Pain Subsequent to Mechanical Loading of the Facet Capsular Ligament Depends on Encoding by Afferents in the Spinal Facet Joint

Author(s):  
Christine L. Weisshaar ◽  
Jeffrey V. Kras ◽  
Kosuke Tanaka ◽  
Beth A. Winkelstein

The cervical facet joint has been identified as the source of neck pain in up to 60% of the cases [1], with the C6/C7 facet joint being particularly susceptible to injury during painful mechanical neck injuries [2]. The facet joint is innervated by both mechanoreceptors and nociceptors (i.e. pain receptors) [3,4]. Both receptor types respond to manipulation of the facet joint and afferent activation is related to the magnitude of joint loading [5]. Also, tensile stretch of the capsular ligament in vivo to magnitudes of strain simulating those during neck injury also produces sustained behavioral sensitivity (pain) and upregulates proteins involved in nociception [6]. Although anatomic and biomechanical studies suggest that facet capsule loading has a role in the development of pain, the relationship between capsule tension, the joint’s innervation, and the production of pain is still unclear.

Author(s):  
Nathan D. Crosby ◽  
Kyle P. Quinn ◽  
Beth A. Winkelstein

Whiplash and other traumatic neck injuries are a primary cause of chronic neck pain in the United States, with the cervical facet joint and its ligament being a common anatomical source of the pain. During these injuries, the facet capsular ligament undergoes excessive stretching that alters the subsequent mechanical function of the facet joint and can also initiate pain [1,2]. Accordingly, defining the mechanical response of the facet capsule requires understanding its microstructural response during loading. Although the macro-mechanical responses of ligaments for many types of loading and injury scenarios have been studied, the microstructural and fibrillar responses in the facet capsular ligament remain largely undefined.


Author(s):  
Kyle P. Quinn ◽  
Kathryn E. Lee ◽  
Beth A. Winkelstein

Whiplash and its associated disorders are significant societal and health problems with half of affected patients reporting neck pain at one year after injury [1]. The cervical facet joint and its capsule have been identified in both biomechanical and clinical studies as a common site of painful injury during whiplash [2]. Also, in vivo joint distractions, which mimic the facet capsule loading reported in human cadaveric whiplash simulations, can produce behavioral hypersensitivity suggestive of chronic pain symptoms in the rat [3]. Increased laxity and decreased stiffness in the capsule are also produced after both painful joint distractions in the rat [4] and whiplash loading of the neck using cadaveric spines [5]. Together, these findings suggest that subfailure loading of the joint and its capsule produces both mechanical changes and pain. Yet, identifying the mechanical response associated with pathophysiological conditions in the capsular ligament requires an understanding of if, and how, its load-bearing microstructure is altered following painful loading.


Author(s):  
Kathryn E. Lee ◽  
Beth A. Winkelstein

Chronic neck pain following whiplash is a substantial problem, affecting as many as 42% of whiplash patients [1]. The cervical facet joint is a common candidate for producing neck pain because it sustains altered kinematics during whiplash, with tensile stretch of its capsular ligament exceeding that during normal motions [2,3]. Altered facet capsule mechanics have been documented for loading conditions below structural failure [4,5]; evidence of both decreased linear stiffness and minor ruptures of the capsule suggest ligament injury prior to failure. In vivo studies have also implicated subfailure capsule injury as a potential source of pain. Capsule nociceptive pain fiber activation and saturation [6], as well as sustained pain symptoms [7], can be produced for facet joint distraction below gross failure.


2012 ◽  
Vol 630 ◽  
pp. 431-435
Author(s):  
Hai Bin Chen ◽  
Yi Wang ◽  
Li Ying Zhang ◽  
Guang Yu Yang ◽  
Xin Ning ◽  
...  

The cervical facet joint capsule is the major origin of neck pain. To in vivo test the cervical facet capsule strain, a flexible, miniature strain gauge was developed. A special liquid metal served as the strain sensitive element, and a tubular structure was selected as the configuration of this miniature strain gauge. Calibration tests and rear-end crash simulation experiments were performed to analyses the behavior of this new gauge. A physical head-neck model or living goat model was used as a human surrogate. Experiment results indicated the good linearity and stability of this miniature strain gauge. With the improvement of structural designs and manufacturing techniques, the miniature strain gauge stated in this paper has the potential to in vivo test the cervical facet capsule strain.


Author(s):  
Kiersten M. Craig ◽  
Kyle P. Quinn ◽  
Beth A. Winkelstein

Epidemiologic reports indicate that over 5 million nonfatal accidents occur annually, with painful injuries being the most common type of injury [1]. The cervical facet joint and its capsule are a common source of pain in these injuries [2]. Biomechanical tolerances of the cervical spine in compression, cervical motion segments in tension, and isolated spinal ligaments have all been reported to vary with age [3, 4]. Although microstructural damage has been shown to occur in the facet capsular ligament well-before the gross failure of that tissue and also has been speculated to relate to painful damage in that ligament [5], there is currently no study investigating ligament damage during tensile loading as function of age.


Author(s):  
Nathan D. Crosby ◽  
Ling Dong ◽  
Beth A. Winkelstein

Traumatic neck injuries are a primary cause of chronic pain, with the cervical facet joint and its capsule being a common source of the pain. During these injuries, the facet capsular ligament undergoes excessive stretching that can initiate pain [1]. Behavioral sensitivity is produced as early as 1 day after facet capsule stretch, which suggests that the excitatory systems in the spinal cord are modulated by certain tissue loading conditions. In particular, the signaling protein PKCε has been implicated in glutamate release in inflammatory pain [2] and is increased in afferents after painful facet injury [3]. Also, neuronal hyperexcitability has been detected after painful, but not nonpainful, facet joint distraction [4]. Despite the involvement of spinal neuronal activation in pain, the time course of its development and its relationship to painful mechanical facet joint injury is unknown.


Spine ◽  
2014 ◽  
Vol 39 (8) ◽  
pp. E514-E520 ◽  
Author(s):  
William J. Anderst ◽  
William F. Donaldson ◽  
Joon Y. Lee ◽  
James D. Kang

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