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MEDSCAPE VI


State of Art Whiplash Care and Certain Realities


I had intended moving on from cervical care when two CME’s appeared in MedScape, followed by a paper published in AAOS Now, that are not helpful to my message. Since anything in print has its influence, I am going to elaborate on them.


My mantra is that nothing replaces fundamentals. Clinical comfort with fundamentals requires accepting anatomy and function of structures as they are. And acceptance may require shedding a generally accepted doctrine.


Somewhere in this series I must have described a sign that was on the pilot’s gate at Santa Barbara Airport, in California, in 1977. It’s likely still there. I’d landed, exited through it and turned back to close it when I read what became a goldmine in my teaching and some subsequent relationships. The sign read, “Keep This Gate Closed At All Times.”


If you haven’t smiled, please stop. And keep reading it until you do.


It’s a benchmark of the authority that is reflexively invested in what seems authoritatively written.


Every time I encounter issues such as this, my memory banks unleash a flood of mostly painful memories how the essentials were frantically obscured - had to be frantically obscured - because to illuminate any of them would expose the Fundamental Flaw: the historic blunder when traditionalism repudiated the basic of hands-on examination and treatment of injured tissues. I shouldn’t be surprised that the reason for this writing has again generated another ‘the dam is broke’ writing consistent with my previous contributions here and complete in Release From Pain.


If a real life analogy is needed, very regretfully one is here daily in Israel. I mention it not to politicize but to best illustrate how universal is the tendency to circumvent truth when it gets in the way of prejudice.


Objectively, no one can deny that $ billions have been donated to the “Palestinian” authority to build their society. For many reasons, vast wealth pours in that would jump start the process, but only if its fundamental ingredients are there! But they aren’t. None of the essentials of a sustainable society are evident:  a central respected, government, dedication of the welfare of the citizens, control of corruption on and on. So the chaos becomes self perpetuating. The failure for truth and sound principles to lead destroys the advance of truth – and so, from the likes of what has been published, and not published,  it is so in general orthopaedic therapy related to neck care .


All that said, let’s examine the papers that precipitated this diatribe and then seek a salve by reexamining principles designed to restore rationality. Hopefully enough whose habits most need change and propagation will consider them dispassionately.


I am also compelled by a persisting memory of my opportunity lost when I should have continued with an important conversation that occurred at an Orthopaedic Surgical meeting  decades ago, again that concerned cervical traction, cervical care in general and an aside comment from a responder in the audience concerning ankle traction. The commentator was Mason Hohl, a former professor of mine at U.C.L.A. when I was a medical student, who later served as President of the American Academy of Orthopaedic Surgery. (I am sure I alluded to this event previously, but for this purpose it is an important elaboration.)


I had risen to comment after a paper on cervical care had been given and briefly related my concerns and issues with standard care including how I believe cervical traction becomes valuable therapy. Dr. Hohl rose to rebut my considerations, and he concluded by saying, “We don’t traction ankles so I see no reason why we should traction necks.” His face colored when he expressed that sentiment, and I wondered why. Regardless, that event became a ‘I wish I’d said’ event in my recurring theme of memories. I shouldn’t have sat down. I should have countered and informed the audience what I had learned more than a decade before that meeting.       


Two recent Medscape CME vignettes focus on the ubiquitous, mischievous “Whiplash.”


I’ve previously described cervical care, and, in fact, that contribution provided the most gratifying comments in this series. If you have not done so, please peruse it (MedScape III - Examining for pains in the neck - "We cannot command nature except by obeying her." Sir Francis Bacon. And MedScape V – Resurrecting Traction [which has not been published at the time of this writing])


As I have stated before, I owe much of the success I have had in treating “Whiplash” and related conditions to my resolve to submit to a credo I slowly evolved decades ago: Principia Primum – Fundamentals First. First Decide the Principles – and then decide what to do about them.


As I repeatedly allude in this collection, a major medical failure, that Orthopaedic Medical practice strives to resolve, is the defensive and self-defeating set of assumptions that arose because of the scars of traditionalism’s having rejected hands-on applications of biomechanics and kinesiology because they smacked of the “C” word. In the light, chiropractic is a still developing profession that focuses on the ancient art. Today, chiropractic has become so ingrained with manipulative practice that when I employ it, many, if not most of my patients, ask if I was performing it instead of the historic generic that emerged from the mists of antiquity. And again I explain that it’s all medicine, all related to reasonable and appropriate care regardless that the bastions of medical authority repudiated it over a century ago in a spasm of perverted self-righteousness that largely produced the present that we are so painfully attempting to extricate ourselves from. I must get off the soap box here, but for your inclination to become satisfied with more grounding of course I invite you to visit my website, which is dedicated to the resolution.


Here, I will visit the CME mini courses as a ground from which to comment on their limitations and what I believe needs to be considered to balance the quandary with sound clinical appreciation of some essential factors. It all follows naturally from certain fundamentals.


The first was a MedScape CME comparing three therapies in the treatment of Whiplash injury. As I read the article, I again placed myself in the position of a clinician seeking to understand the issues, a traditionally trained clinician who is responsible for such common conditions and who has not been successful. Then I again considered the responsibilities of a clinician who decides to write such a paper. And in this case, prime in my memory was another time that I may have described before in this series but that, especially, here bears repeating because of its import. I ask that you not consider it a digression.


Sudek’s Atrophy, also called Reflex Sympathetic Dystrophy (RSD), also called Complex Regional Pain Syndrome (CRPS) is a dread condition that is an emergency at its onset. The dynamics are so wild that it requires immediate, active therapy that is as directed as possible. While it comes in various sizes and degrees any experienced clinician recognizes that fact and well may bear frustrated memories of failure despite best attempts to relieve the suffering despite a number of therapies including sympathetic blockade, Baer blocks etc.


One fact we do know is that RSD does not respond to “simple” modalities. But a search of the “sacred” literature by someone who wanted to write a paper didn’t produce one that proved that ultrasound doesn’t work. So this doctor found her claim to fame. How she obtained departmental authority for the study still makes me shudder because I had enormous respect for it. She assembled a series of such sufferers of lower extremity RSD, randomly divided them according to scientific protocol and then treated them exclusively with ultrasound either turned on or off. And, indeed, she proved that ultrasound doesn’t work. There was no difference in the two groups. Both miserably suffered equally. Her day came. She presented the paper and descended the platform with head held high. She had presented to the Academy and in her eyes contributed to science. And of the desperate patients needing earliest mobilization, sympathetic blocks….. active therapy…


I felt even more repulsed as I scanned the large, silent audience. The faces I could see were so passive. We had heard the ghost of a Mengele experiment! And no visible reaction? I expressed my rage. Afterward no one approached me. But that scene never left me.  Reading this paper provoked a hint of the memory. So much here was different? So why my invoking the my memory and feeling a hint of comparison? And here is a crux of this issue.


Because there is a general lack of appreciation about the fundamentals – not because of individual laxness but because of institutional failure of education for many decades - as I have elaborated as a central theme – most readers lack the sophistication to realize that potentially valuable options have not been included in the study. So, unless something triggers them to suspect the lack, the habit to rush to the proverbial bottom line will likely result in the erroneous conclusion that doing nothing is just as good as any therapy. I would be very grateful to be wrong in that comment and be repudiated, but after 50 years in medicine I know how busy doctors want immediate answers from their reading and how serious the trap is.


Briefly analyzing :  


The main author of the paper reported in MedScape CME is Alice Kongsted, DC, PhD. There are several M.D. co-authors. The study compares three approaches to whiplash and concludes “Immobilization, act-as-usual, and mobilization had similar effects regarding prevention of pain, disability, and work capability 1 year after whiplash injury, according to the results of a randomized, parallel-group, controlled trial reported in the March 15 (2007)issue of Spine.” …an active mobilization program (Mechanical Diagnosis and Therapy; physical therapy twice weekly for 3 weeks).


“At the 1-year follow-up, 48% of participants reported considerable neck pain, 53% reported disability, and 14% were still listed as sick. There were no significant differences noted between the 3 intervention groups.”


. "We find our results adequately sound to conclude that earlier recommendations of active treatment regimens cannot be supported. Moreover, taking the per protocol analyses into account, use of a stiff neck collar should be discouraged as a standard approach."


Study limitations include poor compliance with treatment, frequent use of treatment other than prescribed, and more participants lost to follow-up in the act-as-usual group.


"The present trial shows clearly that active intervention in the first weeks after an injury does not result in a better outcome than an 'act as usual' program when prescribed to a high-risk patient group," the authors conclude. "There might be subgroups that respond to treatment, but in a large group of patients the prognosis was not improved by active treatment. Until such subgroups have been identified, our general recommendation is that advice to act as usual, the less expensive intervention, should be the preferred treatment."


Active Interventions, Act-As-Usual Have Similar Outcomes After Whiplash Injury  CME

News Author: Laurie Barclay, MD
CME Author: Laurie Barclay, MD


Disclosures


April 2, 2007 — Immobilization, act-as-usual, and mobilization had similar effects regarding prevention of pain, disability, and work capability 1 year after whiplash injury, according to the results of a randomized, parallel-group, controlled trial reported in the March 15 issue of Spine.


"Long-lasting pain and disability, known as chronic whiplash-associated disorder (WAD), may develop after a forced flexion-extension trauma to the cervical spine," write Alice Kongsted, DC, PhD, from the University of Southern Denmark in Ringe, and colleagues. "It is unclear whether this, in some cases disabling, condition can be prevented by early intervention. Active interventions have been recommended but have not been compared with information only."


In this study, 458 participants were recruited from emergency units and general practitioners within 10 days after a whiplash injury. They were randomized to receive 1 of the following: immobilization of the cervical spine in a rigid collar followed by active mobilization, advice to act as usual, or an active mobilization program (Mechanical Diagnosis and Therapy). At 3-, 6-, and 12-month follow-ups, treatment effect was measured in terms of headache and neck pain intensity (scale, 0 - 10), disability, and work capability.


At the 1-year follow-up, 48% of participants reported considerable neck pain, 53% reported disability, and 14% were still listed as sick. There were no significant differences noted between the 3 intervention groups. Per-protocol analyses showed results very close to the primary analyses (intent-to-treat), but the neck collar group tended to have a poorer outcome.


"Immobilization, act-as-usual, and mobilization had similar effects regarding prevention of pain, disability, and work capability 1 year after a whiplash injury," the authors write. "We find our results adequately sound to conclude that earlier recommendations of active treatment regimens cannot be supported. Moreover, taking the per protocol analyses into account, use of a stiff neck collar should be discouraged as a standard approach."


Study limitations include poor compliance with treatment, frequent use of treatment other than prescribed, and more participants lost to follow-up in the act-as-usual group.


"The present trial shows clearly that active intervention in the first weeks after an injury does not result in a better outcome than an 'act as usual' program when prescribed to a high-risk patient group," the authors conclude. "There might be subgroups that respond to treatment, but in a large group of patients the prognosis was not improved by active treatment. Until such subgroups have been identified, our general recommendation is that advice to act as usual, the less expensive intervention, should be the preferred treatment."


The Danish Insurance Association, PTU, the Karen Elise Jensens Foundation, and the IMK Foundation supported this study.

Spine. 2007;32:618-626.


Clinical Context


Chronic whiplash-associated disorder, or long-lasting pain and disability, may develop after a forced flexion-extension trauma to the cervical spine, with resultant personal pain and socioeconomic consequences. Early, active, and often costly interventions have been recommended but have not been compared with providing information only.


In various studies, mobilization has been shown to have a somewhat better effect than a soft collar and passive treatment methods; advice to act-as-usual was superior to a soft collar; and immobilization in a semirigid neck collar for 4 weeks was reported to be superior to a mobilization regimen. To evaluate the spectrum of treatment regimens, the current prospective randomized trial focused on prevention of chronic sequelae after a whiplash injury using interventions directed toward soft tissue damage in the cervical spine.


Study Highlights


At 2 university research centers in Denmark, 458 participants were recruited from emergency units and general practitioners within 10 days after a whiplash injury. This trial took place between May 10, 2001, and June 17, 2004, and recruitment ended in June 2003.


Inclusion criteria were 18 to 70 years of age, exposure to a rear-end or frontal car collision, symptomatic within 72 hours, and could be examined within 10 days of the collision. Exclusion criteria were fractures or dislocations of the cervical spine, amnesia or unconsciousness, injuries other than whiplash, self-reported average neck pain during the preceding 6 months of more than 2 on a scale of 0 to 10, significant preexisting somatic or psychiatric disease, and known alcohol or drug abuse.


Those with marked symptoms and an expected increased risk of developing persistent symptoms were included in this trial; those who reported milder symptoms were included in a separate study.


Participants were randomized to receive (1) immobilization of the cervical spine in a semirigid Philadelphia neck collar worn during all waking hours for 2 weeks, followed by active mobilization, (2) advice in a 1-hour session to act as usual, or (3) an active mobilization program (Mechanical Diagnosis and Therapy; physical therapy twice weekly for 3 weeks). All participants received a pamphlet emphasizing a generally good prognosis and simple advice about use of ice and mild analgesics.


At baseline, age, sex distribution, pain intensity, and cervical range of motion were similar in all groups.


Follow-up visits were at 3, 6, and 12 months. Treatment outcome measures were headache and neck pain intensity (scale, 0 - 10), neck disability (15-item Copenhagen Neck Functional Disability Scale, 0 = no neck disability to 30 = extremely disabled), and self-reported work capability. Primary analyses were by intent-to-treat.


Participants lost to follow-up: act-as-usual group, 25; immobilization group, 8; and active mobilization group, 5. Those lost to follow-up did not differ significantly from the others in terms of baseline parameters.


There was good treatment compliance for 80 (53%) of 151 in the collar group and 106 (76%) of 140 in the active mobilization group, and poor compliance in 40 (26%) of 151 and 9 (6%) of 140 in these groups, respectively. Participants with poor compliance in the collar group were less likely to be listed as sick at baseline, but other baseline data did not differ between compliance groups. Poorly compliant participants in the collar group reported a better outcome at 1-year than did others. The outcome of those poorly compliant to active mobilization could not be reliably estimated because only 4 of 9 completed follow-up.


All groups reported reduced headache and neck pain intensity, with improvement occurring mainly during the first 3 months after injury. At 1-year follow-up, 48% of participants had considerable neck pain, 53% reported disability, and 14% were still listed as sick.


There were no significant differences between the 3 groups. Improvement from baseline to 1-year follow-up was reported by 38% in the collar group, 33% in the act-as-usual group, and by 40% in the mobilization group. Worsening was reported by 12%, 17%, and 10%, respectively (P = .60).


Per-protocol analyses showed results close to the primary analyses, but the neck collar group tended to have a poorer outcome, with estimated higher risk for altered working ability in this group vs act-as-usual (odds ratio, 2.3) or mobilization (odds ratio, 3.2; P < .05).


Pearls for Practice


After whiplash injury, patients at high risk for whiplash-associated disorder treated conservatively reported reduced headache and neck pain intensity, with improvement occurring mainly during the first 3 months after injury. At 1-year follow-up, 48% of participants reported considerable neck pain, 53% reported disability, and 14% were still listed as sick.


There were no significant differences noted between the 3 intervention groups. Improvement from baseline to 1-year follow-up was reported by 38% in the collar group, 33% in the act-as-usual group, and 40% in the mobilization group.


Acute Whiplash Subjects Demonstrate Generalized Hypersensitivity

Mindy Hung

Jan. 23, 2004 — Whiplash subjects with higher levels of pain and disability show evidence of sensory disturbance that differentiates them from those with lesser symptoms, according to the results of a study published in the Jan. 15 issue of Spine.


"While those with moderate and severe levels of pain and disability showed greater psychological distress, the main distinguishing feature from those with lesser symptoms was the presence of generalized hypersensitivity to a variety of stimuli," write Michele Sterling, PhD, and colleagues from the University of Queensland in Brisbane, Australia.


"This enhanced sensitivity occurred independently of psychological distress and is likely as a result of changes in central pain processing mechanisms, evident soon after injury," they add.


The investigators enrolled 80 volunteers (24 men, 56 women; mean age, 33.5 ± 14.7 years) who reported neck pain as a result of a motor vehicle crash, as well as 20 healthy asymptomatic volunteers (9 men, 11 women; mean age, 39.5 ± 14.6 years).


Whiplash subjects had met the Quebec Task Force Classification of WAD II or WAD III and were studied less than one month after injury. Investigators excluded those with a classification of WAD IV; those who experienced concussion, loss of consciousness, or head injury as a result of the accident; and those with a previous history of whiplash, neck pain, headaches, or a psychiatric condition that required treatment. Researchers also excluded symptomatic volunteers who had previous pain or trauma to the cervical spine, head, or upper quadrant.


Investigators measured motor functions by recording cervical range of movement (ROM) in three dimensions, joint position error (JPE), and activity of the superficial neck flexors using surface electromyography (EMG).


They also performed quantitative sensory tests including measurement of pressure pain thresholds (PPTs) and thermal pain thresholds. The researchers administered the brachial plexus provocation test (BPTT) and asked subjects to record pain levels on a 10-cm visual analog scale.


Psychological distress was assessed using the Neck Disability Index (NDI). WAD subjects also completed the General Health Questionnaire 28 (GHQ-28), the TAMPA questionnaire for fear of movement/injury, and the Impact of Events Scale (IES) for posttraumatic stress.


Cluster analysis, based on NDI scores, identified three subgroups within the whiplash group: cluster 1 (n = 36, with mild pain or disability; NDI score, 15.6); cluster 2 (n = 32, with moderate pain or disability; NDI score, 39.5); and cluster 3 (n = 12, with severe pain or disability; NDI score, 69.5).


Patients in all three whiplash groups demonstrated significantly less ROM in all directions and increased EMG than control patients (P < .01). The moderate and severe groups (clusters 2 and 3) demonstrated JPEs greater than the group with mild pain (cluster 1) and the control group (P < .01).


The moderate and severe groups had lower PPTs at all test sites except the ulnar nerve site, and they had lower cold pain thresholds with compared with control subjects (P < .01). The severe group also demonstrated a decreased range of elbow extension at pain threshold in the BPPT and higher VAS scores of pain than did control patients and the other two whiplash groups (P < .01).


Total GHQ-28 scores for the moderate (31.4 ± 2.3) and severe (46.8 ± 4.1) groups were above the normal threshold (23/24). Scores were significantly greater than those for the mild group (23 ± 2.4) (P < .01). There was also a significant difference between the three whiplash groups for the TAMPA score (P < .01). All three groups contained subjects with moderate or severe posttraumatic stress reactions, indicated by IES scores of more than 26.


"This is the first study to identify that those with higher levels of pain and disability show objective evidence of sensory disturbance that differentiates them from those with lesser symptoms," write Dr. Sterling and colleagues.


"It is possible that these subjects have alterations in central pain processing mechanisms soon after injury, which impedes their recovery," the authors write. "This may have implications for the medical management of this particular group with acute whiplash injury."


The study was funded by Suncorp Metway General Insurance (Queensland) and the Center for National Research on Disability and Rehabilitation Medicine (CONROD).


Spine. 2004;29:182-188

Reviewed by Gary D. Vogin, MD


A new “pain in the neck”

by Jerrold M. Gorski, MD

A breakthrough in the evaluation and treatment of chronic neck pain and whiplash-associated disorders


Editor’s note:

I promised that AAOS Now would give AAOS members a place to “sound off,” just as Dr. Gorski is doing in this column. Readers are welcome to respond, comment, or critize, as long as you remember that AAOS Now is a “member” publication—not a scientific, peer-reviewed journal. Whether you think Dr. Gorski is ahead of his time or way off base, if there is referred pain from the neck to the shoulder, then I guess it is possible to have referred pain from the shoulder to the neck. (Some nerves, like the median nerve at the wrist, can “go uphill” [proximal pain].) As I recall, I was one of those who said total hips would not work!


Not long after the introduction of the Model T, the term “whiplash” was coined. In the decades since, researchers have never been able to prove the existence of the condition, which affects millions of unhappy patients. Chronic neck pain and whiplash-associated disorders continue to cost up to $20 billion annually, without any hope for a cure…perhaps until now.


Whiplash is not a favorite subject of orthopaedic surgeons, principally because a pathologic lesion has never been found in the neck. We can understand the whiplash mechanism resulting from acceleration/deceleration forces acting on the head and neck in a rear-end collision. We note that the number of whiplash claims continues to increase, despite modern head restraints, seat belts, and airbags. We are disappointed and perplexed when patients don’t improve after surgery. Without a defined neck lesion, we frequently defer the treatment of these patients to others. Every conceivable anatomic structure in the neck has been repeatedly scrutinized for the whiplash lesion and it just doesn’t exist—in the neck.


I think whiplash exists, and this is my hypothesis: No pathologic lesion has been found in the neck because whiplash—and most intractable chronic neck pain—is due to a shoulder problem. The pathologic lesion is asymptomatic shoulder impingement that presents as “neck” pain. In other words, whiplash is a shoulder—not a neck—condition!


More than semantics


The first problem with whiplash and chronic neck pain is largely semantic. The most common “neck” pain is not in the neck, but in the upper back between the neck and the shoulder, and frequently over the supraspinatus muscle. Pain in the upper back may also be ascribed to trapezius spasms, trigger points, thoracic outlet syndrome, and fibromyalgia.

When I see a patient with neck pain localized to the supraspinatus muscle in the upper back, I consider a new referred pain syndrome I call the Referred Shoulder Impingement Syndrome (RSIS), which I first described in the Journal of Bone and Joint Surgery in 2003.1 Patients with whiplash, whiplash-associated disorders, or intractable chronic neck pain frequently have pain here, which my physician’s assistant has named the “G-spot” in my honor.

The second problem is that the shoulder is asymptomatic for many of these patients, and they may deny any shoulder problems. Yamaguchi has recently and definitively shown that shoulder impingement has both asymptomatic and symptomatic presentations.2 He estimates that up to 17 million people have asymptomatic shoulder impingement, and I believe that many of them actually have RSIS, or neck pain referred from the shoulder.


Muddu3 and Chauhan4 have separately shown that the symptomatic shoulder impingement is associated with whiplash (“shoulder whiplash”), even suggesting this as a distinct clinical entity. My own research indicates that asymptomatic shoulder impingement is not only associated with, but frequently is, the underlying etiology in chronic neck pain and whiplash-associated disorders.

What’s behind it?


The pathophysiology of RSIS is largely speculative at this time. MacNab has histologically described the absence of pain fibers in impinged rotator cuff tissue, which may best explain the absence of shoulder complaints in the asymptomatic group.5 This finding is important and somewhat analogous to pressure sores. In chronic impingement, sustained pressure on the blood vessels and nerves of the rotator cuff causes them to become painless and asymptomatic in the shoulder.


I believe that the neck pain is due to pain and spasm in the adjoining supraspinatus muscle. When the shoulder hurts, the cuff is symptomatic, and perhaps some pain fibers are still present or the bursal tissues are painfully involved.


Don’t be surprised if you find yourself checking for RSIS in your own upper back; everyone seems to have this “neck” ache from time to time. The pain is ususally rated at about 3 on a visual analogue scale, on which 10 is maximum pain. For most people, it’s an annoying ache rather than a severe pain; for others, it is sometimes very severe. I think the associated limited neck motion may result from a compensatory reaction by the muscles around the supraspinatus. When patients bob their heads after a shoulder injection—I call it the “head dancing sign”—it is due to the immediate lessening of “neck” pain and spasm. It’s a great prognostic sign.


Don’t sleep on it


How does an insenated rotator cuff from sustained pressure or impingement develop without the patient's being aware of it? The chronicity of the impingement is anecdotally correlated with a common sleep position in which the shoulder remains in the overhead position for prolonged periods “under the pillow.” Although my workers compensation patients deny it, everyone seems to sleep this way. I think this may also be the cause of the nightly sleep disturbances, tossing, turning, and the early morning complaints frequently reported by patients as having “slept funny” on their necks! I think every physician (and throwing/swimming coaches) should recommend avoiding this sleep position. We need much more research on the effect of sleep positions, but you can check it out for yourself tonight.


In my opinion, an acute shoulder injury commonly occurs in a car accident, especially if the driver continues to hold the steering wheel. It likely represents an acute injury to a chronically impinged shoulder if the patient habitually sleeps with the arm in the overhead position.


Furthermore, both the shoulder and neck are likely to be injured in any given accident, and the neck may be whipped back and forth, producing a soft-tissue sprain. In other words, the shoulder impingement likely accompanies a concomitant neck sprain. The neck sprain may subside, leaving the supraspinatus ache in the neck. This is aggravated when the patient sleeps with the arm overhead, resulting in persistent pain.


Making the diagnosis


If your patient winces with the arm overhead and complains of neck pain, suspect RSIS and consider a shoulder injection. In addition to using standard clinical diagnostic tests, the Neer impingement sign, and the Neer injection test to diagnose shoulder impingement, specific radiographic findings have proven essential, especially when the shoulder is asymptomatic. I believe that the radiographic finding of a pseudocyst in the proximal humerus is one key to the diagnosis (Fig. 1 on page 27). Its presence may give you enough reason to try injecting an asymptomatic shoulder.


The triad of a positive referred Neer sign (pain in the upper back with forward elevation of the shoulder), the radiographic pseudocyst, and the positive Neer injection test (relief of neck pain after a shoulder injection) can be used to diagnose RSIS.


The pseudocyst is real

The pseudocyst has been known since Codman’s day, but is rarely recognized and can only be understood along with RSIS. It is usually considered a normal variant or positional anomaly, and its presence is ignored, which is perhaps good considering its similarlity in appearance to a malignancy. But don’t biopsy this lesion! Because I often see the pseudocyst immediately after a motor vehicle accident, I believe it is present as an asymptomatic condition even before the accident. Pseudocysts are so common that I have extrapolated that RSIS is also common.

I think the pseudocyst is very real. It is not a cystic hole, but trabecular atrophy. I hypothesize that it results from increased retrograde blood circulation to the insertion of the rotator cuff into the greater tuberosity. When the rotator cuff is chronically impinged or traumatized, it becomes inflamed, edematous, and hyperemic. The increased blood flow causes demineralization and a radiolucent appearance on X-rays. Although an X-ray isn’t necessary to diagnose symptomatic shoulder impingement, it has helped me to make the diagnosis when the shoulder is asymptomatic.


If you find a pseudocyst in a patient who has chronic neck pain and an equivocally positive Neer sign, go ahead and inject the subacromial space with cortisone and lidocaine. I strongly recommend three injections over a period of 6 weeks to reliably relieve pain by 90 percent or more. Do not give just one injection and then operate when the symptoms recur, as I used to do. The use of three injections has been uncomplicated and will prevent the need for shoulder surgery. Physical therapy has not been required.


With this course of treatment, you will have very happy patients, especially if they suffered “whiplash” for years before being accurately diagnosed. Interestingly, one quarter of the patients I see have bilateral complaints, probably from sleeping with both arms overhead. Whether patients have unilateral or bilateral pain, advise them to avoid the overhead impingement position, especially while they are asleep. Prescribe a shoulder immobilizer to use at night, and ask if it is still on in the morning.


Ahead of my time?


It may appear oxymoronic to describe an aysmptomatic pain syndrome, and preposterous to propose both a pathologic lesion in the shoulder and shoulder treatment for neck pain and whiplash. Describing a new clinical entity in this contentious milieu is an uncertain and challenging process. As a pioneer of the anatomic medullary locking prosthesis and the S-ROM hip prosthesis under Charles A. Engh Sr., MD, and as an investigator who attempted to study bone morphogenic proteins in 1983—years before their use became accepted—I am well aware of how much time new hypotheses need to be tested, understood, and accepted. I expect that it will take a very long time for this new referred pain syndrome to be accepted as a “cure for whiplash” and chronic neck pain. But please don’t wait too long to try this; I predict that you and your patients will be amazed.


Jerrold M. Gorski, MD, is in private practice in Mineola, N.Y. He welcomes your feedback at jgorskimd@hotmail.com or through his Web site, www.gorskimd.com. Links to the studies cited in this article can be found online at www.aaos.org/now.


References

Gorski JM, Schwartz LH. Shoulder impingement presenting as neck pain. J Bone Joint Surg Am. 2003 Apr;85-A(4):635-8.

Yamaguchi K, Ditsios K, Middleton WD, Hildebolt CF, Galatz LM, Teefey SA. The demographic and morphological features of rotator cuff disease. A comparison of asymptomatic and symptomatic shoulders. J Bone Joint Surg Am. 2006 Aug;88(8):1699-704.

Muddu BN, Umaar R, Kim WY, Zenios M, Brett I, Sharma Y. Whiplash injury of the shoulder: is it a distinct clinical entity? Acta Orthop Belg. 2005 Aug;71(4):385-7.

Chauhan SK, Peckham T, Turner R. Impingement syndrome associated with whiplash injury. J Bone Joint Surg Br. 2003 Apr;85(3):408-10.

Macnab I, McCulloch J. Neck Ache and Shoulder Pain. Williams and Wilkens Co: Baltimore: 1983. p. 318-319.



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What Did It?

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Hip Dysfunction

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Tendon Reflex

Malingering

Ask it!

Prolotherapy

Resurrecting Traction

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Sometimes Something Works

The Cervical Exam

What Did It?

Repetitive Bilateral Lateral Bending

Why Orthopaedic Surgery?

Is it a Normal Tendon Reflex?