Non specific low back pain is a neurological movement disorder not a musculoskeletal disorder. Treat the disease not symptoms for success. Defining movement deficiency in relation to low back pain – an observational study of the prevalence of movement deficiency.

Dr David Johnson FRACS Neurosurgery, Spinal Surgery. Mr John Kim M.Phty Physiotherapy.

The observational movement proficiency study consisted of a consecutive random convenient sample of twenty-six subjects working in an inner city tertiary hospital. No subjects declined participation in the study.

Movement Deficiency (MD) is hypothesised to be a significant contributor to the high prevalence of Non-Specific Low Back Pain (NSLBP) in our modern industrialized society. Treatment of low back pain symptoms is conventionally directed towards symptoms. This is clearly apparent by the misguided yet accepted diagnosis and commonly misused label of “Non-Specific Low Back Pain” which itself is not a diagnosis at all but an admission that the disease causing the symptom remains nebulous. This is unacceptable if progress is to be achieved in controlling the rising prevalence and economic burden of this condition. If the aforementioned hypothesis and authors are correct, in that the disease causing NSLBP is spinopelvic Movement Deficiency, a distinctive NSLBP management paradigm shift can be implemented with the treatment targets being those of neurologically corrupted motor patterns manifesting as movement deficiency with secondary musculoskeletal sequelae and back pain symptoms. If low back pain is considered to be a primary neurological movement disorder we can switch our focus away from common, expensive, invasive and often poorly efficacious strategies such as interventional nociceptor blocks, core stability, Pilates, exercise therapy, adjustments and deep tissue release toward restoring the primary condition of corrupted central nervous system controlled movement proficiency.

Presently the critically important definition of MD in relation to low back pain and therefore its prevalence in the community has not been defined in peer reviewed scientific literature. This article defines desired points of performance of healthy movement and highlights the high prevalence of movement dysfunction postulating that this is the root cause disease creating NSLBP symptoms.

Twenty-six consecutive random and convenient subjects were asked to perform a movement task of placing a cap screw top on a drink bottle positioned at knee height. A kinematic pass or fail mark was assigned by proficiency in what we have termed the “NeuroHAB” screening tool.

Only two subjects (eight percent) out of twenty-six scored a pass whilst performing a simple movement task that would be expected to be representative of movement that occurs repetitively through out one’s normal activities of daily living.

Utilising the NeuroHAB screening we are able to characterise MD in a work place highly representative of the normal daily physical activity demands of everyday Australians to be at a surprisingly high prevalence consistent with the high and increasing prevalence of low back pain and supportive of the hypothesis that low back pain is primarily a neurological movement disorder currently being poorly treated by targeting strength and conditioning and secondary musculoskeletal nociceptors rather than the more imperative reversal of corrupted neurologically controlled motor patterns and movement deficiency. (1,2,3,4,5,6,7,8,9,10,11,29,30).

Existing research reveals deranged trunk muscle contraction in the presence of low back pain and even after pain has subsided electromyographic abnormalities in trunk control may remain. (12, 13) The corollary, however, has not been well investigated, that primarily corrupted motor patterns and subsequent movement deficiency over time contribute to reduced functional capacity and the development of NSLBP (14). Mechanisms by which MD may contribute to NSLBP include both mechanical and central processes. The mechanical process involves the transformation of normal non-nociceptive degenerative elements of the lumbar spine into active nociceptors (15). We have termed this transformation “degeneritis”.

We also postulate a central process too that may shed light on chronic disabling NSLBP and other spinal pain in the presence of normal spinal integrity in the absence even of degenerative changes. The presence of persisting MD itself may behave as “physiological nociceptor” manifesting with an obligatory cautionary central nervous system (CNS) signal of pain. Evolution wise, pain serves the purpose of cautioning the organism of real or potential threat. It is implicit that moving poorly leads to injury, therefore it is reasonable and logical that persisting movement deficiency may behave as a nociceptor in the absence of recognizable nociceptive signalling from structural elements such as lumbar discs, facet joints and musculo-ligamentous structures. If this hypothesis is correct, then targeting movement deficiency effectively and scoring well on our proposed 5 point movement screening tool, termed the NeuroHAB Screen would be a novel and exceptionally effective NSLBP treatment target and strategy.

Conceptually it is important to account for individuals with obvious MD who do not suffer from NSLBP. This observation was recognized in our study but does not breach the foundation of our original hypothesis on the premise that the development of pain is unlikely to occur until the functional demand of the individual exceeds their functional capacity. It is intuitive that MD if unresolved, will steadily retard functional capacity, however, pain may not manifest if the individual’s functional demand also declines. This logic can be applied and is observed, for example, in nursing homes or the elderly where by obvious MD exists in the absence of pain because functional demand remains low enough that there is no mismatch between the capacity and demand.

The opposite is seen in a labourer who displays MD in the presence of constant high functional demand. With time the mismatch between functional capacity not meeting the functional demands of work manifests with the development of NSLBP.

Our observation in current general and specialist clinical practice is that all too often when this scenario presents, the treatment choices target “hardware” spinal anatomy elements, such as facet joints, discs, motion segments and the myo-fascia rather than corrupted “software” central nervous system motor pattern driven movement dysfunction (16). We also recognize that excruciating low back pain can occur whilst performing trivial tasks such as picking up a paper clip (17). This reality lends further support to the hypothesis that the motor pattern and movement proficiency is the critical factor that links the individual to the development of pain, not the absolute physical load. Despite this, lifting capacity but not lifting kinematics appears to be the focus of return to work stipulations and certification desired from injured worker insurers. In our clinical practice, we have never been questioned about movement proficiency requirement in contrast to the lifting load limit that is always queried and in our view significantly less relevant.

Justification or explanation for the high prevalence of MD in our society is attributed to modern lifestyle actively suppressing the athletic capabilities of natural human functional movement. Our lifestyles which are plagued with modern conveniences and prolonged inactivity result in a compromise to the three inherent constituents necessary for proficiency of functional movement which are soft tissue mobility, coordination and subsequently strength. With the decline in these domains that constitute movement, maladaptive movements are employed which further compound deficiencies and functional capacity, pushing one cyclically closer to the mismatch between functional capacity and functional demand, and therefore pain, accounting for the exceedingly high prevalence and suffering from NSLBP in industrialized nations distinctively different to third world countries where the toils of labour and functional movement are far more likely to be maintained. (18,19,20, 21)

Assessment of lumbo-pelvic spine movement proficiency in relation to low back pain has not previously been described. Therefore we developed the Functional Movement Training NeuroHAB Screening Tool which is a 5 point screen that determines a pass/fail in our observation of simple movement patterns to perform tasks requiring forward bending and lowering of the torso. A pass is required in criteria 1,2,3,4 to gain an overall pass in terms of a correct and proficient motor pattern for the performance of a task requiring forward bending and lowering. Criterion 5 based on a range of motion is not essential to pass because range of motion may be limited in the presence of a proficient motor pattern. Functional capacity will, however, be limited by poor range of motion and practical tasks are likely to be restricted in the presence of poor range of motion. None the less, the motor pattern initiating movement may still be maintained up to the restricted range.

These criteria for proficient movement were chosen because they represent the points of performance of natural spinal health maintaining powerful functional human movement regardless of age, be they a naturally squatting toddler, an Olympic weightlifting champion or a pain-free and independently functioning elder. Functional capacity, of course, is vastly different for all individuals however motor patterns and virtuosity in executing spino-pelvic movement according to these criteria should be identical and be able to be maintained through out life if low back pain is to be avoided. Other research has shown that motor control of the spine is corrupted in the presence of chronic low back pain and we have observed in clinical practice this being manifested by gross deficiencies in the elements of movement criteria selected in our NeurHAB screening tool. (22, 23, 24)

Low Back Pain Functional Movement NeuroHAB Screening Tool.

1. Hip centric rotation
2. Neutral spine maintenance
3. Post chain activation-weight through heels not through toes (anterior chain)
4. Unloaded knees (avoid anterior knee drive with deactivated posterior chain)
5. Adequate range of motion for the required task.

Overview

The study was an observational study that directly observed healthy hospital staff subjects performing a simple given movement based task, one subject at a time. The study was conducted in vacant spaces of several wards, office departments and the operating theatre at a tertiary metropolitan hospital.

Subjects

A random and convenience sample of twenty-six subjects currently working at a tertiary metropolitan hospital was chosen to participate in the study. Subjects included medical and nursing staff, as well as administration and kitchen/utility department employees. Subjects were recruited one at a time via verbal request during the course of their normal duties, with all subjects agreeing to participate in the study. As the study did not intend to draw causal inferences between the subjects’ performance outcome and their demographic variables, information such as age, occupation and race was not recorded and our fundamental belief that motor patterns and movement proficiency should be able to be maintained in everyone regardless of other demographic variables.

Observation Protocol

Subjects were observed performing the given task during the course of their day shift. One of the study team members recorded the subjects’ task performance using a handheld video recording device, while the other team member assessed their performance as being either a pass or a fail based on the points of performance criteria considered critical for movement proficiency in relation to maintaining a healthy lumbar spine.

NeuroHAB Functional Movement points of performance assessed in performing the movement task.

1. Hip centric rotation
2. Neutral spine maintenance
3. post chain activation (weight on heels)
4. Unloaded knee position
5. Range of motion

A pass or fail rating was applied to each subject upon observing the motor pattern employed by the subject to perform the task. Video replay was also available to the investigators for further close assessment.

The study task comprised replacing a screw cap onto a water bottle placed on top of a plastic box which positioned the top of the bottle at approximately knee height for all study participants. This sequence was verbally explained to the subjects who were then asked to perform the task in their ordinary manner. They were told not to pick up the bottle off the platform thus the task mandated movement downwards and forwards toward the bottle top at approximately knee height. Verbal clarification was given as required but without demonstration. The subjects were given enough space to carry out the task and no verbal feedback was given during or after the task. The observations were conducted with two observers. One observer recorded the task performance using the handheld device while the other observer assessed the performance as being pass or fail based on the above mentioned 5 point performance criteria.

Only 2 of the 26 subjects, or eight percent of a convenient adult population sample in a standard work place of mixed tasks demands, passed the functional movement task with proficiency in movement based upon the 5 point functional movement NeuroHAB screen. Extrapolation of this finding is that only 2 subjects were able to perform the simple movement task proficiently and therefore maintain hip centric rotation, posterior chain activation, a neutral spine and adequate range of motion with no loading of the knee joint. All other subjects in some form precipitated mechanical stress on the lumbar spine or knee joint or promoted the development of further movement deficiency by compensating for inadequate range of motion and/or not affording opportunistic conditioning of the posterior chain musculoligamentous structures whilst performing simple high repetition activities of daily living as a result of a deactivated posterior chain evident while adopting the common kneeling movement in the performance of our representative study task. Ninety-two percent of individuals have elements of movement deficiency based on this biomechanically critically important functional movement NeuroHAB 5 point screening tool.

Low back pain is being recognized as a worldwide leading cause of disability with an associated mounting economic burden, particularly in industrialized nations and this is in spite of increasing technology and research dedicated to arresting the prevalence of this chronic disease. (1,19,20,21,25)

The increasing prevalence strongly points to a lack of efficacious treatment and/or a dramatically increasing incidence or more than likely both processes occurring simultaneously leading to the observation of staggering incidence, persistence and recurrence of low back pain in our society. (1)

This study and few before it suggest that the root cause of low back pain is movement deficiency and not failings of spinal core stability or flexibility which is all too often the conventional target of physical therapy and rehabilitation strengthening and stretching programming. (14,23,25)

Intuitively movement deficiency doesn’t immediately cause pain but does contribute to lowering functional capacity and increasing the substrate level of degeneration, which in its own right may be pain free and regarded as “normal”, but in the presence of persistent movement deficiency promoting reduced functional capacity that may fall below functional demand transform normal pain free degeneration into painful lumbar degeneration or “degenritis”.

The concept of movement deficiency and its role in the development of low back pain warrants further elaboration. We have discussed earlier that the presence of MD does not immediately cause pain until functional demands exceed functional capacity. The caveat is however that in the presence of movement deficiency functional capacity declines steadily due to the progressive incorporation of maladaptations or compensatory movement patterns that become employed in an attempt to maintain a functional capacity which is struggling to meet a functional demand. Once on this brink of tolerance the onset of pain is inevitable as even simple trivial poorly performed movements now have the potential to trigger immense and immobilizing low back pain as the bodies cautionary and protective nociceptor signalling stimulates the cascade of guarding responses that subjects describe as pain. Patient histories of minor trivial bending tasks precipitating immense spasming low back pain will be all too familiar to clinicians and exemplifies this conceptual hypothesis. The presence of pain then feeds positively into the development of even more movement deficiency in a snow balling cyclic manner further compounding and entrenching chronicity estimated to occur at a rate of approximately ten percent for every episode of acute low back pain (26).

Rest and analgesia and the myriad maze of treatment remedies are typically sought and for the majority, pain relief is obtained as nociceptive tissues calm in their signalling potential. However with out restoration and specific attention to reversing the movement deficiency root cause, pain typically recurs in seventy five percent of patients experiencing an acute episode of low back as current and conventional futile symptom based treatments are employed including rest, deep tissue release, adjustments, pain medication, interventional pain blocks and surgery (26).

Restoration of motor patterns which represents a CNS “software” remedy as opposed to a more conventional musculoskeletal “hardware” remedy is given little to no priority due to a distinct lack of specific quality and efficacious movement training programs.

Individuals experiencing an acute episode of low back pain experience a ten percent chance of developing persistence or chronicity as complex central nervous system changes occur to perpetuate the perception of pain despite the resolution of nociceptive tissue injury or inflammation, as evidenced by radiological imaging revealing normal lumbar degeneration.(26,27) Patients that progress to chronicity have been unable to eliminate the mismatch between their functional capacity and functional demand as the pain experienced from the outset perpetrated further movement and motor pattern corruption.

Few studies have focused on optimizing the specific kinematics of movement primarily as a prevention target and secondarily as a treatment target for low back pain. We recognize work place health and safety lifting guidelines to be common place but there is little literature to support the movement pattern that is commonly advocated (28). We were unable to identify any literature that offers practical guidelines that are reproducible and applicable to reverse movement deficiency. One may look to commonly performed motor control exercise (MCE) therapy, posture and Pilates exercise for guidance in this field, however, all of these movement and stability based approaches have been disappointing in the management of non-specific chronic low back pain (24,29,30). We postulate that this may be the factor that has resulted in a lull of research focusing on movement proficiency and NSLBP however we believe these methods should not be specifically regarded as meeting the requirement or criteria of effective central nervous system motor pattern rehabilitation or distinctive movement training for that matter and are overtly non functional in their implementation and for that reason are inherently lacking intensity, which we believe is important in stimulating neuro-endocrine favourable physiological adaptations that promote “healing” and the diminution of pain as the central nervous system’s requirement to signal caution subsides (31,32,33,34). Currently employed movement training approaches can be likened to teaching someone to play golf with substitute exercises and never allowing them to hold a golf club, swing at a golf ball on a golf course.

The term non-specific low back pain that is assigned to the vast majority of chronic low back pain diagnoses implies a nebulous and unexplained causation (35). We demonstrated in our study that ninety-two percent of working individuals fail a simple movement screen based on healthy kinematic movement criteria. Repetition of this poor proficiency movement throughout all activities of daily living intuitively reduces functional capacity. Future studies are required to reverse this defeated attitude implied in the label of “Non-Specific” and a cure for low back pain is desperately needed by invigorating the concept that non-specific low back pain is not nebulous, but in fact “specific low back pain secondary to movement deficiency”. With this notion being held primarily linked to the development, persistence and recurrence of low back pain, effective functional movement based training therapies can be developed. Our study highlights the prevalence of poor movement proficiency in the community and sets the benchmark for movement points of performance research utilising the NeuroHAB Screen that should be specifically targeted with effective functional movement training that is inherently and relatively intense, promoting physiological adaption and arresting the suffering from low back pain. Our group’s future research investigates the correlation between restoring movement proficiency based on the NeuroHAB screening tool and improvement in pain and disability ratings in patients with the diagnosis of NSLBP.

Non-specific Low Back Pain is a symptom, not a disease

The disease causing NSLBP is postulated to be Movement Dysfunction

Proficient movement can be defined with the NeuroHAB screen

Movement dysfunction like low back pain symptoms is widely prevalent in the industrialised community and are postulated to be causally linked

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