LOUISVILLE  ACCIDENT DOCTOR
         Dr. Harold Byers, B.A.,M.S.,D.C. & Associates
                                            
     
 
                                                                          

Harold Byers, Jr., B.A., M.S., D.C. &  Associates
 
We have helped thousands of accident victims!
  

   Dr. Harold Byers, Jr., B.A., M.S., D.C. 

INJURY CARE CHIROPRACTIC

    

  Personal Injury Report



                  FRONT IMPACT OR HEAD ON COLLISION AND WHIPLASH


Collisions are interactions between vehicles with transfer of energy. Both vehicles involved experience impacts, which lead to energy transfer between the vehicles. Based on the direction of impact, collisions can be classified into rear end impacts, frontal impacts or head on collisions, lateral or side impacts and, rarely, roof impacts.


A frontal impact collision is a high energy trauma resulting from collision of vehicles, front end of one vehicle with front end of another vehicle, or front end with a tree or other stationary or moving object. The consequence of such trauma depends on various factors as follows;

  • Velocity of the subject vehicle - energy and velocity bears an exponential relationship.
  • Velocity of the offending vehicle or object
  • Resultant acceleration of the impact
  • Restraints like seat belts or airbags – seat belt syndrome and air bag induced injuries.
  • Reflex reaction of the driver or passengers of the subject vehicle like pushing arms towards the front seat by the rear end passenger out of panic or reflexive, deep breathing or breath holding resulting in hyperinflation of lungs making it prone to trauma.
  • Structure of the front end of the colliding vehicle. A 30 mph collision results in a 0.6m front end crush (13).
  • Size or mass of the vehicle involved. It has been found that a collision between two small cars is worse than that between two large cars (1).
  • Position of the driver
  • Characteristic of the injured tissue (old people whose bones have undergone degenerative changes sustain skeletal injuries like fractures in osteoporosis   and young children with highly elastic tissue are less prone to fractures but more prone to muscle and soft tissue injuries).
  • Windshield, steering column, dash board and rest of the car interior. 

                  


              BIOMECHANICS OF A FRONTAL IMPACT


Understanding the mechanism behind a frontal impact requires a deep understanding of the laws of nature or the physics of colliding objects. Two colliding objects, in this case, the two automobiles seem to obey the three Newtonian laws.  

The above mechanism demonstrates Newton’s principles. The second and third steps of the process obey the first law which states that an object in state of rest or motion continues its action unless stopped by an external force. The final step demonstrates that as a reaction to the backward movement of the wheels, a forward pressure is exerted by the road surface. This corresponds to Newton’s third law of motion.

The below illustration describes some of the factors or situations and the resultant injuries. 


An unrestrained rear seat passenger acts as a flying bullet and may hit other passengers (10). This results in secondary injuries following contact with the ground or hitting an external object.


                                    PATHOLOGY OF A FRONTAL IMPACT


  • Ponto-medullar laceration – fracture of the base of the skull (hinge fractures, pyramidal fractures or ring fractures) result in the laceration of the brain stem. Post mortem findings of 705 head on collision fatalities, revealed head injuries in 63.4% (4) and PML was observed in 15% of the victims. Mandibular fracture increases the risk of ponto- medullar laceration by 2.3 times (4). 


 Rumor has it that the old classic cars were bigger and stronger than cars of today so how would they cope in a head collision with a modern car.

The IIHS (Insurance Institute for Highway Safety) have been running for 50 years now and to celebrate their anniversary they have decided to put an old 1959 Chevrolet Bel Air against a new 2009 Chevrolet Malibu in a head on crash to see if we have made progress in passenger safety over the last 50 years. No contest, the new model destroyed the 1959 model.  


  • Strain on the foramen magnum leading to secondary pathologies.
  • Renal injuries – about 90% of the renal injury victims of frontal impacts were seat belt wearers.
  • Urogenital trauma – rupture of the urinary bladder following flexion injury in seat belt wearers. A full bladder is more susceptible to rupture when compared to an empty bladder.
  • Strain at the level of C3-C4 (5) puts a strain on the supraspinous and infraspinous ligaments and also ligamentum flavum at lower accelerations. There is comparatively less strain on the posterior longitudinal ligament and facer capsular ligament.
  • During the energy transfer following an impact, the spine absorbs most of the energy between the stationary head and moving torso. This causes the classical whiplash phenomenon.  Kalleries et al study states that 13 g acceleration is sufficient to cause a whiplash injury in a frontal impact collision. The pathology behind whiplash following a frontal impact collision is explained below;

Strain on the ligaments of the neck

                

Reflex muscle contraction

                

Increased guarding resulting in a decrease in the range of motion

                

Decreased general functioning of the patient further acclerates ligament injury.

                 

Poor spinal stability

                  

Nerve impingement and cervical disc degneration.

                  

Cervical dorsal root ganglion nerve injury gives rise to cervical pain and whiplash symptoms.


  • About one-third of neck injuries are believed to be of frontal impact origin. In A1S1 injury, the response of the cervical muscles (trapezius) to the frontal impact was directly proportional to the level of acceleration (2). Neck is the primary site of whiplash following low velocity frontal impacts. Cervical muscle injury level is low in people who sat with trunk flexed during the impact (3).
  • Pneumothorax- reflex deep breathing is observed in victims who are caught by surprise during an impact. This hyper-inflates the lung making it prone to injury.
  • When the anterior aspect of the neck strikes the steering column, it results in laryngeal fracture and soft tissue injury.
  • Rotation of the ankle resulting in sprain and ligament tears following a knee impact.
  • Head injuries result from head impacting the roof, windshield, mirror or dashboards. Traumatic brain injury and post concussion symptoms of varying severity are observed.
  • Fractures of lower limb, when lower limb hits against the interiors of the car. Nielson et al (1997) study, states that a delta v of 16 km/hr or higher is required to produce injuries in frontal impacts.


Seat belts and airbags are not dependable when it comes to frontal impacts. About half of the fatalities in frontal impact were belted individuals and among them 48 were the victims of small overlap impact and 23% were victims of a large overlap (6). Seat belts have been a source of compression and hyper-flexion injuries. In 1962, the term seat belt syndrome (11, 12) came into existence. It was characterized by abdominal wall ecchymosis, internal abdominal injuries, spinal fractures and clavicular fractures.

Airbags studies revealed occurrence of corneal abrasion, eyelid laceration and eye lens dislocation. Skin burns and eye burns were observed in cases injured by the release of chemicals and heat during airbag deployment.


Personal Injury Cases

  • Taking a good case history and giving strong documentation of injury for your lawyer and insurance company.
  • Doing a thorough orthopedic and neurological examination
  • Performing all the required neuro-psychological tests. Taking good quality, adequate digital radiographs and or including stress views
  • Creating an accurate diagnosis that can be supported by history, complaints and examination findings
  • Doing standard and thorough daily charting
  • Duties under duress (DUD)
  • Loss of enjoyment of life (LOE)
  • Using standard measurement outcomes, such as pain drawings, Oswestry, Roland Morris, Neck Disability Index, SF-36, algometer, visual analogue scale, etc.
  • Doing periodic (monthly) thorough subjective and objective re-evaluations with follow-up and written report of findings
  • Having referred the patient if needed out for needed diagnostic procedures that are not done in the chiropractic office (MRI, EMG, EEG, SEP, PET, SPECT, etc.)
  • Having referred to other health care providers and/or colleagues for verifying or additional opinions if needed. Pain management for pain control. Being able to determine when the patient has reached a point of maximum improvement, and consequently ending regularly scheduled treatment, so that the case can proceed towards settlement of claim.
  • Being knowledgeable and conversant in the academic concepts of soft tissue injury, such as the phases of injured tissue healing, the relationship of vehicle damage to patient injury, the influence of pre-accident degenerative joint disease, and the influence of variables such as pre-accident awareness or head rotation


            99% of cases we see are accident and injury. This   is why we know this area of practice as well as any one.
  •  

 Injury Care Chiropractic keeps you updated on relevant academic concepts pertaining to whiplash injury patients. I hope that the information is useful in terms of enhanced understanding, as well as helpful for the personal injury attorneys to deal with insurance claim adjusters, dealing with Colossus systems and adverse medical experts.

Injury Care Chiropractic is well informed and trained in these concepts of personal injury and the details of Colossus and will be a valuable asset in personal injury cases, in terms of both academics and treatment.  Additionally, expert chiropractors and your law firm will have access to daily phone consultation with me, to discuss any pertinent issues faced by them, on a particular case.



BIBLIOGRAPHY

  1. M.D. Gilchrist, D. O'Donoghue & T. J. Horgan ; A two-dimensional analysis of the biomechanics of frontal and occipital head impact injuries; pages 253-262

 

  1. Kumar, Shrawan ; Narayan, Yogesh ; Amell, Tyler 

 Analysis of low velocity frontal impacts ; Clinical Biomechanics, 2003, Vol.18(8), pp.694-703 [Peer Reviewed Journal] 



3, Kumar, Shrawan ; Ferrari, Robert ; Narayan, Yogesh ; An Observational Electromyography Study of the Effect of Trunk Flexion in Low-Velocity Frontal Whiplash-Type Impacts ; Archives of Physical Medicine and Rehabilitation, 2006, Vol.87(4), pp.496-503 [Peer Reviewed Journal] 



4 Živković, Vladimir ; Nikolić, Slobodan ; Babić, Dragan ; Juković, Fehim;The significance of pontomedullar laceration in car occupants following frontal collisions: A retrospective autopsy study;Forensic Science International, 2010, Vol.202(1), pp.13-16 [Peer Reviewed Journal] 



5. Panjabi MM, Pearson AM, Ito S, Ivancic PC, Gimenez E, Tominaga Y. Cervical spine ligament injury during simulated frontal impact. Spine 2004;29(21):2395-2403.



6. Lindquist MO, Hall AR, Björnstig UL. Kinematics of belted fatalities in frontal collisions: A new approach in deep studies of injury mechanisms. Department of Surgical and Perioperative Sciences, Division of Surgery, Umeå University, Saab Automobile, Enginuity Services International, Trollhättan, Sweden. 

7.  Staff T, Eken T, Hansen TB, Steen PA, Søvik S, a field evaluation of real life motor vehicle accidents: presence of unrestrained objects and their association with distribution and severity of patient injuries. Norwegian Air Ambulance Foundation, Department of Research, Holterveien 24, PO Box 94, 1441 Drøbak, Norway. 

 

8.Rupp JD, Schneider LW. Injuries to the hip joint in frontal motorvehicle

crashes: biomechanical and real-world perspectives. Orthop Clin North Am. 2004; 35:493-504, vii.


9. Mackay M. Engineering in accidents: vehicle design and injuries. Injury 1994; 25:615-21.


10.. Mayrose J, Jehle D, Hayes M, et al. Infl uence of the unbelted rear-seat

passenger on driver mortality: “the backseat bullet”. Acad Emerg Med2005; 12:130-4.


11. Campbell DJ, Sprouse LR 2nd, Smith LA, Kelley JE, Carr MG.

Injuries in pediatric patients with seatbelt contusions. Am Surg 2003;

69:1095-9.


12. Munshi IA, Patton W. A unique pattern of injury secondary to seatbelt related blunt abdominal trauma. J Emerg Med 2004; 27:183-5.


13. Eid H O, Abu-Zidan F M, Biomechanics of road traffic collision

injuries: a clinician’s perspective; Trauma Group, Faculty of Medicine and Health Sciences, United Arab Emirates University,






                                                                                       Whiplash


Definition:  Is the acceleration-deceleration mechanism of energy transfer to the neck.  The magnitude of the problem is great ... at least one percent of the entire population will experience chronic pain due to whiplash.


The acceleration-deceleration forces which cause whiplash injury are sufficient to permanently disable you. Even in a low speed rear impact collision of 8 mph, your head moves roughly 18 inches, at a force as great as 7 G’s in less than a quarter of a second.  The Discovery space shuttle is only built to withstand a maximum of 3 G’s.


Understand about bumpers and there real function.


The car bumper is designed to prevent or reduce physical damage to the front and rear ends of passenger motor vehicles in low-speed collisions. Automobile bumpers are not typically designed to be structural components that would significantly contribute to vehicle crashworthiness or occupant protection during front or rear collisions.  It is not a safety feature intended to prevent or mitigate injury severity to occupants in the passenger cars. Bumpers are designed to protect the hood, trunk, grille, fuel, exhaust and cooling system as well as safety related equipment such as parking lights, headlamps and taillights in low speed collisions.



Whiplash 




The Four Phases of a Whiplash Injury


During a rear-end automobile collision, the body goes through an extremely rapid and intense acceleration and deceleration.  In fact, all four phases of a whiplash injury occur in less than one-half of a second!  At each phase, there is a different force acting on the body that contributes to the overall injury, and with such a sudden and forceful movement, damage to the vertebrae, nerves, discs, muscles, and ligaments of the cervical spine can be substantial. 


Phase 1                     

During this first phase, car begins to be pushed out from under an individual, causing your mid-back to be flattened against the back of your seat.  This results in an upward force in the cervical spine, compressing the discs and joints.  As the seat back begins to accelerate the torso forward, it head moves backward (as seen above), creating a shearing force in the neck.  If the head restraint is properly adjusted, the distance the head travels backward is limited.  However, most of the damage to the spine will occur before the head reaches the head restraint.  Studies have shown that head restraints only reduce the risk of injury by 11-20%.


Phase 2

During phase two, the torso has reached peak acceleration – 1.5 to 2 times that of the vehicle itself – but the head has not yet begun to accelerate forward and continues to move rearward.  An abnormal S-curve (as seen above) develops in the cervical spine as the seat back recoils forward, much like a springboard, adding to the forward acceleration of the torso. Unfortunately, this forward seat back recoil occurs while the head is still moving backward, resulting in a shearing force in the neck that is one of the more damaging aspects of a whiplash injury.  Many of the bone, joint, nerve, disc and TMJ injuries that occur is seen clinically, occur during this phase.


Phase 3

During the third phase, the torso is now descending back down in the seat and the head and neck are at their peak forward acceleration.  At the same time, the car is slowing down.  If the brake pedal is applied during the first phases of the collision, it will likely be reapplied during this phase. Reapplication of the brake causes the car to slow down even quicker and increases the severity of the flexion injury of the neck.  As the body moves forward in the seat, any slack in the seat belt and shoulder harness is taken up.   


Phase 4

This is probably the most damaging phase of the whiplash phenomenon.  In this fourth phase, the torso is stopped by the seat belt and shoulder restraint and the head is free to move forward unimpeded.  This results in a violent forward-bending motion of the neck, straining the muscles and ligaments, tearing fibers in the spinal discs, and forcing vertebrae out of their normal position.  The spinal cord and nerve roots get stretched and irritated, and the brain can strike the inside of the skull causing a mild to moderate brain injury.  If the occupants are not properly restrained by the seat harness, the individual may suffer a concussion, or more severe brain injury, from striking the steering wheel or windshield.


Several studies have indicated that the zygapophysial joint pain: Is the single most common basis of chronic neck pain after whiplash injury.


2011 Journal Spine

A narrative review discusses the evidence that the cervical zygapophysial joints: The leading source of pain in patient with chronic whiplash-associated disorder. (Acute injury usually starts from injury in extension and rotation, torsion injuries to the cervical spine).



Facet Joints

The cervical facet joints are a common source of neck pain, particularly in chronic whiplash patients. There is strong clinical evidence of facet joint related neck pain which has led to the development of medical diagnostic tests (e.g., facet blocks) and treatment procedures (e.g., radiofrequency neurotomies) that can reduce or eliminate pain for a period of time.

There are two facet joints between each pair of cervical vertebra from C2 to C7. The facet joint is a synovial joint enclosed by a thin, loose ligament known as the facet capsule. A synovial fold on the inner capsule extends between the margins of the articulating bony surfaces. The facet capsule itself lacks the stiffness to alter motion and instead follows the motions of its surrounding bony vertebrae.

The cervical facet joints have the necessary anatomical features to initiate and potentially modulate more widespread neck pain caused by facet joint syndrome.  The motion of the facet joint and capsule during whiplash like impacts have been characterized in both human volunteers and cadaveric specimens. Based on documented joint motion, two mechanisms of facet joint injury have been proposed: pinching of the synovial fold and excessive strain of the capsule. It has been observed that the abnormal motion during a whiplash exposure compresses the posterior facet surfaces together, pinching the synovial fold.

Excessive facet capsule strain during whiplash has been demonstrated by numerous groups. Peak strains of 29 to 40 percent have been measured in the C6/C7 capsule of cadaveric specimens exposed to whiplash dynamics, whereas peak strains experienced during normal bending are only 6 ± 5 percent. Head-turned postures can double peak capsule strain during simulated whiplash loading. Partial ruptures of the facet capsule have been observed in both tension and shear loading of this joint along with capsule elongation during whiplash is a potential mechanism of injury in some individuals.

Their induction, persistence, and relationship to joint/capsule mechanics in painful whiplash loading supports the facet joint’s involvement in whiplash pain.




Ligaments and disc

Magnetic resonance and autopsy studies of whiplash patients have documented injuries to the neck ligaments and intervertebral discs in addition to the facet joints. Ligament injuries may cause acute neck pain and lead to chronic spinal instability, abnormal muscle response patterns and decreased neck mobility.

Ligaments of the upper cervical spine have unique functional and structural anatomy, predisposing them to partial or complete rupture at low strains. Ligaments provide joint position sense during normal motion and combined with discs provide stability and absorb energy during high speed trauma. The specific function of each cervical ligament and disc in resisting whiplash loading is dependent upon its specific anatomical location, orientation, geometry, and unique mechanical properties.

Spinal ligaments and fibers encapsulating the discs can partially or completely rupture when stretched beyond their physiological limit. The whiplash related response of the cervical ligaments and discs of the neck have been quantified using a whole cadaveric cervical spine model with muscle force replication. During rear impacts with the head facing forward, dynamic strains in the anterior longitudinal ligament and annular disc fibers above physiological levels and increased joint laxity were observed. The C5/C6 disc was found to be at highest risk of injury. The disc injuries occurred at lower impact accelerations during rear impacts compared to frontal impacts.

Ligament damage may cause instability resulting in loss of motion segment integrity which can be evaluated with flexion/extension x-rays. The AMA Guides to the Evaluation of Permanent Impairment, 5th edition, Nov. 2000, Chapter 15, pages 378-392 place a high impairment rating on loss of motion segment integrity, equating this damage as equal to a vertebra that has a compression fracture greater than 50%. This ligament instability often interferes with normal neck posture, altering the structure of the cervical spine which may lead to chronic health problems.

Damage to the disc in whiplash injuries may cause an early onset of degenerative disc disease. An article published in Injury. 1991 Jul;22(4):307-9, indicated a significantly higher rate of disc degeneration was found in whiplash patients 10 years after the accident when compared to age matched controls.

It should be noted that a normal MRI study of the neck does not exclude the existence of clinically significant disc disease in whiplash patients suffering chronic neck, head or nerve pain. Internal Disc Disruption is a condition where the internal structure of the disc is disrupted, while the external appearance is essentially unchanged.

The cascade events to synovial joints following whiplash:


      Image above is an example of chronic synovial changes as a result of whiplash.  

•••••

The most recent comprehensive review of the Synovial Fold Entrapment Syndrome is written by Alexandra Webb and colleagues and will be published in the April 2011 issue of the journal Manual Therapy (Epub at this time, 2/15/11) (1).

In this article, Dr. Webb and colleagues note that intra-articular synovial folds are formed by folds of synovial membrane that project into the joint cavity. Cervical spine synovial folds extend 1–5 mm between the articular surfaces. Synovial folds are found in synovial articulations throughout the vertebral column. Synovial folds in the vertebral column were first documented in 1855.

Dr. Webb and colleagues note that the published literature uses a number of names to identify these synovial folds, including:

  • “Synovial fold is the most accurate name to apply to these structures.”
  • Meniscus / Menisci
  • Meniscoid
  • Intra-articular inclusions
  • Intra-articular discs

Anatomically, synovial folds contain an abundant vascular network and sensory nerve fibers (1).

The entrapment hypothesis is usually proposed to explain the clinical presentations of the synovial fold syndrome. “An abnormal joint movement may cause a synovial fold to move from its normal position at the articular margins to become imprisoned between the articular cartilage surfaces causing pain and articular hypomobility accompanied by reflex muscle spasm (1).”

“Synovial fold entrapment has been used to explain the pathophysiology of torticollis and the relief of pain and disability following spinal manipulation.” The traction forces generated during manipulation would cause release of a trapped fibro-adipose synovial fold from between the articular surfaces (1).

Additionally, contusions, rupture and displacement of the synovial folds have been reported at autopsy following fatal motor vehicle trauma; these injuries are not visible at post-mortem using conventional X-ray, CT or MRI (1).

With repeated mechanical impingement between the articular surfaces, the synovial fold may differentiate into fibrous tissue to varying degrees. The fibrous apex of the synovial indents the articular hyaline cartilage, further entrapping the apex of the synovial fold. Manipulative therapy may traction and separate the articular surfaces apart, releasing the entrapped synovial fold. (Drawing below based on #1).

Historically, the entrapped synovial fold syndrome has been written about for decades. In the 1971 translation of their authoritative reference text The Human Spine in Health and Disease, Drs. Schmorl and Junghanns note (2):

“Like other body articulations, the apophyseal joints are endowed with articular capsules, reinforcing ligaments and menisci-like internal articular discs.”

“Like any other joint, the motor segment may become locked. This is usually associated with pain.” Chiropractors refer to such events as subluxations. These motor unit disturbances can cause torticollis and lumbago.

“Various processes may cause such ‘vertebral locking.’ It may happen during normal movement. The incarceration of an articular villus or of a meniscus in an apophyseal joint may produce locking.”

If a joint is suddenly incarcerated within the range of its physiologic mobility, as occurs with the meniscus incarceration of the knee joint, it is an “articular locking or a fixed articular block.”

“Such articular locking is also possible in the spinal articulations (apophyseal joints, intervertebral discs, skull articulations, lumbosacral articulations). They may be mobilized again by specific therapeutic methods (stretching, repositioning, exercises, etc.). Despite many opinions to the contrary, this type of locking is today increasingly recognized by physicians. Many physicians are employing manipulations which during the past decades were the tools of lay therapists only (chiropractors, osteopaths). However, these methods have at times been recommended by physicians. They have also been known in folk medicine and in medical schools of antiquity.”

Schmorl and Junghanns’ text includes two photographs of anatomical sections through the facet joints showing these “menisci-like internal articular discs,” or meniscus. They also included three radiographs and one drawing showing abnormal gapping of an articulation as a consequence of meniscus entrapment in a facetal articulation. They note that such a meniscoid incarceration can cause acute torticollis, and they show a “follow-up roentgenogram after manual repositioning” resulting in “immediate relief of complaints and complete mobility.”

In 1985, 30 distinguished international multidisciplinary experts collaborated on a text titled Aspects of Manipulative Therapy (3). The comments in this text pertaining to the interarticular meniscus (synovial entrapment syndrome) include:

“Histologically, meniscoids are synovial tissue.”

“Their innervation is derived from that of the capsule.”

The current hypothetical model of the mechanism involved in acute joint locking is based on a phenomenon in which the “meniscoid embeds itself, thereby impeding mobility.”

“It is highly probable that the meniscoids do play an important role in acute joint locking, and this is confirmed by the observation that all the joints afflicted by this condition are equipped with such structures.”

In 1986, physical therapist Gregory Grieve authored a text titled Modern Manual Therapy of the Vertebral Column (4). This text boasts 61 international multidisciplinary contributors, contains 85 topic chapters, and is 898 pages in length. In the chapter titled “Acute Locking of the Cervical Spine” the text notes that a cause of acute cervical joint locking includes:

“Postulated mechanical derangements of the apophyseal joint include nipped or trapped synovial fringes, villi or meniscoids.”

In her 1994 text Physical Therapy of the Cervical and Thoracic Spine, professor of physiotherapy from the University of South Australia, Ruth Grant writes (5):

“Acute locking can occur at any intervertebral level, but is most frequent at C2-C3. Classically, locking follows an unguarded movement of the neck, with instant pain over the articular pillar and an antalgic posture of lateral flexion to the opposite side and slight flexion, which the patient is unable to correct. Locking is more frequent in children and young adults. In many, the joint pain settles within 24 hours without requiring treatment (because the joint was merely sprained or because it unlocked spontaneously), but other patients will require a localized manipulation to unlock the joint.”

In his 2004 text titled The Illustrated Guide to Functional Anatomy of the Musculoskeletal System (6), renowned physician and author Rene Cailliet, MD comments on the anatomy of the interarticular meniscus, stating:

“The uneven surfaces between the zygapophyseal processes are filled by an infolding of the joint capsule, which is filled with connective tissue and fat called meniscoids. These meniscoids are highly vascular and well innervated.”

In the fourth edition of his textbook Clinical Anatomy of the Lumbar Spine and Sacrum (7), physician, anatomist, and researcher Dr. Nikolai Bogduk writes:

“The largest of the meniscoid structures are the fibro-adipose meniscoids. These project from the inner surface of the superior and inferior capsules. They consist of a leaf-like fold of synovium which encloses fat, collagen and some blood vessels.”

“Fibro-adipose meniscoids are long and project up to 5 mm into he joint cavity.”

“A relatively common clinical syndrome is ‘acute locked back.’ In this condition, the patient, having bent forward, is unable to straighten because of severe focal pain on attempted extension.”

“Maintaining flexion is comfortable for the patient because that movement disengages the meniscoid. Treatment by manipulation becomes logical.”

The January 15, 2007 publication of the top ranked orthopaedic journal Spine contains an article titled (8):

High-Field Magnetic Resonance Imaging of Meniscoids
in the Zygapophyseal Joints of the Human Cervical Spine

Key Points From this article include:

  1. Pain originating from the cervical spine is a frequent condition.
  2. Neck pain can be caused by pathologic conditions of meniscoids within the zygapophysial joints.
  3. “Cervical zygapophysial joints are well documented as a possible source of neck pain, and it has been hypothesized that pathologic conditions related to so called meniscoids within the zygapophysial joints may lead to pain.”
  4. The meniscoids of the cervical facet joints contain nociceptors and may be a source of cervical facet joint pain.
  5. Proton density weighted MRI image sequence is best for the evaluation of the meniscoid anatomy and pathology.
  6. Meniscoids are best visualized with high-field MRI of 3.0 T strength.
  7. Meniscoids are best depicted in a sagittal slice orientation.
  8. The meniscoids in C1-C2 differ from those in the rest of the cervical spine.
  9. Meniscoids may become entrapped between the articular cartilages of the facet joints. This causes pain, spasm, reduced movement, and “an acute locked neck syndrome.” “Spinal adjusting can solve the problem by separating the apposed articular cartilages and releasing the trapped apex.”

 

 

Clinical Applications

Decades of evidence support the perspective that the inner aspect of the facet capsules have a process that extends into and between the facet articular surfaces. This evidence includes anatomical sections, histological sections, MR imaging, and clinical evaluations. This synovial fold can become entrapped between the facet articulating surfaces, producing pain, spasm, and antalgia. Published terminology for the anatomy includes synovial fold, synovial villus, meniscoid, meniscoid block, and joint locking.

Using the cervical spine as a representative model, a classic clinical presentation would be that of an acute torticollis. If the synovial fold is entrapped on the left side of the cervical spine, the patient would present with an antalgia of right lateral flexion; in other words, the patient bends away from the side of entrapment. The patient’s primary pain symptoms will be on the side of entrapment, in this example, the left side (exactly like our patient Kim). Active range of motion examination will show that the patient is capable of additional lateral flexion to the right, but will not laterally flex to the left because of increased pain; once again this is because the synovial fold is entrapped on the left side and left lateral flexion increases meniscus compression, pain, and spasm. This is also why the patient is antalgic to the right; such positioning reduces left sided synovial fold compression, pain, and spasm.

Additional clinical evaluation will reveal no sings of radiculopathy; no alterations of superficial sensation in a dermatomal pattern, and no signs of motor weakness or altered deep tendon reflexes. An important clinical feature is that although the patient will not laterally flex the cervical spine to the left because of increased pain and spasm, left cervical lateral flexion against resistance without motion (the doctor holds the patient’s head so that there is no motion even though the left-sided cervical muscles are contracting) will not increase the patient’s pain. This is because the involvement is not muscular. Muscle contraction against resistance will not increase pain as long as the joint does not move in the meniscoid block syndrome.

A typical treatment protocol to manage the synovial fold entrapment syndrome is that the patient is manipulated in an effort to free the entrapped meniscus. Post-graduate teachings in chiropractic orthopedics (Richard Stonebrink, DC, DABCO) and clinical experience indicate that the most successful manipulation would induce additional right lateral flexion; in other words, the manipulation would cause further right side antalgia. Such a maneuver would cause both a gapping of the facets on the left side as well as a tensioning of the left side facet capsules, together pulling free the entrapped synovial fold.

When the precise level of synovial fold entrapment is ascertained and that precise level is manipulated in the appropriate direction to cause the intended neurobiomechanical changes, it is referred to by chiropractors as a “spinal adjustment.” The depth and speed of such an adjustment must be sufficient to overcome local muscle spasms that reflexively exist as a consequence of the pain the patient is experiencing. Following this first manipulation/adjustment, the patient may benefit from 10-15 minutes of axial traction to the cervical spine. Experience suggests that most patients will benefit from the application of a soft cervical collar, worn continuously until the following day.

The patient is evaluated and manipulated/adjusted again the second day, followed once again by optional axial cervical traction, but there is no need for the soft cervical collar on the second day. The patient is given the third day off, returning the fourth day for a final evaluation and adjustment/manipulation. It is typical for complete symptomatic resolution to occur in a period of 3 – 5 days following onset and treatment.

An important caution in adjusting/manipulating the meniscoid block lesion is to not do so in such a manner that it straightens the right antalgic lean. Recall that the patient is antalgic to the right because the synovial fold is entrapped on the left side. To attempt to straighten the right antalgic lean out will increase the meniscoid compression, pain and spasm, making the patient truly unhappy. In contrast, the adjustment/manipulation should be made in such a manner that the right antalgic lean is enhanced, gapping the left sided articulations, freeing the entrapped synovial fold, reducing pain and spasm.

As described in the eighth edition of his book (1982) Textbook of Orthopaedic Medicine (9), orthopaedic surgeon Sir James Cyriax describes how the fibers of the multifidus muscles blend with the facet joint capsular fibers. Chiropractic orthopedic training indicates that at the beginning of any joint movement, appropriate local articular proprioception will quickly initiate a contraction of the multifidus muscle, tightening the capsular ligaments, and pulling the meniscus of that joint into such a position that it cannot become entrapped. This suggests that the etiology of the meniscoid block syndrome is a failure of appropriate proprioceptive driven reflexes, indicative of a long-standing biomechanical problem. It is reasonable and appropriate to treat the long-standing biomechanical problem with a more prolonged series of spinal adjustments/manipulations and indicated rehabilitation. Failure to do so often results in frequent reoccurrences of the synovial fold entrapment syndrome following trivial mechanical environmental stresses.

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REFERENCES

1. Daniel J. Murphy, DC 

www.necksolutions.com/whiplash-neck-pain 

2. Webb AL, Collins P, Rassoulian H, Mitchell BS; Synovial folds – A pain in the neck?; Manual Therapy; April 2011; Vol. 16; No. 2; pp. 118-124.

2. Junghanns H; Schmorl’s and Junghanns’ The Human Spine in Health and Disease; Grune & Stratton; 1971.

3. Idczak GD; Aspects of Manipulative Therapy; Churchill Livingstone; 1985.

4. Grieve G; Modern Manual Therapy of the Vertebral Column; Churchill Livingstone; 1986.

5. Grant R; Physical Therapy of the Cervical and Thoracic Spine, second edition; Churchill Livingstone, 1994.

6. Cailliet R; The Illustrated Guide to Functional Anatomy of the Musculoskeletal System, American Medical Association, 2004.

7. Bogduk N; Clinical Anatomy of the Lumbar Spine and Sacrum, fourth edition; Elsevier, 2005.

8. Friedrich KM. MD, Trattnig S, Millington SA, Friedrich M, Groschmidt K, Pretterklieber ML; High-Field Magnetic Resonance Imaging of Meniscoids in the Zygapophyseal Joints of the Human Cervical Spine; Spine; January 15, 2007, Volume 32(2), January 15, 2007, pp. 244-248.

9. Cyriax J; Textbook of Orthopaedic Medicine, Diagnosis of Soft Tissue Lesions, eighth edition; Bailliere Tindall, 1982.