ABC of Rheumatology: PAIN IN NECK, SHOULDER, AND ARMBMJ 1995; 310 doi: https://doi.org/10.1136/bmj.310.6973.183 (Published 21 January 1995) Cite this as: BMJ 1995;310:183
All rapid responses
Thank you, Dr. Hart. If by "neurological component" you mean "pain",
then it is true: not all reversals of the normal cervical lordosis are
However, it is true that there is only a 9% chance that a reversal of
the cervical lordosis is not due to trauma (see Gore, 1986). In other
words, if a lordosis is reversed, the likelihood is that it was
traumatically induced. That likelihood, then, is 91%. Of course, reversal
of the lordosis may be asymptomatic. And in many cases, it is. However,
I believe (and you may find the studies) that this posture is a
significant risk factor for cervical strain and secondary osteoarthrosis.
Gore DR, Sepic SB, Gardner GM: Roentgenographic findings of the
cervical spine in asymptomatic people. Spine 11(6):521-524, 1986.
Competing interests: No competing interests
Although I fail to disagree with any of the eminent authors'
responses, I feel it essential that I add a further perspective to that
presented by the western medical paradigm.
Traditional Chinese Medicine (TCM) not only recognises the anatomical
and physiological derivations of neck, shoulder and arm disorders but also
adds a perspective unique to itself, by nature of it's understanding of
the meridian phenomenon.
Neck problem : whatever the 'mechanical' injury, or indeed if there
has been neither mechanical injury or degenerative changes, TCM always
looks for systemic developments either as cause of, or result of, the neck
problem presented. eg. For pain radiating from the anterior lower cervical
spine one may suspect an accompanying 'stomach' disorder; for pain
radiating from the posterior lateral cervical spine, 'kidney and/or
bladder' problems, possibly small intestine problems; from the lateral
cervical spine and occipital area, liver/gall bladder malfunction.
Arm/shoulder problems: tennis elbow - bowel trouble; golfer's elbow -
potential heart problem; anterior shoulder - intestinal trouble and
possibly lung problem; posterior shoulder - fluid metabolism, small
Although a purely mechanical injury is always possible, it can often
be a result of the combination of stress to a particular area coupled with
constitutional weakness in that area
eg. golfer's elbow in one with familial 'heart' defect; tenosinovitis
(wrist) in one with constitutional lung defect such as asthma; C7 to T3
discomfort/inflammation in one with lung defect (such as asthma or
existing lung infection). T3 to T6 possible pericardium/heart problem.
The list is by no means exhaustive but provides an example of how a
different paradigm can add a new perspective and enhance others. From this
perspective TCM practitioners clear up many such injuries on a daily
basis, often when 'western orthodox' measures have failed. Not only do we
apply physical remedies such as acupuncture & moxibustion, or
acupressure, but also dietary therapy - an obvious choice when faced with
apparent systemic disorders involving liver, gall bladder, small intestine
or kidney/ bladder 'malfunction' etc.
eg. for 'cervical spondylitis/losis' a diet that reduces bile
production is favoured (low fat, low alcohol, no coffee/chocolate/cheese),
also reduces other symptoms such as occipital pain and vertigo.
A word of caution: as TCM reminds us of the potential for systemic
links to these apparent 'mechanical injuries' we are also aware that
treating purely as a 'mechanical' injury, without due consideration that a
systemic defect may exist, we may aggravate a systemic problem whilst
having apparently 'cured' the mechanical injury. Spinal pain is sometimes
a reflection of a systemic defect; taking remedial action at the spine
'shifts' the problem back to the organ creating a more serious outcome.
Arms, hands and shoulders are no different; does one really wish to evoke
a serious heart event by treating say 'carpal tunnel syndrome' without
considering the alleged strong link (according to TCM) between median
nerve and heart muscle function?
Competing interests: No competing interests
Dr. Gregory Wright, a fellow chiropractor, seems to miss an important
point regarding the loss of cervical spine lordosis: The kyphotic neck
may not necessarily have a neurological component. Consequently, the
nervous system should be checked somehow to see if indeed there is nerve
impairment prior to a cervical spine corrective procedure.
John Hart, D.C.
Competing interests: No competing interests
Drs. Barry and Jenner provide an extremely superficial and misleading
review of neck pain resulting from whiplash trauma in the "ABC's of
Rheumatology: Neck, Shoulder and Arm Pain". Articles such as this attempt
to summarize the salient points about different neck conditions, but in
the case of whiplash, have truly botched the job. If this is a reflection
of the quality of thinking and writing in rheumatology, I would suggest
that the authors stay at home to practice their research skills. Please
leave the writing to those who know something about the topic. If that
sounds harsh, read on and open your eyes!
Rather than shedding new light on an old topic by citing the
overwhelming number of new studies on the topic of whiplash, the authors
repeat the same old and tired comments and cliches about whiplash that
have absolutely no basis in the literature, such as "restriction of
movements may be considerable, but investigation often reveals no
pathology". Whose investigation is that? That of a doctor who is
performing "indpendent" medical "examinations" for an insurance company?
Reading further, we find that "the pain...is probably caused by
stretching or tearing of cervical muscles and ligaments", and then
"...principles of treatment are the same as for any acute neck pain, with
early mobilisation and avoidance of prolonged use of a collar". These
comments are not only superficial, but I would add, almost completely
useless. Whiplash-injured patients deserve much better. Will they find
it from their rheumatologist? Not if Barry and Jenner are as deep as it
gets. So we should, as stated so eloquently by one of my patients, "get
real". Here is the reality
The conditions seen in patients secondary to whiplash include:
single and multiple cranial nerve palsies peripheral neuropathy dizziness and otoneurologic disorders thoracic outlet syndrome oculomotor and other visual disturbances posttraumatic stress disorder herniation of cervical discs; rupture of ligaments and adjacent tissues rim lesions (disc-bone interface) spinal cord injury retropharyngeal hematoma damage to subarachnoid space mediastinitis TMJ injury, disruption hypopharyngeal, tracheal, or esophageal perforation brain injury hypothalamic-pituitary-thyroid axis disorder damage to posterior cervical sympathetic nerves menstrual disorders tremor and movement disorders occipital neuralgia cervical dystonia
At least 3 cases cases of retinal angiopathy have been reported in
Fractures, dislocations, subluxations, sprains, and strains are the
more common conditions associated with this injury. Soft-tissue lesions
are particularly prevalent.
Barry and Jenner state that "the start of pain may be delayed for a
few hours or even several days after the accident". That is very weak!
Delay in onset of symptoms after whiplash is extremely common and is well
documented in the literature; it is the RULE not the exception
Generally speaking, more severe lesions are symptomatic very soon after
trauma. However, delays of several months are not uncommon for some
disorders, and they may be quite disabling.
Gotten (17) stated that symptom onset delays of several days were
common. Braaf and Rosner (141) emphasized that the delay may be months or
years. Certainly, if one considers the progression and subsequent
degeneration of disc injuries and the later onset of spondylosis, these
figures seem reasonable. Deans et al. (73) found that 78% of their study
group was symptomatic within 12 hours, whereas 13% became symptomatic
between 12 and 24 hours. Seven percent became symptomatic after 48 hours.
Hildingsson and Toolanen (70), in their study of 95 cases of CAD trauma,
found the following onset of symptoms: 1. within one hour--65 patients, 2.
within five hours--77 patients, 3. within 15 hours--85 patients. One must
be careful in assessing the findings of these two studies, however,
because in both cases, the patients were taken from a hospital outpatient
center rather than from a secondary or tertiary center.
People who might be injured in MVC (this new term replaces the older
"MVA", since "motor vehicle collisions are not really "accidents"; see
NHTSA and SAE) are quite likely to present themselves at an emergency
room, particularly when their pain develops soon after the accident.
However, when symptoms are delayed, the sense of urgency will usually
subside. So the tendency to attend the ER is roughly inversely
proportional to the delay in onset of symptoms. Therefore, these authors
have inadvertently selected a group of patients whose symptom onset was
fairly quick, but who also may not be particularly representative of the
general group of CAD patients.
One of the few studies to account for this problem in its design was
one by two British orthopedists, Gargan and Bannister (529). Even after a
mean post-crash interval of 5.5 days, three patients developed symptoms in
their study and remained symptomatic at three month follow-up. In the 29%
of patients injured in 2.5 mph crashes, and 38% injured in 5.0 mph
crashes, Brault et al. (468) noted that these symptoms always occurred
when the volunteers were not at the testing facility, suggesting some
degree of delay in onset of symptoms.
Barry and Jenner go on to state that "recovery is often slow with
neck pain persisting beyond six months in up to 10% of patients". That
statement is RUBBISH. It is a fact that 50% of patients exposd to these
types of collisions are injured each year in the United States.
Conservatively, epidemiology has shown that 3 million persons are injured
in whiplash trauma each year. Of the persons injured, a full FIFTY per
cent will develop chronic symptoms.
Over the last 40 years there have been at least 30 papers published
on the long-term prognosis of CAD trauma. These studies are summarized in
Table 1 below. While some of the studies represent outliers and probably
represent some type of methodological problem or variation in definition
[e.g., Ellertsson et al. (72) and Pearce (106)], the reader can clearly
see that, still, the prognosis for full recovery is poor in a large
segment of this population.
It should be noted that of these 30 studies, only 9
(72,96g,109,109a,113,169s,476,523,529) evaluated only the rear impact
variety of collisions. The others either concern whiplash injuries of all
types, or the authors did not specify the type of collision. Three of
these studies (109,113,523) followed the same group of patients and
represent the longest follow-up periods (15.5 years) and one of the worst
outcomes (70% still symptomatic). The other longer follow-up (168f) also
showed an 86% symptomatic rate.
Long-term Outcome of CAD Injuries ¦ Author(s) ¦ Date ¦ (n) ¦ Type ¦Follow-up¦Chronic(%)¦ ¦Gotten ¦ 1956 ¦ 100 ¦ Mixed ¦ >1 ¦ 46 ¦ ¦Macnab ¦ 1964 ¦ 266 ¦ Mixed ¦ >2 ¦ 45 ¦ ¦Hohl ¦ 1974 ¦ 146 ¦ Mixed ¦ >5 ¦ 43 ¦ ¦Ellertsson ¦ 1978 ¦ 100 ¦ Rear ¦ 1.5 ¦ 12 ¦ ¦Norris, Watt ¦ 1983 ¦ 61 ¦ Rear ¦ 2 ¦ 44-90 ¦ ¦Ebbs et al. ¦ 1986 ¦ 137 ¦ Mixed ¦ 1 ¦ 26 ¦ ¦Deans et al. ¦ 1987 ¦ 137 ¦ Mixed ¦ 1 ¦ 26 ¦ ¦Miles et al. ¦ 1988 ¦ 73 ¦ Mixed ¦ 2 ¦ 29 ¦ ¦Maimaris ¦ 1988 ¦ 102 ¦ Mixed ¦ 2 ¦ 34 ¦ ¦McKinney ¦ 1989 ¦ 167 ¦ Mixed ¦ 2 ¦ 23-46 ¦ ¦Pearce ¦ 1989 ¦ 100 ¦ Mixed ¦ 1 ¦ 15 ¦ ¦Hodgson ¦ 1989 ¦ 40 ¦ Mixed ¦ 10-15 ¦ 14-62 ¦ ¦Hildingsson ¦ 1990 ¦ 93 ¦ Mixed ¦ 2 ¦ 58 ¦ ¦Olsson et al.¦ 1990 ¦ 33 ¦ Rear ¦ 1 ¦ 41 ¦ ¦Pennie ¦ 1990 ¦ 135 ¦ Mixed ¦ 0.5 ¦ 13 ¦ ¦Gargan and Bannister¦ 43 ¦ Mixed ¦ 10.8 ¦ 88 ¦ ¦Watkinson ¦ 1991 ¦ 35 ¦ Rear ¦ 10.8 ¦ 86 ¦ ¦Kischka et al¦ 1991 ¦ 52 ¦ Mixed ¦ >2 ¦ 44; 61 ¦ ¦Radanov et al¦ 1991 ¦ 78 ¦ Mixed ¦ 0.5 ¦ 27 ¦ ¦Ettlin et al.¦1992 ¦ 21 ¦ Mixed ¦ 2 ¦ 35; 41 ¦ ¦Parmar et al.¦ 1993 ¦ 100 ¦ Rear ¦ 8 ¦ 55 ¦ ¦Robinson ¦ 1993 ¦ 21 ¦ ? ¦ 10-19 ¦ 86 ¦ ¦Hildingsson ¦ 1993 ¦ 38 ¦ Mixed ¦ >1 ¦ 45; 34 ¦ ¦Radanov et al¦ 1993 ¦ 97 ¦ Mixed ¦ 0.5 ¦ 27 ¦ ¦Radanov et al¦ 1993 ¦ 98 ¦ Mixed ¦ 0.5 ¦ 32 ¦ ¦Ono & Kano ¦ 1993 ¦ ? ¦ Mixed ¦ ? ¦ 15-20 ¦ ¦Gargan et al.¦ 1994 ¦ 50 ¦ Rear ¦ 2 ¦ 62 ¦ ¦Ryan et al. ¦ 1994 ¦ 29 ¦ Mixed ¦ 0.5 ¦ 66 ¦ ¦Jónsson et al¦ 1994 ¦ 50 ¦ Mixed ¦ 5 ¦ 32 ¦ ¦Radanov et al¦ 1994 ¦ 117 ¦ Mixed ¦ 1 ¦ 24 ¦ ¦Di Stefano ¦ 1995 ¦ 117 ¦ Mixed ¦ 2 ¦ 18 ¦ ¦Spitzer et al¦ 1995 ¦ 3014¦ Mixed ¦ 6 ¦ ? ¦ ¦Borchgrevink ¦ 1996 ¦ 345 ¦ Rear ¦ >2.5 ¦ 58 ¦ ¦Mayou, Bryant¦ 1996 ¦ 57 ¦ Mixed ¦ 1 ¦ 49 ¦ ¦Squires et al¦ 1996 ¦ 40 ¦ Rear ¦ 15.5 ¦ 70 ¦ ¦Pettersson ¦ 1997 ¦ 39 ¦ Mixed ¦ 2 ¦ 15/44 ¦ ¦Karsborg ¦ 1997 ¦ 39 ¦ Mixed ¦ 0.6 ¦ 71 ¦ ¦Gargan et al.¦ 1997 ¦ 52 ¦ Rear ¦ 2 ¦ 64 ¦ ¦Voyvodic ¦ 1997 ¦ 29 ¦ ? ¦ 0.5 ¦ 62 ¦ ¦Borchgrevink ¦ 1997 ¦ 88 ¦ Mixed ¦ 1 ¦ 28 ¦ ¦Borchgrevink ¦ 1998 ¦ 201 ¦ Mixed ¦ 0.5 ¦ 41-66 ¦
(Adapted from AC Croft, Spine Research Institute of San Diego)
For the most part, studies which did not follow patients for at least one year were excluded from Table 1 as were those providing insufficient data to allow meaningful comparison with other studies. A few exceptions were made based on the relatively high quality of the research. Some of the shortcomings of this work were discussed earlier. Since the selection criteria and outcome measures used by these authors varied from one study to the next, and often were not described in detail, we cannot compare the results in more than a general sense. As noted earlier, the range in outcomes from best (12% still symptomatic) to worst (86% still symptomatic) covers a considerable scale and is most likely attributable to variations in study design and outcome measure. For example, a researcher may decide that patients with only minimal symptoms occurring on an infrequent basis are resolved, while another may include any patient with symptoms, no matter how trivial or infrequent, as still symptomatic.
This part of the study design is rarely described. In general terms, the average of the proportions of patients who are still symptomatic at follow-up in the mixed group studies is about 35%, while for those of the rear impact only groups it is about 55%.
Another important distinction to make is that the patients that remained symptomatic were, in some cases, totally disabled with pain, whereas others complained of only occasional bothersome pain. Most of the recent reports give statistics for disability, as well as symptoms. Many earlier reports did not. It should also be noted that some degree of selection bias exists in nearly all of these studies. Some patient data was obtained from IME doctors' files, which probably selects a more severe set of patients. In other studies, a small number of patients were not injured at all, and should not have been included in an outcome study of injured persons. Still in others, consecutive patients visiting an emergency room were recruited for the study. It is possible that many of these patients were visiting the ER merely at the suggestion of police or family. This may be the most common design flaw in this genre of study, and many of the studies in this series used this design, probably out of convenience.
However, as pointed out by Dolinis (467), who conducted a longitudinal (i.e., prospective) study, only three of 254 injured drivers had been seen at an ER department. This clearly suggests that these ER patients may not be representative of the majority of CAD victims, although we can only speculate as to what important ways they might be different.
Finally, it is important to remember that, for the most part, all of the people in these studies did suffer an acute whiplash. But we know that only about half of those persons exposed to trauma will be injured, so it would clearly be inappropriate to say that 35-55% of persons in these crashes will remain symptomatic.
Barry and Jenner conclude that "psychological disturbance is often seen in such people, who seem to have coped poorly with their injuries and only slowly revert to their previous level of functioning"... this "syndrome is related to a number of factors including the stress of having been involved in an accident, frustration at the lack of improvement despite reassurance and treatment, and resentment at prolonged suffering through no fault of their own".
Actually, if Barry and Jenner had done their homework, they would also know that chronic "psychological disturbance" is SIMPLY due to CHRONIC PAIN AND TRAUMATIC BRAIN INJURY, MILD TO SEVERE. And to say that these victims have "coped poorly" is a bastardization of the truth. Coping with the day-to-day activities of daily living, in spite of great pain, and, I would now have to add, in spite of colossal misunderstanding by rheumatologists (if Barry and Jenner are representative of the field) of their condition, is TRULY COPING WELL. It is Barry and Jenner who are coping poorly with the available knowledge.
Bogduk, Lord, Barnesley and many others have located the lesions found in whiplash responsible for chronic pain, and among others, include the cervical facets (zygophaseal or z-joints), which are responsible for posterior element instability and chronic pain. Damage to the spinal ligaments, such as to the facets, posterior longitudinal ligaments, ligamentum nuchae, ligamentum flavum and interspinous ligaments are responsible for GREAT PAIN in these patients. These are lesions which are not visible on MRI, or static cross-table x-rays so often mis-read in the ER. The University of Minnesota has looked at need for flexion-extension films (motion studies) after whiplash and has concluded that if loss of cervical curve or reversal of the cervical lordosis is present, flexion- extension x-rays MUST be taken to rule out anterior and posterior listhesis (i.e., partial dislocations). Often these films are POSITIVE, but ER doctors and rheumatologists fail to use them. This is clinically illiterate.
Partial dislocations (subluxations, in the medical sense), are common after whiplash, provide hard evidence that the posterior (and often anterior) ligamentous elements have been badly damaged, explain the so- called "bizarre" pain distribution patterns in the upper extremities, head and scapular regions, and are responsible for much of the chronic pain that Ferrari and Russell have branded "part of our whiplash culture", most unfortunately.
If Ferrari really had a handle on whiplash, why has most of his junk science been refuted by almost every whiplash researcher in the past ten years? But he is routinely published in the rheumatology literature (another bad sign). read Freeman and Croft's critique in SPINE (1999) regarding the literature refuting whiplash, it is very good science, unlike the nonsense published by Ferrari and now Barry and Jenner.
But I digress. Pain from ligaments damaged in whiplash is NOT dermatomal unless the nerve roots are involved with disc (and other) injury. However, in our disc-obsessed culture, we just can't seem to accept the idea of referred, or for want of a better term, scleratogenous pain. Referred pain is VERY REAL to its sufferers, and is accepted very well in other branches of medicine. And it should be in whiplash, especially since we have hard evidence on flexion-extension radiographs, referred pain patterns now mapped out in the cervical spine (see Feinstein, Bogduk and others), all of which corresponds to and fits with the most recent crash tests (Ono, Kaneoka, Panjabi, Brault, Siegmund, Cholewicki, etc.).
Persons are often brain-injured in low-speed collisions, most often when there is LITTLE OR NO DAMAGE TO THE VEHICLE. Is it true that MD's pretty much have forgotten their physics? There is a big difference between plastic vs. elastic collisions, and therein lies the big secret to understanding injury mechanisms in low-speed crashes. MTBI is also responsible for cognitive defects and personality changes after whiplash. It is certainly not for the silly reasons suggested by these two authors.
And, let me say that there is absolutely NO EVIDENCE IN THE LITERATURE to suggest that a "litigation neurosis" exists. There is NO relationship between litigation and chronic pain, except that persons WITH chronic pain are suing more than persons without chronic pain. However, just as many non-litigants as litigants have chronic pain (see Khan S, Cook J, Gargan M, Bannister G. A symptomatic classification of whiplash injury and the implications for treatment. Journal of Orthopaedic Medicine 1999;21(1):22-25).
Finally, be sure to refer to your local chiropractic physician for whiplash cases. It is the only proven effective treatment for chronic whiplash (see Woodward MN, Cook JCH, Gargan MF, Bannister GC. Chiropractic treatment of chronic whiplash injuries. Injury 1996;27:643-645. See more importantly Khan S, Cook J, Gargan M, Bannister G. A symptomatic classification of whiplash injury and the implications for treatment. Journal of Orthopaedic Medicine 1999;21(1):22-25).
Recent Crash Test References
Ono K, Kaneoka K, Wittek A, Kajzer J: Cervical injury mechanism based on the analysis of human cervical vertebral motion and head-neck-torso kinematics during low speed rear impacts. 41st Stapp Car Crash Conference Proceedings. SAE paper 973340, 339-356, 1997. Szabo TJ, Welcher JB: Human subject kinematics and electromyographic activity during low speed rear impacts. SAE paper 962432, 339-356, 1996. Szabo TJ, Welcher JB, Haight WR: Analysis of low speed collisions. Texas Engineering Extension Service, Texas A&M University, 2:2, 1998. Brault JR, Wheeler JB, Siegmund GP, Brault EJ: Clinical response of human subjects to rear-end automobile collisions. Archives of Physical Medicine & Rehabilitation 79:72-80, 1998. van den Kroonenberg A, Philippens H, Cappon J, Wismans J, Hell W, Langweider K: Human head-neck response during low-speed rear end impacts. Proceedings of the 42nd Stapp Car Crash Conference, SAE 983157, 207-221, 1998. Dolinis J: Risk factors for 'whiplash' in drivers: a cohort study of rear- end traffic crashes. Injury 28(3):173-179, 1997. Panjabi MM, Cholewicki J, Nibu K, Grauer JN, Babat LB, Dvorak J: Mechanism of whiplash injury. Clinical Biomechanics 13:239-249, 1998. Siegmund GP, King DJ, Lawrence JM, Wheeler JB, Brault JR, Smith TA: Head/neck kinematic response of human subjects in low-speed rear-end collisions. SAE Technical Paper 973341, 357-385, 1997. Grauer JN, Panjabi MM, Cholewicki J, Nibu K, Dvorak J: Whiplash produces an s-shaped curvature of the neck with hyperextension at lower levels. Spine 22(21):2489-2494, 1997. Panjabi MM, Cholewicki J, Nibu K, Babat LB, Dvorak J: Simulation of whiplash trauma using whole cervical spine specimens. Spine 23:17-24, 1998. Cholewicki J, Panjabi MM, Nibu K, Babat LB, Grauer JN, Dvorak J: Head kinematics during in vitro whiplash simulation. Accid Anal and Prev 30(4):469-479, 1998. Panjabi MM, Cholewicki J, Nibu K, Grauer J, Vahldiek M: Capsular ligament stretches during in vitro whiplash simulations. Journal of Spinal Disorders 11:227-232, 1998. Freeman MD, Croft AC, Rossignol AM: Chronic neck pain and whiplash: a case -control study of the relationship between acute whiplash injuries and chronic neck pain. Submitted. Freeman MD, Croft AC, Rossignol AM, Weaver DS, Reiser M: A review and methodologic critique of the literature refuting whiplash syndrome. Spine 24(1):86-98, 1999.
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Gregory T. Wright, D.C. Team Physician Cape Cod League Baseball Harwich Mariners
Tour Physician Winning Medicine International NBC Sports Gravity Games
Tour Physician AVP Professional Beach Volleyball U.S. National Tour
Physician Instructor Back Power Program National Safety Council
Harwich, Massachusetts April 15, 2000
Competing interests: single and multiple cranial nerve palsies peripheral neuropathy dizziness and otoneurologic disorders thoracic outlet syndrome oculomotor and other visual disturbances posttraumatic stress disorder herniation of cervical discs; rupture of ligaments and adjacent tissues rim lesions (disc-bone interface) spinal cord injury retropharyngeal hematoma damage to subarachnoid space mediastinitis TMJ injury, disruption hypopharyngeal, tracheal, or esophageal perforation brain injury hypothalamic-pituitary-thyroid axis disorder damage to posterior cervical sympathetic nerves menstrual disorders tremor and movement disorders occipital neuralgia cervical dystonia
It is clear that the first photograph in Barry and Jenner's article
represents anything but a "normal" cervical lordosis, as subtle a change
as exists. Almost any physician I know would look at this photograph and
immediately see an anterior weight-bearing cervical spine and head (a
vertical line drawn inferiorly from the auditory canal falls several cm
anterior to the center of the glenohumeral mid-line).
I would begin with the suspicion that this photo actually represents
a woman with a history of cervical spine trauma, and I would ask the
appropriate questions in the clinical history. If plain film radiography
was indicated in her condition, it would definitely NOT surprise me if
this woman did indeed have loss or reversal of the cervical lordosis,
especially reversal in the lower cervical spine (C4-T1), in spite of a
lordotic curvature in the upper cervical spine.
This appears to be a most inappropriate photograph to describe as
"normal". If, in fact, a lower cervical reversal exists, that sharp
reversal would me most significantly ABNORMAL.
Really bad choice with which to start.
Grgeory T. Wright, D.C.
Competing interests: No competing interests