Specific Segmental Spinal Thrust Technique

Erl Pettman FCAMPT
IFOMPT Quebec City, 2012

A brief historical perspective:

The proposition that specific spinal segmental thrust technique (SSSTT) is necessary to remedy spinal segmental dysfunction is not new and goes back at least to the writings of Hippocrates (1). Based on architecture and vertebral position a specific thrust on a ‘mal-aligned’ or prominent (gibbus) vertebra could supposedly realign the spine and restore function. In North America, during the 19^th century, this ideology was expanded to suggest that such manipulations could also improve visceral function and general health. Osteopathy and Chiropractic were born within the USA not so much from scientific endeavour as from a general public distrust of the deleterious and sometimes catastrophic effects of treatment from a poorly (scientifically) educated Physician (1).

The ‘springboard’ of each profession’s claim came from a personal experience. Andrew Still supposedly relieved his chronic headaches when, lying on a ‘Y’ shaped branch he was supposedly able to readjust his atlas. Palmer ‘cured’ Henry Lillard’s hearing dysfunction with a thoracic A/P thrust. Faced with the onslaught of modern science each profession has altered it’s ‘official’ philosophy but not so much that we heard John Uplegder state that spinal dysfunction could cause serious systemic dysfunction, even resulting in death (2). Modern science has seriously challenged and repudiated these ideals but, as we all know, they continue to be popular within the general public.

In the mid-20^th century three notable physiotherapists Kaltenborn, Maitland and Paris chose to work with and study under expert manipulators within the three professions of Physical Medicine, Chiropractic and Osteopathy around the world. The conjoint result of their experience was to be the first ‘evolutionary’ change within Manipulative Therapy for over ten thousand years. A new concept was born: specific spinal segmental mobilization and it rapidly gained popularity within the manual orthopaedic community mainly because each system was gentle and non-provocative i.e, in the spirit of Hippocrates to do ‘no more harm’. Using the relatively new science of arthrokinematics the ‘Kaltenborn/Evenjth’ system further evolved orthopaedic manual therapy to include specific spinal segmental assessment and distractive and translatory manipulative thrust techniques.

Specific vs non-specific techniques:

Signs and symptoms of a specific segmental lesion can be treated adequately with a non-specific approach. For example, signs and symptoms of an L5 postero-lateral disc protrusion can be alleviated with the` McKenzie extension protocol`. In the case of foraminal compression C6 nerve root signs and symptoms may be relieved by postural correction. Such postural correction may be enhanced by manipulation of the thoracic spine (3).

In the case of manipulative thrust technique localised lumbar pain can be alleviated by a non-specific rotational (distraction or `gapping`) technique if the patient’s presentation fits the clinical prediction rule (4). However, such a rule relates to a very small proportion of the overall low back dysfunction population and is designed for lesions of recent onset and localised lumbar pain. Suggested reasons for the efficacy of such a technique might be that distraction (more likely de-compression) of the Z-joint may enable a segment to achieve a more normal biomechanical function having exceeded its anatomical neutral zone (5). Another may be the release of an entrapped meniscoid body (6). Both explanations remain hypothetical as are the majority of issues related to spinal manipulative technique.

Relating to the cervical spine, before an argument for SSSTT is put forward it is necessary to ask the questions ‘What lesion, or dysfunction, is actually being manipulated i.e, what causes Zygapophyseal joint (Z-joint) hypomobilty?’ If we do not, at least, have a theoretical patho-mechanical model of how motion is lost then arguments regarding specificity versus non-specificity will be insoluble.

Analysing peripheral joint hypomobility we see a fairly large list of recognized causes including muscle spasm and contracture; intra-articular loose bodies; articular surface disruption e.g, fracture; capsular contracture; ligamentous adhesions. All of these lesions can occur within spinal segments and obviously affect Z-joint motion but it is extremely doubtful that any of them would be amenable to SSSTT. Neither would SSSTT be appropriate for the acute/sub-acute post-traumatic arthritis (within 2 months). All of the preceding pathologies appear to do better with medication, mobilizations and exercises.

The so called chronic Z-joint hypomobility that seems to respond best to SSSTT has certain characteristics:

The lesion only seems to affect one quadrant of motion e.g, a loss of right side bending in extension, whilst the other quadrants remain fully mobile. I believe this type of dysfunction was first described by Stoddard as the ‘Osteopathic lesion’.
The end-feel is hard and painless, at least with regard to the hypomobile joint.
The pre-manipulative hold produces no radiating, long-tracking or neurovascular symptoms.
The pre-manipulative hold produces no localized reactive spasm or pain.

Furthermore, post manipulative response needs to be explained:

Both through passive intervertebral motion testing (PIVMs) and active ROM testing there is an immediate positive response in regaining motion.
It does not appear to matter how chronic the lesion may be, chronicity being determined by a history of trauma and onset of symptoms. Dysfunctions that appear to have their origins many years in the past still respond positively to SSSTT.
With regard to the above, in spite of perhaps years of hypomobility there are no signs, on visual diagnostics, as to any significant segmental deterioration. This would be impossible if multiple quadrants of motion were affected.
SSSTT alone fails in the overall rehabilitation of the patient. Only when segmentally specific and regional neuromuscular re-education is employed is successful resolution of motion to be anticipated. An immediate question arises here that perhaps such neuromuscular re-education is the key, that it alone may resolve the problem. In my experience of working for many years with younger therapists whose only tools are segmental mobilizations and muscle re-education techniques I suspect this is not the case. SSSTT appears to be the ‘key’ that opens the ‘door’ to neuromuscular re-education.

So looking at the above mentioned pre and post-manipulative characteristics of hypomobile Z-joints a theory needs to be proposed as to what creates such a dysfunction initially, and then how SSSTT assists in the rehabilitation of such a dysfunction and why it is such a necessary component.

A hypothesis as to the cause of single quadrant Z-joint hypomobility:

When two or more forces act simultaneously at a single point there will be a resultant force vector (diagram). When one or more of these forces change, the resultant vector will change accordingly. The most common example of this is in patello-femoral mal-tracking (diagram). Inhibition of the VMO, or an imbalance in the hip rotator strength will lead to excessive lateral displacement of the patella, most pronounced at 30 degs of knee flexion (5). In this instance such mal-tracking is occurring in a very mobile articulation. Now imagine the same mal-tracking occurring within a very restricted joint.

Z-joints have very limited ‘joint play’ (6). The capsules and their associated ligaments severely limit any accessory motion. Therefore a Z-joint moves on a very well-defined track.

Now look at the incredible number of muscular vectors that are responsible for moving any one such Z-joint through its well-defined track (diagram).

Muscles reflexly act according to the proprioceptive information relayed to the CNS (7). Such proprioceptive information primarily comes from the articular and peri-articular inert tissues of a joint. Imagine specific and discrete damage to a capsule or its supportive ligaments. Such damage would undoubtedly lead to specific fasciculi of a muscle(s) acting aberrantly, perhaps protectively, when these inert structures are challenged by motion. The scenario for articular mal-tracking is set. However, the available accessory motion in a Z-joint is significantly limited and the joint ‘jams’ (diagram). The joint, however, is not fixated. It can freely move into the other three quadrants thus maintaining cartilaginous nutrition and decreasing the risk of articular malnutrition within the entire segment, but not perhaps in the affected quadrant. Even after years of single quadrant dysfunction the segment, as a whole, most often shows little or no signs of segmental deterioration on visual diagnostics.

An integral part of this discussion must include the question of why chronic and painless Z-joint hypomobility leads to symptoms from adjacent joints and segments. The theory of ‘adaptive hypermobility’ is a seductive one and I confess to having taught it for many years. When a joint gets ‘stuck’, for whatever reason, other joints are somehow made to adapt for this loss of mobility. This suggests that the CNS, at a segmental level, has the ‘intelligence’ to alter muscle patterning so that more motion is gained at other joints/segments within the kinetic chain. There is no evidence within the current literature that supports such a theory. Far more likely is the idea that hypomobility of any component of spinal segmental motion causes a change in its mechanical axis thus producing patho-mechanical motion within the whole segment.

Biomechanics and patho-biomechanics of segmental cervical motion:

Apart from neuromuscular control, motion of any joint or spinal segment must be determined by two factors, those inert anatomical structures that facilitate motion and those that oppose or limit it. In the cervical spine, so little attention seems to have been paid to the uncinate joints (U-joints), otherwise known as the ‘joints of Von Lushka’ (diagram). A recent literature search shows that the scientific community cares little about these joints, they seem unimportant. However, from a biomechanical standpoint, by their mere presence, they must be important since their planar orientation is almost at right angles to that of the Z-joints (diagram).

It is generally accepted that during rotation of the head, within the typical cervical segments (C2/3 to C7/T1), rotation and side bending are ipsilateral. It seems to be assumed that planes of motion are dictated by the Z-joints (9)(diagram). I believe this view needs to be modified. Motion of a bone will be directed according to the plane that the joint’s surfaces are orientated in. Whilst both Z-joints and U-joints incline towards the horizontal, in the case of typical cervical Z-joints their orientation is closer to the coronal plane and will therefore facilitate side bending within the segment whilst, at the same time, resist rotation. The U-joint however, is orientated more into a sagittal plane and will facilitate rotation whilst modifying side bending towards a contra-lateral translation (diagram).

When performing a functional quadrant movement e.g, extension, right side bending the only logical combination of joint motions would seem to be a predominant inferior, medial and posterior (IMP) within the right Z-joint and an accompanying superior, anterior and lateral (SAL) glide within the opposite (left) U-joint (diagram).This means that the actual axis of motion must be far more oblique(diagonal) than previously described (diagram). Disruption of movement through mal-tracking in either joint will lead to hypomobility within the right extension quadrant of segmental motion. When such a hypomobility occurs it will change the axis of motion within that segment for that quadrant of motion. The change in axis will cause abnormal motion to occur within the other articular elements. So it is not so much that the other joints necessarily compensate and become hypermobile as much as the changed axis of motion causes abnormal stresses on inert tissues within the segment. Such abnormal stresses will activate ‘polymodal C fibres’ (10).

Segmental ‘Central Sensitization’ and resultant signs and symptoms:

In spite of the fact there may be no tissue damage to other articular structures within the affected segment the hypomobile component, in changing the normal biomechanical axis, will create repetitive, abnormal afferent input to the spine via the polymodal C fibres from the remaining mobile elements of the segment. This will ultimately cause segmental central sensitization (‘faciltated segment’) (11) within the substantia gelatinosa leading to referred segmental symptoms. It also causes hypertonus of segmental musculature, further challenging efficient neuromuscular tracking of articular motion. It would appear, in the case of the typical cervical segment that this sensitization phenomena occurs on the opposite side to the dysfunctional Z-joint i.e, hypomobility of the left C3/4 sensitizes the right C3/4 hemi-segment.

Recent information suggests that segmental central sensitization can have a more profound effect than just causing referred segmental pain, making segmental inert tissue hypersensitive and segmental and key muscles hypertonic. It appears to have a deleterious effect on axonal transport (12). A decrease of anterograde axonal transport impedes the flow of chemicals essential for synaptic transmission. It also impedes the transport of essential molecules (e.g, actin) (13) to the muscle tissue that the segmental nerve innervates. Though no research has yet proven a direct link between segmental central sensitization and segmental muscle function this recent information is certainly suggestive that muscle dysfunction may occur through a combination of synaptic changes and actual cellular changes within muscle tissue itself. It may certainly be the explanation as to why segmental muscles appear to weaken and atrophy so rapidly in centrally sensitized and unstable vertebral segments (14).

The key to resolving central sensitization and all its deleterious effects would seem to be a restoration of the segments normal biomechanical axis of motion. This suggests that normal tracking of e.g, the hypomobile Z-joint must be regained. Assuming the ‘mal-tracking theory’ is an acceptable working hypothesis the question is posed how best to restore normal motion. A non-specific Z-joint distraction (gapping) manipulation, inevitably incorporating rotation, is perhaps the most popular and widely taught (inter-professionally) technique. It is certainly almost guaranteed to get a ‘crack’ or ‘pop’, and of course very popular with its recipients since they hear and feel that an ‘adjustment’ has been achieved. Unless performed on an unsuitable patient (which most competent manual physical therapists are able to avoid due to extensive assessment screening) there is often an immediate relief of localized neck symptoms and increased active range of motion. Unfortunately, such changes in chronically dysfunctional patients appear to be short lived and the patient will require repetitive manipulations, on a regular basis ad infinitum.

This temporary affect has been explained since the 1970’s (15) when manipulation to the spine was shown to increase activity within (and concurrent increased blood flow to) the peri-aqueductal grey matter of the mid brain, the so-called PAG effect. This phenomenon appears to temporarily decrease abnormal muscle patterning and, through its interactions with the parasympathetic system, induces an endorphin release. This brings us to the most important question. Does spinal manipulation have any biomechanical effect or is it all a temporary neuromuscular, neurochemical and/or neurovascular effect? This, in turn, directs us to the very heart of whether SSSTT is essential, or not, in certain segmental spinal dysfunctions.

What is SSSTT and what does it set out to achieve?:

If hypomobility of a segmental quadrant motion is causing central sensitization because an abnormal biomechanical axis has been created then it seems logical that a corrective spinal technique should be employed in an attempt to restore the normal biomechanical axes of motion within that segment. Since the loss of motion must be, by definition a loss of articular glide, it seems reasonable that the technique should incorporate the lost translatory glide. However, using the above model of articular mal-tracking due to muscular guarding suggests an articular gliding technique must be employed that can overcome the speed of this neuro-muscular barrier. Such a technique will require sensitivity to the motion barrier. It will require a sense, or knowledge of the translational plane of motion. It will require an acceleratory force that exceeds the patient’s muscles’ protective, reactive time. Welcome to the world of SSSTT.

Such a thrust must be a translatory one, following the above model, into either an IMP or SAL glide of the dysfunctional Z-joint or U-joint. It is proposed that once seated into the end range of its normal neutral zone segmental muscle tone and reactivity may be reset, which is why immediate segmental neuromuscular re-education must begin whilst the joint is in this comfortable, neutral position thus minimizing the chance for abnormal muscle activity continuing to cause articular mal-tracking.

There are two methods of delivering such a translational thrust. Direct which thrusts into the restriction or indirect, delivered by longitudinal traction i.e, away from the barrier. Palpation of a motion barrier immediately brings into question the subjective sensitivity and specificity of end-feel, a topic that exceeds the time parameters of this particular discussion.

However, assuming such sensitivity and specificity can be achieved, the starting point at which each thrust is delivered is extremely important (17). Initiating the thrust at the point where muscles can react and create mal-tracking would obviously be inadvisable. With the joint poised close to, but not into the reactive motion barrier, a high acceleration thrust is delivered either directly or indirectly.

It is assumed that the acceleration of such a thrust must achieve the comfortable end range position before the ‘muscle guarding’ can cause articular mal-tracking (direct thrust) (diagram) or create a sufficient stretch reflex vector that the segmental muscles themselves achieve the corrective force (indirect thrust) (diagram). In either case we can conclude that three factors must be essential for a successful result:

Sensitivity to the motion barrier i.e, do not initiate ‘segmental muscle guarding’ prior to the thrust.
Accurate translatory direction.
Adequate velocity (more accurately acceleration).

When considering the above it must be appreciated that, although the ultimate goal of SSSTT is to alter neuro-muscular bias or patterning, the thrust itself requires biomechanical specificity.

Specificity for safety:

Apart from directional specificity of thrust being necessary to achieve a discreet neuro-biomechanical affect the question arises how to make a specific thrust safe, certainly in the case of cervical manipulation. So let’s focus on that for a moment. Roger Kerry has described how certain positions, or movements, may threaten neurovascular tissues passing across or within cervical segments, even within otherwise ‘normal patients’ with no obvious or apparent systemic disorders. The greatest focus has been on the vertebro-basilar artery (VBA) and potential excessive tortuosity (stretching) of the artery. Excessive tortuosity has been cited as the main cause of damage to an artery’s tunica intima (arterial dissection) leading to thrombus formation and potential brainstem stroke and even death (20++). In Canada at least there has seemingly been a furious battle between the Medical (the ‘Stroke Consortium’) and Chiropractic professions as to the dangers of cervical manipulation to the VBA (21++). According to Roger Kerry.s latest figures the risk of serious or catastrophic neurovascular damage is quite small (22). However, as a profession it would seem to be very unwise to ignore evidence as to the possible and even probable links between certain types of manipulation and the cause of VBA trauma. As a summary of the factors mentioned in the literature, having selected a patient suitable for manipulative thrust, the Orthopaedic Manipulative Physical Therapist should pay attention to the following:

Never manipulate into the end range of rotation of the head and neck. Rotational manipulation at this point relies on the elasticity of cervical arteries to avoid arterial dissection. This definitely brings into question an individual patient’s arterial integrity and its ability to adequately stretch without harm (23).
Minimise or obviate any rotation within the thrust itself. Throughout the spine, but especially the cervical and lumbar regions, it is clear that segmental inert tissue resists (or absorbs) torsional forces applied to it. It seems most logical to assume that the ‘weakest link’ will absorb most torsion and in segments that are already structurally unsound this will adversely impact neurovascular structures travelling through, or within, such segments. It also suggests that any ‘cracks’ or ‘pops’ (‘audibles’) are most likely to occur in the most hypermobile segments.
Avoid locking techniques that include a combination of rotation and extension especially in both cranio-vertebral and cervical segments (24). Since most of the studies involved in arterial blood flow to the brain involve extension of both the cranio-vertebral and mid-lower cervical spine i.e, full extension of the head and neck, it is assumed that arterial tortuosity might be relieved by reciprocating motions e.g, cranio-vertebral extension with mid-lower cervical flexion.
Avoid any combined thrust that could create excessive tortuosity of the VBA or carotid artery e.g, traction with rotation and/or extension of the cervical spine. Whilst it is admitted that the studies were performed in vitro ((25) there remains the possibility that such techniques may seriously compromise the VBA blood flow.
Avoid any technique that might cause excessive foraminal compression to the lower cervical segments. Attention should be directed to the MVA studies of Punjabi (26) in which he showed maximum torque stress is applied to the lower cervical segments in moderate momentum assaults from rear end MVA collision. This, combined with reality that segmental deterioration of these segments begins as early as the third decade, should lead the therapist to avoid any thrust technique that might involve foraminal compression to these segments.
From a biomechanical perspective (not including distraction or ‘gapping’ technique) a translatory glide should be employed that most closely simulates what a segmental joint would perform in normal ‘life-like’ physiological motion, for example when regaining rotation at the atlantoaxial joint. Atlantoaxial rotation is a composite movement involving an antero-inferior glide of the contra-lateral (to head motion) joint and a postero-lateral glide of the ipsi-lateral joint. A rotational thrust to the C1/C2 segment is never necessary.
Follow the dictates inherently inferred within Physical Therapy’s definition of a manipulative thrust technique which is ‘a high velocity (acceleration), low amplitude thrust designed to regain normal physiological range of motion’.

Is there an SSSTT that might involve all of the above concerns and considerations?

To answer this I have chosen a clinical scenario that transcends consideration of the PAG effect on spinal motion and neck pain.

C2/3 dysfunction:

I have chosen C2/3 dysfunction as a case needing SSSTT for a number of reasons:

The symptoms of C2/3 dysfunction are least likely to be cervical or upper limb and most likely to be trigeminal i.e, headaches, dizziness, nausea etc.
Of the three spinal segments that can cause trigeminal symptoms C2/3 is easy to differentially diagnose.
C2/3 appears to be one of the most commonly traumatised segments following high momentum trauma to the head and/or neck.
In my own clinical experience patients chronically suffering from this dysfunction have had multiple interventions, including cervical manipulation, without prolonged relieve of trigeminal symptoms.
SSSTT of C2/3 brings about prolonged and commonly permanent relief of trigeminal symptoms.
Commonly in post-traumatic rear-end collision patients the manipulation must be performed in a specific manner to avoid foraminal compression to the segments below.

The technique, as demonstrated in the accompanying video, involves cranio-vertebral locking (to minimise tortuosity of the VBA at the C2 level) from above, and a SAL glide of C3 up into C2 i.e, extension of the C2/3 joint. Care must be taken to fixate the manipulator’s stabilising elbow by leaning on it, thus removing the risk of traction to the lower cervical spine i.e, the VBA length remains unchanged.