordosis, with an associated lack of hip flexion
– Arc of pain into flexion and a tendency to use the hands to return from flexion
– During backward bending there is a tendency to extend above the symptomatic segment
– Inability to anterior pelvic tilt independently of upper lumbar and low thoracic extension
– Jerky staccato movements rather than smooth controlled ones
– Movement tests of squatting, sit to stand, sitting with knee extension and hip flexion reveal an inability to control segmental lordosis and an anterior pelvic tilt position, with a tendency to flex and posterior pelvic tilt instead
– Inability to reposition within the neutral zone and a tendency to over-shoot into flexion
– Inability to activate lumbar multifidus and psoas in co-contraction with the transverse abdominal wall
– Unable to initiate a start position of neutral lumbar spine in 4-point kneeling and sitting, and particular difficulty initiating an anterior pelvic tilt and lordose the low lumbar spine
– Attempts to activate these muscles are commonly associated with Valsalva manoeuvres and bracing of abdominal muscle with loss of breathing control and excessive co-activation of the thoracic erector spinae

2. Lateral shift pattern
– Usually associated with a flexion/lateral shift movement disorder
– In the history commonly complain of an injury into flexion and rotation
– Commonly relate to difficulty reaching and rotating in one direction associated with flexion
– Report relief in extended or lordotic postures
– Report the with minimal precipitation their spine may deviate into a lateral shift position in flexion
– Loss of segmental lumbar lordosis at the affected level with an associated lateral shift
– Atrophy/absence of the lumbar multifidus muscle on the contralateral side to the shift
– Shift is accentuated when standing on the ipsilateral foot of the shift during gait and Stork test
– Tendency to deviate at mid-range flexion and is commonly associated with an arc of pain
– Side bending in the direction of the shift reveals a translatory motion rather than side bending at the unstable level
– Dominant activation of the lumbar multifidus and thoracic erector spinae on the ipsilateral side of the shift and a loss of rotatory and lateral trunk control seen in 4-point kneeling whilst flexing one arm and supine lying lateral leg lowering
– Single leg standing reveals an inability to load the thoracolumbar spine vertically over the pelvis
– Sit-to-standing and squatting reveal a tendency to lateral trunk shift
– Inability to reposition the pelvis with a tendency to overshoot into flexion and lateral deviation
– Attempts to dynamically stabilize the lumbar spine tend to be carried out by dominant activation of the lumbar erector spinae, quadratus lumborum and in some cases the lumbar multifidus on the side of the shift along with the diaphragm and abdominal muscles

3. Active extension pattern
• Lumbar spine is held actively into extension with high levels of concentric muscle activity from the erector spinae and iliopsoas
• Commonly report a single or repetitive extension mechanism of injury, however sometimes they report a flexion incident where they actively fix their spines into extension
• Provocative activities include, standing, erect sitting, forward bending postures (where there is a tendency to hold the lumbar spine in fixed extension), carrying out overhead activities, and an inability to walk fast, run or swim
• Symptoms are relieved in flexion postures such as crook lying in supine
• Segmental hyperlordosis at the unstable level , the pelvis is often in anterior pelvic tilt and the thorax is positioned forward of the pelvis
• Forward bending reveal excessive hip flexion and a tendency to maintain the lumbar hyperlordosis with or without a sudden loss of hyperlordosis at mid-range accompanied by an arc of pain
• Return to neutral accompanied by hyperlordosis and a tendency to need to use the hands
• In sitting there is a tendency to maintain lumbar lordosis and difficulty in posterior pelvic tilting
• Inability to posterior pelvic without the use of hip flexors, rectus abdominis, and external obliques in standing and supine lying
• Hip extension with knee flexion in prone reveals a tendency to hyperextend at the unstable segment with loss of co-contraction of the abdominals and inner range activation of erector spinae and iliopsoas
• Position sense in sitting and 4 point kneeling reveal a tendency to overshoot into extension
• Inability to co-contract segmental lumbar multifidus with transverse abdominal muscles in a neutral lumbar posture, tendency to hyperextend and over-activate segmental extensors, abdominals and inability to control diaphragmatic breathing

4. Passive Extension pattern
• Present with very low tone of the lumbar multifidus, iliopsoas and erector spinae muscles
• Mechanism of injury associated with extension. Similarly aggravating positions involve extension. Flexion positions relieve symptoms
• Unlike the ‘active’ group the ’passive’ group do not report aggravation of symptoms with forward bending activities and postures as they do reverse their lordosis
• Tendency to sway the thorax posterior to their pelvis, with resultant ‘hinging’ of the unstable spinal segment into extension
• This ‘passive’ posture results in deactivation of transverse abdominal muscles, multifidus, gluteals, and erector spinae, with increased tonic activation of the rectus abdominis and external oblique muscles (O’Sullivan 2002)
• In sitting, unlike the ‘active’ group they sit in a slumped posture
• Position sense testing reveals a tendency to overshoot into extension
• Inability to posterior pelvic tilt without dominant activity of the upper abdominal wall and flexion of the thorax


5. Multidirectional pattern
• Most debilitating with high levels of pain,
• Usually of traumatic onset,
• Excessive segmental shifting and hinging patterns may be observed in all movement
directions

Clearly, there are some movement patterns which are best avoided, as they represent the potential to create neurological compromise. Other patterns to avoid are those which initially were avoided in the acute stage and then later in the subacute phase become the chronic irritating movement pattern. Hence, in those cases the logical arguement is to use the directional preference of movement which reduces pain, rather than the inherent movement (motor pattern) which keeps on biomechanically generating more pain.

13 September 2012


 

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However, the following clinical variables are considered factors at increasing risk. These include prior history of concussion, sex (females more prominant), younger age, history of cognitive dysfunction, and affective disorders such as anxiety and depression (Leddy et al 2012, Sports Health, 4, 2, 147-154). Unlike the 'old days' which recommended a dark room and rest for several weeks post concussion, the consensus appears to be a graded return to exercise in order to restore metabolic homeostasis. Incredibly, highly trained young individuals can find even exercises in bed extremely demanding. Kozlowski et al (2013, J Ath Train, 48, 5, 627-635) used 34 people 226 days post injury to conclude significant physiological annomalies in response to exercise which may be the result of 'diffuse cerebral swelling'. Researchers have noted lower systolic and higher diastolic blood pressure in PCS (Leddy et al 2010, Clin J Sports Med, 20, 1, 21-27). 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Cognitive deficits with school work were reported to becoming more apparent. Assessment using various one leg standing tests employing oscillatory movement aroud the hips and knees for kinetic limb stability and lumbopelvic stability, which had been employed 6 months previously for his Basketball injuries were exhibiting deficits, despite these being 'somewhat good' previously. Physical Examination : cervical and thoracic spine Due to the Joint Hypermobility Syndrome (JHS) it was difficult to ascertain neck dysfunction based on range of movement testing. ROM were unremarkable except for lateral flexion which demonstrated altered intervertebral motion in both directions. Palpation using Australian and New Zealand manual therapy techniques such as passive accessory glides (upslopes and downslopes and traction) exhibited muscles spasms in the upper right cervical spine. Eye - Neck proprioceptive assessment using blind folds and laser pointer also  revealed marked variance from the normal. Repositioning error using the laser pointer with rotation demonstrated marked inability to reposition accurately from the left, tending to be short and at times completely missing the bullseye. Gaze stability with body rotation was NAD. Gaze stability whilst walking displayed some difficulty. Laser pointer tracing of the alphabet was wildly inaccurate. Thoracic ring relocation testing also revealed several annomalies, which may have also accounted for some autonomic dysfunction.  Occulomotor assessment and training Headache : Commonly referred to as cervicogenic headaches, one in five headaches in the general population are thought to be due to the cervical spine. The Upper Cervical Spine is particularly vulnerable to trauma because it is the most mobile part of the vertebral column, with a complex proprioceptive system connecting the vestibular apparatus and visual systems. It also coincides with the lower region of the brainstem and fourth ventricle. The brainstem houses many neurones associated with autonomic responses to pain and balance. Imaging of the fourth ventricle for swelling of the 'tonsils' and Arnold Chiari malformations are recommended when symptoms persist. In particular, children and adolescents are more vulnerable to neck contusions due to the proportionately larger head and less developed musculature. Cervical vertigo and dizziness after whiplash can mimic symptoms of PCS.. Mechanoreceptor dysfunction and vertebrobasilar artery insufficiency should be part of the differential diagnosis. Mechanical instability of the Upper Cervical Spine should also not be missed. Cervicogenic Headaches Further Interventions : Neurocognitive rehabilitation of attention processes. Psychological intervention using cognitive behavioural therapy (CBT). Neuro-opthalmologist to assess and treat smooth pursuit eye tracking. Naturopath for food intolerances and dietician for the optimisation of diet. Diet :  In cases with chronic fatiguing factors, nutrition can be become a vital aspect into the reparative process. This may include energy and mineral rich foods such as bananas, green leafy vegetables for iron and magnesium (200-300mg), oranges for vitamin C (anit-oxidant and helps with the absorption of iron), anti-oxidant rich foods such as EPA/DHA (1000mg) fish oil, curcumin (tumeric), Cats Claw, Devils Claw, Chia seeds, fruits of the forest (berries), and CoQ10 with Vitamin B. Folate and Ferritin levels should also be checked. Calorific energy intake should balance with energy exependiture. However, as we are often dealing with young individuals, as in this case, some form of comfort food may be appropriate such as, nuts, legumes, homus and sushi. Protein intake prior to carbohydrate intake may help ameliorate any blood suger fluctuations due to Glycemic Index factors, however simple carbohydrates (high GI) should be avoided wherever practical. Even oats need to be soaked overnight and cooked briefly, otherwise they become a high GI food and may even affect the absorption of iron. The type of rice used can also influence GI, hence the addition of protein such as fish. Protein supplementations are generally over-used. Daily protein intake should not exceed 1.2g per kg of body weight per day. Dosage for children is less than that for adults. See Nutritional Section of this Site Conclusion  Investigations, into people with persisting PCS, demonstrated that they applied more force over time to control balance. Helmich et al (2016, Med Sc Ex Sp, 48,  12, 2362-2368) proposed that in regard to cognitive processes, the increase of cerebral activation indicates an increase of attention demanding processes during postural control in altered environments. This is relevant in so far as individuals with post concussive symptomatology have a variety of symptoms including headache, dizziness, and cognitive difficulties that usually resolve over a few days to weeks. However, a subgroup of patients can have persistent symptoms which last months and even years. Complications in differential diagnosis, can arise clinically, when neck dysfunction and altered motor control occur concurrently due to both neck and cerebral pathology. For example, Whiplash and other traumatic head and neck injuries can result in pathology to both regions, whereas, more discreet altered cognitive processing from concussion can result in altered neck motor control. Musculoskelatal Physiotherapy can play a vital part in the treatment of neck dysfunction including the re-establishment of occulomotor proprioception and managing localized strength and cardiovascular exercise regimes. A total body, multi-disciplinary approach which is well co-ordinated amongst practitioners is vital to an optimal outcome.    Uploaded : 17 October 2017 Read More
  • Thu 24 Aug 2017

    Pain in the Brain - neural plasticity

    Pain in the Brain and Neural Plasticity by Martin Krause There are several mechanisms that can create a sensation of pain, which has been described as 'an unpleasent sensory and emotional experience in response to perceived or potential tissue damage'. Pain can be the result of peripheral sensitisation from peripheral inflammation, vascular compromise, necrosis, swelling, etc. Importantly, higher centres of the central nervous system not only perceive such sensitization of the peripheral nerve receptors, they can also modulate and control the intensity and tolerability of the perceived sensation through descending modulation at the peripheral receptor and in the spinal cord and through transcortical mechanisms depending on the 'meaning' and 'context given to the pain. Moreoever, the higher centres can create a 'state' of perceived 'threat' to the body through emotions such as fear and anxiety. Rather than the brain acting as a filter of unwanted sensation, in the higher centre induced pain state, rumination and magnification of sensations occur to create a pathological state.  Paradoxically, representation of body parts such as limbs and individual muscles can reduce in perceived size. In such instances the pain doesn't represent the sensation of pathology but rather pain has become the pathology. Hence, the brain generates pain in the brain, where the pain is perceived to be some sort of non-existant inflammatory or pathological sensation in the periphery. Evidence for this neural plasticity comes from imaging studies, where brain white matter structural properties have been shown to predict transition to chronic pain (Mansour et al 2013, Pain, 154, 10, 2160-2168). Specifically, differential structural connectivity to medial vs lateral prefrontal cortex and connectivity between medial prefrontal cortex and nucleus accumbens has been shown in people with persistent low back pain. In this case the back pain becomes the inciting event and given the persons' structural propensity, establishes specific functional coonectivity strength.  further reading Peripheral input is a powerful driver to neuroplasticity. Information gathered by touch, movement and vision, in the context of pain can lead to mal-adaptive plasticity, including the reorganisation of the somatosensory, and motor cortices, altered cortical excitability and central sensitisation. Examples of somatosensory reorganisation come from the work of Abrahao Baptista when investigating chronic anterior knee pain, who not only demonstrated reduced volume of Vastus Medialis but also is cortical translocation to another part of the cortex. ndividuals with patellofemoral pain (PFP) had reduced map volumes and an anterior shift in the M1 representations, greater overlap of the M1 representation and a reduction in cortical peaks across all three quadriceps (RF, VL, VMO) muscles compared with controls.(Te et al 2017 Pain Medicine, pnx036, https://doi.org/10.1093/pm/pnx036)   AKP = anterior knee pain The same researcher (Abrahao Baptista) has shown that maximal tolerable electrical stimulation (eg TENS) of muscles can induce normalisation of the cortical changes through a process called 'smudging'. Transcortical stumilation has also been applied as a cortical 'primer' prior to the application of more traditional therapy such as motor re-training, exercise, and manipulation. Body illusions are another novel way to promote the normalisation of cortical function through adaptive neuroplasticity. Examples come from people with hand athritis, whose perception of their hand size is underestimated (Gilpin et al 2015 Rheumatology, 54, 4, 678-682). Using a curved mirror, similar to that in theme parks, the visual input can be increased to perceive the body part as larger (Preston et al 2011 DOI: 10.1093/rheumatology/ker104 · Source:PubMed ) . Irrespective of size, watching a reflection of the hand while performing synchronised movements enhances the embodiment of the reflection of the hand (Whitkopf et al 2017, Exp Brain res, 23, 5, 1933-1944). These visual inputs are thought to affect the altered functional connectivity between areas of the brain thereby affecting the 'pain matrix'. Another, novel way of looking at movement and pain perception is the concept of the motor engram. This has been defined as motor skill acquisition through the modification and organisation of muscle synergies into effective movement sequences. The learning process is thought to be acquired as a child through experientially based play activity. The specific neural mechanisms involved are unknown, however they are thought to include motor map topography reflecting the capacity for skilled movement reorganisation of motor maps in a manner that reflects the kinematics of aquired skilled movement map plasticity is supported by a reorganisation of cortical microcircuitry involving changes in synaptic efficacy motor map integrity and topography are influenced by various neurochemical signals that coordinate changes in cortical circuitry to encode motor experience (Monfils 2005 Neuroscientist, 11, 5, 471-483). Interestingly, it is an intriguing notion that accessing motor engrams from patterns aquired prior to the pain experience might lead a normalisation of brain activity. My personal experience of severe sciatica with leg pain, sleepness nights and a SLR of less than 30 degrees, happened to coincide with training my 9 year old sons soccer training. I was noticing that the nights after i trained the children, I slept much better and my range of movement improved. I commenced a daily program of soccer ball tricks which i had been showing the kids, including 'juggling', 'rainbows' and 'around the worlds'. Eventually, I even took up playing soccer again after a 30 year abscence from the sport. Other than new activity related pain issues (DOMS), four years on, the sciatica hasn't returned. I can only conclude that this activity activated dormant childhood motor engram, worked on global balance, mobilised my nerve, encouraged cross cortical activity and turned my focus into finctional improvement. Further explainations for my expereience comes from evidence suggesting that a peripheral adaptive pain state is initiated, whereby transcortical inhibiton occurs by the contralaleral hemisphere to the one which controls the affected limb. Additionally, excitation cortical (M1) drive of the muscles of the contralateral limb to the one which is in pain also occurs. In such cases re-establishement of motor drive to the affected side is important. In terms of tendon rehabilitation, external audtory and visual cues using a metronome have been employed and are showing promising results (Ebonie Rio et al 2017 Personal communication). In terms of my experience with the soccer ball tricks, the external visual cues and the cross talk from using left and right feet, head, shoulders, and chest during ball juggling manouvers, whilst calling the rhythm to the kids may have been the crucial factor to overcome the dysfunctional brain induced pain - muscle inco-ordination cycle, which I was in. Additionally, I was cycling which allowed me to focus on motor drive into the affected.limb. However, work by Lorrimer Moseley on CRPS has established that 'brain laterality' must be established before commencing trans-cortical rehabilitation techniques. Lorrimer's clinical interventions use 'mirror imaging' techniques which are only effective once the patient is able to discriminate the left and right sides of the affected body parts, presented visually, in various twists and angles.   Alternatively, the altered pain state can result in a hostage like situation, whereby the pain takes control. Similar to the 'Stockholm Syndrome' where the hostage begins to sympathise with their captors, so do some peoples brain states, where it begin to sympathise with the pain, creating an intractable bondage and dysfunctional state. One screening question which may reflect commitment to the process of rehabilitatation is to question whether they were able to resist the cookie jar when they were a child? Or were they committed to any sporting endeavours as a child? This may give some indication for the presence of motor engrams which can be used to overcome dysfunctional pain induced muscle synergies (neurotags), but also indicate an ability to be self disciplined, as well as being able to reconcile and identify goal oriented objectives, in spite of the cognitive pain processes? Remember that neurons that fire together, wire together. Uploaded : 18 October 2017 Read More
  • Thu 03 Aug 2017

    Sickle Cell Trait and Acute Low Back Pain

    Researchers believe that lumbar paraspinal myonecrosis (LPSMN) may contribute to the uncommon paraspinal compartment syndrome and that sickle cell trait (SCT) may play a role. Sustained, intense exertion of these lumbar paraspinal muscles can acutely increase muscle size and compartment pressure and so decrease arterial perfusion pressure. This same exertion can evoke diverse metabolic forces that in concert can lead to sickling in SCT that can compromise perfusion in the microvasculature of working muscles. In this manner, they believe that SCT may represent an additional risk factor for LPSMN. Accordingly, they presented six cases of LPSMN in elite African American football players with SCT. See link below http://journals.lww.com/acsm-msse/Fulltext/2017/04000/Acute_Lumbar_Paraspinal_Myonecrosis_in_Football.1.aspx Read More
  • Thu 03 Aug 2017

    Ibuprofen, Resistance Training, Bone Density

    Taking Ibuprofen immediately after resistance training has a deleterious effect on bone mineral content at the distal radius, whereas taking Ibuprofen or undertaking resistance training individually prevented bone mineral loss. http://journals.lww.com/acsm-msse/Fulltext/2017/04000/Effects_of_Ibuprofen_and_Resistance_Training_on.2.aspx Read More
  • Tue 11 Jul 2017

    Mitochondrial Health and Sarcopenia

    The aging process (AKA 30 years of age onwards), in the presence of high ROS (reactive oxygen species) and/or damaged mitochondrial DNA, can induce widespred mitochondrial dysfunction. In the healthy cell, mitophagy results in the removal of dysfunctional mitochondria and related material. In the abscence of functional removal of unwanted mitochondrial material, a retrograde and anterograde signalling process is potentially instigated, which results in both motor neuronal and muscle fibre apoptosis (death) (Alway, Mohamed, Myers 2017, Ex Sp Sc Rev, 45, 2, 58-69). This process is irreversible. Investigations in healthy populations, have shown that regular exercise improves the ability to cope with regular oxidative stress by the buffering and 'mopping up' of ROS agents which are induced as a result of exercise. It is plausible and highly probable that regular exercise throughout life can mitigate against muscle fibre death (Sarcopenia). Importantly, this process of muscle fibre death can commence in the 4th decade of life. and be as much as 1% per year. Reduction of muscle mass can result in immune and metabolic compromise, including subclinical inflammation, type II diabetes as well as the obvious reduction in functional capacity for activities of daily living. Published 11 July 2017 Read More
  • Thu 22 Dec 2016

    Ehlers Danlos Syndrome

    Is your child suffering Ehlers Danlos Syndrome? Hypermobile joints, frequent bruising, recurrent sprains and pains? Although a difficult manifestation to treat, physiotherapy can help. Joint Hypermobility Syndrome (JHS) by Martin Krause When joint hypermobility coexists with arthralgias in >4 joints or other signs of connective tissue disorder (CTD), it is termed Joint Hypermobility Syndrome (JHS). This includes conditions such as Marfan's Syndrome and Ehlers-Danlos Syndrome and Osteogenesis imperfecta. These people are thought to have a higher proportion of type III to type I collagen, where type I collagen exhibits highly organised fibres resulting in high tensile strength, whereas type III collagen fibres are much more extensible, disorganised and occurring primarily in organs such as the gut, skin and blood vessels. The predominant presenting complaint is widespread pain lasting from a day to decades. Additional symptoms associated with joints, such as stiffness, 'feeling like a 90 year old', clicking, clunking, popping, subluxations, dislocations, instability, feeling that the joints are vulnerable, as well as symptoms affecting other tissue such as paraesthesia, tiredness, faintness, feeling unwell and suffering flu-like symptoms. Autonomic nervous system dysfunction in the form of 'dysautonomia' frequently occur. Broad paper like scars appear in the skin where wounds have healed. Other extra-articular manifestations include ocular ptosis, varicose veins, Raynauds phenomenon, neuropathies, tarsal and carpal tunnel syndrome, alterations in neuromuscular reflex action, development motor co-ordination delay (DCD), fibromyalgia, low bone density, anxiety and panic states and depression. Age, sex and gender play a role in presentaton as it appears more common in African and Asian females with a prevalence rate of between 5% and 25% . Despite this relatively high prevalence, JHS continues to be under-recognised, poorly understood and inadequately managed (Simmonds & Kerr, Manual Therapy, 2007, 12, 298-309). In my clinical experience, these people tend to move fast, rely on inertia for stability, have long muscles creating large degrees of freedom and potential kinetic energy, resembling ballistic 'floppies', and are either highly co-ordinated or clumsy. Stabilisation strategies consist of fast movements using large muscle groups. They tend to activities such as swimming, yoga, gymnastics, sprinting, strikers at soccer. Treatment has consisted of soft tissue techniques similar to those used in fibromyalgia, including but not limited to, dry needling, myofascial release and trigger point massage, kinesiotape, strapping for stability in sporting endeavours, pressure garment use such as SKINS, BSc, 2XU, venous stockings. Effectiveness of massage has been shown to be usefull in people suffering from chronic fatigue syndrome (Njjs et al 2006, Man Ther, 11, 187-91), a condition displaying several clinical similarities to people suffering from EDS-HT. Specific exercise regimes more attuned to co-ordination and stability (proprioception) than to excessive non-stabilising stretching. A multi-modal approach including muscle energy techniques, dry needling, mobilisations with movement (Mulligans), thoracic ring relocations (especially good with autonomic symptoms), hydrotherapy, herbal supplementaion such as Devils Claw, Cats Claw, Curcumin and Green Tee can all be useful in the management of this condition. Additionally, Arnica cream can also be used for bruising. Encouragment of non-weight bearing endurance activities such as swimming, and cycling to stimulate the endurance red muscle fibres over the ballistic white muscles fibres, since the latter are preferably used in this movement population. End of range movements are either avoided or done with care where stability is emphasized over mobility. People frequently complain of subluxation and dislocating knee caps and shoulders whilst undertaking a spectrum of activities from sleeping to sporting endeavours. A good friend of mine, Brazilian Physiotherapist and Researcher, Dr Abrahao Baptista, has used muscle electrical stimulation on knees and shoulders to retrain the brain to enhance muscular cortical representation which reduce the incidence of subluxations and dislocations. Abrahao wrote : "my daughter has a mild EDS III and used to dislocate her shoulder many times during sleeping.  I tried many alternatives with her, including strenghtening exercises and education to prevent bad postures before sleeping (e.g. positioning her arm over her head).  What we found to really help her was electrostimulation of the supraspinatus and posterior deltoid.  I followed the ideas of some works from Michael Ridding and others (Clinical Neurophysiology, 112, 1461-1469, 2001; Exp Brain Research, 143, 342-349 ,2002), which show that 30Hz electrostim, provoking mild muscle contractions for 45' leads to increased excitability of the muscle representation in the brain (at the primary motor cortex).  Stimulation of the supraspinatus and deltoid is an old technique to hemiplegic painful shoulder, but used with a little different parameters.  Previous studies showed that this type of stimulation increases brain excitability for 3 days, and so we used two times a week, for two weeks.  After that, her discolcations improved a lot.  It is important to note that, during stimulation, you have to clearly see the humerus head going up to the glenoid fossa" Surgery : The effect of surgical intervention has been shown to be favourable in only a limited percentage of patients (33.9% Rombaut et al 2011, Arch Phys Med Rehab, 92, 1106-1112). Three basic problems arise. First, tissues are less robust; Second, blood vessel fragility can cause technical problems in wound closure; Third, healing is often delayed and may remain incomplete.  Voluntary Posterior Shoulder Subluxation : Clinical Presentation A 27 year old male presented with a history of posterior shoulder weakness, characterised by severe fatigue and heaviness when 'working out' at the gym. His usual routine was one which involved sets of 15 repetitions, hence endurance oriented rather than power oriented. He described major problems when trying to execute bench presses and Japanese style push ups.  https://youtu.be/4rj-4TWogFU In a comprehensive review of 300 articles on shoulder instability, Heller et al. (Heller, K. D., J. Forst, R. Forst, and B. Cohen. Posterior dislocation of the shoulder: recommendations for a classification. Arch. Orthop. Trauma Surg. 113:228-231, 1994) concluded that posterior dislocation constitutes only 2.1% of all shoulder dislocations. The differential diagnosis in patients with posterior instability of the shoulder includes traumatic posterior instability, atraumatic posterior instability, voluntary posterior instability, and posterior instability associated with multidirectional instability. Laxity testing was performed with a posterior draw sign. The laxity was graded with a modified Hawkins scale : grade I, humeral head displacement that locks out beyond the glenoid rim; grade II, humeral displacement that is over the glenoid rim but is easily reducable; and grade III, humeral head displacement that locks out beyond the glenoid rim. This client had grade III laxity in both shoulders. A sulcus sign test was performed on both shoulders and graded to commonly accepted grading scales: grade I, a depression <1cm: grade 2, between 1.5 and 2cm; and grade 3, a depression > 2cm. The client had a grade 3 sulcus sign bilaterally regardless if the arm was in neutral or external rotation. The client met the criteria of Carter and Wilkinson for generalized liagmentous laxity by exhibiting hyperextension of both elbows > 10o, genu recurvatum of both knees > 19o, and the ability to touch his thumbto his forearm Headaches Jacome (1999, Cephalagia, 19, 791-796) reported that migraine headaches occured in 11/18 patients with EDS. Hakim et al (2004, Rheumatology, 43, 1194-1195) found 40% of 170 patients with EDS-HT/JHS had previously been diagnosed with migraine compared with 20% of the control population. in addition, the frequency of migraine attacks was 1.7 times increased and the headache related disability was 3.0 times greater in migraineurs with EDS-HT/JHS as compared to controls with migraine (Bendick et al 2011, Cephalgia, 31, 603-613). People suffering from soft tissue hypermobility, connective tissue disorder, Marfans Syndrome, and Ehler Danlos syndrome may be predisposed to upper cervical spine instability. Dural laxity, vascular irregularities and ligamentous laxity with or without Arnold Chiari Malformations may be accompanied by symptoms of intracranial hypotension, POTS (postural orthostatic tachycardia syndrome), dysautonomia, suboccipital "Coat Hanger" headaches (Martin & Neilson 2014 Headaches, September, 1403-1411). Scoliosis and spondylolisthesis occurs in 63% and 6-15% of patients with Marfans syndrome repsectively (Sponseller et al 1995, JBJS Am, 77, 867-876). These manifestations need to be borne in mind as not all upper cervical spine instabilities are the result of trauma. Clinically, serious neurological complications can arise in the presence of upper cervical spine instability, including a stroke or even death. Additionally, vertebral artery and even carotid artery dissections have been reported during and after chiropractic manipulation. Added caution may be needed after Whiplash type injuries. The clinician needs to be aware of this possibility in the presence of these symptoms, assess upper cervical joint hypermobility with manual therapy techniques and treat appropriately, including exercises to improve the control of musculature around the cervical and thoracic spine. Atlantoaxial instability can be diagnosed by flexion/extension X-rays or MRI's, but is best evaluated by using rotational 3D CT scanning. Surgical intervention is sometimes necessary. An interesting case of EDS and it's affect on post concussion syndrome can be read elsewhere on this site. Temperomandibular Joint (TMJ) Disorders The prevelence of TMJ disorders have been reported to be as high as 80% in people with JHD (Kavucu et al 2006, Rheum Int., 26, 257-260). Joint clicking of the TMJ was 1.7 times more likely in JHD than in controls (Hirsch et al 2008, Eur J Oral Sci, 116, 525-539). Headaches associated with TMJ disorders tend to be in the temporal/masseter (side of head) region. TMJ issues increase in prevelence in the presence of both migraine and chronic daily headache (Goncalves et al 2011, Clin J Pain, 27, 611-615). I've treated a colleague who spontaneously dislocated her jaw whilst yawning at work one morning. stressful for me and her! Generally, people with JHD have increased jaw opening (>40mm from upper to lower incisors). Updated 17 October 2017  Read More
  • Fri 09 Dec 2016

    Physiotherapy with Sharna Hinchliff

    Physiotherapy with Sharna Hinchliff    Martin is pleased to welcome the very experienced physiotherapist Sharna Hinchliff to Back in Business Physiotherapy for one on one physiotherapy sessions with clients in 2017.  Sharna is a passionate triathelete and mother and has had several years experience working locally and internationally (New York and London) in the field of physiotherapy. Originally from Western Australia, Sharna graduated from the world renowned Masters of Manipulative Physiotherapy at Curtin University. read more Read More

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Updated : 10 May 2014

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Copyright Martin Krause 1999 - material is presented as a free educational resource however all intellectual property rights should be acknowledged and respected