HVT is not everything (again)

Facilitated Segments: a critical review



Key words: Facilitated segments, manual therapy, osteopathy

The concept of spinal facilitated segments has dominated osteopathic
neurophysiology for over half this century. This concept has been at the
heart of osteopathic teachings and is often used both in clinical diagnosis
and as part of the rationale of treating different musculo-skeletal and
visceral conditions. Surprisingly, such an important subject has never been
criticised: the existence of facilitated segments and their relevance to
manual therapy or osteopathic medicine has never been questioned. This
article re-examines the original studies of Korr, Denslow and their
co-workers, aim to identify what has been demonstrated in these studies and
to reinterpret their findings in the light of current knowledge of
neurophysiology.

The spinal facilitation concept
In principle, the facilitated segment was described as a specific area of
the spinal cord that was capable of organising disease processes. It was a
very simplistic model: it had two input and two output routes. The input
routes were sensory from musculo-skeletal and viscera. The output routes
were the motor efferents to muscle and autonomic motor to sweat glands,
blood vessels and viscera. Inside the spinal cord it was suggested that
abnormal activity in one area of the spinal cord could spread to adjacent
areas. The facilitation process would be initiated when aberrant sensory
information from an area of damage or pathology (muscle or viscera) was
conveyed via the afferents to the spinal cord. This would alter the neuronal
activity at the same segmental level and might spread to adjacent areas of
the spinal cord affecting spinal centres not directly related to the
original injury. For example, a musculoskeletal injury could reach the
spinal cord through its afferent connection causing spinal facilitation or
sensitisation to take place. Because of the anatomical proximity of the
motor and autonomic spinal centres, this spread of excitation would
eventually involve these lateral centres. This in turn would alter the
segmental autonomic activity leading to changes in vasomotor, sudomotor and
visceral activity. The reverse could happen too: through the same
neurological mechanisms a pathological condition in the viscera could end up
affecting skeletal muscle activity.
Even before examining the original research, we can see that there are
several problems with the facilitated segment model:
a. The descending influences from higher centres were not included in the
model, although they have profound segmental influences. This omission is
unrealistic - the spinal centres do not work in isolation from the higher
centres. Both movement and autonomic activity are heavily organised from
above the spinal cord (Sherrington, 1906; Folkow, 1956; Bard, 1960; Brown,
1968; Ganong, 1981; Schmidt, 1991).
b. Outside the spinal cord afferent and efferent connections are,
anatomically, highly segmental. However once in the spinal cord all
anatomical specificity is lost (Luscher & Clamann, 1992). Motoneurons of
several muscles are intermingled within the ventral horn and distributed
over several segments up or down from the point of exit (efferent peripheral
nerve). Similarly afferents from one area or muscle, once in the spinal
cord, tend to diverge up and down over several segments terminating on many
different motoneurons and interneurons (Luscher & Clamann, 1992). For
example, spindle afferents from one muscle connect with motoneurons of other
muscle groups (Eccles et al, 1957; Eccles & Lundberg, 1958). This implies
that if lateral spread of sensitisation does take place, it will not
necessarily be segmentally specific.
c. The facilitation model creates a biological paradox which is not
supported either by research or by clinical observations. If damage in
muscle caused spinal facilitation and consequently visceral dysfunction, it
would mean that each time we damage our muscles it would automatically
result in some visceral dysfunction. In this scenario common conditions,
such as delayed-onset muscle soreness which is associated with muscle damage
(Bobbet et al, 1986; Ebbeling & Clarckson, 1989), would inevitably lead to
visceral dysfunction. Yet, 'viscerally' speaking, most sports people are
fairly healthy. They do not seem to develop visceral dysfunction in response
to acute or chronic musculo-skeletal conditions.

The original research
Korr, Denslow and their co-workers were the first to describe the
facilitated segments in osteopathic medicine. The original research
consisted of several studies which were carried out on a large number of
normal healthy subjects. They used different experimental set-ups and were
able to demonstrate the following findings:

1. Varying motor thresholds - pressure over the spinous processes produced
reflex muscle contraction at and close to the segment. In some segments this
response was exaggerated (Denslow et al, 1947). Every person had an
individual pattern of response.
2. Varying levels of skin conductivity - there were differences in the
sweating pattern of the backs of all normal individuals (Korr et al, 1958).
This suggests increased activity of the sweat gland, implying altered
sympathetic activity.
3. Varying levels of vasomotor activity - using temperature and light
sensors they were able to demonstrate that all normal subjects have
individual vasomotor activity which is changed in different parts of the
back (Wright et al, 1960).
4. Viscerosomatic changes - sometimes, known visceral pathologies manifested
segmentally as increased skin conductivity (Korr et al, 1964).
5. Each individual had a unique thermal pattern with some common patterns
shared by all normal subjects (Wright & Korr, 1965).

Contrary to commonly held belief, they did not demonstrate the following:
1. They did not show facilitation - most of the studies were carried out on
normal healthy subjects. In all subjects they found varying levels of
neurological activity at different segmental levels. This is a complex
situation to begin with: if the subjects were healthy how come they all
displayed a supposedly neuropathological state of facilitation? If the
biological norm is that healthy subjects all show signs of facilitation, it
implies that the regional changes observed probably represent the normal
variability of a highly complex system rather than a facilitation
phenomenon. Such variability can be demonstrated anywhere in the body. For
example, if you prod different parts of your own leg, you will find some
areas are more tender, with the muscles feeling stiffer, and if you press
hard enough you may make the muscle contract to evade pain and discomfort.
When this procedure was applied to the spine, as Denslow et al (1947) did,
it was very attractive to view it as segmental facilitation.
Spinal facilitation does occur and can be seen following musculoskeletal
injuries. It is well established that inflammation produces both peripheral
sensitisation of the afferents (such as free nerve endings) and central
sensitisation within the spinal cord (Dunbar & Ruda 1992, Hylden et al 1989,
Cook et al 1987, Woolf & Walters 1991). This sensitisation means that the
threshold of different neurons is reduced, so they respond to mechanical
stimuli to which they were impervious before injury. This process tends to
spread laterally in the spinal cord but in a selective way; not all neurons
are sensitised. The selectivity of the spread seems to be functional in
character supporting the process in some way. For example, lateral
sensitisation has been shown to spread to the motoneurons which supply the
muscles in the affected area (He et al, 1988). This may have a functional
role in the muscle guarding often observed at the site of damage. It is very
difficult to imagine what would be the functional role of a lateral spread
to autonomic-visceral centres in musculo-skeletal damage. It should also be
noted that the sensitisation process seems only to take place when
nociceptors are excited by pain or inflammation and not when proprioceptors
are stimulated, such as during a manual treatment.
A similar sensitisation phenomenon was demonstrated by Korr and his
co-workers (1962), by introducing chemical insults to different spinal
structures. They demonstrated that this lateral spread could alter
sympathetic activity to the segmental sweat glands. This change only took
place when pain was inflicted. However, the spread was not always 'neatly'
segmental; some of the changes were general or remote from the segmental
distribution. This finding is not surprising in the light of what has been
discussed about afferent divergence within the spinal cord. These changes in
sympathetic activity may not necessarily have been due to facilitation. They
may arise as a secondary functional physiological process, e.g. to support
changes in muscle activity or the inflammation process at the site of
damage. Furthermore, such sympathetic changes in sudomotor activity have no
clinical relevance to osteopathic practice. More important clinically are
changes in motoneuron threshold by spinal sensitisation as described by He
et al (1988).
When Korr et al (1962) introduced postural insults, such as heel lifts on
one side, or having the subjects sit on a tilted chair, they observed
changes in the pattern of sweating. The changes were general but sometimes
more noticeable as an exaggeration of the pattern observed before the
insult. Again, they concluded that these changes were due to facilitation.
However this is also doubtful: the changes were probably due to whole body
adjustments to changes in posture rather than a locally organised change in
the spinal cord. Here too the leg can be used as an example. If you ask a
subject to stand on one leg there will be considerable differences in the
muscle activities of the two legs. Naturally the blood supply and sweat
gland activity will also vary considerably between the two legs with an
increase in activity in the balancing leg. These are whole body postural
adjustments incorporating complex patterns of neuromuscular and supportive
autonomic changes. These patterns of recruitment are organised within the
whole system rather then segmentally by the limited and local processes of
facilitation.
All the changes that were demonstrated were during separate studies on
different individuals: one study showed that in normal subjects there may be
a variable pattern of muscle response to pressure (Denslow, 1947). Another
showed changes in skin conductivity (Price & Korr, 1957), and a third showed
variability of vasomotor tone (Wright & Korr, 1960). They never took the
logical step of examining all three phenomena of facilitation in the same
group of subjects! This is equivalent to seeing three different patients,
one with joint pain, one with conjunctivitis and another with urethritis,
and diagnosing them all as having Reiter's Syndrome! Eventually they did
examine the three manifestations of facilitation in a group of subjects with
musculoskeletal injuries. However, for some reason not all subjects had the
full test procedure, e.g. some had skin conductivity but not EMG
examination. In this study they claimed that "frequently" the exaggerated
patterns were segmentally related to the site of injury. This suggests that
the nervous system does not respond in a stereotypic manner to injury.
Unfortunately no statistical analysis was carried out on the data and their
use of terminology such as "frequently" is not very helpful; does it mean
10% or 90% of subjects? Furthermore they never compared the findings of this
study (subjects with musculoskeletal injuries) to the extensive control
group of the previous studies (normal subjects). Interestingly, when one
compares the photographs of skin conductivity of subjects with injury (Korr
et al, 1964, pages 68-70) to those of normal subjects (Korr et al, 1958,
pages 35-37), they don't seem to be different. The results in this study
could be interpreted like the results of their other studies - they
demonstrated individual variability rather than facilitation.Overall, given
that the studies did not exclud the influences of higher centres and made no
direct recordings from the spinal cord it can be argued that all the changes
observed in the studies were not due to local segmental facilitation but
were in fact organised by the total nervous system (with the prominent role
of supra spinal centres).
2. They did not demonstrate somatovisceral reflexes - These early studies
did not show that abnormal muscle activity or skeletal abnormalities will
spread to affect the viscera by the process of facilitation. This is a very
important point: they assumed (along with many generations of osteopaths)
that sympathetic changes to sweat glands of the skin mean that the whole
segmental autonomic system has been affected including the autonomic centres
controlling visceral activity (Korr, 1948; Korr et al, 1962; Korr 1978).
This conclusion is a fantastic hypothetical leap, one which was never
demonstrated in humans with intact nervous systems. Furthermore, they did
not show that stimulation of mechanoreceptors (proprioceptors) would cause a
change in visceral activity. They simply observed the triad of muscle tone,
local tenderness and local sympathetic changes (skin conductivity and
vasomotor). The generally held belief that stimulation of different groups
of proprioceptors can alter visceral activity was never demonstrated in
these studies. They have demonstrated the reverse: that sometimes, known
visceral pathologies manifested segmentally as increased skin conductivity.
However, that does not mean that the reverse is true, i.e. that stimulation
of the soma will alter the activity in the viscera. This would be comparable
to suggesting that since we reflexively close our eyes during sneezing, we
would sneeze each time we close our eyes.
3. They failed to demonstrate relevance to osteopathic manual therapy -
Another interesting point is that there is no mention in all these studies
of which form of manual technique could bring about autonomic changes. The
logical next step of these studies was never taken and was totally
side-stepped in the articles, i.e., testing the effect of different forms of
manual techniques on spinal facilitation. Without discussing techniques, the
concept of facilitated segment has no meaning to an osteopath. The osteopath
needs to know how to change the activity of the facilitated segment. So many
generations of osteopaths have assumed that high velocity thrusts (HVT) are
the most appropriate form of manipulation for normalising or resetting the
facilitated segment.
Recent studies into the effects of manual techniques on neuromuscular
activity have strongly suggested that passive manual techniques are unlikely
to affect this system (Sullivan et al, 1991; Kukulka et al, 1986; Leone &
Kukulka 1988; Belanger et al, 1989; Goldberg, 1992; Sullivan et al, 1993;
Lederman, 1997; Newham & Lederman, 1997). They only produce a transient
artefact event that has no permanent influence on, or ability to bring about
functional changes in overall motor processes. Even if one accepts the
possibility of facilitated segments as described by Korr, Denslow and their
co-workers, it is extremely doubtful that passive stimulation of the soma
would result in the resetting of neurological activity (Lederman, 1997). All
neuromuscular activity is organised centrally to spread centrifugally to the
periphery (Schmidt, 1991). The peripheral receptors (proprioceptors /
mechanoreceptors) provide feedback rather than control the motor system.
Fascinating segments
The criticism in this article is not about the quality of the research but
the interpretations of the results and the far-reaching conclusions that
were drawn. Overall in their studies, Korr, Denslow and their co-workers did
not demonstrate the facilitation phenomenon. In the light of our current
understanding of neurophysiology it is doubtful whether the facilitated
segment model as described by Korr, Denslow and their co-workers has any
neurological basis or clinical application.
An interesting question arises: what was and still is so attractive in the
concept of facilitated segments? The answer I believe lies in the high
velocity thrust (HVT) and segmental adjustments. The concept of the
facilitated segment provides the justification for performing a very
accurate HVT on particular segments. It gives the HVT a physiological depth
beyond the biomechanical structural fixing of the spine. The osteopath is
now able to reach deep into the interior of the patient to affect visceral
pathologies. This was done at a great cost to osteopathy - osteopathic
understanding of neurophysiology has starts and ended at the facilitated
segment. In my view, the principle of the facilitated segment has stifled
the development of osteopathic neurophysiology for the last 50 years.
Important issues such as neuromuscular rehabilitation following
musculoskeletal injuries, central nervous damage, posture and movement
guidance, the psychodynamics of touch and psychophysiological processes and
pain management have never been addressed in depth. Some of these issues
and their relevance to osteopathy and manual therapy have been discussed in
detail by Lederman (1997).

The way forward
There is a need in osteopathy to develop a better understanding of
neurophysiology; to see the wider picture rather than concentrate on a
single fraction of the total system / person. There also needs to be a
better understanding of how osteopathic manual approaches can be developed
to become effective therapeutic processes for treating the nervous system.
This is essential for working with a wide range of clinical conditions which
have a neurophysiological element in them. Some of these are common clinical
conditions that osteopaths see in daily practice such as postural and
movement changes, neuromuscular changes following musculoskeletal injuries
and the neurophysiological aspects of pain.
In order to influence the nervous system treatment should imitate natural
processes that bring about changes in the nervous system. Most important is
the use of cognition, volition and repetition and avoiding the use of
reflexive type treatments that have been demonstrated to have no long term
effects (Lederman 97, Newham & Lederman 97). Lederman (1997), has discussed
in detail how these elements of neurophysiology can be incorporated into and
expand osteopathic practice enabling the treatment of a wider range of
conditions. Some of these points will be discussed in future articles.

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