Friday, December 28, 2012

Crucial Issues

Crucial Issues

In our opinion, the most powerful arguments against the inclusion of PRI in the Guides are that (1) PRI assessments are likely to be unreliable and (2) they might lead to systematic errors in assessment, such that persuasive patients can “game the system” and get inappropriately high impairment awards. Both of these arguments derive from the permise that it is very difficult for examiners to determine the extent to which patients are affected by their pain. These difficulties were succinctly captured by Scarry when she said: “To have great pain is to have certainty; to hear that another person has pain is to have doubt.” The problem of reliability and validity of PRI assessment is much more than an academic problem in measurement theory. The Guides serves the societal role of providing the equitable method of compensation individuals who ability to function has been compromised by a medical condition. For the Guides must employ assessment procedures that are reliable and valid, rather than capricious ones that can be manipulated by persuasive patients. Thus, regardless of how severely pain affects individuals with various medical conditions, a PRI assessment system must have reasonable reliability and validity to accomplish the societal goal of fairly compensating them.

In fact, the key issue separating proponents and opponents of impairment due to pain is the weight they place on ease of measurement of PRI vs. relevance of PRI. Advocates for PRI emphasize that pain has great relevance to the ability to function of individuals who have various medical conditions, but these advocates tend to downplay the problems of measuring PRI. Opponents tend to emphasize problems in measurement but ignore the issue of relevance. In principle, empirical research could be performed to determine the strength of the independent contribution that pain makes to the burden of illness borne by individuals with various medical condition, and whether examiners can reliably and validly assess PRI. Considerable research has been done on the first issue, at least for some common painful conditions such as disorders of the lumbar spine. Unfortunately, though, essentially no research has been done on the issue of determining the reliability and validity of PRI assessments. Construct validation research is greatly needed in this area. At this time, as a practical matter, decisions regarding PRI for purposes of the Guides’ Sixth Edition must be based on judgment rather than empirical data.

Monday, December 24, 2012

Chronic Pain Syndrome

Chronic Pain Syndrome

In both the Fourth and Fifth Editions of the Guides, a definition of chronic pain syndrome (CPS) was included that captured the major biopsychosocial characteristics of chronic pain. Indeed, the biopsychosocial approach to chronic pain and disability is currently viewed as the most heuristic perspective to the understanding, assessment, and treatment of chronic pain disorders, and has replaced the outdated biomedical reductionist perspective. This biopsychosocial approach views chronic pain as a complex and dynamic interaction among biological, psychosocial, and social factors that perpetuates, and may even worsen, the clinical presentation. Each person will experience a chronic pain condition uniquely, this accounting for the great individual difference in how pain is expressed. The complexity of a chronic pain disorder is especially evident when it persists over time, as a range of psychosocial and economic factors can interact with pathophysiology to modulate a patient’s report of discomfort and disability healing occurs, all patients experience some degree of physical deconditioning associated with stiffness and muscle atrophy in the injured area. Risk factors for profound deconditioning with the injured area becoming a “weak link” include extended periods of inactivity, inhibition of function due to pain, and fear avoidance. In striking contrast, the traditional and outdated biomedical approach assumes that all pain symptoms have specific physical causes, and attempts to eradicate the cause directly by identifying and rectifying the presumed pathophysiology. However, chronic pain can rarely be understood by the linear, nociceptive mechanism. As will be discussed later in this chapter, there is often an absence of a document-able relationship between pain and pathophysiology.

With the above biopsychosocial perspective in mind, CPS can be described as pain that continues beyond the normal healing time for the patient’s diagnosis and includes significant psychosocial dysfunction. It should be noted that this definition does not include any specific time frame to use in making the diagnosis of CPS. This omission is intentional and reflects clinical reality, in that some conditions would be expected to resolve in several days and others in several months or even years. The diagnosis of CPS should then be temporally connected to the point at which a given condition or conditions were expected to have resolved, rather than to any arbitrary time period for an injury or event. Regardless of when it occurs, CPS is a condition that ultimately adversely affects the patient’s well being, level of function, and quality of life. The major characteristics associated with CPS include the following with 3 or more required for a diagnosis:

Ÿ  Use of prescription drugs beyond the recommended duration and/or abuse of or dependence on prescription drugs or other substances.
Ÿ  Excessive dependence on health care providers, spouse, or family.
Ÿ  Secondary physical deconditioning due to disuse and/or fear-avoidance of physical activity due to pain.
Ÿ  Withdrawal from social milieu, including work, recreation, or other social contacts.
Ÿ  Failure to restore pre-injury function after a period of disability, such that the physical capacity is insufficient to pursue work, family, or recreational needs.
Ÿ  Development of psychosocial sequelae after that initial incident, including anxiety, fear-avoidance, depression, or nonorganic illness behaviors.

Saturday, December 22, 2012

Definition of Pain

Definition of Pain

The International Association Study of Pain defines pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.” Pain is a prominent symptom in many acute injuries and illnesses, and often subsides as the medical condition resolves. Since such acute pain is usually short lived, it is not a problem that is considered in an impairment rating system. However, chronic pain is a problem that potentially could be the cause for an impairment rating. The definition of chronic pain is imprecise but, in a general way, it refers to pain that persists over time. For the purposes of the Guides, chronic pain is defined as pain that persists beyond the expected healing time of the medical disorder thought to have initiated the pain. For many sections inthe Guides, chronic pain will be pain that persists beyond 3 months, as most common conditions affecting the musculoskeletal and other organ and systems will substantially heal in this time frame. The nervous system is a notable exception. Although any time point is arbitrary, 3 months should encompass the expected healing time in most situations where there is tissue injury but will allow for situations in which there is no expected healing time. 

Wednesday, December 12, 2012


Medical causality is imputed when the association between a medical condition and a given exposure (physical, biologic, or chemical) is such as to lead one to believe that the condition would not have occurred in the absence of the exposure. The temporal relationship between the exposure or injury and the medical condition (or symptoms suggestive of the condition) is the first factor that must be assessed. The illness or disease should occur after the exposure (referred to as “temporal ordering”) and within a time period that is reasonable given the nature of the exposure (temporalcontiguity). In certain situations (such as asbestos, lead, and benzene exposure) there is a long latency between the time of exposure and the appearance of disease. Hence, regardless of whether a temporal relationship appears to be present, determining causality also requires one to assess whether a causal relationship is biologically plausible.
               A causal relationship is biologically plausible when:

               1. The relationship between the medical condition and the exposure or injury can be explained anatomically or physiologically.
               2. The duration, intensity, or mechanism of exposure or injury was sufficient to cause the illness or injury in question.
               3. There is evidence suggesting that the exposure is consistently or reliably associated with the process under investigation in the population under investigation or in peer-reviewed literature.
               4. Cause and effect are contiguous--ie, there is a readily understandable relationship between the two, in which an increase in the magnitude of the exposure reliably leads to an increase in the severity of its alleged effect upon the injured or exposed person, and vice versa.
               5. There is literature providing biologic or statistical evidence indicating that the symptoms or disorder could develop as a result of the exposure (coherence).
               6. There is specificity of the association for the injury (ie, the absence of other factors, especially pre-existing disease, that could have caused or contributed to the problem).

               The independent examiner is obligated to evaluate the validity and strength of all postulated causal mechanism. Mechanisms that appear weak, or are clearly flawed, must be identified as such and accepted as likely only when at least two other criteria for biologic plausibility have been met. Optimally one would wish to satisfy all criteria. There are, however, circumstances when contiguity cannot be demonstrated, as some exposures lead to disease in a noncontiguous fashion. Specificity of association is also difficult to illustrate definitively given the multifactor nature of many disease processes. Literature supportive of causality is generally available, but must be closely scrutinized before relying upon it as it is often poor quality.

Monday, December 10, 2012

Muscle Strains

Muscle Strains
Muscle strains are probably the most common type of injury to the myotendinous unit (MTU). A muscle strain is an acute stretch-induced injury secondary to excessive indirect force generated by eccentric muscular contraction. Muscle strains may occur anywhere in the body, but the most frequent muscles involved are the quadriceps femoris, biceps femoris, semimembranosus, semitendinosis, and gastronomies-soleus complex. Muscles that cross two joints and have a high proportion of fast twitch fibers are more prone to muscles stabilizing the hip, shoulder, and elbow joints. The pain elicited from an acute muscle strain is typically experienced during an athletic activity or immediately at its termination. The pathologic changes in an acutely strained muscle include disruption of the muscle fibers near the myotendinous junction along with edema and hemorrhage. The grade of a muscle strain depends on the degree of fiber disruption and the clinical findings.
               The appearance of a grade 1 muscle strain on MRI is similar to the findings of a grade 1 muscle contusion. There may be enlargement of the muscle due to interstitial edema and hemorrhage and, on a spin-echo T2-weighted or STIR sequence, there will be increased signal intensity within the muscle. Muscle strains are frequently located near the muscle’s myotendinous junction. The tendon of a multipennate muscle extends into the muscle belly; therefore, the symptoms elicited by a strain may be located anywhere within a muscle and not merely at its ends. MRI has provided excellent documentation of the extent and position of these injuries. Fleckenstein et al reported on the MRI appearance of the natural history of acute muscle strains. Acutely, the abnormal signal intensity was identified throughout the muscle, but on follow-up studies the abnormal signal intensity was most prominent in the periphery of the muscle. In one patient there was persistent abnormal signal intensity within the muscle after complete resolution of symptoms.
               A grade2 muscle strain manifests clinically as muscle pain associated with a loss of strength. Pathologically there is a macroscopic partial tear of the MTU. On an MRI study, there will be a partial tear of the muscle fibers associated with edema and/or hemorrhage. With a grade 3 strain there is a complete disruption of the MTU. Plain films provide little useful information in the evaluation of most muscle strains. Only if there is a grade 3 strain that results in gross instability or malalignment (e.g., a quadriceps rupture) will plain films be helpful. CT has also been used to evaluate muscular strain injuries, but it provides less useful clinical information compared to an MRI examination.
               In addition to the evaluation of acute or delayed muscle injuries, MRI is an ideal imaging modality to follow the evolution of the inflammatory and reparative processes within a muscle. With MRI it is possible to detect any sequelae from a MTU injury (e.g., muscle atrophy or fibrosis). Clinically it can be extremely difficult to determine when a muscle has completely healed, and if an athlete or worker returns to his or her athletic activity or job too soon after injury, he or she may be predisposed to repeat injury. MRI has detected acute MTU injuries that were superimposed on sub acute or chronic injuries that may be predisposed the muscle to reinjury.

Saturday, December 8, 2012

Muscle Injuries

Muscle Injuries
Muscle Contusions and Tears

Muscle injuries may result from a direct or indirect application of force to the muscle. A direct blow to a muscle may cause a muscle contusion with disruption of muscle fibers. Acute disruption of muscle fibers and capillaries may precipitate soft tissue hemorrhage and a hematoma along with a secondary inflammatory response. With the acute pain associated with muscle injury, it may be difficult on a physical examination to determine the precise location, extent, and severity of an injury. Prior to the implementation of MRI, radiologic imaging studies were of little value in the evaluation of acute muscle injuries. On plain films there may be obscuration of the fat planes surrounding an injured muscle secondary to the perimuscular edema. With CT there may be an alteration of the size or contour of a muscle but detection of intramuscular hemorrhage, edema, or a hematoma is difficult. With the excellent soft tissue contrast resolution provided by MRI, it is now possible to obtain the following important clinical information related to a muscle injury: (1) the extent of muscle edema and/or hemorrhage; (2) is a focal hematoma is present, including its size and location; (3) the degree and extent of muscle fiber disruption; (4) if there is complete disruption of the muscle, whether there is associated muscle retraction; (5) whether there is interruption of the overlying fascia and if there is a muscle herniation; (6) the degree of muscle swelling and the detection of a possible concomitant compartment syndrome; and (7) whether single or multiple muscles are injured. Muscle contusions occur most frequently in the lower extremities, particularly involving the quadriceps mechanism.

               On an MRI examination, a muscle contusion is detected by abnormal signal intensity and morphology of the muscle. On spin-echo sequences, normal muscle demonstrates intermediate signal intensity on T1-weighted sequences and intermediate to low signal intensity on T20weighted sequences. Because hemorrhage infiltrates through the muscle, and mixes with the interstitial edema, it is not possible to separate it from the edematous muscle tissue. With a grade 1 contusion (i.e., microstructural fiber failure) there may be a slight increase in the size of the muscle and the margins of the muscle may have a feathery appearance due to the extension of interstitial edema into the perimuscular tissue. Edematous changes in the adjacent subcutaneous fat are also frequently detected. With a grade 2 muscle contusion (ie, partial tear) there will be a focus of disrupted muscle fibers in addition to the altered signal intensity from the interstitial edema and hemorrhage. A grade 3 muscle contusion will appear similar to a grade 2 contusion, except there will be complete disruption of the muscle fibers. With a muscle hematoma, there will be a focal accumulation of blood within a muscle. A hematoma demonstrates intermediate or high signal intensity on a T1-weighted sequence, depending on the chemical composition of the hematoma, and high signal intensity on a T2-weighted sequence. The sequelae of a muscle contusion may include muscle atrophy, fibrosis, calcification, or ossification.

Wednesday, December 5, 2012

Causality Assessment

Causality Assessment
Before making any impairment or disability determination, the physician is obligated to understand how an organ system (or body part under study) normally functions in the absence of disease. This is then coupled with a thorough understanding of the mechanism of the disease process under investigation. Causality is possible--ie, biologically plausible--if the nature of the adverse effects produced by a given physical, chemical, biologic, or psychological stressor is sufficient to alter the anatomy or physiology of the system or body part involved in a fashion that results in the disease under investigation. There also must be an appropriate temporal relationship between the alleged causal event and the disease manifestations. Furthermore, in situations where there is trauma, the mechanical forces involved must be sufficient to cause the alleged physiologic or anatomic stress.

               One should then look for studies supporting the causal relationship between the type of exposure or injury the claimant sustained and the disease process or injury under investigation in the medical literature. If they exist, the next step is to assess whether the epidemiologic and statistical principles used in these studies suggest that the causal association is real, or whether these studies are merely anecdotal or otherwise without scientific basis or validity. If the association between an exposure or injury and the postulated “effect” meets epidemiologic, physiological, and mechanistic criteria for imputing causality, or the injury is a clear sequela of direct trauma, it is then reasonable to assume that a causal relationship between an alleged exposure or injury and the disease process actually exists.

               These types of determinations must not be made solely on the basis of the claimant’s history. The medical records provide a more accurate and defensible history and must support the occurrence of the injury and the appearance of symptoms orsigns of pathology within a time frame that is consistent with the disease process under investigation. Those records from immediately after the injury are best for this purpose, as they are regarding the claimant’s status both before and after a trauma, and often provide the most accurate description of what actually occurred. Emergency room records, police and accident reports, and the employer’s report of occupational injury or disease (for workers’ compensation claims) are examples of documents that are particularly useful in this regard. If these records are not available or are ambiguous, it is best to describe the assessment of causality as provisional rather than definitive, even if the mechanism of injury, the physical examination, and the literature review indicate that a causal relationship may indeed be present.

               Combinations of direct trauma and a preexisting disease process are more difficult to assess for causality and apportionment. One must determine, again, if the requirements of temporal relationship, biologic plausibility, literature support, and sufficient injury have been met. This includes an assessment of whether the trauma would have caused the disease in the absence of the preexisting process or whether the injuries caused by the trauma or whether the injuries caused by the trauma or exposure would ordinarily decrease over time, because these answers provide grounds for apportionment. It is equally important to assess whether the trauma would have progressed on its own accord to a point where the claimant would have has the same clinical presentation; if so, one can argue that the accident only caused an acceleration of an inevitable process.

               When dealing with preexisting conditions, it is mandatory to examine all the records carefully, paying particular attention to the records of those providers who treated the claimant immediately after the accident. These are often the most accurate rendition of the incident and treatment that can be found. Records prior to the accident are even more critical, as they may be the only source of information regarding preexisting conditions. When there are no medical records from before and immediately after an accident, one cannot definitely establish that a causal relationship between current complaints and the accident exists--only that the claimant’s history supports the causal relationship. If the examiner believes that additional information, records, or tests are needed to support conclusions regarding relatedness, then it is necessary to state this and to describe exactly what information or testing is required.
               In conclusion, the examiner can only provide an accurate determination of causality if he or she applies accurate determination of causality assessment, within an objective framework, in which the claimant’s statements have validity only to the extent that they are supported by the medical records. In those instances where the medical records in inadequate, the examiner can make preliminary conclusions regarding causality, especially if the elements of temporal relationship and biologic plausibility have been met, but should reserve final judgment until the entire relevant medical record is available for review.

Monday, December 3, 2012



Little is known about the individual and societal economic burden of WAD. For instance, little is known about the prevalence of long-lasting work disability due to WAD, which probably the most costly part. This burden is probably largely dependent on the legislation in different countries. In 2002, an independent and temporary Commission on whiplash-related injuries was informed in Sweden, initiated by the four largest motor vehicle insurers. The mandate of the 3-year commission was an examination of the problems of WAD from road safety, medical care, insurance and societal aspects. One of the conclusions of the final report was that the yearly cost for society and for the insurance industry was approximately SEK 1.5 billion (US$201 million), while projected costs (i.e. what new cases of WAD arising in a particular year will cost society and insurers by the time the person reaches retirement age) amounted to SEK 4.6 billion (US$648 million). These calculations were based on an annual incidence of 30,000 WAD cases (324 per 100,000 inhabitants) in the year 2002. Since the report’s publication, the number of WAD cases have decreased dramatically to about 16,000 claims in 2008 (173 per 100,000 inhabitants), which, of course, has an impact on the overall costs.
Comparable data has not been found, but there is some evidence from a study that addressed the incidence of WAD in 10 European countries. The administrative data suggests that the total claims cost in Switzerland was 500 million Swiss francs (US$467 million). Switzerland’s population is 80% that of Sweden. Expenditures in addition to the claims cost was not reported in that study.

In summary, as in almost all other diseases and injuries, factors that are involved in the risk or prognosis of WAD are multifactorial and constitute a web of biological, psychological and social components.

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2.      Gay J. Abbott K. Common whiplash injuries of the neck. JAMA 1953; 152:1698-704.
3.      Benson BW, Mohtadi NG, Rose MS, Meeuwisse WH. Head and neck injuries among ice hockey players wearing full face shields vs half face shields. JAMA 1999; 282(24):2328-32.
4.      Versteegen GJ, Kingma J, Meijler WJ, ten Duis HJ. Neck sprain not arising from car accidents: a retrospective study covering 25 years. Eur Spine J 1998;7(3):201-5.
5.      Lorish TR, Rizzo TD, Jr., Ilstrup DM, Scott SG. Injuries in adolescent and preadolescent boys at two larger wrestling tournaments. Am J Sports Med 1992;20(2):199-202.
6.      Spitzer WO, Skovron ML, Salmi LR, et al. Scientific Monograph of the Quebec Task Force on whiplash-associated disorders: redefining “whiplash” and its management. Spine 1995;20(8 Suppl):1S-73S.
7.      Holm LW, Carroll LJ, Cassidy JD, Ahlbom A. Factors influencing neck pain intensity in whiplash-associated disorders in Sweden. Clin J Pain 2007;23(7):591-7.
8.      Ferrari R, Russell AS, Carroll LJ, Cassidy JD. A re-examination of the whiplash-associated disorders (WAD) as a systematic illness. Ann Rheum Dis 2005:1337-42.
9.      Berglund A, Alfredsson L, Jensen I, et al. Occupant- and crash-related factors associated with the risk of whiplash injury. Ann Epidemiol 2003;13(1):66-72.
10.   Bylund P-O, Bjornstig U. Sick leave and disability pension among passenger car occupants injured in urban traffic. Spine 1998;23(9):1023-8.
11.   Versteegen GJ,Kingma J, Meijler WJ, ten Duis HJ. Neck sprain in patients injured in car accidents: a retrospective study covering the period 1970-1994. Eur Spine J 1998;7(3):195-200.

Friday, November 30, 2012




Course of Recovery
Understanding the course and prognosis in WAS is critical. Will people recover from this common injury? Is so, when? If the injury is transient and self-limiting, there would be no need for major prevention and intervention strategies. The natural course and prognosis of WAD has been a controversial matter. Some claim that the prognosis is solely determined by the physical injury and its severity, and that pre- and post-psychosocial factors are not relevant in recovery. Others claim that persistent WAD is mainly a ‘psycho-cultural’ illness, and refer to studies from Lithuania and Greece where there is no or little awareness or reporting of WAD resulting from a whiplash mechanism. Studies from these countries report that 2% or less of study participants report long-lasting symptoms after car collisions. However, drawing firm conclusions based on the findings of these studies is inappropriate, since ‘psychocultural’ factors were not studied per se. Nevertheless, when persons who do not experience neck pain following a car collision have been asked to report on which symptoms they would expect after neck injury or minor head injury, those from Lithuania and Greece do not expect to have as many symptoms or do not have as long-lasting symptoms compared to persons in Canada.
In the majority of studies, the recovery rate is substantially lower than recovery rates reported in Greece and Lithuania. Some report a 66-68% recovery rate at one year after the injury, whereas others report a less than 40% recovery rate at a similar time point. Differences in recovery rates are at least partially due to selection bias. For instance, in the study by Miettinen et al., only 58% of the invited study population was followed up 12 months post injury, so it was unknown what the recovery rate was for the 42% of participants who could not be contacted at follow-up.

Prognostic Factors
A prognostic factor is a factor that is independently associated with the prognosis, and which can contribute to or work against recovery from a condition. Some factors known to contribute to a poor prognosis in WAD are similar to those for other forms of persistent neck pain. These factors include, among others, passive coping strategies, poor mental health, high level of stress, high pain intensity and more ‘associated’ symptoms, such as arm pain, headache and nausea. Similar to the literature on neck pain in the general population, gender does not seem to be a clear prognostic factor in WAD, after adjustments have been made for psychosocial factors. This suggests that the observed poor prognosis in females in some studies might be explained in terms of the psychosocial factors rather than the biological factors of gender. Furthermore, societal factors, such as insurance systems with possibilities to claim for pain and suffering, and extensive healthcare utilization in the early stage of the injury, have been suggested to be associated with delayed recovery in WAD.
Surprisingly, the bulk of evidence suggests that crash-related factors (e.g. impact direction, awareness of collision, head position) are not associated with the prognosis.
There is evidence that people’s lowered expectations of recovery and return to work, assessed early in the process of recovery, are an important predictor for long-lasting WAD, even after controlling for other factors, such as prior health, pain areas and acute post-traumatic stress symptoms. An expectation is defined as a degree of belief that some as being tied to an outcome, such as a recovery state or return to work, rather than the individual behaviors required to achieve that outcome (self-efficacy expectations). It is believed to be influenced by personal and psychological features, such as anxiety, self-efficacy, coping abilities and fear, and recent studies have demonstrated that in those with WAD, initial pain, depressive symptomatology, and some crash and demographic factors were associated with recovery and return-to-work expectation.
Health expectations are postulated to be primarily learned from the cultural environment, and based on ‘prior knowledge’. The mechanism by which expectations influence emotional and physical reactions may also actually affect the autonomic nervous system, involving biochemical processes, which may explain some of the power observed in studies of the placebo and nocebo effect. These mechanisms help to explain why persons who strongly anticipate they will recover really do, and why strong expectations about bad health actually lead to bad health. A concept that is closely related to expectations is a person’s belief—the lens through which a person views the world—which is shaped by the environment. In a study where injured persons were asked about their belief of the origin of their neck pain (casual belief), those who believed that something serious had happened to their neck had greater perceived disability during follow-up compared to those who did not have such beliefs.

WAD and Widespread Pain
One important aspect about the course of recovery from WAD is whether the neck injury is a trigger for subsequent widespread body pain. This has been suggested from cross-sectional studies, but knowing whether widespread pain came before the neck injury remains unclear from this type of study design. A potential aetiological explanation is a neurophysiological disturbance in the peripheral and central nervous system, which, in some stances, leads to an increased sensitivity to pain in other ‘uninjured’ areas. Another possible explanation for widespread pain is that new tissue damage may result from an altered pattern of movement in the body due to the neck pain. The exact aetiology of widespread pain is that new tissue damage may result from an altered pattern of movement in the body due to the neck pain. The exact aetiology of widespread pain is probably complex and multifactorial, but there are no indications that it would be specific to WAD. It can also occur after surgical intervention or any tissue damage. In addition, large prospective studies on pain of other aetiology have demonstrated that psychosocial factors at work, repetitive strains or other physical strains at work, awareness of symptoms and illness behavior may increase the risk of development of widespread pain. Thus, it seems that biological as well as psychological and social factors contribute to the development of widespread pain.
Prospective studies on WAD and its association with widespread pain are sparse and the evidence is not clear. The results from one study suggest a relationship between the onset of neck pain or other associated symptoms as well as self-perceived injury severity, after an MVC, and subsequent widespread pain. However, age, gender, health behavior and somatic symptoms prior to collision were at least as important. Another study investigated the incidence of onset of more extensive pain during 12 months of follow- up of WAD claimants, and associated factors with such an outcome. In that study, a less conservative definition of widespread pain was used and probably have resulted in higher incidences. The main conclusions were that widespread pain was common over a 12-month period (21%), but most improved over the follow- up period. Female gender, poor prior health, greater initial symptomatology (including pain intensity) and more depressive symptoms were associated with the development of extensive pain. The authors also found that local neck/ back pain, raising the question of the potential cause of widespread pain in other studies.

Work absenteeism and work disability
Many persons with acute WAD also have some absence from work, and no clear difference occurs between ‘blue’ and ‘white’ collar workers. In one population- based study, 46% persons had been off work due to the injury. A similar figure (49%) was seen in a Dutch study. The majority of people returned to work within a few days and only 4-9% were reported to be off work at six months past injury. In a study form the Netherlands, factors associated with not returning to work were older age and concentration problems. There was no association between degrees of manual labor, (‘blue’ or ‘white’ collar work). 

Tuesday, November 27, 2012



WhiplashA risk factor for an outcome (i.e. disease/injury) is a factor that is independently associated with the outcome or condition in question. Knowledge of the etiology (cause) of WAD is limited. One reason for this is the difficulty in obtaining accurate and appropriate denominators to calculate risks. Rather than using persons exposed to collisions as the denominator, researchers have used proxies, such as registered licensed drivers, population censuses, or persons involved in collisions where at least one person was injured. Some studies have adjusted for possible confounding factors, while others have not. A confounding factor is an independent risk factor for the outcome and is also associated with the exposure/risk factor of interest. Examples of possible confounding factors include gender, age, pre-collision physical and mental health, and severity and direction of crash impact.

Risk factors for WAD reported in published studies include presence of neck pain prior to the collision, being the driver or the front-seat passenger (compared to the rear-seat passenger), and being exposed to a rear-end collision or frontal collision rather than a side collision. Female gender has been suggested to be associated with a slightly higher incidence of WAD in some studies, but other studies have found no gender differences. All these studies have weaknesses, primarily, the lack of ‘true’ denominators and/or the limited possibility to control for potential confounding factors.

One possible risk factor for WAD is the severity of the crash (impact). The biomechanical research on WAD is mainly based on experimental studies using cadavers, volunteers and simulation experiments. So far, the injury mechanism has not been established as a known risk factor. Reasons for this may be that there are different injury mechanisms occurring with different crash types. Car occupant acceleration, velocity and rebound are all factors that should be considered. In much of the research, a major focus is on rear-end injury mechanisms despite consistent findings that rear-end collisions are only responsible for 40-55% of all cases of WAD in MVCs. However, there are some promising results from actual rear-end collisions in that the redesign of headrests and seats so that head/neck extension is limited in rear-end collisions has reduced the incidence of WAD. Before firm conclusions about the magnitude of such preventive interventions can be drawn, larger studies with well-defined outcome measures and controls for potential confounding factors are needed.

Risk Factors for WAD


A risk factor for an outcome (i.e. disease/injury) is a factor that is independently associated with the outcome or condition in question. Knowledge of the etiology (cause) of WAD is limited. One reason for this is the difficulty in obtaining accurate and appropriate denominators to calculate risks. Rather than using persons exposed to collisions as the denominator, researchers have used proxies, such as registered licensed drivers, population censuses, or persons involved in collisions where at least one person was injured. Some studies have adjusted for possible confounding factors, while others have not. A confounding factor is an independent risk factor for the outcome and is also associated with the exposure/risk factor of interest. Examples of possible confounding factors include gender, age, pre-collision physical and mental health, and severity and direction of crash impact.

Risk factors for WAD reported in published studies include presence of neck pain prior to the collision, being the driver or the front-seat passenger (compared to the rear-seat passenger), and being exposed to a rear-end collision or frontal collision rather than a side collision. Female gender has been suggested to be associated with a slightly higher incidence of WAD in some studies, but other studies have found no gender differences. All these studies have weaknesses, primarily, the lack of ‘true’ denominators and/or the limited possibility to control for potential confounding factors.

One possible risk factor for WAD is the severity of the crash (impact). The biomechanical research on WAD is mainly based on experimental studies using cadavers, volunteers and simulation experiments. So far, the injury mechanism has not been established as a known risk factor. Reasons for this may be that there are different injury mechanisms occurring with different crash types. Car occupant acceleration, velocity and rebound are all factors that should be considered. In much of the research, a major focus is on rear-end injury mechanisms despite consistent findings that rear-end collisions are only responsible for 40-55% of all cases of WAD in MVCs. However, there are some promising results from actual rear-end collisions in that the redesign of headrests and seats so that head/neck extension is limited in rear-end collisions has reduced the incidence of WAD. Before firm conclusions about the magnitude of such preventive interventions can be drawn, larger studies with well-defined outcome measures and controls for potential confounding factors are needed.

Friday, November 23, 2012



The cumulative incidence is the number of new cases of an event or outcome occurring in a population over a certain time period. Some evidence from the literature indicates that the incidence of WAD differs between countries. There is also some evidence that the incidence of WAD has increased from the beginning of the 1990s to after the year 2000, with the annual incidence for the latter period being about 300 per 100,000 inhabitants in the studies where emergency setting visits are used. In some instances, the increase is between three and tenfold. It is not known if this increase is partly due to a change in care-seeking behavior.
There are also some indications from administrative insurance claims database in different European countries (e.g. Norway, the Netherlands and Sweden) of a reduction in the number of WAD claims, whereas such decreases have not been seen in Denmark or the United Kingdom. Sweden, for instance, has seen a 33% decrease in personal motor vehicle crash (MVC) injury claims between 2002 and 2008. The relative decrease is similar between the incidence of WAD and other types of injuries, with WAD constituting about 50% of all MVC injury claims. This decrease is not due to reduction in the number of MVCs, and nor has the insurance system in Sweden changed. Instead, this decrease is likely to be due to a combination of reasons. For example, some care manufacturers have developed whiplash-protection devices for new car models, which presumably will result in fewer cases of WAS as a result of rear-end collisions. Secondly, during the second half of the 1990s, police personnel in Sweden showed an increased awareness that there is no need to advise car occupants to seek healthcare if no symptoms are present. Thirdly, the mass media focus in Sweden on whiplash has decreased substantially from over 800 articles in the beginning of the 2000s to only about 200 articles in 2008.

WhiplashIncidence calculation through insurance claims may be prone to other forms of bias. For instance, insurance systems where there are no benefits for the person responsible for a collision may underestimate the frequency of injuries, since fewer claims would be reported. This would also happen with insurance systems where insurance claim access us limited, or where payments for compensation result in a significant increase in the insurance premium. On the other hand, healthcare data may also be prone to bias, since such data only captures those who seek the type of healthcare utilization in question (e.g. emergency care).

Monday, November 19, 2012


Atlanta Injury Clinics

      The term whiplash injury has been used since the late 1920s, when H.E. Crowe coined the term at a medical meeting in San Francisco. It was originally described as an injury mechanism to the neck, but was later also used to define the actual symptoms after such an event. The first known case report was published in the Journal of the American Medical Association in 1953, when Gay and Abbot described 50 patients who had been exposed to whiplash mechanism in car collisions. It was reported that the majority had been exposed to rear-end collisions and that the majority were also examined between one and 24 months after the collision, thus representing a mix of patients with acute or persistent symptoms. Cervical pain with radiation into the occipital region of the skull, shoulder girdle or upper extremities were reported as common symptoms, but irritability, poor concentration and subjective vertigo were also described.
People who are exposed to energy transfer to the neck, in sports, falls or other mishaps, may also experience cervical pain. After such events, however, it is less common that the injury is labeled “whiplash”, but instead other terms, such as neck strain, neck sprain or simply neck injury, are used. The term whiplash associated disorder (WAD) was introduced in 1995 by the Quebec Task Force (QTF), who published the first systematic review on whiplash injuries. The term was intended to reflect that whiplash is an injury mechanism, and the consequences of the mechanism were the spectrum of symptoms (disorders). The QTF formulated the following conceptual definition:
      Whiplash is an acceleration-deceleration mechanism of energy transfer to the neck. It may result from rear-end or side-impact motor vehicle collisions, but can also occur during diving or other mishaps. The impact may result in bony or soft-tissue injuries (whiplash injury) which in turn may lead to a variety of clinical manifestations (whiplash-associated disorders). The reason for excluding frontal collisions from the definition is not discussed in the report and is likely to be an error, since it is known that 25-30% of whiplash injury occurs in such impact direction. The QTF also suggested a classification of WAD into five categories based on clinical signs and symptoms. This classification is mostly used to classify WAD in the acute phase.
Since the publication of the QTF findings, the term WAD has been increasingly used in the medical literature, and it is also a frequently used term in insurance medicine.

Thursday, November 15, 2012

Information about Lilburn, Georgia

Lilburn, Georgia

Introduction to Lilburn, Georgia
Lilburn, Georgia, in Gwinnett county, is 13 miles E of Sandy Springs, Georgia and 17 miles NE of Atlanta, Georgia. The city is conveniently located inside the Atlanta metropolitan area. There are an estimated 11,307 people in Lilburn.
Lilburn History
Prior to 1817, the area now known as Lilburn was inhabited by Native Americans. The Seaboard Airline Railway established the city in 1890. Originally, the area was known as McDaniel. The first church of the region was established in 1823. Lilburn was incorporated on July 27, 1910.
Lilburn and nearby Attractions
  • Yellow River Game Ranch
  • Stone Mountain Park
  • Mountain Park Aquatic Center & Activity Building
  • Southeastern Railway Museum
  • Zoo Atlanta Playspace
  • Georgia Aquarium
Things To Do In Lilburn
There are several parks, playgrounds and scenic trails in Lilburn. You can visit the Lilburn City Park and the Camp Creek Greenway Trail during your leisure hours. Family day trips can also be planned at the Yellow River Game Ranch. The Mockingbird Lake, Sturdivant Lake and Spences Lake offer facilities for fishing and boating. There are also ample shopping opportunities in Lilburn.
Lilburn Transportation
Dobbins Air Reserve Base Airport can be reached within a few minutes.
Lilburn Higher Education
Higher educational facilities are provided by the Gwinnett College of Business, Devry Institute of Technology, Garmon Beauty College and Emory University.

Sunday, November 11, 2012

Clinical Pearl

Clinical Pearl

A straight-leg-raising test this is positive under 30 degrees reveals a large disc protrusion. The nerve root is stretched long before it would normally be. The straight-leg-raising test is most useful for identifying L5-S1 disc lesions because the pressures on the nerve root are highest at this level. During straight leg raising, L4-L5 is not as apt to give as much pain as L5-S1 because the pressure between the disc and the nerve root at L4-L5 is half that at L5-S1. Therefore the L5-S1 disc lesion gives more pain in the lower back and leg than does the L4-L5 disc lesion. No movement on the nerve root occurs until straight leg raising reaches 30 degrees. No movement on L4 occurs during a straight leg raising test. From this, the presence of Turyn’s sign indicates a large disc protrusion at the level of the L5-S1 nerve root.

Wednesday, November 7, 2012



The origin of sciatica includes the following:
Neck/Back Pain- Chiropractor1.      Prolapsed intervertebral disc pressure, infection, and traumatic sciatic neuritis, perineural fibrositis, infections and tumors of the spinal cord.
2.      Lumbosacral and sacroiliac sprain and strain, degenerating intervertebral discs, fibrositis, osteomyelitis, hip joint disease, and secondary carcinomatous deposits in bone.
3.      Nephrolithiasis, prostatic, renal, and anal disease.
4.      Toxic and metabolic disorders, conversion hysteria, and arterial insufficiency.

1.      When the patient is in the supine position with both lower limbs resting straight out on the table, dorsiflexion of the great tor elicits pain in the gluteal region.
2.      The sign is significant for sciatic radiculopathy.

Saturday, November 3, 2012

Lumbar Disc Disease Classification

Turyn’s Sign

Lumbar Disc Disease Classification

Disc Pain/ Lower Back Pain

Variation of the lumbar disc disease classification model is as follows:
1.      Disc protrusion:
a.      Type I: Peripheral annular bulge
b.      Type II: Localized annular bulge
2.      Disc herniation:
a.      Type I: Prolapsed intervertebral disc
b.      Type II: Extruded intervertebral disc
c.      Type III: Sequestered intervertebral disc

Categories of Low Back Pain
The following are five categories of low back pain:
1.      Viscerogenic pain: Pain that originates from the kidneys, sacroiliac, pelvic lesions, and retroperitoneal tumors. This type of pain is neither aggravated by activity nor relieved by rest.
2.      Neurogenic pain: Pain commonly caused by neurofibromas, cysts, and tumors of the nerve roots in the lumbar spine.
3.      Vascular pain: Pain characterized by intermittent claudication from aneurysms and peripheral vascular disease.
4.      Spondylogenic pain: Pain directly related to the pain originating from soft tissues of the spine and sacroiliac joint.
5.      Psychogenic pain: Pain that is quite uncommon and ascribed to nonorganic causes.

Wednesday, October 31, 2012

Distraction Test

Distraction Test

The complaints of patients with chronic or degenerative conditions of the cervical disc are quite different from those of patients with acute conditions. Patients with chronic conditions experience intermittent episodes of pain, discomfort, and muscle spasm. Exacerbations come from exertion. Pain and stiffness may result from weather changes or unexplained causes. Radiculopathy is not always present. Hyporeflexia, motor weakness, and sensory disturbance (especially paresthesia) are common.

1.  Delay in the onset of symptoms.  If the symptoms are not written down and documented within a few hours or days after the crash, then it is very difficult for the patient to say he/she had pain when there is no written evidence.  This can be a critical issue in a case, for example, the first doctor to note that the patient had a traumatic brain injury was made 8 to 10 months after the collision.

2.  Delay in seeing the first doctor.  Any significant delays between the date of the crash and seeing the doctor may create credibility issues for the case.  The patient needs to have a good explanation for waiting for several days to weeks for the first appointment.  There may be legitimate issues such as, some doctors have very busy schedules and may not have appointments available for several days.  The reasons for delays should be noted in the file.  The doctor or patient may have a vacation or work trip scheduled, be out of town for a medical emergency, may have an unrelated surgery that made it impossible to make an appointment, or may simply have not transportation available.

3.  There were conflicts in the history given by the patient in the records.  For example, patient stated in his deposition that he had never been involved in a crash before.  Records from 1989 indicate that the patient was involved in a rear-end crash.  The ER doctor notes that the patient did not use a seatbelt and the orthopedist noted that the patient did use a seatbelt.

4.  Little-to-no damage to vehicle.  The defense will advocate that the damage to the vehicle equals the injury potential (see Chapter 15 for crash speed thresholds for injuries).  There are generally few photographs taken of the vehicles that adequately show the extent of the damage.  Most jurors are going to see poor quality blow-ups of the vehicles or as the parts are removed for repairs.

5.  Impact forces not sufficient to cause any injury or was sufficient enough to have caused only mild muscular strain that would have healed without treatment within a few days may have occurred.  No mechanism of injury was possible in this collision.

6.  No objective findings to prove injuries.  No bruises, bleeding, lacerations, fractures, or photographic evidence of the injury to show the jury.

7.  The treatment that was provided was passive and has not been proven to work.  Patient’s condition would have been the same with or without treatment.  Exercise is the only thing that works.  Patient had only palliative benefits from the treatment.  No long-term benefits noted in file.  May look at deposition.  If patient states in the deposition that the treatment only helped for one to two weeks but the patient continued to have treatment for an additional four months. The case may have challenges.

8.  The duration of treatment was too long, was excessive, or was duplicative, and therefore is not justified from doctor’s experience.  The treatment costs were thus unreasonable for the mild nature of the injuries.  The osteopath, chiropractor, and physical therapist were doing similar things, and therefore the treatments were unnecessary.

9.  Gaps in treatment indicate that the patient did not have any pain.  That a reasonable person in pain would see a doctor is a common attack.

10.  Healing and full recovery takes two to four weeks.  This opinion is simply a hoax for most cases (see Chapter 7 for more about soft tissue healing).

11.  Every person will have full recovery following whiplash injuries.  Doctors and attorneys are to blame.  This is another hoax (see Chapter 13 for a review of prognostic studies).

12.  Patient saw too many providers, consistently self-referred himself or herself, and had a history of psychological problems.

13.  Documentation was poor.  The doctors did not note symptoms, or there are inconsistent statements made by the doctors.

14.  New injuries, including MVCs, falls, etc., or simply flared-up bending over are responsible for the problems.

15.  Prior injuries resulted in all of the problems.  The defense may attack the case by telling the jury that the injuries sustained 8 to 15 years earlier were responsible for the current pain, although there is not evidence of the patient being seen by any health providers for the past five to six years for any musculoskeletal pain.

16.  Prior pain and / or treatment for this pain within the past couple years clearly indicates that the patient’s pain was long-term and would have been present despite the crash.

17.  No justification for the amount of time off work.  May state that the typical patient is back to work within one week (see Chapter 12 for more information).

18.  The MRI scan results showing a bulging or herniated disc are also seen in the general population and are not related to the accident.  Typically, if any degeneration or spurring is noted in the radiology report, the defense medical and biomechanics expert will use that as his/her basis for that opinion using a “Natural Progression” theory.

19.  Future treatment is not needed.  The defense attorney may tell the jury in the opening statement that “Everyone knows that once the case settles the plaintiff’s pain will go away.”

20.  Conservative jurors who have a “Hollywood mentality” can make a case extremely difficult even with the best documentation, proof of bulging discs, and great doctors.  The jury may perceive the plaintiff as looking healthy and there are no photographs of blood and guts.  Some court districts are known as being very conservative, thus making it difficult to get any significant awards.  Some jurors may see that there is monetary motivation for the plaintiff.

Tuesday, October 30, 2012

1994 Press Release: Fast Facts About Stone Mountain Park

1994 Press Release: Fast Facts About Stone Mountain Park

GEORGIA'S STONE MOUNTAIN PARK Public Relations Department
P. O. Box 778
Stone Mountain, Georgia 30086
404/498-5633 (FAX) 404/498-5607For More Information, Contact K" Thweatt or Mauri Spalding (404) 498-5637

Georgia's Stone Mountain Park encompasses one of the world's most amazing works of nature.

Known as a place of scenic beauty, historic remembrance, recreation and enjoyment, following are some little known, yet interesting facts about Georgia's Stone Mountain Park:
* Millions of people visit the Park annually, making it one of the most-visited attractions in the United States.

* Stone Mountain is the world's largest monolith.

* Stone Mountain was formed approximately 300 million years ago by a surge of molten lava beneath the earth's surface. Initially, a two-mile thick overlay of the earth's surface covered the cooling granite. The layer eroded over the next 200 million years exposing the smooth surface of the dome-shaped rock. The mountain is 825 feet high, rises 1,683 feet above sea level and covers 583 acres of land. The surrounding 3,200-acre Park includes woodlands, lakes, recreation areas, museums, and other attractions.

* The Memorial Carving on the north face of the mountain is the world's largest bas-relief sculpture, measuring 90x190, or three acres. The figures of Confederate President Jefferson David, General Robert E. Lee and General "Stonewall" Jackson mounted on horseback depict the South's historic past. In 1912, the Memorial Carving existed only in the mind of Mrs. Helen Plane, charter member of the Daughters of the Confederacy. The first of the three sculptors to work on the project, Mr. Gutzon Borglum began work on the carving in 1923. He left two years later taking his sketches and designs, and went to carve the famous Mount Rushmore sculpture in South Dakota. After remaining untouched for 36 years, the carving was completed in 1972.

* In 1845, the newly completed Georgia Railroad allowed for the extraction of granite from Stone Mountain for commercial use. Granite quarried from Stone Mountain has been used in construction projects throughout the world, including the locks of Panama Canal, the U.S. Capitol Building, and the Imperial Hotel in Tokyo, Japan.

* Although no major Civil War battles were fought on the soil of Stone Mountain, Sherman destroyed the Georgia Railroad line between Stone Mountain and Decatur during his destructive "March to the Sea." The Union army came within close range of the mountain when it burned New Gibraltar, the small town at the base of the mountain. Today, the rebuilt town is known as the Village of Stone Mountain.

* The first written records of the mountain date back to 1567 when Captain Juan Pardo of Spain was sent to set up forts in the New World. He and his group believed the quartz surface of what they called "Crystal Mountain" was made of diamonds and rubies.

* Unique clams and fairy shrimp live in clear freshwater pools formed in the craters on the mountain. In addition to these crustaceans, rare plants and flowers, such as the Confederate Yellow Daisy, grow in the mountain's crevices.

* The Park is home to a variety of animals and endangered species; however, there is little wildlife living on the rock itself.

* John W. Beauchamp was the first person to claim ownership of the mountain when he traded with Indians for possession. Later, he traded the mountain to Andrew Johnson and Aaron Cloud for a muzzle-loading gun and twenty dollars. Because half of Georgia and part of North Carolina rest on the mountain's base, it is widely believed that Stone Mountain may be formed like some icebergs--larger underneath the ground's surface than it is above ground.

Monday, October 29, 2012

Chiropractic Care Assisting With Fertility/Infertility

Chiropractic Care Assisting With Fertility/Infertility

Can a Chiropractor help you get pregnant?

The question, “Can a chiropractor help you get pregnant?” may sound like the setup to a joke, but when a woman is having trouble conceiving it’s no laughing matter. If you’re having problems getting pregnant, you might want to consider visiting a chiropractor for a series of treatments – but keep in mind that this should just be one part of your overall strategy to deal with fertility issues.
Chiropractic and Pregnancy – How it Works

The potential connection between chiropractic care and getting pregnant is related to the nerves that run through the spine and extend to the female body’s reproductive system. According to chiropractic theory, any blocked or pinched nerves result in spinal misalignment, also referred to as subluxations or spinal distortions. Chiropractors believe that when the nerves involved in the reproductive system are blocked or otherwise not working properly, this might result in a hormone imbalance or other malfunction which could lead to infertility. Chiropractic treatment involves manipulating and readjusting the spine, relieving the pressure on nerves running through the spinal column. Once the subluxations are corrected, it is believed that a woman’s reproductive system will function better, possibly resulting in a successful pregnancy.

Chiropractic and Pregnancy – Promising Studies

The majority of published research on the connection between chiropractic treatment and pregnancy can be found in the Journal of Vertebral Subluxation Research (JVSR). A three-part series of case studies published in 2003 showed a successful correlation between women receiving chiropractic care and increased fertility. Some of the women in the study visited a chiropractor specifically for help becoming pregnant, while others went for spinal adjustments due to other concerns – and then became pregnant during the time they were treated by the chiropractor. One of the JVSR studies, from May 2003, reported “successful outcomes on reproductive integrity, regardless of factors including age, history and [prior] medical intervention.” It is not clear how chiropractic treatment can specifically benefit fertility, but one suggestion is that spinal adjustment enhances peristalsis – the contraction of smooth muscles in the body that moves material through the digestive tract and other internal systems. With regard to fertility, peristalsis is necessary to move an egg from the ovary through the fallopian tubes into the uterus. Nerve blockage could inhibit the egg’s movement, keeping it from being fertilized or even possibly preventing a fertilized egg from making it safely from the fallopian tubes to the uterus.

Chiropractic and Pregnancy – Important to Remember

While these published reports make encouraging claims, it’s important to keep in mind that the JVSR studies are not scientifically conclusive and were based on results from a relatively small number of women. Larger clinical trials, comparing chiropractic care to more conventional infertility treatments, have yet to be performed to make a definitive scientific claim about a beneficial connection between chiropractic spinal adjustments and attempts to get pregnant. At the same time, seeing a chiropractor is worth considering if you’re having problems getting pregnant.

Sunday, October 28, 2012

Adjustments For Newborns

                                Adjustments For Newborns

Greater complications during delivery result in greater neurological insult to the newborn due to injury to the head and neck. Even after vaginal births, 4.6% of term neonates suffer unexplained brain bleeds and 10% suffer neonatal encephalopathy. Because so many children had been injured with forceps deliveries, (facial nerve palsy, tearing of cervical spine musculature) vacuum extraction was developed. Suction cups are placed on the newborn's head, and the baby is literally sucked out of the mother.

When utilized, 120 pounds of pressure goes through the baby's head and neck. Decapitation occurs at 140 pounds of pressure, to give you an idea of the high forces involved. Remember when you were a little girl or boy and there was a new baby you were being introduced to? Our parents always said, "Watch his head-you don't want to hurt him." We're careful because the fontanel's of the skull are so pliable, and the neck and brain are fragile and unprotected. This is why so many babies sustain injuries to their heads and neck during vacuum extraction-the force is far greater than their little bodies can tolerate.

Adjustments to newborns contain only ounces of force. But that force is directed into the spine to facilitate health and remove subluxations. We adjust babies as soon after birth as possible, to alleviate subluxations caused by in-utero constraint and the journey down through the birth canal. There has been a lot in the media lately about children not needing Chiropractic care, but there is no better way to get a head start in life. As you all know, Chiropractic care is not a cure for anything-it is a system of wellness to help us be who we're supposed to be. It is not a cure for ear infections, for colic, for allergies, for asthma, for frequent colds, nor for ADD/ADHD.

When we listen to mothers' stories of their pregnancy, labor and delivery, the children who suffer the most from the above complaints, are the ones who've had the greatest trouble with their births. Even relatively easy deliveries can result in subluxations. That's why every child should be checked, before problems with their health even develop. That's preventive care in the truest sense-preventing subluxations in mothers to prevent subluxations in their babies during childbirth. This is why every woman needs Chiropractic through pregnancy-so that the arrival of their baby is a wonderful experience. -Dr. Martha Collins, Family Chiropractor practicing in Kingston, Ontario.