As trauma, especially trauma associated with motor vehicle accidents, becomes implicated as a frequent precipitating factor in temporomandibular disorders medical/legal disputes arise. This occurs specifically because of the separation between casualty insurance carriers and personal health insurance. The general topic of temporomandibular disorders has raised its own level of dispute within the world of personal health insurance secondary to lack of specificity in identifying these disorders and lack of standardization of protocol in treating them. This stands somewhat separate however from the issue of traumatic causation as casualty insurance carriers stand more vulnerable to responsibility for treatment delivered if causation is assessed to be a result of trauma to persons insured by these companies. While many of the same issues, e.g. diagnostic accuracy, need for treatment, specific treatment protocol and prognosis are enjoined responsibility is more firmly asserted in these cases as no exclusion clauses exist in these policies to allow the insurance company to deny treatment and financial responsibility. Thus, at one time or another all of these issues come to be argued.
The key issue here is that a TMD exists only if there are symptoms. Treatment is not recommended for asymptomatic individuals even in the presence of signs indicating less than optimal jaw function. To date, there are no predictive signs for the eventual development of a TMD. This includes malocclusion, bruxism, temporomandibular joint clicking and temporomandibular joint remodeling. Patient history, including record review, stands as the key issue in developing a causation statement and may very well identify a precipitating event as causative and then identify other factors as perpetuating or even predisposing. The ability to accurately identify and then clearly demonstrate the precipitating event will determine the strength of the causation statement.
MECHANISM OF INJURY - WHIPLASH INDUCED TMD
It appears most probable that immediate damage to the temporomandibular joints themselves is produced by a combination of mechanical forces resulting from the vehicular collision and abnormal or accelerated muscular forces acting during joint movement produced by the collision. That is, abnormal muscular forces encountered during the collision are capable of producing injurious forces within the joint which may be disproportionate to the force of the impact of the collision. Certain predisposing factors such as pre-impact disc position may also effect the nature and degree of injury.
Normally, the mechanics of mouth opening occurs so as to protect the internal environment of the temporomandibular joint from undue compression during both rotation and translation.
The first movement which occurs during mouth opening is depression of the mandible secondary to relaxation of the elevator muscles and the effect of gravity. This allows for a minimum of joint compression during condyle rotation and translation thereby minimizing wear and tear on, or even frank injury to, the discal and cartilaginous components of the joint. Theoretically, if mouth opening, even partial opening, occurred without this decompression then forces would be placed on the components of the temporomandibular joint which could produce tissue damage in the joint. In point-of-fact, during the whiplash event it is quite possible that the elevator muscles contract as both rotational and translatory movements take place between the condyles and their respective mandibular fossae. This then would increase rather than decrease joint compression as the mandible and skull move relative to each other during the whiplash event. However, even if muscular tonicity was only maintained during joint movement, this would represent abnormal joint mechanics.
Furthermore, during the whiplash event, it is the 8 to 14 pound skull which moves relative to a less actively displaced 4 to 6 ounce mandible which is held in place by the hyoid muscles and other anchoring tissues. This is the reverse of the normal kinematics for the temporomandibular joint. Finally, these movements occur at an accelerated rate which adds to the stress on the region. The whiplash event then most probably produces frank tissue damage to the temporomandibular joints by:
I would note here that the investigation into the mechanics of the mechanism of temporomandibular joint injury from whiplash is ongoing. Please note that in the UCLA computer model, while abnormal mechanics were noted which support the statement that abnormal temporomandibular joint mechanics were observed, questions concerning tissue tolerances remain. Once again, while the mechanics of the injury are interesting, the historical relationship of symptoms to event remains at the heart of the causation statement.
Frank tissue damage is not the only factor involved in the mechanism of injury for the temporomandibular joints however, although it is the most immediate. Other factors may subsequently act on the inflamed temporomandibular joint and perpetuate or even escalate what then becomes an inflammation/scarring process. Some of these factors are a result of the whiplash event e.g. cervical injury, and yet other influences may represent predisposing architectural, psychological, chemical and postural qualities possessed by the individual injured prior to the whiplash event. These predisposing and/or perpetuating factors frequently involve the very same patient profile pointed to by the defense as causative: malocclusion, bruxism, psychometric profile, tissue weakened by prior injury, arthritides, allergies and chronic pain issues. Care taken in identifying these factors will improve your treatment results and sustain your causation statement.
MECHANISM OF TMJ INJURY FROM A WHIPLASH EVENT SHOULD BE VIEWED AS A FUNCTION OF THE FOLLOWING FORMULA:
Frank tissue damage to TMJ apparatus affected by:
Many medical/legal arguments concerning the proposed pathogenesis for a temporomandibular disorder center around radiography of the temporomandibular joints. Radiography (tomograms, transcranial views, panographic views, etc.) may provide useful information concerning fracture, tumor invasion and specific arthritides. Absent these factors x-rays should not be used to make a statement concerning the prior existence of, presence of or probable development of a temporomandibular disorder. While this is clearly referenced in the literature, x-rays are routinely used inappropriately to discount trauma as the causation in a temporomandibular disorder. Specific statements generally reference alterations in cortical bone shape of the mandibular fossa and condylar head despite the fact that longitudinal studies as well as electron microscopic studies of the temporomandibular joints have stated clearly that alteration in bone shape within the temporomandibular joints will occur within a normally functioning joint and that these joints are capable of extensive remodeling without pathologic process. Temporomandibular joint tomograms have demonstrated a statistically significant relationship between posterior condyle position in centric occlusion and anterior disc position. This has not however been linked to the symptom expression of TMD.
MECHANISM OF INJURY
One of the most frequent arguments made opposing the concept that whiplash precipitates TMD is that injury to the temporomandibular joints is impossible absent mandibular contact. A substantial body of literature stands in opposition to this perspective. In one review of 113 cases of temporomandibular disorders reported to arise from vehicular collisions only one person reported contact of the mandible within an interior structure of the car. In another study comparing whiplash victims without facial/head contact, whiplash victims with facial/head contact and overt facial/head trauma cases general symptom expression was seen to be similar, however, there were distinct differences noted concerning specific clinical findings. The proposed pathogenesis of temporomandibular joint injury from a whiplash event absent mandibular contact has been confirmed by computer study. Studies of whiplash patient populations and a population of temporomandibular joint surgical candidates supports this position.
TIMING OF ONSET OF THE DISORDER
Another issue frequently raised concerns the timing of the onset and/or identification of the temporomandibular disorder following the trauma in question. There are multiple issues involved here yet this point is frequently oversimplified with the statement made that if a temporomandibular injury was truly sustained as a result of a vehicular collision, the disorder would manifest immediately or at least within 24 hours of the trauma. In point of fact, this argument should be divided up into:
1. ONSET OF DISORDER
Under this heading one must consider the definition of a temporomandibular disorder and differentiate local symptom expression from peripheral symptom expression. The temporomandibular joint injury is a complex affair which may involve injury to support ligaments, articular tissue, synovial tissue, muscular and neurological elements of the temporomandibular apparatus. Injury to this region may well produce peripheral symptoms such as headache, neck and shoulder pain/spasm, ear symptoms and vertigo before producing local signs and symptoms of dysfunction. This is in large part due to the fact that the discs and articular surfaces of the temporomandibular joints have no nociceptive neurology. That is, while the internal environment of the temporomandibular joint is rich in proprioceptive neurology, local pain perception secondary to injury may be poor and further may be mediated by the central nervous system. Inflammation within the temporomandibular joint may well then irritate neurology which, while not producing local symptomatology, may well influence the brain stem and produce peripheral symptoms. These peripheral symptoms may well dominate the symptom picture until synovial tissue stimulated by the inflammatory process grows over the articular surfaces producing local pain. Local symptoms may also be delayed until scar tissue organizes to produce local destabilization of the joint. This may take weeks to months. The argument is frequently made that an injury to the temporomandibular joints would produce swelling within the joint that distends the pain sensitive capsule thus producing local symptoms. This level of injury would most certainly be considered severe and appears to be a phenomena limited to a minority of cases.
2. DELAY IN PATIENT RECOGNITION
Patients injured during a whiplash event are frequently subject to multiple sites of injury. These injuries produce a constellation of symptoms which can and frequently do mask the presence of a temporomandibular joint injury. Of particular note is the tendency for the symptoms expressed by cervical injury to overlap with those peripheral symptoms produced by a temporomandibular joint injury, e.g. headache, neck and shoulder muscle pain. This frequently leads to delay in patient awareness of jaw involvement in the symptom picture. Thus, the patient is frequently slow to report the involvement of the jaw to the treating or examining doctor. Complicating this issue is the fact that the relatively non-pain sensitive temporomandibular joint may produce local signs before local symptoms and those signs such as clicking, popping and intermittent/ partial locking of the temporomandibular joints may not be appreciated as signs of a substantial disorder by the patient. Thus, once again delaying report to the treating physician.
3. DIAGNOSIS OF DISORDER
As TMD has long been considered a subset of dental/chronic pain disorders and due to the focus on spinal, paraspinal and primary neurologic injury following the whiplash event the portal of entry physician frequently fails to examine the temporomandibular joints in the post trauma scenario. This includes failure to question the patient concerning this region and to perform the routine tests appropriate for evaluation of the region. This stands at the heart of many medical/legal issues and frequently leads to under appreciation of the whiplash event in question as the precipitating factor for TMD. This not only compromises the plaintiff's case on causation grounds but raises potential malpractice issues for the treating doctor on grounds of failure to examine and failure to diagnose. Doctors should be aware that within the scope of the paradigm shift toward rapid management of traumatically induced temporomandibular disorders these issues of standard of care responsibilities will be raised more frequently. The question of whether earlier identification of the temporomandibular disorder following trauma and the appropriate treatment and referral of the patient would have obviated the need for an eventual surgical resolution has been raised frequently over the past year. Questions of malpractice have arisen over this issue. Specific to the assignation of causation in an alleged temporomandibular joint injury, failure to identify the TMD component of symptom expression may well lead to claims being denied and appropriate compensation lost. This is a very difficult problem to overcome even with appropriate and accurate retrospective analysis. Portal of entry examination and re-examination during the first four months post trauma will serve to avoid this problem only if findings are documented. Undocumented suspicions are useless. Do not speculate, however, not every whiplash produces TMD and over-diagnosis is inappropriate. Diagnosis should proceed from history and findings and only a specific TMD diagnosis should lead to treatment, monitoring and/or referral. Support your findings.
OTHER IMPORTANT MEDICOLEGAL ISSUES
The treating and/or examining doctors are frequently asked to describe the effect of the trauma induced temporomandibular disorder on the lifestyle of the patient. It should be made clear that temporomandibular disorder patients, especially those who suffer from symptom expressive internal derangement, suffer and suffer greatly when the disorder is acute. The doctor should not be shy about expressing this both in reports and at trial. The doctor should accurately and fully describe the disorder and its effects during the time of treatment, but should not overstate future suffering in healed patients. Overstatements of future suffering serve to discredit the doctor and diminish the appreciation of the suffering that has occurred. Overstatement of future suffering and need for treatment may well also inappropriately color the record of the patient in the event of future trauma and/or other insurance related questions. The main issues to be addressed in expressing the effect on the patient's lifestyle include:
In this last regard, disabilities and specific work preclusions occur as a result of temporomandibular joint injuries. This may involve restricted capacity to use the mandible or may be a result of peripheral symptoms of the TMD. These symptoms include: neck pain, upper extremity pain/paresthesia, dizziness, tinnitus, headache and/or fatigue. These symptoms may individually or jointly compromise the patient's work capacity. While each case must be considered individually, the occupations most affected are those that require repetitive mandibular use. These occupations as well as those that strain the cervical region threaten to perpetuate and even escalate the disorder. Specific work preclusions frequently include:
Specific occupations which are affected most frequently by temporomandibular disorders include teachers, telephone operators, telemarketing personnel, sales persons and others who must speak repetitively and expressively as part of their job description. Issues of temporary and total disability will frequently be addressed and it is recommended that persons who fit this occupational profile should be put on temporary total disability or at least be reassigned with a job modification to eliminate the need for repetitive speech during the active treatment in the acute stage's of the symptom expressive internal derangement. Temporary total disability is generally extended to all patients during the first two to three weeks postoperatively. Issues of partial permanent disability and vocational rehabilitation are uncommon for TMD patients but do arise. Patients who require these more extreme ratings should be thoroughly examined to determine if an improved M.M.I. status can be reached.
Temporomandibular disorders have historically been considered chronic pain presentations arising from malocclusion, bruxism and stress. This view of temporomandibular disorders prevails in our society and serves to discriminate against the patient who has developed a temporomandibular disorder secondary to trauma. Effective treatment of the trauma induced temporomandibular disorder requires a treatment protocol which stands separate from the treatment protocol for chronic pain disorders including insidious onset TMD. Effective medical/legal management of the trauma induced TMD requires an understanding of the literature which supports this position. The doctors involved in treating these disorders will facilitate the medical/legal process by:
Temporomandibular disorders are a serious health problem in the United States with billions of dollars spent every year treating the chronic expression of these disorders. With the evolving evidence that many of the more serious temporomandibular disorders begin following a traumatic event, including whiplash, identification of the trauma induced TMD becomes an important issue in our motorized society. In the adversarial environment within which these disorders are handled the medical/legal management of these disorders becomes equally important with the medical management of the disorder. Ineffective medical/legal management discourages doctors from actively treating these disorders and causes great hardship in the life of the injured person. This unfortunate situation need not exist and it is hoped that the guidelines established in this workbook will help to make this difficult problem more manageable.
MEDICOLEGAL CONSIDERATIONS AND TECHNIQUES
B) Preliminary Diagnosis:
C) Obtain past films and/or take good quality films as needed
D) Obtain lien and authorization for information release:
A) Develop good reporting habits and train your staff to record accurately, thoroughly and clearly:
B) Act as though a defense IME is looking over your shoulder.
C) Record all symptoms, complaints and exacerbating events (who, what, when, where, how, why as to each):
D) As to EACH treatment provided (state the type, duration, strength and location of application of each modality):
E) It is the Plaintiff's duty:
A) Help determine early on:
B) Recommend books and treatises on the pertinent ailment, organize a study group library and updated bibliography.
C) Provide reports requested by the attorney:
E) Prepare with the attorney for your deposition or arbitration or trial testimony.
A) Often the doctor is not as well prepared for a deposition as at trial, thereby enhancing the attorney's prospect of successfully attaining the goals of a successful deposition.
B) Lawyers will consider the following to be points in favor of taking a deposition and goals to reach in taking the deposition:
C) Opposing counsel will consider the following to be reasons NOT to take a doctor's deposition:
D) Often a deposition will be scheduled by a notice accompanied by a written request to produce the following documents:
E) The examining attorney will generally cover the following areas in a deposition:
F) Plaintiff's attorney ideally does the following in advance preparation for the witness's deposition:
G) Deposition fees (per CCP 2034(i) (2) in California):
H) Opposing counsel can ask about all information considered and reviewed by the witness:
I) Outline of Deposition Inquiry
5. Trial Testimony of the Health Care Witness
A) Pretrial Conference with Attorney:
B) At trial, wear: Suit, white shirt, and tie or dark dress, modest and small amount of jewelry, and a new haircut, do not talk so as to be overheard by jurors during breaks.
C) Five Rules to
Remember When Questioned:
D) General Considerations to Effectively Handle Cross-Examination:
E) Outline of Presentation of Trial Testimony:
F) The jury is apt
to accept the medical opinions of the doctor who has the superior qualifications,
unless the basis of opinion lacks sufficient plausibility. If qualifications
are reasonably equal and the jury receives conflicting medical opinions,
it is apt to accept the one with the most plausible basis.
6. The Health Care Professional Employed as an Expert
A) Purpose of Expert to Attorney:
B) In as much as the expert must have all pertinent data - it should be clarified who is to gather it. If there is more than one expert in related fields who will be testifying on the same side each should be aware of the conclusions of each and the bases for their opinions.
C) If there is more than one expert in related fields who will be testifying on the same side each should be aware of the conclusions of the other[s] and the bases for their opinions.
D) Attributes of a good expert:
E) An attorney may have his own expert to provide:
F) The cross-examination will probe for the following:
A summary discussion of the problematic nature of whiplash injuries, tmj injuries, insurance and legal issues:
Medicolegal issues frequently arise when whiplash is considered to be the cause of a temporomandibular disorder. This paper serves as an overview of the key issues central to any case where whiplash is purported to cause TMD. The first part of the paper deals with specific points of argument frequently encountered in whiplash induced TMD cases. The second part of the paper presents general guidelines for your P.I. practice from patient intake to testimony. Feel free to read, print out, use and share this information as you see fit.
The emerging recognition of whiplash and other traumatic events as precipitating factors for the development of temporomandibular disorders (TMD) has led to multiple disputes between insurance carriers and claimants. This is due in large part to the perpetuated supposition that temporomandibular disorders exist only as a subclass of chronic pain disorders and occur secondary to architectural dis-relationships, psychobiologic imbalances and other insidiously developing noxious influences. A substantial amount of research has developed a clearer picture of the pathogenesis of these disorders and has led to a paradigm shift in the diagnosis and treatment of TMD. This has included new classification systems as well as new treatment models and has been affected by evolution in diagnostic and treatment modalities available to the treating doctors. It is this paradigm shift that has led to many of the adversarial disputes which arise and which result in heated and costly litigation.
Widely diversified treatment models still exist in this field despite current research which substantially challenges the need for them and their efficacy. Further, this paradigm shift has not obviated certain of the older treatment techniques, but has placed them in a new perspective. Included in this group are oral orthotics, physiotherapy, stress management, chronic pain counseling, Phase II dentistry, behavioral modifications and exercise regimens. In many of the classic treatment models for temporomandibular disorders architectural dis -relationships were managed by oral orthotic therapy and permanent occlusal change. This was frequently orchestrated with spinal postural alterations via manipulation, spinal exercises, massage and home care instructions. Patients who demonstrated poor stress management techniques and tendencies toward bruxism where frequently given biofeedback training and medications such as the tricyclic antidepressants. The substantial body of these patients were considered to be victims of insidious decompensation of their adaptive capacity over time and, depending on the perspective of the discipline of the doctor in charge of the case, various combinations of the aforementioned therapies would be prescribed. A substantial portion of these patients would undergo permanent alteration of their developed occlusion. These treatment programs continue to date despite questions raised concerning scientific validation of these proposed pathogenic pathways as causative of temporomandibular disorders. Specifically highlighted issues of contention include malocclusion and bruxism. Over the past six years at least three authoritative studies have discounted malocclusion as related to the onset of temporomandibular disorders. Most recently a well orchestrated study by Pullinger et al has confirmed earlier studies which disclaim bruxism, with specific reference to nocturnal grinding of the teeth as evidenced by tooth wear, as a cause of temporomandibular disorders. Despite these findings treatment frequently proceeds as it has for decades addressing these issues as the driving force behind any temporomandibular disorder regardless of the history of its onset. There is no doubt that multifactorial, insidious decompensation produces a body of patients whose needs are met by these treatment programs, however, treating trauma victims within this model may produce rather than control chronic pain.
Patient history is the key to effective management of TMD and to effective medical/ legal assessment. The importance of this statement cannot be overvalued. Temporomandibular disorders are a substantial cause of chronic pain and these disorders result in billions of dollars of treatment each year and an inestimable amount of suffering. It is well agreed among the practitioners treating these disorders that early identification of TMD following its onset leads to more effective treatment as many of the chronic pain issues can be avoided. This is, in point of fact, the driving force behind the effort to identify causation or causations. As data surfaces which leads us to believe that trauma is frequently the precipitating event for the onset of many temporomandibular disorders, portal of entry doctors are being alerted to identify the onset of these disorders at the earliest possible opportunity. The hope is that this early identification will lead to effective referral patterns and early management patterns which will more effectively control these disorders and avoid the onset of chronic pain issues.
At the heart of this paradigm shift is the dispute over whether the majority of temporomandibular disorders are extracapsular (driven by psychobiologic and/or muscular phenomena)or intracapsular (inflammation/derangement within the joint). Prior to the advent of arthroscopic surgical techniques and investigation into the character of the temporomandibular joints proper, this distinction was somewhat problematic as there was no way of directly addressing pathology within the temporomandibular joints without aggressive surgical technique. The somewhat quiet yet rapid evolution of arthroscopic surgical potential for the temporomandibular joints has changed this perspective substantially. We now have the capacity to enter the temporomandibular joints with a relatively nonmorbid technique and improve the environment of the temporomandibular joints so that the balance of degenerative and reparative phenomena is tilted toward the reparative process. However, this does not eliminate the need for many of the aforementioned techniques which are aimed at stabilizing function in this region and stimulating repair such as the oral orthotic, chiropractic care, physiotherapy and home care. When whiplash is suspected of causing intracapsular TMJ damage a course of appropriate conservative care should be initiated as early on as possible. Early intervention in these cases portends to minimize or eliminate the chronic pain formation which complicates the treatment issues and may well head off surgical necessity, allow for shorter treatment regimens, improve results and, when viewed in the long term, constrain costs.
These issues are
of particular importance in a motorized society such as ours as the all
too frequent phenomena of whiplash has been linked to the onset of symptomatic
expressive internal derangement of the temporomandibular joints. There
are an estimated 4 million reported whiplash injuries in the United States
per year. This addresses only the whiplash injuries reported to the police
following the collision and represents a fraction of the true number of
cases which occur per year. When it is considered that referenced studies
have estimated that as many as 50% of these cases result in a dysfunction
of the temporomandibular joints the importance of this paradigm shift
becomes obvious. It is hoped that linking the research which implicates
trauma as a frequent precipitator of these disorders with accurate diagnosis
will result in more timely and effective treatment as well as a decrease
in chronic pain formation.
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