FROM: J Manipulative Physiol Ther 1998 (May); 21 (4): 267-280 ~ FULL TEXT
David R. Seaman, D.C. and James F. Winterstein, D.C.
Research and Development,
Hendersonville, North Carolina, USA.
This article is reprinted with the permission of National College of Chiropractic and JMPT. Our special thanks to the Editor, Dr. Dana Lawrence, D.C. for permission to reproduce this article exclusively at Chiro.Org!
Background and Objectives: Since the founding
of the chiropractic profession, very few efforts have been made to
thoroughly explain the mechanism(s) by which joint complex
dysfunction generates symptoms. Save for a few papers, only vague
and physiologically inconsistent descriptions have been offered.
The purpose of this article is to propose a precise and
physiologically sound mechanism by which symptoms may be
generated by joint complex dysfunction.
Data Sources: The data was accumulated over a
years by reviewing contemporary articles and books, and
subsequently retrieving relevant papers. Articles were also
selected from volumes 1-4 of the Chiropractic Research Archives
Collection. The Nexus, published by the David D. Palmer
Health Sciences Library, and In Touch, published by Logan
College of Chiropractic Library, were reviewed and relevant
articles were retrieved. Medline searches were found to be
ineffective because appropriate key indexing terms were difficult
Data Synthesis: The symptoms generated by joint
dysfunction, such as pain, nausea and vertigo, are probably
caused by increased nociceptive input and/or reduced
Conclusions: Joint complex dysfunction should
included in the differential diagnosis of pain and visceral
symptoms because joint complex dysfunction can often generate
symptoms which are similar to those produced by true visceral
Key Indexing Terms: Allodynia; Central
Dysafferentation; Joint Complex Dysfunction; Mechanoreception;
Nociception; Nociceptor Sensitization
In a recent article, the term joint complex
dysfunction was suggested as a replacement for subluxation
complex . Joint complex dysfunction refers to pathological and
functional changes that occur in joint complex structures
including (a) the negative effects of hypomobility/immobility,
(b) functional imbalances such as muscle tightening or shortening
and (c) myofascial trigger points. In short, the article
demonstrated how the term joint complex dysfunction allows for a
more descriptive and pathophysiologically precise discussion of
spinal dysfunction compared with the term subluxation/subluxation
complex. The author also proposed that the chiropractic
profession adopt the term "dysafferentation" to describe the
neuropathophysiological effects of joint complex dysfunction that
act to generate symptoms .
The topic of symptom generation remains a source for
within the chiropractic profession. For example, B. J. Palmer,
who was often referred to as the "developer" of chiropractic,
maintained "a peculiar belief in the perfection of the incoming
(afferent) sensory system" . In his writings, Palmer indicated
that subluxations only affected efferent pathways and not the
afferent system . Many modern-day chiropractors still promote
this notion. They believe that subluxations impinge upon spinal
nerves at the level of the intervertebral foramina and interfere
with the conduction of impulses innately generated within the
brain and which subsequently pass through neural tissue, with the
result that tissue supplied by the affected nerves could suffer
some form of functional insult .
Another popular notion is that upper cervical
misalignments can somehow impinge upon the medulla and interfere
with the transmission of "the mental impulse life force" . To
our knowledge, at the present time, there is no evidence to
support such opinions about this type of relationship between
joint complex dysfunction and efferent nerve function. However,
as will be discussed in this article, a great deal of information
suggests that joint complex dysfunction affects the afferent
system by altering the function of nociceptors and
mechanoreceptors found within the structures of the joint
complex. The purpose of this article is to describe the sensory
receptors and their relationship to afferent input and to
describe possible symptoms that can develop in response to
enhanced nociceptor input and reduced mechanoreceptor input,
which has been referred to previously as dysafferentation . We
should mention that much confusion exists regarding sensory
receptor terminology . Consequently, a discussion about
receptors and their function can lead to unnecessary arguments
[6, 7]. For this reason and for the sake of clarity in general,
pertinent terminology will be discussed in appropriate sections
of this article.
Afferentation and Deafferentation
Afferentation refers to the transmission of afferent nerve
impulses; deafferentation is defined as the elimination or
interruption of afferent nerve impulses, as by destruction of
the afferent pathway . In neurological literature, the word
"deafferentation" is typically reserved for conditions in which
peripheral nerves are either damaged, completely severed or
avulsed [9-11]. Because joint complex dysfunction is very rarely
associated with peripheral nerve injury, it is not appropriate to
use the word deafferentation.
Dysafferentation refers to an imbalance in afferent
such that there is an increase in nociceptor input and a
reduction in mechanoreceptor input . Notice that
proprioceptors are not mentioned; this is because contemporary
texts do not consider proprioceptors a category of receptor. A
recent article explained why 'proprioceptor' is actually an
obsolete, inaccurate word .
According to standard texts in neurology, there are two
categories of somatic receptors: nociceptors and mechanoreceptors
[5, 12-14]. At the present time, an emerging body of research
indicates that abnormal joint complex function can alter the
activity of nociceptors [15-19] and mechanoreceptors [20-23],
such that nociceptive activity increases and mechanoreceptive
activity decreases. Many authors and researchers involved in
joint adjusting and manipulation realize this and use the terms
"altered afferent input," "abnormal afferent input" or similar
terms when discussing the neuropathophysiological component of
joint complex dysfunction [24-32]. For example, Peterson stated
that, "somatic dysfunction and/or joint dysfunction induce
persistent nociceptive input and altered proprioceptive input"
. Peterson and Bergmann described vertebral joint
dysfunctions and their associated mechanical alterations, pain
and potential local inflammation as lesions capable of inducing
chronically altered nociceptive and proprioceptive input" .
Hooshmand illustrated how restricted joint mobility results in
decreased firing of large diameter mechanoreceptor axons (A-beta
fibers) and increased firing of nociceptive axons (A-delta and C
fibers) . Henderson used the term "altered somatic afferent
input theory" to classify a neurophysiologic theory of
chiropractic subluxation . He proposed that chiropractic
adjustment might normalize articular afferent input to the
nervous system, which reestablishes normal nociceptive and
kinesthetic reflex thresholds.
The information in the previous paragraph demonstrates
researchers in different professions have acknowledged the fact
that compromised joint function will alter afferent input, such
that nociception is enhanced and mechanoreception is reduced. In
the biomedical literature, the prefix "dys" is used to describe
activity that is abnormal, bad, difficult or disordered . For
this reason, we propose that the chiropractic profession adopt
the word 'dysafferentation' to describe the abnormal afferent
input associated with joint complex dysfunction .
The remainder of this article will discuss potential
that may develop as a consequence of dysafferent input (i.e.,
increased nociception and reduced mechanoreception). To
accomplish this task, both the neuroanatomy and physiology
related to nociceptors and mechanoreceptors will be discussed and
then related to symptom generation.
Dr. Seaman kindly supplied us with this figure for your reference.
Many believe that spinal
tissue nociceptors can be found in:
- subcutaneous and adipose tissue,
- fibrous capsules of the apophyseal and sacroiliac joints,
- spinal ligaments,
- the periosteum covering vertebral bodies and arches (and
attached fascia, tendons and aponeurosis),
- the dura mater and epidural fibro-adipose tissue,
- the walls of blood vessels supplying the spinal joints,
sacroiliac joints and the vertebral cancellous bone,
- the walls of epidural and paravertebral veins and
- the walls of intramuscular arteries and at least the outer
third of the annulus fibrosis [34-41].
Wyke provides the most vivid anatomical description of
nociceptive receptor system . He described interstitial
nociceptors as "a continuous tri-dimensional plexus of
unmyelinated nerve fibers that weaves (like chicken-wire) in all
directions throughout the tissue." A similar plexus of
unmyelinated nerve fibers is embedded in the adventitial sheath
and encircles each blood vessel. Commenting on nociceptive C
fiber innervation, Charman stated that the "network of each C
fibre innervates a three-dimensional receptive field of between 6
and 15 mm in diameter and of variable depth with extensive field
overlapping between adjacent C-fibers" . Thus, we can
envision the presence of an almost unending meshwork of
nociceptors within the various tissues described earlier.
Nociceptors are classified as mechanical nociceptors,
mechanothermal nociceptors and polymodal nociceptors, depending
on the type of energy used to activate them in the nociceptive
range. Polymodal nociceptors are activated by noxious mechanical
and thermal stimulation, as well as by chemical mediators
released from the injured tissues .
Recent research has demonstrated the presence of
nociceptors with thresholds so high that they cannot be excited
by acute noxious stimulation, for example, mechanical injury to
the joint [17-19, 43]. Thus, these nociceptors are normally
mechano-insensitive and have been characterized as solely
chemosensitive . This special category of nociceptors is
called silent or sleeping nociceptors. Sleeping nociceptors are
thought to awaken in the presence of chemical mediators released
from injured tissues [17, 18, 43], at which time they become
mechanosensitive. It is thought that the activation of these
afferents may not only represent an extra source of nociceptive
input but may also be important in promoting central
Generally speaking, mechanical and mechanothermal
are innervated by A-delta axons, whereas polymodal and silent
nociceptors receive their innervation from C fibers. Within the
spinal cord, nociceptive afferents send collaterals to supra- and
infra-adjacent segments. For example, A-delta fibers spread
collaterals three to six segments rostrally and an equal number
caudally, whereas C fibers spread two to three (or possibly more)
segments above and below the level of entry .
A recent review by Charman provides a vivid description
central connections of nociceptive afferents . Nociceptive
afferents travel up the anterolateral system and ultimately
terminate in the spinal cord, a variety of brainstem nuclei, the
limbic system, frontal lobes, parietal lobes, insula cortex and
Peripheral nociceptive sensitization
Nociceptors have high thresholds of activation,
means that, under normal circumstances, only stimuli that are
either potentially or overtly tissue-damaging can depolarize a
nociceptor [45, 46]. Normally, light touch and normal joint
motion cannot depolarize a nociceptor .
Although nociceptors normally have high thresholds, certain
physiological environments can result in the lowering of
nociceptive thresholds, such that light touch and normal movement
patterns can cause nociceptor depolarization and excitation of
nociceptive afferent pathways. Peripheral sensitization is the
term used to describe the process by which nociceptor thresholds
are lowered , thus enhancing the transmission of nociceptive
impulses into the spinal cord. The driving force behind the
sensitization process seems to be the chemical mediators released
after tissue injury. Prostaglandin E-2, leukotriene B-4,
bradykinin, histamine and 5-hydroxytryptamine are thought to be
the main chemical mediators that can sensitize nociceptors [10,
47]. Local tissue acidity is also thought to be capable of
participating in the sensitization process [47 49].
Recent research suggests that norepinephrine release from
sympathetic terminals into the area of tissue injury can also
sensitize nociceptors [47, 50-52]. The exact mechanism by which
this occurs is not well understood. It is possible that
norepinephrine released from sympathetic terminals activates
alpha-1-adrenergic receptors found on the nociceptor membrane
. It is also possible that sympathetic discharge into the
area of tissue injury promotes the release of prostaglandins
It is not clear whether substance P is directly involved
the sensitization process [10, 47, 54]. We know that substance P
is produced in the dorsal root ganglion cells and then
transmitted to the spinal cord and to the nociceptor. Substance P
is released from nociceptors after they are activated by noxious
input. The activity of substance P in this local environment can
cause further accumulation of bradykinin and the release of
histamine from mast cells and 5-hydroxytryptamine from platelets,
all of which can promote the sensitization of local nociceptors
It is thought that chemical mediators depolarize and/or
sensitize a nociceptor through their interaction with
chemosensitive receptors on the membrane of the nociceptor, which
influences the flow of sodium, calcium and potassium ions Some of
the chemical mediators have receptors linked directly to ion
channels, whereas the receptors for other mediators are linked to
second messenger systems that modulate ion channels. For more
details, see Rang et al. .
It is important to consider the degree to which
sensitization can influence the activity of the associated
afferent fibers and the spinal cord. Hanesch et al. provide a
vivid example of afferent fiber function after nociceptor
sensitization . They studied the medial articular nerve in
cats and discovered that, in normal joints, the afferent volley
during a simple flexion movement comprises approximately 4,400
impulses per 30 seconds, including resting discharges. During
inflammation, which promotes nociceptor sensitization, the
afferent volley comprises some 30,900 impulses per 30 seconds,
which represents about a sevenfold increase compared with normal
conditions. They indicated that, "in individual afferents that
have been studied consecutively under both normal and inflamed
conditions, the afferent discharges sometimes increased more than
It is thought that an increased nociceptive barrage
sensitized nociceptors plays a role in the development of central
nociceptive sensitization. Researchers have yet to discover all
of the details about central sensitization. Nonetheless, we will
attempt to provide the most relevant data in the next
Central nociceptive sensitization
After tissue injury, nociceptors exhibit
activity, lowered thresholds and increased responsiveness to
noxious stimuli, which leads to hyperexcitability and altered
neuronal processing in the spinal cord and brain . The term
'central sensitization' refers to this increased excitability of
nociceptive neurons in the central nervous system (CNS) . Of
importance to the chiropractic profession is the fact that joint
nociceptors, as with nociceptors in other tissues, can be
sensitized . In addition, joint and muscle nociceptors are
much more capable of producing central nociceptive sensitization
than cutaneous nociceptors .
In 1942, Denslow and Hassett reviewed the literature and
demonstrated that the concept of spinal cord hyperexcitability
had been around since at least the 1930s . At that time, the
term central excitatory state was used to describe central
sensitization. Denslow and Hassett were the first to suggest and
demonstrate that spinal dysfunction (i.e., joint complex
dysfunction) was associated with central sensitization. They
credited Charles Sherrington for developing the concept of the
central excitatory state. They state that the evocation of
additional activity by a stimulus which, in the normal would be
ineffective, is explained by Sherrington's concept of a
motoneuron pool in which there is an enduring subliminal central
excitatory state (CES) created by sub-threshold stimuli .
In 1947, Denslow et al. used the terms facilitation and
central facilitation in an effort to describe what is now
referred to as central sensitization . Recently, Patterson
indicated that Irvin Korr is credited with coining the term
facilitated segment , about which Korr wrote numerous
articles [61 -67].
In 1983, and apparently without knowledge of the work by
Denslow et al., Woolf hypothesized and then experimentally
demonstrated the presence of a hyperexcitable central component
in post-injury pain hypersensitivity . In 1987, Woolf
provided a clear explanation of central sensitization: "C fiber
input to the spinal cord, in addition to producing input
concerning the onset, location and duration of the peripheral
noxious stimuli, also produces a prolonged increase in the
excitability of the spinal cord" . Research demonstrated that
brief conditioning stimuli of nociceptive C -fibers (up to 20
sec) at low frequencies (1 Hz) can produce a prolonged excitation
(up to 90 minutes) of the spinal cord. Additionally, it was shown
that C fibers innervating deep structures, such as joints or
muscles, can more readily produce central facilitation than can
cutaneous C fibers - . The activation of nociceptive C
afferents can also produce profound changes in the receptive
field properties of dorsal horn neurons, such as an expansion of
the receptive field size, an increase in spontaneous activity,
and an increase in response to innocuous stimuli .
Since Woolf's initial article in 1983, a great deal of
research has been devoted to understanding the process of central
sensitization [55, 56, 69-81]. Most authors now agree that
central sensitization manifests in CNS neurons as increased
spontaneous activity, reduced thresholds or increased
responsiveness to afferent inputs, which are prolonged after
discharge from repeated stimulation, and expanded receptive
fields of -dorsal horn neurons . Many think that these CNS
changes are caused by an increase in excitatory inputs and/or a
loss of inhibitory inputs, which result in a net excitation of
the dorsal horn .
At the present time, an emerging impression is that
cord plasticity is responsible for the development of central
sensitization [55, 56, 69-71, 82]. In general, plasticity refers
to an adaptation of the nervous system in response to changes in
the associated internal or external environment . Kandel
states-that plasticity is a "change in the effectiveness of
specific synaptic connections" . Research suggests that the
physiological basis of plasticity involves an increase in gene
expression, particularly intermediate-early genes, such as
c-fos and c-jun [70, 85]. With respect to central
sensitization, plastic changes begin after the release of various
excitatory transmitter substances from nociceptive afferents,
such as substance P, calcitonin gene-related peptide, aspartate
and glutamate, and their subsequent action at
N-methyl-D-aspartate receptor sites. Dubner and Ruda provide a
review of this proposed mechanism .
It is thought that central sensitization extends to
the dorsal and anterior horns of the spinal cord, the thalamus
and even higher centers [56, 86, 87]. In other words, noxious
input leads to the hyperexcitability of alpha-motoneurons,
preganglionic sympathetic neurons, spinal cord nociceptive
projection neurons, thalamic projection neurons and other neurons
in the brain. A variety of symptoms and conditions can develop in
response to these changes. For example, it is known that
nociceptor sensitization and central nociceptive sensitization of
projection neurons causes increased pain . From a clinical
perspective, chiropractors routinely encounter pain associated
with a sensitized nociceptive system. It is common to discover
that gentle or normal palpation of spinal tissues results in the
experience of pain. The word allodynia is used to describe this
state, in which normally painless stimuli result in pain
Considering the fact that nociceptive input reaches
subcortical areas, such as the brainstem hypothalamus , it is
also likely that -a wide variety of neuro-endocrine responses and
seemingly unrelated symptoms could develop in response to a
sensitized nociceptive system. The following two sections discuss
these relationships in some detail.
Neuro-endocrine responses caused by nociceptive input to
We know that nociceptive afferent input travels
anterolateral pathway, which contains the spinoreticular and
spinothalamic tracts. -Bonica provides a succinct explanation of
the neuroendocrine responses associated with such activity
Suprasegmental reflex responses result from nociceptive
induced stimulation of medullary centers of ventilation and
circulation, -hypothalamic (predominantly sympathetic) centers of
neuroendocrine function and some limbic structures. These
responses consist of hyperventilation, increased hypothalamic
neural sympathetic tone and increased secretion of catecholamines
and other catabolic hormones. The increased neural sympathetic
tone and catecholamine secretion add to the effects of spinal
reflexes and further increase cardiac output, peripheral
resistance, blood pressure, cardiac workload and myocardial
oxygen consumption. In addition to catecholamine release, there
is an increased secretion of cortisol, adrenocorticotrophic
hormone, glucagon, cyclic AMP, antidiuretic hormone, growth
hormone, renin and other catabolically acting hormones, with a
concomitant decrease in the anabolically acting hormones insulin
and testosterone.--- Cortical responses, in addition to and
including the perception of pain as an unpleasant sensation and
negative emotion, initiate the psychodynamic mechanisms of
anxiety, apprehension and fear. These, in turn, produce
cortically mediated increases in blood viscosity, clotting time,
fibrinolysis and platelet aggregation. Indeed, cortisol and
catecholamine responses to anxiety usually exceed the
hypothalamic response that is provoked directly by nociceptive
impulses reaching the hypothalamus.
Bonica demonstrates the degree to which nociceptive
metabolically compromise the host. As implied above, subcortical
responses can occur with or without the experience of pain.
Perhaps such asymptomatic neuroendocrine responses, induced by
nociceptive input, play a role in the pathogenesis of
degenerative diseases, such as cardiovascular disease, cancer,
diabetes, -arthritis and Alzheimer' 5 disease. We need more
research in this area, which becomes more obvious when the
devastating effects of hypercortisolemia are considered.
Cortisol levels are increased by nociception, pain,
inflammation, trauma, anxiety, fear, apprehension, prolonged and
strenuous exercise and hypoglycemia [87, 88]. When stressors are
present for protracted periods of time, feedback suppressibility
of cortisol can be impaired .
The damaging effects of excess endogenous cortisol are
jeopardizing as those associated with exogenous intake in the
form of medication. Such a relationship can be better appreciated
when we understand that -cortisol secretion can rise 20-fold when
the adrenal gland is chronically stimulated .
Excess cortisol produces a continuous drain on body
stores, most notably in muscle, bone, connective tissue and skin.
Hypercortisolemia causes a variety of tissue-specific changes,
including a reduction in rapid-eye-movement sleep; a reduction of
cell-mediated immunity by inhibiting the production of
interleukin- 1, interleukin-2 and gamma-interferon; a decrease in
the proliferation of osteoblasts; and a reduction in collagen
synthesis. We know cortisol antagonizes the action of insulin,
which results in decreased glucose use. Cortisol stimulates
lipogenesis in specific body locations, including the abdomen,
trunk and face .
Chronic hypercortisolemia may play a role in spinal
degeneration. We know that cortisol preferentially reduces the
ratio of slow oxidative type I muscle fibers to fast glycolytic
type Il-B -fibers . This may enhance the deconditioning -of
spinal muscles that occurs as a consequence of sedentary living
and aging and may promote spinal injury and chronic joint complex
There are also a number of diseases that are driven by
hypercortisolemia. Dilman and Dean actually characterize
hypercortisolemia as a disease . They coined the term
hyperadaptosis to describe a state characterized in its latent
stage -by an excessive and -prolonged elevation of cortisol
levels in response to stressors, and in its overt stage by an
elevation of basal cortisol levels in the absence of apparent
stressors. Several conditions are known to develop as a
consequence of hypercortisolemia, including heart disease,
various cancers, hypertension, depression, obesity and diabetes
Symptoms caused by nociceptive input to subcortical centers
Feinstein et al. were the first to clearly
some symptoms associated with noxious irritation of spinal
tissues . They injected hypertonic saline into interspinous
tissues and paraspinal muscles of normal volunteers for the
purpose of characterizing local and referred pain patterns that
might -develop. What they discovered was surprising:
The pain elicited from muscles was accompanied by a
characteristic group of phenomena which indicated involvement of
other than segmental somatic mechanisms. The manifestations
were pallor, sweating bradycardia, fall in blood pressure,
subjective 'faintness," and nausea, but vomiting was not
observed. Syncope occurred in two early procedures in the series
of paravertebral injections and was subsequently avoided by
quickly depressing the subject's head or by having him lie down
at the first sign of faintness. These features were not
proportional to the severity of or to the extent of radiation; on
the contrary, they seemed to doimnate the experience of subjects
who complained of little pain, but who were overwhelmed by this
distressing complex of symptoms.
Feinstein et al. -referred to these symptoms as
concomitants . It is likely that these autonomic concomitants
were caused by nociceptive stimulation of autonomic centers in
the brainstem, particularly the medulla . Fein stein et al.
indicate that "this is an example of the ability of deep noxious
stimulation to activate generalized autonomic responses
independently of the relay of pain to conscious levels" . In
other words, pain may not be the symptomatic outcome of
nociceptive stimulation of spinal structures. Such a conclusion
has profound implications for the chiropractic profession.
Clearly, patients do not need to be in pain to be candidates for
Nansel and Szlazak published the most recent article
devoted to autonomic concomitants associated with nociceptive input
- . They explained -that it is now well-established that
nociceptive input from somatic and visceral structures "converges
on common pools of interneurons within the spinal cord and
brainstem." As -a consequence, nociceptive input from somatic
structures can "create complex patterns of signs and symptoms
-that can often be virtually identical to and, therefore, easily
mistaken for those induced by primary visceral disease." They
have collected more than 200 scientific articles that deal with
various somatic visceral disease mimicry syndromes.
In summary, there are many neuroendocrine and -symptomatic
presentations that can occur in response to nociceptive input. It
is very likely that no two patients will present in the exact
same fashion, even if joint complex dysfunction exists in the
same spinal location. The symptomatic picture can become even
more complex when the consequences of reduce mechanoreception
Mechanoreceptors are located in the skin, muscles,
structures and the intervertebral disc [13, 14, 92]. Examples of
mechanoreceptors include muscle spindles, golgi tendon organs
(GTOs) and a variety of corpuscular mechanoreceptors, such as
Ruffini endings, Merkel cell complexes, Meissner's corpuscles,
Pacinian corpuscles and many others .
Many believe that, as a group, mechanoreceptors respond only
to weak mechanical stimuli, such as touch and joint movement, and
not to nociceptive stimuli with higher frequencies [l8, 19, 42,
93]. -As would be expected, several authors suggest that reduced
joint movement results in less mechanoreceptor activation
[20-23]; however, the degree to which mechanoreceptor input would
be compromised by joint hypomobility is unknown at the present
time. Although it may be difficult to quantify such
mechanoreceptor deficits in the laboratory, research suggests
that a reduction in mechanoreceptor afferent input can result in
the development of symptoms that can be identified in the
clinical setting. For example, de Jong et al. injected human
subjects with lidocaine in the area halfway between the mastoid
process and carotid tuberde at the level of the second and third
cervical vertebrae . Injections were made unilaterally.
Immediately after injection, symptoms of dysequilibrium began to
appear. Symptoms included ataxia, hypotonia of the ipsilateral
arm and leg and a strong sensation if ipsilateral falling or
tilting. The symptoms were more pronounced on the side of
injection and lasted for about an hour. The authors suggested
that the injection of local anesthetics interrupts the flow of
afferent information from neck and muscle receptors," which can
affect vestibular nuclei function and promote a variety of
vestibular symptoms . Presumably, the receptor types to which
de Jong et al. refer include corpuscular mechanoreceptors, muscle
spindles and GTOs.
A brief review of mechanoreceptor subtypes, their basic
functions and the neuroanatomical pathways associated with
mechanoreceptors will help to outline potential symptoms that may
develop because of joint complex dysfunction.
Corpuscular mechanoreceptors are found in the
joint structures and muscles [14, 21, 95]. in general, -people
believe that corpuscular mechanoreceptors are associated with
A-beta fibers [12, 13].
Mechanoreceptor afferents (A-beta fibers) influence the
nervous system in many ways. For example, at the spinal cord
level, mechanoreceptor input can inhibit nociception [14, 20,
96-99]. Thus, it is very likely that reduced mechanoreceptive
activity will enhance the nociceptive input associated with joint
complex dysfunction. Also, mechanoreceptor afferents can reduce
sympathetic hyperactivity [20, 99, 100]. Thus, it is reasonable
to suggest that reduced mechanoreception will enhance segmental
sympathetic hyperactivity and somatomotor output.
Clearly, mechanoreceptor afferents have important functions in
the CNS. It seems that it would be ideal to have an abundance of
mechanoreceptors functioning at an optimal level at all times.
Unfortunately, it also seems that there are relatively few
corpuscular mechanoreceptors compared with nociceptors.
The precise concentration of corpuscular
somatic tissues is unknown. Recent research suggests that the
concentration of nociceptors far exceeds that of corpuscular
mechanoreceptors. Schmidt et al. discus-s the percentage of fiber
types in the medial articular nerve and posterior articular nerve
of the cat . Only 9% of the fibers in the medial articular
nerve and 26% in the posterior articular nerve were
mechanoreceptive. Such a low percentage of mechanoreceptive
afferents suggests that maintaining prQper joint mobility is very
Muscle spindles are classically described as
that send information into the CNS about muscle length or the
rate of change of muscle length. It is generally believed that
muscle spindles lie parallel to extrafusal fibers in the center
of a muscle. Muscle spindles have primary endings associated with
a group Ia afferent fiber and secondary endings associated with a
group II afferent fiber. Both group Ia and II fibers are thought
to have numerous connections within the spinal cord.
Group Ia afferents are involved in several cord reflexes
modulate extrafusal muscle function, such as the stretch reflex,
recurrent inhibition, reciprocal inhibition and the cross
extensor reflex . All of these reflexes are very important
for promoting smooth and controlled movements. Group II afferents
are not as well described as Ia afferents. It is generally
believed that group II afferents primarily affect the static
component of the stretch reflex.
In general, the greatest concentration of muscle
located in muscles involved in fine movements and posture,
whereas the lowest concentration is found in muscles involved in
gross movement . Research has demonstrated that the digits
and neck contain the greatest density of muscle spindles. Indeed,
it has been stated that the neck muscles contain a "bewildering
number of muscle spindles" . Dvorak and Dvorak indicate
that, per gram of muscle tissue, the rectus femoris contains 50
muscle spindles, whereas the suboccipital muscles contain
approximately 150-200 muscle spindles and the intertransverse
muscles in the cervical spine contain between 200-500 muscle
spindles . Some have suggested that the intertransverse
muscles of the neck and lower back may actually function as
mechanoreceptors and not as muscles .
The distribution of muscle spindles within muscles is
varied and complex than the classic description. Richmond et al.
indicated that muscle spindles can be associated with one another
in several ways, including:
(a) paired associations, in which two or more spindles lie side-by-side,
(b) parallel associations, in which two or more intrafusal fiber bundles are contained within a common capsule for some part of their -length and
(c) tandem associations, in which two or more spindle units are linked in series by a common intrafusal fiber that runs through each spindle unit in succession."
It is not uncommon to find muscle spindles linked in
arrays that span the length of an intervertebral muscle. Some
spindles are also found in close contact with Paciniform
corpuscles and GTOs .
GTOs are usually described as muscle tension
receptors. Many believe that GTOs lie in series with extrafusal
fibers. In other words, GTOs are found at the junction of a
muscle and its tendon.
GTOs are stimulated when muscle contraction generates tension
in a muscle. The frequency of firings increase in proportion to
the increasing muscle tension . GTOs are innervated by a
group lb afferent fiber. The lb afferent enters the cord and
excites an interneuron located in the intermediate region of
spinal cord gray matter. This so-called lb inhibitory interneuron
serves to inhibit the alpiha-motoneuron that innervates the same
muscle that was contracted and created the tension. It should be
mentioned that the lb inhibitory intemeuron receives convergent
input from -Ia afferents from muscle spindles and A-beta
afferents from cutaneous and joint receptors [100, 105].
GTOs are highly concentrated in neck muscles. Their
distribution tends to be nonuniform. They are found -along
internal aponeurosis and where muscles attach to the vertebral
process. In both the deep and more superficial neck muscles,
spindles and -GTOs are often clustered in complex receptor arrays
In recent years. it has been shown the GTOs have a
sensitivity and are more suited to signaling rapidly changing
tensions rather than static levels of tension. Research has shown
that GTOs respond to forces as low as 4 mg.
We know that afferent input from corpuscular
mechanoreceptors, muscle spindles and GTOs can influence brain
-function. Researchers have stated that mechanoreceptive input is
partially responsible for proprioception [14, 96] and
suprasegmental motor control . Indeed, it seems that many
supraspinal centers depend on afferent input, including the
cerebellum and cerebral cortex. For example, Carpenter states
that afferent fiber input to the cerebellum exceeds efferent
fibers by a ratio of-approximately 40:1, which demonstrates the
degree to which afferent input is needed by the CNS . With
this information in mind, it is important to consider -the
probability that joint complex dysfunction is associated with the
degeneration, atrophy and deconditioning of mechanoreceptor rich
tissues, such as muscles and joint structures [1, 107-109].
The following sections describe the main afferent and
subsequent efferent connections of the cerebellum and cerebral
cortex. Based on these connections and related research findings,
a variety of potential symptoms that may manifest in response to
the reduced mechanoreceptive input associated with joint
dysfunction will be described.
Brodal provides a detailed description of
mechanoreceptive input to the cerebellum . Afferents enter
the cerebellum through all three cerebellar peduncles. Whereas
the superior peduncle contains mostly efferent fibers and some
afferent fibers, the middle peduncle contains only afferent
fibers and the inferior peduncle contains mostly afferent fibers
and some efferent fibers. The discussion that follows focuses on
afferent information that travels through the middle and inferior
Afferents entering the middle cerebellar peduncle come
the cerebral cortex via the corticopontocerebellar tract, which
contains some 20 million fibers . The majority of these
fibers project to the lateral cortex of the cerebellum, which is
involved in the coordination and regulation of sequential and
volitional motor activities initiated by the cerebral cortex [95,
110]. Clearly, without afferent input, the lateral cortex could
not properly modulate motor control.
The lateral cortex is often called the cerebrocerebellum
because it receives input exclusively from the cerebral cortex by
way of the pontine nuclei . The heaviest projections come
from the primary motor area (Brodmann area 4), the primary
sensory area (Brodmann areas 3, 1 and 2), a somatosensory
association area (Brodmann area 5) and from parts of the visual
areas related to the peripheral visual field . Areas 3, 1 and
2, the primary sensory area, each receive afferents from specific
receptors . Group Ia muscle spindle afferents project to
area 3a. Cutaneous afferents project to area 3b. Joint afferents
project to area 2. Area 1 receives input from both cutaneous and
deep tissue receptors. This information makes it clear that a
significant level of mechanoreceptor afferent input indirectly
reaches the cerebellum by way of the cerebral cortex.
The inferior peduncle contains some 0.5 million fibers
most of which originate from receptors in axial and appendicular
structures. -Afferents from spinal structures end in the
cerebellar vermis, whereas afferents from the extremities end in
the intermediate cortex, which is also referred to as the
paravermal region. It is important to note that this input is
somatotopically organized. Nolte indicates that the principal
sources of afferent input to the vermis and intermediate cortex
come via the -spinal cord from mechanoreceptors in the skin,
muscles and joints . For this reason, the vermis and
intermediate cortex are often referred to as the spinocerebellum.
It should be mentioned that both the vermis and intermediate
cortex also receive afferent input from the motor cortex by way
of the corticopontocerebellar tract. This input is
somatotopically organized so that the cortical fibers end in the
same pattern as those from mechanoreceptor afferents [1-10].
As far back as 1960, researchers determined that the
spinocerebellar tract conveys information to the vermis and
intermediate cortex from muscle spindles, GTOs and corpuscular
mechanoreceptors in the skin. Later, it was determined that the
dorsal spinocerebellar tract also conveys information from joint
receptors . We know that the dorsal spinocerebellar tract
conveys mechanoreceptive information from the lower half of the
body and the cuneocerebellar tract relays mechanoreceptor
afferent input from the upper half [95, 107]. The importance of
the spinocerebellar pathways is demonstrated by the conduction
velocity of its component fibers. We know that impulses are
transmitted at velocities up to 120 rn/sec for the purpose of
instantaneously apprising the cerebellum of peripheral movements
. Additional afferents that travel through the inferior
cerebellar peduncle to end in the spinocerebellum arise from the
inferior olive and central-cervical nucleus.
The inferior olive also provides input to the cerebellum from
mechanoreceptor afferents that end somatotopically in the olive
. Carpenter  indicated that afferents from cutaneous
receptors and lb afferents from GTOs contribute to the
spino-olivary tract. Proske indicated that the principal
supraspinal site of termination for OTO afferents is the
cerebellum . The major -projection is from the
spinocerebellar tracts and the secondary projection comes from
the inferior olive via the spino-olivary tract . If the
spino-olivary tract fis consistent with other ascending
mechanoreceptive tracts, it is likely that all types of
mechanoreceptor afferents project to the inferior olive. Brodal
states that "the quantitatively most important contingents of
afferents mediate spinal impulses" .
The inferior olive is a very important structure and far
complex to discuss in this article. In brief, we know that the
inferior olive projects -to all parts of the cerebellar cortex
and all deep cerebellar nuclei (i.e., the dentate, globus,
emboliform (nucleus interpositus) and fastigial). There are even
reciprocal connections between each cerebellar nucleus and the
olive. In addition to mechanoreceptor afferents, the inferior
olive also receives -input from the cerebral cortex (chiefly the
motor cortex), red nucleus, mesencephalic reticular formation,
superior colliculus and pretectum . The symptoms associated
with experimental oblation of the inferior olive are similar to
those associated with destruction of the entire contralateral
The central cervical nucleus (CCN), located in lamina
the first four cervical segments, projects to the cerebellar
vermis . Originally, the CCN was thought to receive only
upper cervical mechanoreceptor afferents [95, 112]. Recent
research suggests that the CCN may receive mechanoreceptor
afferents from as low as the lumbar spine . However, there
is evidence to suggest that the CCN is most powerfully influenced
by receptors in deep neck muscles .
The vermis functions to control equilibrium, posture,
tone and locomotion [12, 95, 107]. Ghez states that the vermis is
involved in axial and proximal motor control . It must be
remembered that, without proper afferent input, these functions
would be compromised.
Assuming that the vermis receives sufficient
input, it will modulate motor function by projecting to a variety
of nuclei. The vermis projects somatotopically organized
information to the fastigial nucleus, which then projects
bilaterally to the lateral vestibular nucleu and reticular
formation nuclei , particularly the nucleus reticularis
pontis caudalis and the nucleus reticularis gigantocellularis
. The tracts associated with these nuclei include the lateral
vestibulospinal tract, the medial reticulospinal tract and the
lateral reticulospinal tract. respectively. We know the fastigial
nucleus also projects to the thalamus and, ultimately, to the
motor cortex [95, 111].
The intermediate cortex mainly coordinates the actions
distal extremities [95, 107, 111]. It accomplishes this task by
projecting to nucleus interpositus, which projects mainly to the
red nucleus and motor cortex, affecting the rubrospinal tract and
corticospinal tract, respectively. Many believe that the
intermediate cortex compares commands emanating from the motor
cortex with the actual position and velocity of the moving part
(it receives this information from mechanoreceptors); then, by
way of the nucleus interpositus, the intermediate cortex issues
correcting signals . Without adequate mechanoreceptor input,
the ability of the intermediate cortex to modulate motor control
would be compromised.
Thus far, both the cerebrocerebellum and spinocerebellum
been discussed. The third division of the cerebellum is known as
the vestibulocerebellum, so named because it receives afferent
input from the vestibular nerve and vestibular nuclei. The
flocculonodular lobe is the specific area of the cerebellum
referred to as the vestibulocerebellum. Afferents to the
vestibulocerebellum also travel through the inferior cerebellar
Most texts indicate that only vestibular afferents end
flocculonodular lobe [11, 110, 111]; however, this is not the
case. Guyton alluded to the fact that mechanoreceptor afferents
from the neck also gain access to the flocculonodular lobe .
He explains that mechanoreceptors from the neck and body transmit
information directly into the vestibular nuclei and indirectly,
by way of the cerebellum, into the flocculonodular lobe.
Apparently, mechanoreceptor input from the neck transmits signals
that oppose the signals from the vestibular apparatus, which
prevents a person from developing dysequilibrium when the head is
laterally flexed or rotated. Guyton further stated that, "by far
the most important proprioceptive information needed for the
maintenance of equilibrium is that derived from the joint
receptors of the neck" . Although not described by Guyton,
several other authors describe a specific relay nucleus by which
mechanoreceptor afferents gain access to the vestibulocerebellum
[95, 113, 114].
Brodal states that mechanoreceptor afferents project to
flocculonodular lobe via the group X nucleus located in the
region of the vestibular nuclei . Bakker and Abrahams explain
that the neurons of group X seem to serve as a primary relay for
cervical mechanoreceptor afferent input to the cerebellum .
Research also suggests that thoracic and lumbar mechanoreceptor
afferents project to group X .
In summary, the flocculonodular lobe receives input from
vestibular apparatus in the inner ear and mechanoreceptor
afferents, and then projects ipsilaterally to the middle,
superior and inferior vestibular nuclei. Relatively few fibers
project to the lateral vestibular nucleus 
Most authors agree that the medial vestibulospinal tract
originates in the medial vestibular nucleus and descends
bilaterally into the cervical and perhaps upper thoracic cord
[95, 110, 111]. Ghez stated that, "this tract participates in the
reflex control of neck movements so that the position of the head
can be maintained accurately and is correlated with eye
The medial longitudinal fasciculus (MLF) is believed to
originate in the superior and medial vestibular nuclei. Fibers in
the MLF project to abducens. trochlear and oculomotor nuclei.
which allow a person 5 gaze to stay fixed on an object while the
head is moving . This is known as the vestibulo-ocular
reflex; Maeda has demonstrated that the cervical spine
mechanoreceptors participate in this reflex by projecting to the
group X nucleus .
The MLF also projects to the interstitial nucleus of
. It is thought that this nucleus probably plays an important
role in mediating the effects of optic and vestibular impulses on
the neck and body musculature and may also influence certain
central effects on the autonomic system .
The vestibular nuclei also project to the cerebral
both direct and indirect pathways. Animal experiments have
revealed that within the facial region of the primary sensory
area, there is a marked convergence of vestibular and
somatosensory impulses arising from muscle spindles and from
mechanoreceptors in the skin and joints . These connections
may exist in humans; Nolte indicates that each superior
vestibular nucleus sends projections bilaterally to the facial
region of the primary sensory area . Through these
connections, it is likely that the vestibular nuclei play a role
in the conscious appreciation of body position [95, 110].
The vestibular nuclei also have extensive reciprocal
connections with the reticular formation. "The vestibuloreticular
connections are presumably involved in vomiting and
cardiovascular reactions observed on vestibular irritation"
In a classic sense, the vestibulocerebellum is primarily
thought to play a role in equilibrium. This is because lesions to
the flocculonodular lobe can result in general dysequilibrium and
vertigo . However, the vestibular nuclei have widespread
connections; therefore, lesions within the vestibulocerebellum
may also result in conditions such as nystagmus and a variety of
autonomic concomitants . It is quite possible that similar
symptoms could develop when -adequate mechanoreceptive input does
not reach the vestibular nuclei and flocculonodular lobe.
As mentioned in the cerebellum section, each
the primary somatosensory region receives afferents from specific
receptors . Group Ia muscle spindle afferents project to
area 3a. Cutaneous afferents project to area 3b. Joint afferents
project to area 2. Area 1 receives input from both cutaneous and
deep tissue receptors. It is well-known that the dorsal columns
and medial lemniscus carry this mechanoreceptive information. The
importance of such mechanoreceptor afferent input to the cerebral
cortex is described by many neuroanatomists.
Carpenter states that although impulses generated in-neurons
in the primary motor area (M I), the premotor area, and in the
supplementary motor area (M -II) are responsible for movement,
motor control, changes in muscle tone and maintenance of posture,
these motor activities are initiated by inputs that arise from
the thalamus, other cortical areas and peripheral receptors
According to Masdeu and Brazis, sensorimotor control is
carried out by various thalamic nuclei, such as the ventrolateral
nucleus, which predominantly coordinate the finer distal motor
movements - : "The ventrolateral nucleus integrates input
-from the cerebellum, basal ganglia and mechanoreceptors from the
musculoskeletal system; it projects to the pericentral cortex or
primary motor cortex (area 4). " Wyke maintained that Type I
joint receptors, which are similar to Ruffini spray endings,
excite the paracentral and parietal regions of the cerebral
cortex and make a significant contribution to the perceptual
experiences of postural sensation and kinesthesis . Clearly,
appropriate mechanoreceptor afferent input is required by the
cerebral cortex to perform a host of conscious and subconscious
Other authors indicate that afferent input plays a role
extends beyond that of motor control. Both Guyton  and Nolte
 indicated that if afferent signals are eliminated, the
cerebrum would be incapable of functioning in a conscious manner
and would actually approach a permanent state of coma.
A more precise anatomical look at the cerebral cortex reveals
that somatosensory input plays an additional role in human
function, such that mechanoreceptor input is actually needed to
help us function as humans. The human neocortex accounts for more
than 90% of the total cortical area  and is divided into six
separate layers . Layer 1, the molecular layer, is the most
external. Layer II is the external granular layer. Layer III is
the external pyramidal layer. Layer IV is the internal granular
layer. Layer V is the internal pyramidal layer. Layer VI, the
deepest layer, is known as the multiform layer.
Generally speaking, layers II and IV receive afferent
and layers III and V receive mainly efferent data . Layer II
receives cortical afferents and, depending on the location in the
neocortex, layer IV receives afferents from somatosensory
receptors, the medial geniculate body for audition and the
lateral geniculate body for vision (see discussion below on
primary sensory areas). Layer III projects ipsilaterally and
contralaterally to other areas of the cerebral cortex via
association fibers and commissural fibers. Layer V gives rise to
corticostriate fibers, corticopontine fibers, corticobulbar
fibers and corticospinal fibers . Layer VI is also thought
to be largely -efferent and to mainly project fibers to the
thalamus. Cortical interneurons allow the various layers in a
specific area to communicate with one another .
The term 'great sensory pathways' has often been used to
describe the somatosensory, optic-and acoustic systems . Each
has an individual primary sensory area in the cerebral cortex.
Area 17 in the occipital lobe is for-vision. Area 41 in the
temporal lobe is for audition, and areas 3,1 and 2 in the
parietal lobe are for sornatosensory input. Once afferent input
is received in a specific primary sensory area, the information
is integrated and then communicated to other parts of the brain
via commissural and association fibers. The great majority of
commissural fibers travel in the corpus callosum, which is
thought to contain about 180 million fibers. The projections
between homotopic regions are thought to be very precise. For
example, the commissural connections of the primary and secondary
sensory areas seem to be extremely specific .
Association fibers are ipsilateral, and four main fiber
pathways are typically described. One passes through the
cingulate gyms and is known as the cingulum. The superior
longitudinal fasciculus connects the frontal lobe to the
occipital lobe. The inferior longitudinal fasciculus connects the
occipital lobe to the temporal lobe. The uncinate fasciculus
passes from the temporal lobe to the frontal lobe [95, 110]. It
should be understood that none of the association pathways are
discrete, point-to-point pathways. Fibers freely enter and leave
along the course of the pathways . Thus, the association
pathways allow for an almost unimaginable number of connections.
We know that the primary sensory areas (for somatosensory input,
vision and audition) all communicate in various association
areas, such as the parieto-occipital-temporal association area
and the prefrontal association area, via the commissural and
association pathways [95, 112].
The prefrontal association area also receives input from
limbic system; thu-s, this association area receives information
about all sensory modalities as well as information regarding
motivational and emotional states . All of this input is
integrated, which allows one to appropriately engage a given
environmental situation. A reduction in limbic input, visual
input, auditory input or somatosensory input would necessarily
compromise--one's ability to function.
Janse provided a most elegant commentary on the
mechanoreceptor afferent input : Numerically, the somatic
sensory factors comprise by far the major activating vehicle of
the nervous system, and the overtones of the body's conduct are
significantly conditioned and controlled by their input."
Regarding the total sensorial experience of humans, which
includes mechanoreceptive, nociceptive and special senses, Janse
stated that humans are provided "with sentiencies [sic] of
emotional, mental and spiritual affectivities that defy total
comprehension." Janse suggested that an divergence in the
totality of sensory input could ultimately result in pathology,
or symptoms of pathology, in seemingly unrelated tissues and
Symptoms associated with reduced mechanoreceptor input
Mechanoreceptive information reaches numerous
in the CNS. Consequently, a reduction in mechanoreceptor input
caused by joint complex dysfunction has the potential to promote
numerous symptoms that could mimic lesions of the vestibular
nuclei, cerebellum, cerebral cortex and basal ganglia. Although
much more research is still needed in this area, evidence exists
to support this contention. For example, as early as 1845,
"Longet reported that surgical damage of neck muscles in a wide
range of species led to generalized but transient motor
disturbances characterized by an ataxia similar to that which
followed cerebellectomy" . More recently, a study of
patients with soft tissue injuries in the neck led the authors to
conclude that oculomotor abnormalities may be caused by abnormal
mechanoreceptor input .
Fitz-Ritson found that 112 of 235 patients with cervical
tmuma experienced cervical vertigo . The definition of
vertigo used in this study included both "subjective vertigo,
i.e., the patient feels that he/she is rotating, [and] objective
vertigo, i.e., the feeling that the room or environment is
rotating." After 18 treatments, which involved chiropractic
adjustments to restore mobility to restricted joints, 101 of the
112 patients (90.2%) were symptom-free. This finding is
consistent with the findings of Lewit, who stated that
manipulation is very effective for reducing vertigo and dizziness
It seems that symptoms of enhanced nociception often
symptoms associated with reduced mechanoreception. For example,
Weeks and Travell demonstrated that a clinical syndrome
characterized by postural vertigo or dizziness, imbalance and,
usually, headache may be caused by dysfunction of the
sternocleidomastoid muscle . Gray reported on a series of
case histories that described how injured cervical muscles can
play a role in the production of vertigo, pain, nausea and
In a article titled Cervical Vertigo, Wing and
HargraveWilson described 80 patients, all of whom had some form
of vertigo, varying from the severe rotary type to generalized
unsteadiness . All patients had a thorough examination of
the ears, nose and throat, and the results were normal in 96% of
the cases. Electronystagmographic abnormalities were found in all
patients. Some 69% of the patients also had either occipital
headaches or cervical pain. All patients had "tender muscle
guarding" in the upper cervical region, which was thought to
exist because of "partial fixation of the involved vertebra." The
authors stated that manipulation was a "bastion" of treatment.
After treatment, electronystagmographic recordings were
significantly improved in 73% of the patients. A total of 53% of
patients had complete relief of symptoms, and 36% had significant
improvement to the point where they required no medication and
could return to normal activities.
Several additional authors have discussed the
between a dysfunctional cervical spine and symptoms of pain,
vertigo and dizziness [123-126]. Research also suggests that
joint complex dysfunction in the lumbar spine can affect
Reduced mechanoreception may also impact the nonmotor
functions of the cerebellum. In 1978, Watson explained how
traditional concepts of cerebellar physiology emphasize motor
control functions; however, he also points out that an emerging
body of literature demonstrates a relationship between the
cerebellum and psychological processes .
Specifically, data have suggested that this brain
participate in sensory integration activities, motor skills
learning, visual and auditory discrimination performance, emotion
and motivation control, and reinforcement processes .
Many articles have discussed the cerebellum's
emotional expression [128-132]. The most dramatic work was
completed by Heath during the 1970s .
Through experimentation, Heath demonstrated that brain
for emotional expression are anatomically connected and
functionally related to sensory relay nuclei for all modalities
and also to sites involved in facial expression and motor
coordination . His research demonstrated that efferent
pathways from the vermis/fastigial nucleus could stimulate
pleasure centers located in the septal nuclei of the hypothalamus
and corticomedial amygdala, and simultaneously inhibit adversive
emotion centers located in the hippocampus and dorsolateral
amygdala. Heath applied electrical stimulation to the vermis to
activate this pathway in his treatment of psychiatric patients.
To access the cerebellum, suboccipital craniotomy was performed
and 2-mm electrodes were implanted subtentorially over the
rostral vermal and paravermal regions of the cerebellum. A
pace-making device delivered a stimulus at selected time
intervals. Heath used this method on 11 patients with intractable
psychiatric illness, all of whom were pronounced incurable by at
least two physicians. The length of illness varied from 6 to 23
yr. Of the 11 patients, four had uncontrollable
violence-aggression (two with no demonstrable organic brain
disease and two with brain pathology), five were schizophrenics,
and two had lifetime patterns of severe neurosis. After
treatment, 10 of the 11 patients were out of the hospital and
functioning without medication or other treatment [except for
cerebellar stimulationT. Some were symptom-free, and others
demonstrated significant improvements. The one patient who failed
to respond had an adhesion between the tentorium and the rostral
vermis that extended 2.5 cm to either side of midline, which
apparently damaged the targeted cerebellar neurons.
Heath's work is important for chiropractors because the
rostral vermal and paravermal neurons of the cerebellum receive
axial and appendicular mechanoreceptor input from all levels of
the spinal cord (see earlier discussion on the cerebellum).
Although this does not prove that dysafferentation caused by
joint complex dysfunction is a cause of psychiatric illness, it
is clear that interesting implications do exist and should be
The information presented in this article
demonstrates that the CNS is greatly influenced-by somatosensory
input. Numerous, seemingly unrelated symptoms can be generated
when nociceptive input is enhanced and mechanoreceptive input is
reduced. Research evidence leads us to believe that such
dysafferent input is associated with joint complex dysfunction,
which explains why so many seemingly bizarre symptoms respond to
As stated earlier, according to classic neuroanatomy,
great sensory systems include the visual system, the auditory
system and the somatosensory system. At the present time, there
are specialists devoted to -the visual and auditory systems. As
of yet, no profession has effectively stepped forward to
specialize in treating somatosensory system dysfunction (i.e.,
dysafferentation induced by joint complex dysfunction). That
chiropractic has not assumed such a role is surprising. Indeed,
it seems that Janse envisioned chiropractors filling this role .
Apparently, Janse was so convinced that the chiropractic
profession would pursue research in the field of somatosensory
neurology that he wrote, "Let us be a trifle bold and quite
foolish; let us try to imagine what a symposium on Principles of
Sensory Communication might be like in 10 or 15 years hence"
. Janse went on to discuss numerous aspects of somatosensory
function that could have served as research topics for
chiropractors. Unfortunately, save for a few scattered articles,
the idea that chiropractors should be the doctors or care takers
of one of the great sensory systems has not been pursued. Janse
warned future generations of chiropractors about neglecting the
somatosensory system. He stated:
It is not to be forgotten that essentiatly man is a
organism. Re ftinctions by vintue of the in-puts he experiences
via the cutaneum, the subdermal, the myofascial planes, the
dianthrodial complexes of the musculoskeletal system, especially
the spine; the related proprioceptive phenomena .
Suggestions for Chiropractic Education
At the present time, the basic sciences-in most
chiropractic colleges are taught in the same fashion as in
medical school. Students are taught to view anatomy, physiology
and diagnosis based solely on a pathology model. In other words,
a differential diagnosis involves ruling out pathological changes
in anatomical structures and metabolic pathways. This approach
should not be abandoned; however, joint complex dysfunction and
dysafferentation must be included in every differential diagnosis
whenever it is determined that nociceptive and mechanoreceptive
input can directly or indirectly influence the structures from
which the symptoms are generated. This demands that students and
practitioners be well versed in the details of the central
connections of the many neuroanatomical pathways related to
nociceptive and mechanoreceptive input.
Without this knowledge, it will be impossible for
doctors to understand and explain how joint complex dysfunction
can affect the many conditions that afflict the human body.
At the present time, only a few articles explain how to
include joint complex dysfunction in the differential diagnosis,
all of which focus on the topic of dizziness and vertigo [99,
118, 133, 134]. This must change if chiropractic is to ever
become a truly mainstream profession that reaches a majority of
Seaman D. Joint complex dysfunction, a novel term
to replace subluxation/subluxation complex: Etiological and
treatment considerations J Manipulative Physiol Ther 1997;
Waagen G, Strang V. Origin and development of traditional
chiropractic philosophy. In: Haldeman S, editor. Principles and
practice of chiropractic. 2nd ed. Norwalk: Appleton &
Practice guidelines for straight chiropractic. Proceedings of
the International Straight Chiropractic Consensus Conference.
Chandler (AZ): World Chiropractic Alliance; 1992. p.98.
Kale Clinic & Research Center. Houston control (patient
pamphlet). Spartanburg: South Carolina; 1993.
Seaman D. Proprioceptor: an obsolete, inaccurate word. J
Manipulative Physiol Ther 1997; 20:279-84.
Seaman D. Letter to the editor. Top Clin Chiropr 1997; 4(1)
Cramer G, Darby S. Letter to the editor. Top Clin Chiropr
Deafferentation. Dorland's Medical Dictionary. 25th ed.
Philadelphia: WB Saunders; 1974. p.409.
Burchiel K. Deafferentation syndromes and dorsal root entry
zone lesions. In: Fields H, editor. Pain syndromes in neurology.
Boston: Butterworth-Heinemann; 1990. p.201-22.
Fields H. Pain. New York: McGraw-Hill; 1987.
Tasker R. Management of nociceptive, deafferentation and
central pain by surgical intervention. In: Fields H, editor. Pain
syndrome in neurology. Boston: Butterworth-Heinemann; 1990.
Guyton A. Basic neuroscience. 2nd ed. Philadelphia: WB
Martin J, Jessell T. Modality coding in the somatic sensory
system. In: Kandel E, Schwartz J, Jessell T, eds. Principles of
neural science. 3rd ed. New York: Elsevier; 1991. p.341-52.
Willis W, Coggeshall R. Sensory mechanisms of the spinal
cord. 2nd ed. New York: Plenum Press; 1991.
Schaible H, Schmidt R. Direct observation of the
sensitization of articular afferents during an experimental
arthritis. In: Dubner R, Gebhart G, Bond M, editors. Proceedings
of the Fifth World Congress on Pain: 1987 Aug 2-7; Hamburg,
Germany. New York: Elsevier; 1988. p.44-SO.
Guilbaud G. Peripheral and central electrophysiological
mechanisms of joint muscle pain. In: Dubner R, Gebhart G, Bond M,
editors. Proceedings of the Fifth World Congress on Pain; 1987
Aug 2-7; Hamburg, Germany. New York: Elsevier; 1988. p.
Hanesch U, Heppelmann B, Messlinger K, Schmidt R.
Noci-ception in normal and arthritic joints: structural and
functional aspects. In: Willis W, editor. Hyperalgesia and
allodynia. New York: Raven Press; 1992. p.81-106.
Schaible H, Grubb B. Afferent and spinal mechanisms of joint
pain. Pain 1993; 55:5-54.
Schmidt R, Schaible H Messlinger K. Heppelmann B, Hanesch U,
Pawlak M. Silent and active nociceptors: structure, functions,
and clinical implications. In: Gebhart G, Hammond T, Jensen T,
editors. Proceedings of the 7th World Congress on Pain:
Progress in Pain Research and Management; 1993; Paris,
France. Seattle: IASP Press; 1994. p.213-SO.
Hooshmand H. Chronic pain: reflex sympathetic dystrophy,
prevention and management. Boca Raton (FL): CRC Press; 1993.
Jozsa L, Balint J, Kannus P, Jarvinen M, Lehto M.
Mechanoreceptors in human myotendinous junction. Muscle Nerve
Lephart S. Reestablishing proprioception, kinesthesia, joint
p0sition sense, and neuromuscular control in rehabilitation. In:
Prentice W, ed. Rehabilitation techniques in sports medicine. 2nd
ed. St. Louis: Mosby; 1994. p.118-37.
Parkhurst T, Burnett C. Injury and proprioception in the
lower back. J Orthop Sports Phys Ther 1994; 19:282-95.
Slosberg M. Effects of altered afferent input on sensation,
proprioception, muscle tone and sympathetic reflex response. J
Manipulative Physiol Ther 1988; 11:400-8.
Jones M, Christensen N, Carr J. Clinical reasoning in
orthopedic manual therapy. In: Grant R, editor. Physical therapy
of cervical and thoracic spine. 2nd ed. New York:
Churchill-Livingstone; 1994. p.89-108.
Peterson D. Principles of adjustive technique. In: Bergmann
T, Peterson D, Lawrence D, editors. Chiropractic technique. New
York: Churchill-Livingstone; 1993. p.123-95.
Peterson D, Bergrnann T. Joint assessment principles and
procedures. In: Bergmann T, Peterson D, Lawrence D, editors.
Chiropractic technique. New York: Churchill Livingstone; 1993.
Henderson C. Three neurophysiologic theories on the
chiropractic subluxation. In: Gatterman M, editor. Foundations of
chiropractic-subluxation. St. Louis: Mosby; 1995. p.225-33.
Murphy D. The locomotor system: Korr's "primary machinery of
life." J Manipulative Physiol Ther 1994; 17:562-4.
Denslow J, Hassett C. The central excitatory state associated
with postural abnormalities. J Neurophysiol 1942; 5:393-402.
Korr I. The neural basis of the osteopathic lesion. J Am
Osteopath Assoc 1947; 47:191-7.
Patterson M. A model mechanism for spinal segmental
facilitation. J Am Osteopath Assoc 1976; 76:62-72.
Miller B, Keane C, editors. Encyclopedia and dictionary of
medicine, nursing and allied health. Philadelphia: WB Saunders;
Bogduk N. Innervation patterns of the cervical spine. In:
Grant R, editor. Physical therapy of the cervical and thoracic
spine. 2nd ed. New York: Churchill-Livingstone; 1994.
Bogduk N, Valencia F. Innervation patterns of the thoracic
spine. In: Grant R, editor. Physical therapy of the cervical and
thoracic spine. 2nd ed. New York: Churchill-Livingstone; 1994.
Bogduk N. Innervation, pain patterns, and mechanisms of pain
production. In: Twomey L, Taylor J, editors. Physical therapy of
the low back. 2nd ed. New York: Churchill-Livingstone; 1994.
Charman R. Pain and nociception: mechanisms and modulation in
sensory context. In: Boyling J, Palastanga N, editors. Grieve's
modern manual therapy: the vertebral column. 2nd ed. New York:
Churchill-Livingstone; 1994. p.253-70.
Grieve G. Common vertebral joint problems. 2nd ed. New York:
Churchill-Livingstone; 1988. p.51-2.
Haldeman S. The neurophysiology of pain. In: Haldeman S,
editor. Principles and practice of chiropractic. 2nd ed. Norwalk
(CT): Appleton-Century-Crofts; 1992. p.165-84.
Wyke B. The neurological basis of thoracic pain. Rheumatol
Phys Med 1970; 10:356-67.
Wyke B. Neurological aspects of pain therapy. In: Swerdlow M,
editor. The therapy of pain. Philadelphia: JB Lippincott; 1980.
Price D. Psychological and neural mechanisms of pain. New
York: Raven Press; 1988. p.76-99.
McMahon S, Koltzenburg M. Novel classes of nociceptors:
beyond Sherrington. Trends Neurosci 1990; 13:199-201.
Bonica J. Anatomic and physiologic basis of nociception and
pain. In: Bonica J, editor. Management of pain. 2nd ed.
Philadelphia: Lea & Febiger; 1990. p.28-94.
Bonica J. Definitions and taxonomy of pain. In: Bonica J,
editor. The management of pain. 2nd ed. Philadelphia: Lea &
Febiger; 1990. p.18-27.
Maciewicz R. Organization of pain pathways. In: Ashbury A,
McKhann G, McDonald W, editors. Diseases of the nervous system:
clinical neurobiology. Philadelphia: WB Saunders; 1992.
Casey K. Nociceptors and their sensitization: overview. In:
Willis W, editor. Hyperalgesia and allodynia. New York: Raven
Press; 1992. p.13-S.
Randwerker H, Peeh P. Nociceptors: chemosensitivity and
sensitization by chemical agents. In: Willis W, editor.
Hyperalgesia and allodynia. New York: Raven Press; 1992.
Steen KH, Reeh PW, Anton F, Handwerker HO. Protons
selectively induce lasting excitation and sensitization to
mechanical stimulation of nociceptors in rat skin, in vitro.
J Neurosci 1992; 12:86-95.
Campbell J, Meyer R, Davis K, Raja S. Sympathetically
maintained pain: a unifying hypothesis. In: Willis W, editor.
Hyperalgesia and allodynia. New York: Raven Press; 1992.
Levine J, Coderre T, Basbaum A. The peripheral nervous system
and the inflammatory process. In: Dubner R, Gebhart 0, Bond M,
editors. Proceedings of the Fifth World Congress on Pain; 1987
Aug 2-7; Hamburg, Germany. New York: Elsevier; 1987.
Levine J, Taiwo Y, Heller P. Hyperalgesic pain: inflammatory
and neuropathic. In: Willis W, editor. Hyperalgesia and
allodynia. New York: Raven Press; 1992. p.117-23.
Rang H, Bevan S, Dray A. Chemical activation of nociceptive
peripheral neurones. Br Med Bull 1991; 47:534-48.
Reeh P. Chemical excitation and sensitization of nociceptors.
In: Urban L, editor. Cellular mechanisms of sensory processing.
Berlin: Springer-Verlag; 1994. p.119-31.
Dubner R. Spinal cord neuronal plasticity: mechanisms of
persistent pain following tissue damage and nerve injury. In:
Vecchiet D, Albe-Fessard D, Lindbolm U, Giamberardino M, editors.
New trends in referred pain and hyperalgesia. New York: Elsevier;
Coderre T, Katz J, Vaccarino A, Melzack R. Contribution of
central neuroplasticity to pathological pain: review of clinical
and experimental evidence. Pain 1993; 52:259-85.
Light A. The initial processing of pain and its descending
control: spinal and trigeminal systems. New York: Karger; 1992.
Woolf C. Physiological, inflammatory and neuropathic pain.
Adv Tech Stand Neurosurg 1987; 15:39-62.
Denslow 1, Korr I, Krems A. Quantitative studies of chronic
facilitation in human motoneurons. Am J Physiol 1947; 150:
Patterson M. The spinal cord: participant in disorder. Spinal
Manipulation 1993; 9(3):2-11.
Korr I. Symposium on the functional implications of segmental
facilitation: a research report. J Am Osteopath Assoc 1955;
Korr I. The facilitated segment: a factor in injury to the
body framework. Osteopath Ann 1973; 1:10-12, 17-18.
Korr I. Andrew Taylor Still memorial lecture: research and
practice-a century later. J Am Osteopath Assoc 1974;
Korr I. Proprioceptors and somatic dysfunction. I Am
Osteopath Assoc 1975; 74:638-50.
Korr I. Sustained sympathicotonia as a factor in disease. In:
Korr I, editor. The neurobiologic mechanisms in manipulative
therapy. New York: Plenum Press; 1978. p.229-68.
Korr I. Somatic dysfunction, osteopathic manipulative
treatment, and the nervous system: a few facts, some theories,
many questions. I Am Osteopath Assoc 1986; 86:109-14.
Korr I. Osteopathic research: the needed paradigm shift. I Am
Osteopath Assoc 1991; 91:156-71.
Woolf C. Evidence for a central component of post-injury pain
hypersensitivity. Nature 1983; 306:686-8.
Dubner R. Neuronal plasticity in the spinal and medullary
dorsal horns: a possible role in central pain mechanisms. In:
Casey K. Pain and central nervous system disease: the central
pain syndromes. New York: Raven Press; 1991. p.143-55.
Dubner R, Ruda M. Activity-dependent neuronal plasticity
following tissue injury and inflammation. Trends Neurosci 1992;
Dubner R, Basbaum A. Spinal cord plasticity following tissue
or nerve injury. In: Wall R, Melzack R, editors. Textbook of
pain. 3rd ed. New York: Churchill-Livingstone; 1994.
Hoheisel U, Mense S. Long-term changes in discharge behavior
of cat dorsal horn neurones following noxious stimulation of deep
tissues. Pain 1989; 36:239-47.
Ren K, Rylden 3, Williams G, Ruda M, Dubner R. The effects of
a non-competitive NMDA receptor antagonist, MK-801, on behavioral
hyperalgesia and dorsal horn neuronal activity in rats with
unilateral inflammation. Pain 1992; 50:331-44.
Richmond C, Bromley L, Woolf C. Preoperative morphine
pre-empts postoperative pain. Lancet 1993; 342:73-5.
Roberts W. A hypothesis on the physiological basis for
causalgia and related pains. Pain 1986; 24:297-311.
Wall P, Woolf C. Muscle but not cutaneous C-afferent input
produces prolonged increases in the excitability of the flexion
reflex in the rat. I Physiol 1984; 356:443-58.
Woolf C. Long term alterations in the excitability of the
flexion reflex produced by peripheral tissue injury in the
chronic decerebrate rat. Pain 1984; 18:325-43.
Woolf C. Generation of acute pain: central mechanisms. Br Med
Bull 1991; 47:523-33.
Woolf C. Excitability changes in central neurons following
peripheral damage: role of central sensitization in the
pathogenesis of pain. In: Willis W, editor. Hyperalgesia and
allodynia. New York: Raven Press; 1992. p.221-243.
Woolf C. The dorsal horn: state-dependent sensory processing
and the generation of pain. In: Wall P, Melzack R, editors. The
textbook of pain. 3rd ed. New York: Churchill-Livingstone; 1994.
Simone D. Neural mechanisms of hyperalgesia. Curr Opin
Neurobiol 1992; 2:479-83.
Gillette R. Spinal cord mechanisms of referred pain and
related neuroplasticity. In: Gatterman M, editor. Foundations of
chiropractic: subluxation. St. Louis: Mosby; 1995.
Huttenlocher P. Neural plasticity. In: Ashbury A, McKhann G,
McDonald W, editors. Diseases of the nervous system: clinical
neurobiology. Philadelphia: WB Saunders; 1992. p.63-71.
Kandel E. Cellular mechanisms of learning and the biological
basis of individually. In: Kandel E, Schwartz I, Jessell T,
editors. Principles of neural science. 3rd ed. New York:
Elsevier; 1991. p.1009-31.
Teyler T, Grover L. Forms of long-term potentiation induced
by NMDA and non-NMDA receptor activation. In: Baudry M, Thompson
R, Davis I, editors. Synaptic plasticity: molecular, cellular
aspects. Cambridge (MA): MIT Press; 1993. p.73-86.
Bonica I. Introduction: semantic, epidemiologic, and
educational issues. In: Casey K, editor. Pain and central nervous
system disease: the central pain syndromes. New York: Raven
Press; 1991. p.13-29.
Bonica 3. Clinical importance of hyperalgesia. In: Willis W,
editor. Hyperalgesia and Allodynia. New York: Raven Press; 1992.
Berne R, Matthew L. Physiology. 3rd ed. St. Louis: Mosby Year
Book; 1993. p.949-79.
Dilman V, Dean W. The neuroendocrine theory of aging and
degenerative disease. Pensacola: The Center for Bio-Gerontology;
Feinstein B, Langton I, Iameson R, Schiller F. Experiments on
pain referred from deep somatic tissues. I Bone loint Surg Am
Nansel D, Szlazak M. Somatic dysfunction and the phenomenon
of visceral disease simulation: a probable explanation for the
apparent effectiveness of somatic therapy in patients presumed to
be suffering from true visceral disease. I Manipulative Physiol
Ther 1995; 18:379-97
Mendel T, Wink C, Zimny M. Neural elements in human cervical
intervertebral discs. Spine 1992; 17:132-5.
Willis W. Central plastic responses to pain. In: Gebhart G,
Hammond D, Iensen T, editors. Proceedings of the 7th World
Congress on Pain; 1993; Paris, France. Seattle: IASP Press; 1994.
De long P, de long I, Cohen B, Jongkees L. Ataxia and
nystagmus induced by injection of local anesthetics in the neck.
Ann Neurol 1977; 1:240-6.
Brodal A. Neurological anatomy. 3rd ed. New York: Oxford
University Press; 1981.
Wyke B. Articular neurology and manipulative therapy. In:
Glasgow E, Twomey L, Scull E, Kleynhans A, Idczak R, editors.
Aspects of manipulative therapy. 2nd ed. New York:
Churchill-Livingstone; 1985. p.72-7.
Gillette R. Potential antinociceptive effects of high level
somatic stimulation- chiropractic manipulation therapy may
coactivate both tonic and phasic analgesic systems. Some recent
evidence. Trans Pac Consortium Res 1986; 1:A4(1)-A4(9).
Woolf C. Segmental afferent fibre-mediated analgesia:
transcutaneous electrical nerve stimulation (TENS) and vibration.
Wall P, Melzack R, editors. Textbook of pain. 2nd ed. New
York: Churchill-Livingstone; 1989. p.884-96.
Dvorak I, Dvorak V. Manual medicine: diagnostics. 2nd ed. New
York: Thieme Medical Publishers; 1990.
Gordon I. Spinal mechanisms of motor coordination. In: Kandel
E, Schwartz I, lessell T. editors. Principles of neural science.
3rd ed. New York: Elsevier; 1991. p.581-95.
Sato A. Spinal reflex physiology. In: Haldeman S, editor.
Principles and practice of chiropractic. 2nd ed. Norwalk (CT):
Appleton & Lange; 1992. p.87-103.
Fitz-Ritson D. The anatomy and physiology of the muscle
spindle, and its role in posture and movement: review. ICCA 1982;
Richmond F, Bakker D, Stacey M. The sensorium: receptors of
neck muscles and joints. In: Peterson B, Richmond F, editors.
Control of head movement. New York: Oxford University Press;
Bogduk N, Twomey L. Clinical anatomy of the lumbar spine. 2nd
ed. New York: Churchill-Livingstone; 1991. p.86.
Proske U. The golgi tendon organ. In: Dyck P, Thomas P,
Griffin I, Low P, Podusko I, editors. Peripheral neuropathy. 3rd
ed. Philadelphia: WB Saunders; 1993. p.141-8.
Masdeu I, Brazis P. The anatomic localization of lesions in
the thalamus. In: Brazis P, Masdeu I, Biller I, editors.
Localization in clinical neurology. 2nd ed. Boston: Little, Brown
and Company; 1990. p.319-43.
Carpenter M. Core text of neuroanatomy. 4th ed. Baltimore:
Williams & Wilkins; 1991. p.224-49.
Lantz C. The vertebral subluxation complex. ICA Rev Chiropr
Lantz C. The vertebral subluxation complex. In: Gatterman M,
editor. Foundations of chiropractic: subluxation. St. Louis:
Mosby; 1995. p. 149-74.
Nolte 3. The human brain. 3rd ed. St. Louis: Mosby; 1993. p.
Ghez C. The cerebellum. In: Kandel E, Schwartz 3, Jessell T,
editors. Principles of neural science. 3rd ed. New York:
Elsevier; 1991. p. 626-46.
Brodal P. The central nervous system: structure and function.
New York: Oxford University Press; 1992.
Fitz-Ritson D. Neuroanatomy and neurophysiology of the upper
cervical spine. In: Vernon H, editor. Upper cervical spine:
chiropractic diagnosis and treatment. Baltimore: Williams &
Wilkins; 1988. p.48-85.
Bakker D, Abrahams V. Central projections from nuchal
afferent systems. In: Peterson B, Richmond F, editors. Control of
head movement. New York: Oxford University Press; 1988. p.
Maeda M. Neck influences on the vestibulo-ocular reflex arc
and the vestibulocerebellum. Prog Brain Res 1979; 50:551-9.
Janse 3. The integrative purpose and function of the nervous
system: a review of classical literature. 3 Manipulative Physiol
Ther 1978; 1:182-91.
Hildingsson C, Wenngren B, Toolanen G. Eye motility after
soft-tissue injury of the cervical spine: a controlled,
prospective study of 38 patients. Acta Orthop Scand 1993;
Fitz-Ritson D. Cervicogenic vertigo. 3 Manipulative Physiol
Ther 1991; 14:193-8.
Lewit K. Manipulative therapy in rehabilitation of the
locomotor system. 2nd ed. Boston: Butterworth Heinemann; 1991.
Weeks V, Travell 3. Postural vertigo due to trigger areas in
the sternocleidomastoid muscle. 3 Pediatr 1957; 47:315-27.
Gray L. Extra labyrinthine vertigo due to cervical muscle
lesions. 3 Laryngol Otol 1956; 70:352-61.
Wing L, Hargrave-Wilson W. Cervical vertigo. Aust N Z 3 Surg
Caranasos G, Israel R. Gait disorders in the elderly. Hosp
Revel M, Andre-Deshays C, Minguet M. Cervicocephalic
kinesthetic sensibility in patients with cervical pain. Arch Phys
Med Rehabil 1991; 72:288-91.
Revel M, Minguet M, Gergory P, Vaillant 3, Manuel 3. Changes
in cervicocephalic kinesthesia after a proprioceptive
rehabilitation program of in patients with neck pain: a
randomized controlled study. Arch Phys Med Rehabil 1994;
Hulse M. Disequilibrium, caused by a functional disturbance
in the upper cervical spine: clinical aspects and differential
diagnosis. Man Med 1983; 1:18-22.
Hinoki M, Ushio N. Lumbomuscular proprioceptive reflexes in
body equilibrium. Acta Otolaryngol Suppl (Stockh) 1975; 330:
Watson P. Nonmotor functions of the cerebellum. Psychol Rev
Courchesne E, Yeung-Courchesne R, Press G, Hesselink J,
Jernigan T. Hypoplasia of cerebellar vermal lobules VI and VII in
autism. N Engl 3 Med 1988; 318:1349-54.
Gutzmann H, Kuhl K. Emotion control and cerebellar atrophy in
senile dementia. Arch Gerontal Geriatr 1987; 6:61-71.
Lalonde R, Botez M. The cerebellum and learning processes in
animals. Brain Res Rev 1990; 15:325-32.
Heath R. Modulation of emotion with a brain pacemaker. 3 Nerv
Ment Dis 1977; 165:30047.
Douglas F. The dizzy patient: strategic approach to history,
examination, diagnosis, and treatment. Chiropr Technique 1993;
Schimp D. A diagnostic algorithm for the dizzy patient.
Chiropr Technique 1994; 6:123-37.
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