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Author: admin | 10.01.2014 | Category: Tinnitus Hearing Loss

We will be provided with an authorization token (please note: passwords are not shared with us) and will sync your accounts for you. The aim of this review is to focus the attention of clinicians and basic researchers on the association between psycho-social stress and tinnitus.
Stress stimulates neuroendocrine axes such as hypothalamus-pituitary-thyroid axis (Mebis and van den Berghe, 2009), hypothalamus-pituitary-gonadal axis (Whirledge and Cidlowski, 2010) and hypothalamus-pituitary-adrenal axis (HPA axis) (Lupien et al., 2007). Tinnitus is a subjective perception of sound without external acoustic signal caused by inappropriate activation of auditory cortex. In this review, we will describe some of HPA axis-mediated effects induced by stress and will discuss their possible influence on the auditory system with special focus on tinnitus. HPA-induced steroids signal trough their respective receptors: glucocorticoid and mineralcorticoid receptors. Glutamate is an abandoned neurotransmitter in CNS and is involved in the process of memory, learning, and also in the auditory processing. Post-synaptic neuronal plasticity can be induced by changes in the expression and trafficking of glutamate receptors AMPAR. Taken together, peripheral and central auditory systems express molecules, which are modulated by stress in the limbic, memory, and learning centers of CNS. Extended presence of stressor such as inability to escape from a stressing situation (chronic stress) or a high impact stressor (acute stress) may induce allostatic load reflected by pathological reactions or conditions. Taken together, caution needs to be taken when designing, interpreting, and comparing experiments that use various animal stress models. In the auditory research, influence of stress on the auditory processing was often studied using physical acute stress. Under special circumstances, the administration of corticosteroids can also have adverse effects on the auditory system. In addition to physical stress, psycho-social stress model was also used in the auditory research. Interesting for the issue tinnitus and stress is the HPA axis, which seems to be disturbed in tinnitus patients. The link between tinnitus and negative emotional arousal was proposed many years ago by Jastreboff and Hazell to explain why is tinnitus perceived as unpleasant or even dangerous sound (Jastreboff and Hazell, 1993). Scientists in the field currently agree that tinnitus may be triggered by an injury to the inner ear causing decreased activity of the auditory nerve and lastly in plastic changes in central auditory system (Kaltenbach, 2011).
Furthermore, information collected here, indirectly implies the requirement for psychological assessment during the diagnosis of tinnitus patients, with focus on perceived stress and psychological comorbidity. Second, stress-activated HPA corticosterone release may affect mineralcorticoid receptor function in cochlea and possibly influence the concentration of potassium secreted by stria vascularis, resulting in tinnitus.
Third, stress-induced activation of HPA axis and corticosteroid release could provoke pre- or post-synaptic neuronal plasticity of the auditory system (Figure 5). Exploring the above models and obtaining a clear-cut animal model, which would combine an appropriate stress type and tinnitus read-out, is a challenging task. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
AbstractThe use of conventional modalities for chronic neck pain remains debatable, primarily because most treatments have had limited success.
The capsular ligaments are the main stabilizing structures of the facet joints in the cervical spine and have been implicated as a major source of chronic neck pain. When the capsular ligaments are injured, they become elongated and exhibit laxity, which causes excessive movement of the cervical vertebrae. Therefore, we propose that in many cases of chronic neck pain, the cause may be underlying joint instability due to capsular ligament laxity.
In the realm of pain management, an ever-growing number of treatment-resistant patients are being left with relatively few conventional treatment options that effectively and permanently relieve their chronic pain symptoms.
Treatment protocols for acute and sub-acute neck pain are standard and widely agreed upon [1, 2].
In light of the poor treatment options and outcomes for chronic neck pain, we propose that in many of these cases, the underlying condition may be related to capsular ligament laxity and subsequent joint instability of the cervical spine. The diagnosis of chronic neck pain due to cervical instability is particularly challenging. In that context, comprehensive dextrose prolotherapy offers a promising treatment option for resolving cervical instability and the subsequent pain and disability it causes. The cervical spine consists of the first seven vertebrae in the spinal column and is divided into two segments, the upper cervical (C0-C2) and lower cervical (C3-C7) regions. The upper cervical spine consists of C0, called the occiput, and the first two cervical vertebrae, C1 and C2, or atlas and axis, respectively. The intrinsic, passive stability of the spine is provided by the intervertebral discs and surrounding ligamentous structures.
The lower cervical spine, while less specialized, allows for the remaining 50% of neck flexion, extension, and rotation. In addition to the discs, multiple ligaments and the two synovial joints on each pair of adjacent vertebrae (facet joints) allow for controlled, fully three dimensional motions.
Three other ligaments, the ligamentum flavum, anterior longitudinal ligament (ALL), and posterior longitudinal ligament (PLL), help to stabilize the cervical spine during motion and protect against excess flexion and extension of the cervical vertebrae.
A spinous process and two transverse processes emanate off the neural arch (or vertebral arch) which lies at the posterior aspect of the cervical vertebral column. The inferior articular process of the superior cervical vertebra, except for C0-C1, and the superior articular process of the inferior cervical vertebra join to form the facet joints of the cervical spine; in the case of C0-C1, the inferior articular process of C1 joins the occipital condyles. There is some dissimilarity in facet joint anatomy between the upper and lower cervical spine. In contrast, the facet joints of the lower cervical spine are positioned at more of an angle. Nevertheless, injury to any of the facet joints can cause instability to the cervical spine. The capsular ligaments are extremely strong and serve as the main stabilizing tissue in the spinal column.
While much has been reported about the strength of the capsular ligaments as related to cervical stability, when damaged, these ligaments lose their strength and are unable to support the cervical spine properly. Capsular ligament laxity can occur instantaneously as a single macrotrauma, such as a whiplash injury, or can develop slowly as cumulative microtraumas, such as those from repetitive forward or bent head postures. Furthermore, the capsular ligaments surrounding the facet joints are highly innervated by mechanoreceptive and nociceptive free nerve endings.
In a clinically unstable joint where neurologic insult is present, it is presumed that the joint has undergone more severe damage in its stabilizing structures, which may include the vertebrae themselves. Clinical instability can be classified as mild, moderate or severe, with the later being associated with catastrophic injury.
Cervical instability is a diagnosis based primarily on a patienta€™s history (ie, symptoms) and physical examination because there is yet to be standardized functional X-rays or imaging able to diagnose cervical instability or detect ruptured ligamentous tissue without the presence of bony lesions [24].
However, functional computerized tomography (fCT) and magnetic resonance imaging (fMRI) scans and digital motion x-ray (DMX) are able to adequately depict cervical instability pathology [46, 47].
Functional imaging technology, as opposed to static standard films, is necessary for adequate radiologic depiction of instability in the cervical spine because they provide dynamic imaging of the neck during movement and are helpful for evaluating the presence and degree of cervical instability (Fig.
Although not usually apparent radiographically, injury to the ligaments and soft tissues of C0-C2 from head or neck trauma is more likely than are cervical fractures or subluxation of bones [50, 51].
Due to its lack of osseous stability, the upper cervical spine is also vulnerable to injury by high velocity manipulation. Excessive tension on the capsular ligaments can cause upper cervical instability and related neck pain [56].
According to the International Association for the Study of Pain (IASP), cervical spinal pain is pain perceived as anywhere in the posterior region of the cervical spine, defining it further as pain that is a€?perceived as arising from anywhere within the region bounded superiorly by the superior nuchal line, inferiorly by an imaginary transverse line through the tip of the first thoracic spinous process, and laterally by sagittal planes tangential to the lateral borders of the necka€? [59]. The IASP defines radicular pain as that arising in a limb or the trunk wall, caused either by ectopic activation of nociceptive afferent fibers in a spinal nerve or its roots or by other neuropathic mechanisms, and may be episodic, recurrent, or sudden [59]. With capsular ligament laxity, hypertrophic facet joint changes occur (including osteophytosis) as cervical degeneration progresses, causing encroachment on cervical nerve roots as they exit the spine through the neural foramina. The neural foramina lie between the intervertebral disc and the joints of Luschka (uncovertebral joints) anteriorly and the facet joint posteriorly. Cadaver studies have demonstrated that cervical nerve roots take up as much as 72% of the space in the neural foramina [61]. Cervical radiculopathy from a capsular ligament injury typically produces intermittent radicular symptoms which become more noticeable when the neck is moved in a certain direction, such as during rotation, flexion or extension. When disc herniation is the cause of cervical radiculopathy, it typically presents with acute onset of severe neck and arm pain unrelieved by any position and often results in encroachment on a cervical nerve root.
Spondylosis has previously been described as occurring in three stages: the dysfunctional stage, the unstable stage, and the stabilization stage (Fig. Damage to cervical ligaments from whiplash trauma has been well studied, yet these injuries are still often difficult to diagnose and treat. MRI and autopsy studies have both shown an association between chronic symptoms in whiplash patients and injuries to the cervical discs, ligaments and facet joints [42, 80]. Multiple studies have implicated the cervical facet joint and its capsule as a primary anatomical site of injury during whiplash exposure to the neck [55, 57, 82, 83].
In whiplash trauma, up to 10 times more force is absorbed in the capsular ligaments versus the intervertebral disc [30]. Injury to the facet joints and capsular ligaments has been further confirmed during simulated whiplash traumas [91]. In other simulations, whiplash trauma has been shown to reduce cervical ligament strength (ie, failure force and average energy absorption capacity) compared with controls or computational models [30, 87]; this is especially true in the case of capsular ligaments, since such trauma causes capsular ligament laxity. Each year in the United States, approximately 1.7 million people are diagnosed with traumatic brain injury (TBI), although many more go undiagnosed because they do not seek out medical care [95].
While most individuals recover from a single concussion, up to one-third of those will continue to suffer from residual effects such as headache, neck pain, dizziness and memory problems one year after injury [99]. Despite unique differences in the biomechanics of concussion and whiplash, both types of trauma involve an acceleration-deceleration of the head and neck. Debate over the veracity of PCS or WAD symptomology has persisted; however, there is no single explanation for the etiology of these disorders, especially since the onset and duration of symptoms can vary greatly among individuals. The occipito-atlanto-axial complex has a unique anatomical relationship with the vertebral arteries. Considering the position of the vertebral arteries in the canals of the transverse processes in the cervical vertebrae, it is possible to see how head positioning can alter vertebral arterial flow.
Proper blood flow in the vertebral arteries is crucial because these arteries travel up to form the basilar artery at the brainstem and provide circulation to the posterior half of the brain. Whiplash injury itself has been shown to reduce vertebral artery blood flow and elicit symptoms of VBI [118, 119]. Various tensile forces place strains with differing deformations on a variety of viscoelastic spinal structures, including the ligaments, the annulus and nucleus of the intervertebral disc, and the spinal cord. The posterior ligamentous structures of the human spine are innervated by four types of nerve endings: pacinian corpuscles, golgi tendon organs, and ruffini and free nerve endings [40]. As described earlier, the nucleus pulposus is designed to sustain compression loads and the annulus fibrosus that surrounds it, to resist tension, shear and torsion. There are a number of treatment modalities for the management of chronic neck pain and cervical instability, including injection therapy, nerve blocks, mobilization, manipulation, alternative medicine, behavioral therapy, fusion, and pharmacologic agents such as NSAIDS and opiates.
The literature contains many reports on injection therapy for the treatment of chronic neck pain. In the case of manipulative therapy, the results of a randomized trial disputed the hypothesis that supervised home exercises, combined or not with manual therapy, can be of benefit in treating non-specific chronic neck pain, as compared to no treatment [7]. Cervical disc herniation is a major source of chronic neck and spinal pain and is generally treated by either surgery or epidural injections, but their effectiveness continues to be debatable. Collectively, these interventions for the treatment of chronic neck pain may each offer temporary relief, but many fall short of a cure.
To date, there is no consensus on the diagnosis of cervical spine instability or on traditional treatments that relieve chronic neck pain.
Chronic neck pain and cervical instability are particularly difficult to treat when capsular ligament laxity is the cause because ligament cartilage is notoriously slow in healing due to a lack of blood supply.
While the most studied type of prolotherapy is the Hackett-Hemwall procedure which uses dextrose as the proliferant, there are multiple other choices that are suitable, such as polidocanol, manganese, human growth hormone, and zinc.
It is important to note that prolotherapy not only involves the treatment of joints, but also the associated tendon and ligament attachments surrounding them; hence, it is a comprehensive and highly effective means of wound healing and pain resolution. Prolotherapy has a long history of being used for whiplash-type soft tissue injuries of the neck.
Evidence that prolotherapy induces the repair of ligaments and other soft tissue structures has been reported in both animal and human studies. Studies have also been published on the use of prolotherapy for resolving chronic pain, [152, 178, 179] as well as for conditions specifically related to joint instability in the cervical spine [163, 180] In our own pain clinic, we have used prolotherapy successfully on patients who had chronic pain in the shoulder, elbow, low back, hip, and knee [181-186].
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Although tinnitus is an auditory symptom, its onset and progression often associates with emotional strain. Schematic representation of two main types of stress and different stress models used in basic research. Further, stress can also activate sympathetic nervous system (Ulrich-Lai and Herman, 2009).
Most representative stress-induced pathways and hypothetical involvement in the induction of allostatic load. This activation has been documented in tinnitus patients by using either positron emission tomography (PET) or functional magnetic resonance imagining (fMRI) (Lanting et al., 2009).
Accumulating evidence suggests that changes induced by these diverse conditions may result in similar phenotype, which is inappropriate activation of the auditory cortex. In addition, we will attempt to transfer some of the in vitro knowledge into a clinical practice.
HPA-induced stress hormone release and their signaling via respective receptors induce genomic (slow) and non-genomic (rapid) changes.
In contrast to ubiquitously expressed GRs, expression of mineralcorticoid receptors is restricted to selected tissues including brain, eye, intestine, kidney, mammary gland, pancreas, pituitary gland, and the inner ear. Not surprisingly, mineralcorticoid receptor was found to be predominantly localized in stria vascularis and in the spiral ganglion neurons (Furuta et al., 1994).
Special feature of glutamate circuits is their involvement in the process of plasticity, for the reason that glutamate and glutamate receptors NMDAR (N-methyl-D-aspartate receptor) and AMPAR (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor) regulate the strength and function of neuronal synapses.
AMPAR are multimers composed of various subunits, quantity, and ratio of which influences the synaptic strength.
However, the outcome of allostatic load not only depends on duration and category of stress but also on age, gender and the genetic makeup of stressed organism (Joels and Baram, 2009). Majority of stress research requiring information regarding histology, molecular or cell biology has been preformed with use of different animal stress models.
Physical type of stressor (restraint) in the acute settings (4 h of duration) increased the concentration of corticosterone in blood and as a consequence, protected the animals form the noise-induced trauma.
Prenatal, long-term administration of glucocorticoids, increased the susceptibility of the of the Sprague-Dawley offspring rats to noise trauma (Canlon et al., 2003).
However, little is known about the other side of this interaction—that is about stress inducing tinnitus. The first study demonstrated that the probability of developing tinnitus is approximately the same for highly stressed persons as it is for persons exposed to occupational noise (Baigi et al., 2011). Recent review of Kraus and Canlon delineates known to date anatomical connectivities between the auditory and limbic systems (reviewed in detail by Kraus and Canlon, 2012).
Resulting plastic changes in central auditory activity are coupled with altered attention and negative emotions.
Importantly, biomarkers and mechanisms are being indentified in a process of stress definition (Piazza et al., 2010).
Such assessment may be performed in form of a self-filled questionnaire or by a clinical psychologist. Model of stress-induced neuronal plasticity, which has been accepted in memory, learning, and emotional systems—can it also be truth to explain the induction of auditory pathologies by stress?
In addition, designing and conducting large epidemiological studies, where individuals would be monitored for stress parameters and followed audiometrically for decades, would be an expensive and a time-consuming mission. We conducted a review of the literature published up to December 2013 on the diagnostic and treatment modalities of disorders related to chronic neck pain and concluded that, despite providing temporary relief of symptoms, these treatments do not address the specific problems of healing and are not likely to offer long-term cures.
In the upper cervical spine (C0-C2), this can cause a number of other symptoms including, but not limited to, nerve irritation and vertebrobasilar insufficiency with associated vertigo, tinnitus, dizziness, facial pain, arm pain, and migraine headaches.
Currently, curative treatment options for this type of cervical instability are inconclusive and inadequate. Chronic cervical spine pain is particularly challenging to treat, and data regarding the long-term efficacy of traditional therapies has been extremely discouraging [1]. However, conventional treatments for chronic neck pain remain debatable and include interventions such as use of nonsteroidal anti-inflammatory drugs (NSAIDs) and narcotics for pain management, cervical collars, rest, physiotherapy, manual therapy, strengthening exercises, and nerve blocks.
Should this be the case and joint instability is the fundamental problem causing chronic neck pain, a new treatment approach may be warranted.
In most cases, diagnostic tools for detecting cervical instability have been inconsistent and lack specificity [11-15], and are therefore inadequate. The distinct anatomy of the cervical spine and the pathology of cervical instability described herein underlie the rationale for treating the condition with prolotherapy.
Despite having the smallest vertebral bodies, the cervical spine is the most mobile segment of the entire spine and must support a high degree of movement.
The upper cervical spine is stabilized solely by ligaments, including the transverse, alar, and capsular ligaments. Each vertebra in this region (C3-C7) has a vertebral body, in between which lies an intervertebral disc, the largest avascular structure of the body. Capsular ligaments wrap around each facet joint, which help to maintain stability during neck rotation.
From C1-C2 to the sacrum, the ligamentum flava run down the posterior aspect of the spinal canal and join the laminae of adjacent vertebrae while helping to maintain proper neck posture. The transverse processes are bony prominences that protrude postero-laterally and serve as attachment sites for various muscles and ligaments. Researchers have found there is a continuum between the amount of trauma and degree of instability to the cervical facets, with greater trauma causing a higher degree of facet instability [26-28]. They lie close to the intervertebral centers of rotation and provide significant stability in the neck, especially during axial rotation [29]; consequently, they serve as essential components for ensuring neck stability with movement.
For instance, in an animal study, it was shown that sequential removal of sheep capsular ligaments and cervical facets caused an undue increase in range of motion, especially in axial rotation, flexion and extension with caudal progression [31]. In either case, the cause of injury occurs through similar mechanisms, leading to capsular ligament laxity and excess motion of the facet joints, which often results in cervical instability.


Hence, the facet joint has long been considered the primary source of chronic spinal pain [36-38].
In general, instability implies a pathological condition with resultant symptoms, whereas joint hypermobility alone does not (Fig.
In contrast, joints that are hypermobile demonstrate increased segmental mobility but are able to maintain their stability and function normally under physiological loads [41]. Minor injuries of the cervical spine are those involving soft tissues alone without evidence of fracture and are the most common causes of cervical instability. For example, in one autopsy study of cryosection samples of the cervical spine, [42] only one out of ten gross ligamentous disruptions was evident on x-ray. Studies using fCT for diagnosing soft tissue ligament or post-whiplash injuries have demonstrated the ability of this technique to show excess atlanto-occipital or atlanto-axial movement during axial rotation [48, 49]. Ligament laxity across the C0-C1-C2 complex is primarily caused by rotational movements, especially those involving lateral bending and axial rotation [52-54]. The capsular ligaments of the atlanto-axial joint are especially susceptible to injury from rotational thrusts, and thus, may be at risk during mechanically mediated manipulation. Capsular ligament tension is increased during abnormal postures, causing elongation of the capsular ligaments, with magnitudes increased by up to 70% of normal [57]. Similarly, cervical pain is divided equally by an imaginary transverse plane into upper cervical pain and lower cervical pain. Clinically, there is a 30% rate of radicular symptoms during axial rotation in those with rotator instabilities [60].
These movements can cause encroachment on cervical nerve roots and subsequent paresthesia along the pathway therein of the affected nerve and may be why evidence of cervical radiculopathy does not show up on standard MRI or CT scans. While disc herniation can easily be seen on routine (non-functional) MRI or CT scans, evidence of radiculopathy from cervical instability cannot.
Animal models used for initiating disc degeneration in research studies have shown the induction of spinal instability through injury of the facet joints [68, 69]. Standard x-rays often do not reveal present injury to the cervical spine and as a consequence, these injuries go unreported and patients are left without proper treatment for their condition [76].
Success in relieving neck pain in whiplash patients has been documented by numerous clinical studies using nerve block and radiofrequency ablation of facet joint afferents, including capsular ligament nerves, such that increased interest has developed regarding the relationships between injury to the facet joints and capsular ligaments and post-whiplash dysfunction and related symptoms [36, 81]. Others have shown that injury to the cervical facet joints and capsular ligaments are the most common cause of pain in post-whiplash patients [84-86]. Maximum capsular ligament strains occur during shear forces, such as when a force is applied while the head is rotated (axial rotation). One study conclusively demonstrated that whiplash injury to the capsular ligaments resulted in an 85% to 275% increase in ligament elongation (ie, laxity) compared to that of controls [30]. Such symptoms characterize a disorder known as post-concussion syndrome (PCS) and are much like those of WAD; both disorders are likely due to cervical instability.
This overlap in symptomology may be due to a common etiology of underlying cervical instability that affects the cervical spine near the neck. This impact to the head can not only cause injury to the brain and skull, but can also damage surrounding ligaments of the neck since these tissues undergo the same accelerating-decelerating force. Many of the symptoms of PCS and WAD tend to increase over time, especially when those affected are engaged in physical or cognitive activity. In the lower cervical spine, the vertebral arteries lie in a relatively straight-forward course as they travel through the transverse foramina from C3-C6.
Even normal physiological neck movements (ie, neck rotation) have been shown to cause partial occlusion of up to 20% or 30% in at least one vertebral artery [110]. In one study, the authors concluded that patients with persistent vertigo or dizziness after whiplash injury are likely to have VBI if the injury was traumatic enough to cause a circulation disorder in the vertebrobasilar arterial system [118]. Further to this, cadaver experiments have shown that the spinal cord and the intervertebral disc components carry considerably lower tensile forces than the spinal ligament column [129, 130]. These receptors monitor joint excursion and capsular tension, and may initiate protective muscular reflexes that prevent joint degeneration and instability, especially when ligaments, such as the anterior and posterior longitudinal, ligamentum flavum, capsular, interspinous and supraspinous, are under too much tension [131, 135].
The stress in the annulus fibers is approximately 4-5 times the applied stress in the nucleus [136, 137]. However, these treatments do not address stabilizing the cervical spine or healing ligament injuries, and thus, do not offer long-term curative options. Cervical interlaminar epidural injections with or without steroids may provide significant improvement in pain and function for patients with cervical disc herniation and radiculitis [140]. In a systematic review of therapeutic cervical facet joint interventions, the evidence for both cervical radiofrequency neurotomy and cervical medial branch blocks is fair, and for cervical intra-articular injections with local anesthetic and steroids, the evidence is limited [142]. The study found that there were no differences in primary or secondary outcomes among the three groups and that no significant change in health-related quality of life was associated with the preventive phase.
In a randomized, double-blind, controlled clinical trial assigning patients to treatment with epidural injections with lidocaine or lidocaine mixed with betamethasone, 72% of patients in the local anesthetic group and 68% of patients in the local anesthetic with steroid group had at least a 50% improvement in pain and disability at 2 years, indicating that either protocol may be beneficial in alleviating chronic pain from cervical disc herniation [146]. Aside from these conventional treatment options, there are pain medications and pain patches, but their use is controversial because they offer little restorative value and often lead to dependence. Most treatment options do not address this specific problem, and therefore, have limited success in providing a long-term cure. In a five-part series evaluating the strength of evidence supporting WAD therapies, Teasell, et al. In addition to the Hackett-Hemwall procedure, there is another procedure called cellular prolotherapy, which involves the use of a patienta€™s own cells from blood, bone marrow, or adipose tissue as the proliferant to generate healing.
The Hackett-Hemwall prolotherapy technique was developed in the 1950s and is being transitioned into mainstream medicine due to an increasing number of studies reporting positive outcomes [155-158].
In separate studies, Hackett and his colleagues early on had remarkably successful outcomes in treating ligament injuries; more than 85% of patients with cervical ligament injury-related symptoms, including those with headache or WAD, reported they had minor to no residual pain or related symptoms after prolotherapy [125, 159, 160].
Animal research conducted by Hackett [174] demonstrated that proliferation and strengthening of tendons occurred, while Liu and associates [175] found that prolotherapy injections to rabbit ligaments increased ligamentous mass (44%), thickness (27%), as well as ligament-bone junction strength (28%) over a six-week period.
In the upper cervical spine (C0-C2), this can cause symptoms such as nerve irritation and vertebrobasilar insufficiency with associated vertigo, tinnitus, dizziness, facial pain, arm pain, and migraine headaches.
Furthermore, we contend that the use of comprehensive Hackett-Hemwall prolotherapy appears to be an effective treatment for chronic neck pain and cervical instability, especially when due to ligament laxity.
Neck pain clinical practice guidelines linked to the international classification of functioning, disability, and health from the orthopaedic section of the American Physical Therapy Association. Recent epidemiological studies have provided evidence for a direct relationship between the emotional status of subjects and tinnitus. Adaptation of neuronal system to stress-induced condition is reflected by neuronal plasticity. The results of animal and human studies have helped to determine various possible causes of inappropriate activation of auditory cortex leading to neuronal plasticity. Finally, release of ACTH to blood causes secretion of stress hormones from the adrenal glands (Lupien et al., 2007). It consists of locally produced corticotropin-releasing factor (CRF), CRF1-receptor and ACTH. To date, mechanisms determined as responsible for the synaptic plasticity are glutamate receptors (NMDAR)—related long-term potentiation (LTP) and long-term depression (LTD).
The mechanism that mediates HPA-induced changes in AMPA receptors trafficking is attributed to the genomic and non-genomic effects of glucocorticoids (Figure 4). If stress and activated HPA axis could induce plastic changes in the auditory pathway via modification of glutamate neurotransmission, remains to be established.
The goal of animal stress models is to mimic and study stress experienced by people under certain conditions.
Similar protective effects had the administration of glucocorticoid-based drugs prior to acoustic trauma (reviewed in Meltser and Canlon, 2011). However, these findings could not be reproduced by other group in Wistar rats, possibly reflecting inter-strain genetic differences in stress and corticosteroid susceptibility (Hougaard et al., 2007).
This implies that chronic, psycho-social stress may influence the function of auditory pathway.
It has been a frequent observation made by otologists and audiologists that many tinnitus patients complain of psycho-social distress prior to or during the onset and progression of tinnitus.
Importantly, the authors also have noticed that psycho-social stress contributes to worsening of tinnitus symptoms. In addition, patients who had disturbing tinnitus for a longer time (on average 14.7 years) were shown to develop improper HPA responses to an experimental, psycho-social stress (Hebert and Lupien, 2007). In addition, this important work collected evidence supporting the notion of noise generating synaptic plasticity in the limbic structures. Can stress induce such critical injury to the inner ear or induce plasticity in higher auditory structures? This provides the researchers and clinicians not only with more basic knowledge about stress-induced processes but also with more diagnostic power. Psychological intervention with a goal of stress-management strategies appears to be an indispensable element in tinnitus treatment, especially important to use in very early stages of tinnitus, before the chronification of plastic changes has taken place. Nevertheless, step-by step understanding of how and to what degree the psycho-social or physical stress could affect our peripheral and central auditory system should become a goal in the basic and clinical auditory research. The anti-inflammatory action of glucocorticoids is mediated by cell type specific regulation of apoptosis.
Cell-specific regulation of apoptosis by glucocorticoids: implication to their anti-inflammatory action.
Focal metabolic activation in the predominant left auditory cortex in patients suffering from tinnitus: a PET study with [18F]deoxyglucose. The objectives of this narrative review are to provide an overview of chronic neck pain as it relates to cervical instability, to describe the anatomical features of the cervical spine and the impact of capsular ligament laxity, to discuss the disorders causing chronic neck pain and their current treatments, and lastly, to present prolotherapy as a viable treatment option that heals injured ligaments, restores stability to the spine, and resolves chronic neck pain.
Based on clinical studies and experience with patients who have visited our chronic pain clinic with complaints of chronic neck pain, we contend that prolotherapy offers a potentially curative treatment option for chronic neck pain related to capsular ligament laxity and underlying cervical instability. The prevalence of neck pain in the general population has been reported to range between 30% and 50%, with women over 50 making up the larger portion [1-3]. Furthermore, the literature on long-term treatment outcomes has been inconclusive at best [5-9]. A better understanding of the pathogenesis of cervical instability may better enable practitioners to recognize and treat the condition more effectively.
Consequently, it is highly reliant on ligamentous tissue for stabilizing the neck and spinal column, as well as for controlling normal joint motion; as a result, the cervical spine is highly susceptible to injury.
The transverse ligament runs behind the dens, originating on a small tubercle on the medial side of a lateral mass of the atlas and inserting onto the identical tubercle on the other side. This disc is a piece of fibrocartilage that helps cushion the joints and allows for more stability and is comprised of an inner gelatinous nucleus pulposus, which is surrounded by an outer, fibrous annulus fibrosus. Each vertebra in the lower cervical spine (in addition to C2) contains a spinous process that serves as an attachment site for the interspinal ligaments.
With the exception of C7, each of these processes has a foramen which allows for passage of the vertebral artery towards the brain; the C7 transverse process has foramina which allow for passage of the vertebral vein and sympathetic nerves [22]. 2), the facet joints are diarrthrodial, meaning they function similar to the knee joint in that they contain synovial cells and joint fluid and are surrounded by a capsule.
Each facet joint has articular cartilage, the synovium where synovial fluid is produced, and a meniscus.
At C0-C1, the convex shape of the occipital condyles enables them to fit into the concave surface of the inferior articular process. As the cervical spine extends downward, the angle of the facet joint becomes bigger such that the joint slopes backwards and downwards. The capsular ligaments have a high peak force and elongation potential, meaning they can withstand large forces before rupturing.
Human cadaver studies have also indicated that transection or injury of joint capsular ligaments significantly increases axial rotation and lateral flexion [32, 33]. Additionally, injury to these nerves has been shown to affect the overall joint function of the facet joints [39].
When minor or moderate spinal instability occurs, treatment with prolotherapy may be of benefit in alleviating symptoms and restoring normal cervical joint function. Mild or moderate clinical instability is that which is without neurologic (somatic) injury and is typically due to cumulative micro-traumas. Furthermore, there is often little correlation between the degree of instability or hypermobility shown on radiographic studies and clinical symptoms [43-45]. This is especially pertinent when patients have signs and symptoms of cervical instability, yet have normal MRIs in a neutral position.
There are also specialized physical examination tests specific for upper cervical instability, such as the Sharp-Purser test, upper cervical flexion test, and cervical flexion-rotation test. C1-C2 instability can easily be seen in the patient, as 70% of C1 articular facet is subluxed posteriorly (arrow) on C2 facet when the patient rotates his head (turns head to the left then the right).
With severe neck traumas, especially those with rotation, up to 25% of total lesions can be attributed to ligament injuries of C0-C2 alone.
The capsular ligaments in the occipto-atlantal joint function as joint stabilizers and can also become injured due to excessive or abnormal forces [46]. Such excessive ligament elongation induces laxity to the facet joints, which puts the cervical spine more at risk for further degenerative changes and instability. Suboccipital pain is that pain located between superior nuchal line and an imaginary transverse line through the tip of the second cervical spinous process. Cervical nerve roots there are vulnerable to compression or injury by the facet joints posteriorly or by the joints of Luschka and the intervertebral disc anteriorly. However, if the cervical spine and capsular ligaments are injured, facet joint hypertrophy and degeneration of the cervical discs can occur. Neural foraminal narrowing is shown at two levels during lateral extension versus lateral flexion.
Most cases of acute radiculopathy due to disc herniation resolve with non-surgical active or passive therapies, but some patients continue to have clinically significant symptoms, in which case surgical treatments such as anterior cervical decompression with fusion or posterior cervical laminoforaminotomy can be performed [62]. Spondylosis begins with repetitive trauma, such as rotational strains or compressive forces to the spine. When symptoms of cervical spondylosis do develop, they are generally nonspecific and include neck pain and stiffness [66].
In similar models, capsular ligament injuries of the facet joints caused multidirectional instability of the cervical spine, greatly increasing axial rotation motion correlating with cervical disc injuries [31, 28, 70, 71]. Part of the difficulty lies in the fact that major injury to the cervical spine may only produce minor symptoms in some patients, whereas minor injury may produce more severe symptoms in others [77].
Cinephotographic and cineradiographic studies of both cadavers and human subjects show that under the conditions of whiplash, a resultant high impact force occurs in the cervical facet joints, leading to their injury and the possibility of cervical spine instability [84]. Ultimately, the capsular ligaments become elongated, resulting in abnormal motions in the spinal segments affected [30, 87].
While capsular ligament injury in the upper cervical spinal region can occur from compressive forces alone, exertion from a combination of shear, compression and bending forces is more likely and usually involves much lower loads to cause injury [92]. The study also reported evidence that tension of the capsular ligaments is requisite for producing pain from the facet joint.
A concussion is considered a mild TBI and is defined as any transient neurologic dysfunction resulting from a biomechanical force, usually a sudden or forceful blow to the head which may or may not cause a loss of consciousness. According to the International Classification of Diseases, 10th Revision (ICD-10), the diagnosis of PCS is made when a person has had a head injury sufficient enough to result in loss of consciousness and develops at least three of eight of the following symptoms within four weeks: headache, dizziness, fatigue, irritability, sleep problems, concentration difficulties, memory issues, and problems tolerating stress [100, 101]. Data has revealed that over half of patients with damage to the upper cervical spine from whiplash injury had evidence of concurrent head trauma [103]. Chronic neck pain is often described as a long-term result of both concussion and whiplash, indicating that the most likely structures to become injured during these traumas are the capsular ligaments of the cervical facet joints. Studies have shown that contralateral neck rotation is associated with vertebral artery blood flow changes, primarily between the atlas and axis; such changes can also occur when osteophytes are present in the cervical spine [111, 112]. VBI usually occurs in the presence of atherosclerosis or cervical spondylosis, but symptoms can also arise when there is intermittent vertebral artery occlusion induced by extreme rotation or extension of the head [113, 114]. Other researchers have surmised that excessive cervical instability, especially of the upper cervical spine, can cause obstruction of the vertebral artery during neck rotation, thus compromising blood flow and triggering symptoms [120-122].
There is considerable overlap in symptoms amongst these conditions, possibly because they all appear to be due to cervical instability. Encapsulated mechanoreceptors and free nerve endings have been identified in the periarticular tissues of all major joints of the body including those in the spine, and in every articular tissue except cartilage [131].
Collectively, the cervical region of the spinal column is at risk to sustain deformations at all levels and in all components, and when the threshold crosses a particular level at a particular component, injury is imminent owing to the relative increased flexibility or joint laxity. In addition, annulus fibers elongate by up to 9% during torsional loading, but this is still well below the ultimate elongation at failure of over 25% [138].
In a later corresponding systematic review, the same group of authors concluded that the strength of evidence for diagnostic facet joint nerve blocks is good (a‰?75% pain relief), but stated the evidence is limited for dual blocks (50% to 74% pain relief), as well as for single blocks (50% to 74% pain relief) and (a‰?75% pain relief.) [6]. Participants in the combined intervention group did not have less pain or disability and fared no better functionally than participants from the two other groups during the preventive phase of the trial. Furthermore, they found evidence against a long-term benefit for medial branch block of facet joints with steroids and against a short-term benefit for botulinum toxin-A compared to saline, concluding that there is a lack of evidence for most pharmacological interventions.
If joint instability is the fundamental problem causing chronic neck pain and its associated autonomic symptoms, prolotherapy may be a treatment approach that meets this challenge. Prolotherapy is one such treatment which is intended for acute and chronic musculoskeletal injuries, including those causing chronic neck pain related to underlying joint instability and ligament laxity (Fig. Similar favorable outcomes for resolving neck pain were reported recently by Hauser, et al.
The technique is safe and relatively non-invasive as well as efficacious in relieving chronic neck pain and its associated symptoms.
In addition, studies of function, morphology, and gene and protein expression in the auditory system of animals exposed to stress support the notion that the emotional status can influence the auditory system. Generally speaking, stress is a positive reaction because it increases the chance of survival by initiating adaptation and coping with new situation (Lupien et al., 2009). These causes include changes in spontaneous firing rate, increased gamma band reflecting synchronous firing of auditory cortex and tonotopic reorganization (Nava and Roder, 2011). Stress hormones comprise glucocorticoids (corticosterone, cortisol) and mineralocorticoids (aldosterone) (de Kloet et al., 2005).
Interestingly, deletion of CRF1-receptor gene resulted in auditory impairment of knock-out animals (Graham and Vetter, 2011).
In addition, changes in AMPAR composition and density on the synapses were shown to be essential for the plasticity process.
In the prefrontal cortex, stress has been demonstrated to activate in a non-genomic way the glucocorticoid-inducible kinase SGK (Popoli et al., 2011).
From the perspective of allostatic model, one could hypothesize that the acute physical stress is unable to induce allostatic load in auditory pathway.
One of the earliest published observations connecting the onset of tinnitus with psycho-social distress was made by John Harrison Curtis, the surgeon of the Royal Dispensary for Diseases of the Ear in London (the first hospital in England offering specialized care for ear diseases, est. Interestingly, exposure to high level of stress and occupational noise doubles the probability of developing tinnitus. HPA axis in tinnitus patients under stress seems to be activated later and to a lesser extend than in the healthy controls, consistent with glucocorticoid inefficiency (Yehuda et al., 1996).


Induction of limbic plasticity is possible due to multi-level projections of the auditory system to the limbic structures. An important hint was recently delivered by a group studying mild stress model of depression in Sprague-Dawley rat with PET imaging technique.
Stress is no longer an undefined, sad state of mind but an important, distinct factor in precipitation and amplification of mental and mood disorders (Holsboer and Ising, 2010). In either case, the presence of excessive motion between two adjacent cervical vertebrae and these associated symptoms is described as cervical instability. Although many of these cases resolve with time and require minimal intervention, the recurrence rate of neck pain is high, and about one-third of people will suffer from chronic neck pain (defined as pain that persists longer than 6 months), and 5% will develop significant disability and reduction in quality of life [2, 4]. Chronic neck pain due to whiplash injury or whiplash associated disorder (WAD) is particularly resistant to long-term treatment; conventional treatment for these conditions may give temporary relief but long-term outcomes have been disappointing [10]. For instance, when cervical instability is related to injury of soft tissue (eg, ligaments) alone and not fracture, the treatment modality should be one that stimulates the involved soft tissue to regenerate and repair itself. C2 has a prominent vertebral body called the odontoid process or dens which acts as a pivot point for the C1 ring [16]. Thus, the transverse ligament restricts flexion of the head and anterior displacement of the atlas. The nucleus pulposus is designed to sustain compression loads and the annulus fibrosus, to resist tension, shear and torsion [19]. The ALL begins at the occiput and runs anteriorly to the anterior sacrum, helping to stabilize the vertebrae and intervertebral discs and limit spinal extension. The transverse processes of the cervical vertebrae are connected via the intertransverse ligaments; each attaches a transverse process to the one below and helps to limit lateral flexion of the cervical spine.
They also contain a meniscus which helps to further cushion the joint, and like the knee, are lined by articular cartilage and surrounded by capsular ligaments, which stabilize the joint.
The C1-C2 facet joints are oriented cranio-caudally, meaning they run more parallel to their transverse processes. Thus, the facet joints of the lower cervical spine have progressively less rotation than those of the upper cervical spine. This was demonstrated in a dynamic mechanical study in which the capsular ligaments and ligamentum flavum were shown to have the highest average peak force, up to 220 N and 244 N, respectively [30].
Specifically, the largest increase in axial rotation with damage to a unilateral facet joint was 294% [33]. Creep refers to a time-dependent increase in strain and causes ligaments to "stretch out" over time. Therefore, injury to the capsular ligaments and subsequent nerve endings could explain the prevalence of chronic pain and joint instability in the facet joints of the cervical spine.
Clinical instability refers to a loss of motion stiffness in a particular spinal segment when the application of force to it produces greater displacement(s) than would otherwise be seen in a normal structure. Even after severe whiplash injuries, plain radiographs are usually normal despite clinical findings indicating the presence of soft tissue damage.
Although some ligament injuries in the C0-C2 region can cause severe neurological impairment, the majority involve sub-failure loads to the facet joints and capsular ligaments, which are the primary source of most chronic pain in post-neck trauma [26, 55].
Therefore, capsular ligament injury appears to cause upper cervical instability because of laxity in the stabilizing structure of the facet joints [58]. Likewise, cervico-occipital pain is perceived as arising in the cervical region and extending over the occipital region of the skull. Cervical radiculopathy is also strongly associated with spondylosis, a disease generally attributed to aging that involves an overall degeneration of the cervical spine. Only rarely do neurologic symptoms develop (ie, radiculopathy or myelopathy), and most often they occur in people with congenitally narrowed spinal canals [67].
Using human specimens, surgical procedures such as discectomy have been shown to cause an immediate increase in motion of the segments involved [72].
This sequence has been documented with both in vitro and in vivo studies of segmental motion characteristics after torsional loads and resultant disc degeneration [88-90]. However, if the head is turned during whiplash trauma, the peak strain on the cervical facet joints and capsular ligaments can increase by 34% [93].
Concussion induces a barrage of ionic, metabolic, and physiologic events [96] and manifests in a composite of symptoms affecting a patienta€™s physical, cognitive, and emotional states, and his or her sleep cycle, any one of which can be fleeting or long-term in duration [97]. Of those treated for PCS who had mild head injury, 80% report having chronic daily headaches; surprisingly, of those with moderate to severe head injury, only 27% reported having chronic daily headaches [102].
It was shown that whiplash can cause minor brain injuries similar to that of concussion if it occurs with such rapid neck movement that there is a collision between the brain and skull. Direct head trauma has been shown to produce forces between 10,000 and 15,000 N on the head and between 1,000 and 1,500 N on the neck, depending on the angle at which the object hits the head [104, 105]. In light of this, we propose that the best scientific anatomical explanation is cervical instability in the upper cervical spine, resulting from ligament injury (laxity). The vertebral artery emerges from the transverse process of C2 and sweeps laterally to pass through the transverse foramen of C1 (atlas). This mechanical compression of the vertebral arteries can occur along with other anomalies, including cervical osteophytes, fibrous bands, and osseous prominences [115, 116] These anomalies were seen in about half of the cases of vertebral artery injury after cervical manipulation, as reported in a recent review [117]. Symptoms include neck pain, headaches, dizziness, vertigo, visual and auditory disturbances, memory and cognitive impairment, and migraines. Any innervated structure that has been injured by trauma is a potential chronic pain generator; this includes the intervertebral discs, facet joints, spinal muscles, tendons and ligaments [132-134]. Pressure within the nucleus is approximately 1.5 times the externally applied load per unit of disc area. As mentioned earlier in this paper, most treatments have shown limited evidence in their efficacy or are inconsistent in their results. In another systematic review evaluating cervical interlaminar epidural injections, the evidence indicated that the injection therapy showed significant effects in relieving chronic intractable pain of cervical origin; specific to long-term relief the indicated level of evidence was Level II-1 [143]. Another randomized clinical trial comparing the effects of applying joint mobilization at symptomatic and asymptomatic cervical levels in patients with chronic nonspecific neck pain was inconclusive in that there was no significant difference in pain intensity immediately after treatment between groups during resting position, painful active movement, or vertebral palpation [8]. Furthermore, they state that immobilization with a soft collar is ineffective to the point of impeding recovery, saying that activation-based therapy is recommended instead, a conclusion similar to that of Hauser et al. Such a response initiates a healing cascade that duplicates the natural healing process of poorly vascularized tissue (ligaments, tendons, and cartilage) [40, 153].
Prolotherapy has also been found effective for other ligament injuries, including the lower back, [164-166] knee, [167-169] and other peripheral joints, [170-172] as well as congenital systemic ligament laxity conditions [173]. Additional randomized clinical trials and more research into its use will be needed to verify its potential to reverse ligament laxity and correct the attendant cervical instability. The data provided by clinical and basic research with use of animal stress models offers valuable clues for an improvement in diagnosis and more effective treatment of tinnitus. The process of coping with conditions altered by stress is called allostasis and means a change from the usual, homeostatic status into a status, in which the organism can adapt to changes (McEwen and Gianaros, 2011). This impairment was accompanied by reduced expression of glutamine synthetase together with abnormal innervation features and was attributed to the developmental role that CRFR1 potentially plays in the inner ear. SGK1 is also expressed in stria vascularis, spiral ligament, spiral limbus, organ of Corti, Reissner's membrane and in the spiral ganglion of rats (Zhong and Liu, 2009) but role of SGK1 in the inner ear has not yet been experimentally addressed.
To the physical stress models belongs between many others the immersion in cold water, restrain, cold-water restrain, electric foot shock, and food deprivation. From the perspective of allostatic model, one could postulate that chronic physical stress may induce the allostatic load in auditory pathway.
On the contrary, activation of HPA axis resulting in the production of corticosteroids protects the auditory system against the noise trauma. In the second study, a self-completion questionnaire was used to inquire about work- and health-related stressors and hearing problems, such as tinnitus.
Recent research has implicated that living in a city affects stress processing and may be responsible for increased incidence of anxiety disorders in the cities, as opposed to rural communities (Lederbogen et al., 2011).
Tinnitus in the general population with a focus on noise and stress: a public health study. For this group of chronic pain patients, modern medicine offers few options for long-term recovery.
In rotation, the wall of the vertebral foramen of Cl decreases the opening of the spinal canal between Cl and C2.
The left and right alar ligaments originate from the posterior dens and attach to the medial occipital condyles on the ipsilateral sides.
The annulus fibrosus is thought to determine the proper functioning of the entire intervertebral disc [20] and has been described as a lamellar structure consisting of 15-26 distinct concentric fibrocartilage layers that constitute a criss-crossing fiber matrix [19]. The PLL also helps to stabilize the vertebrae and intervertebral discs, as well as limit spinal flexion.
These capsular ligaments hold adjacent vertebrae to one another, and the articular cartilage therein is aligned such that its opposing tissue surfaces provide for a low-friction environment [23].
Furthermore, the presence of intervertebral discs helps give the lower cervical spine more stability. This was reported as considerably greater than the force shown in the anterior longitudinal ligament and middle third disc. While this constitutes low-level subfailure ligament injuries, it may represent the vast majority of cervical instability cases and can potentially incapacitate people due to disabling pain, vertigo, tinnitus or other concomitant symptoms of cervical instability.
In clinical instability, symptoms such as pain and muscle spasms can thus be experienced within a persona€™s range of motion, not just at its furthest extension point. The disorder is characterized by degenerative changes in the intervertebral disc, osteophytosis of the vertebral bodies, and hypertrophy of the facet joints and laminar arches. The dysfunctional phase is characterized by capsular ligament injuries and subsequent cartilage degeneration and synovitis, ultimately leading to abnormal motion in the cervical spine. Physical exam findings are often limited to restricted range of neck motion and poorly localized tenderness. Stabilization procedures such as neck fusion have been known to create increased pressure on the adjacent cervical spinal segments; this is referred to as adjacent segment disease. In one study reporting on an automobile rear-impact simulation, the magnitude of the joint capsule strain was 47% to 196% higher in instances when the head was rotated 60A° during impact, compared with those when the head was forward facing [94]. The impact of the brain on the skull is believed to be the cause of the symptoms of both concussion and PCS, although the specific mechanisms underlying neural tissue damage are still being investigated. Cervical capsular ligaments can become lax with as little as 5 N of force, although most studies report cervical ligament failure at around 100 N [30, 55, 91, 106].
From there it passes around the posterior border of the lateral mass of C1, at which point it is farthest from the midline plane at the level of C1 [108, 109].
It has been surmised that cervical arthritis or injury provokes an irritation of both the vertebral and sympathetic nerves.
As such, the nucleus is relatively incompressible, which causes the intervertebral disc to be susceptible to injury in that it bulges under loads - approximately 1 mm per physiological load [139].
In a systematic review of the literature from January 2000 to July 2012 on physical modalities for acute to chronic neck pain, acupuncture, laser therapy, and intermittent traction were found to provide moderate benefits [5]. In doing so, tensile strength, elasticity, mass and load-bearing capacity of collagenous connective tissues become increased [152]. They also found a linear ligament orientation similar to what is found in normal ligaments. Abuse or chronic deregulation of allostatic processes (such as prolonged or repeated stress) may lead to so-called allostatic load, which is a negative physiological and behavioral effect of stress (Figure 2) (McEwen and Wingfield, 2003). Future experiments should determine the connection between cochlear and systemic HPA systems.
Lastly, there are models that mix different types of acute and chronic stress in an unpredictable way (Jaggi et al., 2011). This endogenous corticosteroid protection is comparable to the application of synthetic corticosteroids, used in therapy of acute hearing loss (Meltser and Canlon, 2011). If these projections are activated by stress and if this activation could induce plastic changes in the auditory system, remains to be determined. After 4 weeks of random mixed stressing, brain PET analysis revealed the activation of left auditory cortex and deactivation of left inferior colliculus in stressed animals. 1), coupled with the lack of intervertebral discs in the upper cervical spine, allows for more movement and rotation of the joint, thus facilitating mobility rather than stability [17].
They work to limit axial rotation and are under the greatest tension in rotation and flexion.
It extends from the body of the axis to the posterior sacrum and runs within the anterior aspect of the spinal canal across from the ligamentum flava.
Such symptoms can be caused by elongation-induced strains of the capsular ligaments; these strains can progress to subsequent subfailure tears in the ligament fibers or to laxity in the capsular ligaments, leading to instability at the level of the cervical facet joints [35].
These muscle spasms can cause intense pain and are the bodya€™s response to cervical instability in that the ligaments act as sensory organs involved in ligamento-muscular reflexes. In the event of another ligament injury, instability of the hypertrophied bones can occur and further reduce the patency of the neural foramen. Since more than one cervical spine segment is usually affected in spondylosis, the symptoms of radiculopathy are more diffuse than those typical of unilateral soft disc herniation and present as neck, mid-upper back, and arm pain with paresthesia. Clinical symptoms commonly manifest when a new cervical ligament injury is superimposed on the underlying degeneration. This can develop when the loss of motion from cervical fusion causes greater shearing and increased rotation and traction stress on adjacent vertebrae at the facet joints [73-75].
The impact was greatest in the ipsilateral facet joints, such that head rotation to the left caused higher ligament strain at the left facet joint capsule. Even low speed rear impact collisions at as little as 7 mph to 8 mph can cause the head to move roughly 18 inches at a force as great as 7 G in less than a quarter of a second [107].
This pathway creates extra space which allows for normal head rotation without compromising vertebral artery blood flow. As a result, current treatment now centers on resolution of cervical instability and its effects on the posterior sympathetic nerves [124]. As the disc degenerates on bulging (herniates), it looses elasticity, further compromising its ability to compress.
Evidence was reported as a€?not stronga€? [144] in one randomized trial comparing groups receiving massage treatment for neck pain versus those reading a self-care book, while another found that cupping massage was no more effective than progressive muscle relaxation in reducing chronic non-specific neck pain [9].
This occurs because the increased glucose concentration causes increases in cell protein synthesis, DNA synthesis, cell volume, and proliferation, all of which stimulate ligament size and mass and ligament-bone junction strength, as well as the production of growth factors, which are essential for ligament repair and growth [154].
Allostatic load can affect various tissues and organs and include neuronal atrophy, impaired immunity, atherosclerosis, obesity, bone demineralization and mood disorders (McEwen, 2003). The genomic reactions occur due to the fact that both GRs and mineralcorticoid receptors are cytoplasmic, ligand-activated transcription factors (Funder, 1997). Curtis has noticed that in two of five cases, affected patients attributed the beginning of tinnitus to a psycho-social strain caused by death in immediate family (Curtis, 1841). In addition, prevalence of sleeping problems was significantly higher in subjects with tinnitus, than in the tinnitus-free subjects.
It is, however, possible that the observed changes in HPA axis of tinnitus patients may be a result and not a cause of tinnitus. Changes in the auditory system correlated significantly with the depressive symptoms of experimental animals (Hu et al., 2010). Including stress as factor of future investigations in the auditory, tinnitus-related research seems to be a logical consequence of above observations. Collectively, the upper cervical spine is responsible for 50% of total neck flexion and extension at the atlanto-occipital (C0-C1) joint, as well as 50% of total neck rotation that occurs at the atlanto-axial joint (C1-C2) [16]. By holding C1 and C2 in proper position, the transverse and alar ligaments help to protect the spinal cord, brain stem, and nervous system from excess movement in the upper cervical spine [18]. A microdissection study using cadavers reported that the cervical annulus fibrosus does not consist of concentric laminae of collagen fibers as it does in lumbar discs. The ligamento-muscular reflex is a protective reflex emanating from mechanoreceptors (ie, pacinian corpuscles, golgi tendon organs, and ruffini endings) in the ligaments and transmitted to the muscles. In patients with spondylosis and underlying capsular ligament laxity, cervical radiculopathy is more likely to occur because the neural foramina may already be narrowed from facet joint hypertrophy and disc degeneration, enabling any new injury to more readily pinch on an exiting nerve root. Thus, instability can a€?travela€? up or down from the fused segment, furthering disc degeneration. Numerous experimental studies have suggested that certain features of injury mechanisms including direction and degree of acceleration and deceleration, translation and rotation forces, position and posture of head and neck, and even seat construction may be linked to the extent of cervical spine damage and to the actual structures damaged [23, 27, 35, 50, 61]. Shock absorption is no longer spread or absorbed evenly by the surrounding annulus, leading to greater shearing, rotation, and traction stress on the disc and adjacent vertebrae. Acupuncture appears to have better results in relieving neck pain but leaves questions as to the effects on the autonomic nervous system, suggesting that acupuncture points per se have different physical effects according to location [145].
Binding of steroids to GRs or mineralcorticoid receptors induces translocation of the ligand-receptor complex to the nucleus, where the transcription of selected genes is either induced or suppressed (Datson et al., 2008).
Importantly, the authors found linear association between tinnitus and the magnitude and duration of stress, such as for instance occupational stress (Hasson et al., 2011).
This motion is possible because the atlas (C1) rotates around the axis (C2) via the dens and the anterior arch of the atlas. Instead, the authors contend that the three-dimensional architecture of the cervical annulus fibrosus is more like that of a crescentic anterior interosseous ligament surrounding the nucleus pulposus [21]. Subsequent activation of these muscles helps to preserve joint stability, either directly by muscles crossing the joint or indirectly by muscles that do not cross the joint but limit joint motion [40]. During this progression, ongoing degeneration is occurring in the intervertebral discs, along with other parts of the cervical spine. These findings support the theory that iatrogenic-introduced stress and instability at adjacent spinal segments contribute to the pathogenesis of cervical spondylosis [74]. The severity of disc herniation can range from protrusion and bulging of the disc without rupture of the annulus fibrosus to disc extrusion, in which case, the annulus is perforated, leading to tearing of the structure. Both studies were performed with more than 10,000 subjects each, thus, providing statistical strength. Ankylosis (stiffening of the joints) can also occur at the unstable cervical spine segment, and rarely, causes entrapment of nearby spinal nerves.
Non-genomic responses induced by corticosteroids and mineralocorticoids are extremely rapid (seconds to minutes) and are not mediated by a cytoplasmic but by a minor, membrane-bound form of GRs or mineralcorticoid receptors (Groeneweg et al., 2012). The stabilization phase occurs with the formation of marginal osteophytes as the body tries to heal the spine.
Both receptors were shown to be localized to the lipid rafts—more precisely to caveolae on a cell surface. Caveolae are rich in signaling proteins such as G-proteins and kinases, thus, they support formation of various signalosomes.
The precise signaling pathways induced by corticosteroids and mineralocorticoids remain to be confirmed but it is already apparent that the kinase pathways are predominant (Groeneweg et al., 2012).



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