(Pain is an unpleasant sensation; nociception). Mechanical Neck pain usually is a response to joint or soft tissue overload. The most mobile joint in the neck(Cervical spine) is the C1/C2 joint.(Atlas/Axis).  This joint supplies 50% of global rotation of the neck.  50% of Flexion and Extension(forward/backward motion) is supposed to occur at the C0/C1 joint, the Occiput(base of skull) and first vertebra(C1). Because this joint is next to the most mobile joint in the neck it has a tendency to become lazy and restricted or fixated.                                                                                                                                       

Most individuals demonstrate restriction at the Transition zones. The transition zones are regions where Mechanical function changes  dramatically. The Second Transition zone is where the rib cage attaches at the base of the neck. C7/T1/1st rib.  The neck joints/segments in the middle of the neck  tend to become Hyper-mobile (Too much mobility at the C4/5, C5/6. C6/7 Motion Segments). These are the areas where we see Osteoarthritic changes(Lipping and Spurring on X-ray). It is important when getting adjustments to the Cervical spine to have the correct joints Adjusted. Most of the time we start with adjustments to the two transition zones mentioned above. Once mobility to the Transition Zones are restored the cause of the pain and nerve root irritation is eliminated. Adjusting the hypermobile joints will not get long term results and will often increase the pain.               EMAIL QUESTIONS TO Doctorrazz@sc.rr.com

Examples of a typical hypermobile mid-cervical spine in Digital Motion Video of the cervical Spine can be found at.

http://www.dmxworks.com/html/pop/video/imagevid1b.html

http://www.dmxworks.com/html/pop/video/imagevid2b.html

The Scalene Triangle &  elevation of the first Rib can cause nerve impingement & Vascular impingement

Arterial Compression of the Subclavian artery

Here is a great video Look at Cervical neck pain and Chiropractic Care .

http://www.viddler.com/explore/drdebbie/videos/5/111.811/

Bone spurs, also called osteophytes, are an enlargement of the normal bone structure that protrude into your spine (and in other areas of your body). Bone spurs do not actually create a point but they are smooth structures formed and pulled over time by muscle spasms. Muscle spasms are a protective mechanism in your body to prevent further injury from any number of causes (see below).

FREE - Chiropractic  REVIEW AND SECOND OPINION

Over time, the tendons (that hold muscle to bone) and ligaments (that hold bone to bone) can actually start pulling the bone from where it should be, creating bone spurs. Bones will conform to any pressure applied to them. As these bone spurs grow and form, they will sometimes impinge on a nerve causing the pain and debilitating symptoms.

Bone spurs that form along the spinal column of your neck or back can lead to nerve impingement causing severe pain, restricted movement, radiating arm and leg pain, weakness in the extremities, numbness and, in some cases, disability.

Prevention of bone Spurs:   Early intervention and Good Chiropractic care, Adjusting the Transition Zones above and below the hypermobile mid-cervical spine can prevent the bone spurs from occurring, or after the process has begun, we can slow down and minimize the damage and changes.

Pinched nerves in the cervical region:

Pinched nerve at C5 - This can cause shoulder pain, deltoid weakness, and possibly a small area of numbness in the shoulder. On physical exam, a patient's biceps reflex may be diminished. Dorsal Scapular nerve Pain  is very Common

Pinched nerve at C6 - This can cause weakness in the biceps and wrist extensors, and pain/numbness that runs down the arm to the thumb. On physical exam, the brachioradialis reflex (mid-forearm) may be diminished.

Pinched nerve at C7 - This can cause pain/numbness that runs down the arm to the middle finger. On physical exam, the triceps reflex may be diminished.

Pinched nerve at C8 - This can cause hand dysfunction (this nerve supplies innervation to the small muscles of the hand). Pain/numbness can run to the outside of the hand (little finger) and impair its reflex.

Most painful shoulder syndromes have a AC joint component. If the AC joint is restricted, the rotator cuff muscles(SITS muscles) will impinge on horizontal abduction.  Release of the AC joint will get rid of this impingement.

Risk of Vertebrobasilar Stroke and Chiropractic Care

Results of a Population-Based Case-Control and Case-Crossover Study

J. David Cassidy, DC, PhD, DrMedSc,*†‡ Eleanor Boyle, PhD,* Pierre Coˆte´, DC, PhD,*†‡§

Yaohua He, MD, PhD,* Sheilah Hogg-Johnson, PhD,†§ Frank L. Silver, MD, FRCPC,¶

and Susan J. Bondy, PhD†

 

Study Design. Population-based, case-control and case-crossover study.Objective. To investigate associations between chiropractic

visits and vertebrobasilar artery (VBA) stroke and to contrast this with primary care physician (PCP) visits and VBA stroke.Summary of Background Data.

Chiropractic care is popular for neck pain and headache, but may increase the risk for VBA dissection and stroke. Neck pain and headache

are common symptoms of VBA dissection, which commonly precedes VBA stroke.Methods. Cases included eligible incident VBA

strokes admitted to Ontario hospitals from April 1, 1993 to March 31, 2002. Four controls were age and gender matched to each case. Case and control

exposures to chiropractors and PCPs were determined from health billing records in the year before the stroke date. In the case-crossover analysis, cases acted as

their own controls.

Results. There were 818 VBA strokes hospitalized in a population of more than 100 million person-years. In those aged 45 years, cases were about three times

more likely to see a chiropractor or a PCP before their stroke than controls. Results were similar in the case control and case crossover analyses. There was no

increased association between chiropractic visits and VBA stroke in those older than 45 years. Positive associations were found between PCP visits and VBA

stroke in all age groups. Practitioner visits billed for headache and neck complaints were highly associated with subsequent VBA stroke.Conclusion. VBA stroke is

a very rare event in the population. The increased risks of VBA stroke associated with chiropractic and PCP visits is likely due to patients

with headache and neck pain from VBA dissection seeking care before their stroke. We found no evidence of excess risk of VBA stroke associated chiropractic

care compared to primary care.Key words: vertebrobasilar stroke, case control studies, case crossover studies, chiropractic, primary care,

complications, neck pain. Spine 2008;33:S176–S183

Understanding Pain:

An overview of pain.  Keith Charlton   06.06.06

I apologise if what follows is old hat familiar stuff, especially for students for whom it probably is not news. I did need to review pain neurobiology myself, however and enjoyed doing it. (I did my DC back in the days of steam radio). Much of what follows is modified from Nik Bogduk’s chapter 1.1 in the textbook “Integrated Basic Surgical Sciences” ISBN 0 340 700912, with added bits from elsewhere. Nik has a gift for explanatory power that is quite astonishing!

The IASP definition is instructive: “Pain is an unpleasant sensory and emotional experience, associated with actual or potential tissue damage or described in terms of such damage.” The second clause reveals that we cannot always find a tissue damage cause for pain, but that does not mean the individual is not suffering. When elaborated in terms of the physiological mechanisms involved, this definition allows pain to be classified as nociceptive, neurogenic (neuropathic) or psychogenic.

Nociceptive pain is the archetypal mechanism where the experience of pain is evoked by damage to somatic or visceral tissues (a pin prick to the skin is a good example here). Notably, my copy of the late Sir Sydney Sunderland’s huge tome “Nerves and Nerve Injuries” (he was Prof of Neurology at U Melbourne) from the eighties does not even mention the term nociception! Nociceptive pain may be felt locally or referred. Neurogenic pain is different: it arises not from peripheral stimulation, but from abnormal activity in nerves that would otherwise be transmitting nociceptive pain. Psychogenic pain is thought to arise from influences in the subject’s mind, such as memory and association with past stressful events (it technically includes malingering).

We are endowed with nerves designed to detect tissue damage, but they do not transmit pain….. they transmit info about noxious stimuli. It may evoke pain when the message gets to the cortex, but not unless and until it does so will the person experience pain. Importantly for understanding pain generation is the understanding that four key processes are involved in nociception:

1.transduction

2.peripheral transmission

3.central transmission

4.modulation.

1. Transduction:

Tissue damage is detected by free nerve endings distributed throughout the external epithelial tissues of the body (skin etc), and all fibrous connective tissues, including skeletal and smooth muscle. These nociceptive nerve endings are absent from the parenchyma of solid viscera, but are present in their capsules. They are absent from the serosa of hollow viscera but are present under the epithelium and in the muscularis.

I won’t get into the chemistry much (too much to cover in overview, and it may be enough to comment on events in the first nociceptive synapse with neurotransmitters … mostly glutamate … and receptors like amino-hydroxy-methylisoxazole-propionic acid receptor … known by its Mum as AMPA, and N-methyl, D-aspartate known as NMDA … see you didn’t want to know anyway).

Free nerve ending nociceptors can be stimulated either chemically or mechanically. Most common algogenic (pain-producing) chemicals are hydrogen and potassium ions, bradykinins and serotonin, the guys released by damaged cells or produced by the inflammatory response to tissue damage, surprise surprise! The mechanism of mechanical nociception is poorly understood. It occurs whenever collagenous tissues are stretched, like with rapid expansion of the capsules of solid viscera, stretching of periosteum by underlying blood, infection or tumour, and strain in ligaments or joint capsules and tendons in biomechanical disorders of the musculoskeletal system. It thus seems reasonable to infer that transduction here involves compression of free nerve endings woven into the lattice-work of collagen in these tissues as it is deformed under tension.

2. Peripheral Transmission:

As I have said, there are no specialised pain fibres in the human body … no specifically and uniquely nociceptive nerves. All nociception is mediated by nerves that subserve other functions (almost as if contributing to the pain generation activity was a moonlighting job for them!). There are several types of nerve fibres, with differing diameters and conduction rates.  All involved in nociception are either C fibres, or A delta fibres, some of the latter of which normally mediate mechanical sensations at low intensity of stimulation, but evoke pain at higher intensity. In humans, all C fibres are polymodal in that they respond to all of mechanical, thermal and chemical stimuli to provide nociceptive stimulus. Both C fibres and some A delta fibres that normally mediate temperature sensation can evoke pain when the stimulus reaches 45 degrees Celsius. There is much more to say about this interesting aspect of neurobiology, but not here.

Most nociceptive afferents enter the spinal cord through dorsal roots, although some take a peculiar circuitous route through ventral roots, but they do not immediately enter the grey matter, but are first distributed rostrally and caudally along the cord in the dorsolateral tract. From here, multiple collaterals from each individual nociceptive afferent enter the dorsal column of grey matter. Thus, any one nociceptive afferent will ramify in the dorsal horns of segments anywhere between one to three levels rostral and caudal to the segment of entry.

Nociceptive afferents ramify in Rexed’s Laminae I, II and V of the dorsal horn. Here they make many differing connections with inter-neurons and second order neurons in the grey matter, again beyond what I wish to include here. It’s a good time to ask why a synapse is needed in a place like this, if simple transmission of information is all that is needed. Why would you (God?) interrupt a perfectly good wire with a junction? The ubiquity of synapses in the nervous system results from the need for control, or modulation. In the nociceptive system, the junction between peripheral afferents and second order transmission neurons in the dorsal horn is the first site of such control.

3. Central Transmission:

Resident in the dorsal horn are large, so-called “marginal” neurons (MNs) in Lamina I, which are nociceptive only, and transmit only nociceptive information they get from nociceptive afferents. In Lamina V of the dorsal horn are other large neurons, known as “wide dynamic range” (WDRs) because they code for pressure and touch as well as nociception. There is, again, more than this to know, but not for this time. It’s just important to realise that this is all for more capacity for control.

The axons of the MNs and WDRs leave the grey matter and mainly cross the midline of the cord in the anterior white commissure to form the anterolateral funiculus (a few ascend in ipsilateral pathways). The ALF is what used to be known as the anterior and lateral spinothalamic tracts (new research shows no basis for functional separation of these tracts). Axons of WDRs are dispersed throughout these regions, and that is why touch and nociception are conveyed by both pathways.

Ascending axons have two destinations. Those of the neo(new)spinothalamic (follow the words) system relay to the ventral posterior lateral (VPL) and central lateral (CL) nuclei of the thalamus. From the VPL nucleus the info is conveyed to the parietal lobe, conveying the location of the origin of the stimulus. The CL nucleus projects through the reticular (from the Latin for net .. the Romans in the days of Big Juli … Caesar that is … used to call the Internet the Interretinaculum….. ;-) ) formation of the thalamus to the limbic system. This pathway gives emotional dimension to the stimulus … aversion and the like. Axons of the paleo(old)spinothalamic system relay to the reticular formation of the brainstem, mostly to the appallingly named nucleus reticularis gigantocellularis  (NRGC), where they are joined by collaterals from the neo system. Significance? Ascending projections from the reticular formation reinforce the aversive effects of the CL nucleus and local projections activate modulating influences (via synapses, of course).

4. Modulation:

This is where a lot of the foregoing comes together. Various nuclei in the brainstem exert tonic inhibitory effects on the spinal cord by preventing the cord and CNS being overloaded with too much traffic (sensory info). By modulating this inhibition, the CNS can accept and even amplify the information in which it is interested, and suppress the noise which might otherwise compete for attention and impair the clarity of the message to which the CNS wants to listen. It’s like an old AM radio not quite on the station because the dial is not where it should be… the news is unclear, and much of the actual sound is drowned out by static. Noxious stimuli are obviously messages in which the CNS should be interested, so when it receives nociceptive information, it can modulate descending inhibition to enhance the clarity of the prime message.

Ascending nociceptive axons activate the NRGC which activates the nucleus raphe magnus (NRM), the periaqueductal grey matter (PAG … Latin for ‘around the aqueduct, or water channel’), and other sites such as the locus coeruleus and the lateral medullary reticular formation (LMRF). From these sites, neurons descend into the spinal cord where they exert inhibitory effects on ascending traffic. This negative feedback produces what is known as centre-surround inhibition. BUT the inhibition is not at the segment through which the nociception is being conveyed but at the adjacent segments (maybe like funny-named traffic cops  ... NRM, LMRF etc controlling speeds and kind of vehicle that gets through the road block, so that the ambulance, the vehicle we want unhindered, can get through faster and safer?). Centre-surround inhibition thus enhances the signal-to-noise ratio.

Referred Pain

Referred pain is felt elsewhere than the location innervated by the nerves which are the actual source of the pain. Bogduk makes the interesting point that referred pain is the norm and local pain the exception! The nociceptive system is poorly organized somato-topically. There is usually poor correlation between the sites of stimulation and the neurons transmitting the stimulus in the CNS, particularly for pain from deep tissues. 

Deep pain is sensed over a wide area with poorly defined borders, but centred over a particular region. It makes sense (or maybe it doesn’t… what do you think?) for an animal (like a human) to know that it suffers from deep pain, but no point teleologically in its knowing the precise location because there is stuff all it can do about it. One cannot escape the pain of renal lithiasis, or angina. No point in cluttering the CNS with all that extra wiring. All one needs to know is that the limb hurts, not whether it is precisely the knee or the thigh: the limb needs rest. That contrasts with pain on the surface of the body, in which you can learn to stay away from fire because of your burn, or you can remove the thorn from your foot or the arrow from your arm, so thoughtlessly planted there by a hostile neighbour!

This should make clear the difference between local pain and referred pain: it’s not a special mechanism difference, just a difference between cutaneous pain and deep pain. Deep pain is misread as referred pain. Note that when one attempts to elicit a more precise diagnosis in, say, right upper quadrant abdominal pain with deep palpation, one is adding to the sensory input and the perceptions are of both deep and cutaneous inputs! The surface of the body is being touched and the parietal lobe can process more accurately the localizing of the pain source.

Neurogenic Pain

This is an important topic to grasp, as most pain chiropractors see is not nociceptive, but neuropathic, or neurogenic. The nociceptive system is designed, as we have seen, to detect damage in peripheral tissues. BUT damage to the nerves of the nociceptive system also evokes pain perception. The messenger suffers damage, not just the message of damage from somewhere else (if that helps … maybe not….). Instead of the pain arising from the tissues in which it’s perceived it’s evoked from nerves innervating these regions. Nociceptive activity arising from the axons of peripheral nerves is called neuropathic pain, which means pain due to a disorder of a nerve (peripheral). Pain from the CNS is called central pain, in order to ensure that sources lie in the CNS and not the periphery.

Neuropathic pain can be caused by a peripheral neuropathy such as diabetes, post-herpetic neuralgia and neuroma (these mechanisms are poorly understood yet: hypotheses include ectopic discharge from the damage site, or loss of inhibition in the spinal cord). Pain from neuromata is better understood. When a nerve is transected, axons sprouts emerge within hours and attempt to regenerate the nerve. If they fail to connect with the distal stump of the rest of the nerve, they form a tangle which is the neuroma. They are exquisitely sensitive to mechanical stimulation and to circulating noradrenalin and become spontaneously active, being massively aggravated by touch. It hurts!

Central pain happens with 2nd or 3rd order neurons in the nociceptive system become spontaneously active, most typically when they lose their accustomed afferent input, hence the term deafferentation (a synonym for central pain). Most common examples are brachial plexus avulsion, chronic post-herpetic neuralgia and spinal cord injury pain. Rarer is thalamic pain from infarction of cells that inhibit nociceptive thalamic nuclei. When deafferented, CNS neurons undergo membrane alteration such that the neuron throws a tantrum since nobody will talk to it anymore (it thinks), and it no longer maintains the apparatus to listen. The nerve cell fails to manufacture receptors, its membrane becomes unstable and the cell discharges impulses spontaneously. The pain is felt in the region that is denervated, paradoxically. This explains why if one has chronic or severe pain that one cannot ask a surgeon just to cut the nerve to relieve the pain. The result is neurological chaos, and usually worsening of the pain, perhaps permanently. Other invasive approaches like radiofrequency neurotomy (heat coagulating the nerve) avoid deafferentation, and in the neck, is the only really proven (so far!!) relief for chronic neck pain.

Psychogenic Pain

There are no diagnostic criteria for this, as it is really only a concept, not a diagnosis. It is real. Remember that 50 years ago, psychiatry texts listed ulcerative colitis and rheumatoid arthritis as psychosomatic disorders. Fewer than 20 years ago, the pain of spinal cord injury was called psychogenic, and only 15 years ago, peptic ulcer was caused by stress!

Summary

If we consider the four components of nociceptive pain generation, then, the sequence of interventions at each stage might look something like this:

1.Initiating disease or injurytreat the disease or allow healing

2.Transduction          corticosteroids, NSAIDs

3.Peripheral Transmission           local anaesthetic blocks, cryo or RF neurotomy

4.Central Transmission              spinal cord stimulation, spinal opioids

5.Modulation          parenteral opioids, TCAs, acupuncture, etc

6.Perception of pain

I now invite rumination on where spinal manipulation might play a role (I dunno, but I suspect we release endorphins which might function at the Central Transmission level, or Modulation, but it must be said we may be helping at initiation or transduction). Over to some thinkin’ on that.

Pain killing drugs, including local anaesthetics, are not curative. The analgesic potency of NSAIDs derives not from any capacity to inhibit prostaglandins, but more likely operates in the CNS. They have no peripheral action on mechanical nociception and offer no greater analgesic potency than paracetamol (acetaminophen) in chronic musculoskeletal disorders. A series of coagulating or cryo blocks can be used after fracture or post-surgically while natural healing occurs. Some use transcutaneous electrical nerve stimulation (TENS) for pain control, but this works beyond placebo only when the electrodes can be interposed between the pain generator and the CNS, for instance in a limb. For back pain and obstetric pain, it simply does not work. TENS appears to produce analgesia by stimulating large diameter afferents which inhibit small diameter nociceptive afferents.

Most medical techniques of pain management interfere in some way with descending modulation of nociception. Low dose opioids, oral or injected, act by a peculiar effect on descending inhibition, not blocking nociception but by reducing tonic descending inhibition, which impairs centre-surround inhibition and decreases the signal-to-noise ratio of nociception. The noxious stimulation is still present and bouncing around the CNS, but is obscured by surrounding noise. My personal experience with post-surgical and dental opioid use is that I still felt the pain, sort of, but didn’t give a stuff about it! Notably, opioids injected at high concentration (but low dose) into the epidural space behave quite differently: they exert a direct effect on the cord, where they mimic the inhibitory effect of enkephalin on primary afferents and 2nd order neurons, blocking nociception.

Tricyclic anti-depressants (TCAs) are thought to exert a similar effect by enhancing the inhibitory action of serotonin in the dorsal horn. Paracetamol (acetaminophen) sites of action are unknown, but seem to be in the CNS, not the periphery.

Acupuncture seems to work by diffuse noxious inhibitory control … the stimulus evokes widespread activation of descending inhibition to all segments of the spinal cord, reducing any ongoing nociceptive traffic. You might say that acupuncture works the same way as opioids, in reverse.

Spinal cord stimulation involves implantation of wires in the epidural space to stimulate ascending and descending tracts. It interferes with the transmission of nociception, perhaps by yielding a tingling feeling and by evoking descending inhibition.

Deep brain stimulation involves the implantation of electrodes under stereotactic control into the PGM and used to increase descending inhibition to all levels of the spinal cord. It’s heroic stuff, for serious pain from cancer and stroke unresponsive to other therapy.

Thankyou for thinking with me!

Keith Charlton

http://www.aafp.org/afp/980215ap/fongemie.html

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Home Page > News & Publications > Journals > American Family Physician® > Vol. 57/No. 4 (February 15, 1998)

Articles | Departments | Patient Information

Management of Shoulder Impingement Syndrome and Rotator Cuff Tears

ALLEN E. FONGEMIE, M.D., DANIEL D. BUSS, M.D.,
and SHARON J. ROLNICK, PH.D.
Minneapolis, Minnesota

Rotator cuff impingement syndrome and associated rotator cuff tears are commonly encountered shoulder problems. Symptoms include pain, weakness and loss of motion. Causes of impingement include acromioclavicular joint arthritis, calcified coracoacromial ligament, structural abnormalities of the acromion and weakness of the rotator cuff muscles. Conservative treatment (rest, ice packs, nonsteroidal anti-inflammatory drugs and physical therapy) is usually sufficient. Some patients benefit from steroid injection, and a few require surgery.

Anatomy

The rotator cuff comprises four muscles--the subscapularis, the supraspinatus, the infraspinatus and the teres minor--and their musculotendinous attachments. The subscapularis muscle is innervated by the subscapular nerve and originates on the scapula. It inserts on the lesser tuberosity of the humerus. The supraspinatus and infraspinatus are both innervated by the suprascapular nerve, originate in the scapula and insert on the greater tuberosity. The teres minor is innervated by the axillary nerve, originates on the scapula and inserts on the greater tuberosity. The subacromial space lies underneath the acromion, the coracoid process, the acromioclavicular joint and the coracoacromial ligament. A bursa in the subacromial space provides lubrication for the rotator cuff (Figure 1).

FIGURE 1. Anatomy of the shoulder and rotator cuff, showing (left) anterior and (right) posterior view.

Functional Anatomy
Understanding the functional anatomy of the rotator cuff assists in understanding its disorders. The rotator cuff is the dynamic stabilizer of the glenohumeral joint. The static stabilizers are the capsule and the labrum complex, including the glenohumeral ligaments. Although the rotator cuff muscles generate torque, they also depress the humeral head. The deltoid abducts the shoulder. Without an intact rotator cuff, particularly during the first 60 degrees of humeral elevation, the unopposed deltoid would cause cephalad migration of the humeral head, with resulting subacromial impingement of the rotator cuff.1 In patients with large rotator cuff tears, the humeral head is poorly depressed and can migrate cephalad during active elevation of the arm. This migration is sometimes evident even on plain radiographs.2

Etiology of Rotator Cuff Dysfunction

The space between the undersurface of the acromion and the superior aspect of the humeral head is called the impingement interval. This space is normally narrow and is maximally narrow when the arm is abducted. Any condition that further narrows this space can cause impingement. Impingement can result from extrinsic compression or from loss of competency of the rotator cuff. Possible causes of impingement are outlined in Table 1.

TABLE 1

Possible Causes of Shoulder Impingement

Outlet impingement

Subacromial spurs

Type 2 and type 3 acromions

Osteoarthritic spurs of acromioclavicular joint (includes subacromial spurs)

Thickened or calcified coracoacromial ligament

Nonoutlet impingement

Loss of rotator cuff causing superior migration of humerus (tear, loss of strength)

Secondary impingement from unstable shoulder

Acromial defects (os acromiale)

Anterior or posterior capsular contractures (adhesive capsulitis)

Thick subacromial bursa

Normal anatomic variants can cause compression. Three distinct types of acromion (Figure 2) can readily be seen on radiographs, especially on the angled outlet Y view. The type I acromion, which is flat, is the "normal" acromion. The type II acromion is more curved and downward dipping, and the type III acromion is hooked and downward dipping, obstructing the outlet for the supraspinatus tendon.3 Cadaveric studies have shown an increased incidence of rotator cuff tears in persons with type II and type III acromions.2,3

The coracoacromial ligament can also calcify, usually secondary to trauma, and cause impingement. In most cases, acromioclavicular joint arthritis is the culprit, resulting from previous trauma (separations) or, most often, nontraumatic osteoarthritis. The os acromiale (an unfused acromial apophysis) has also been associated with impingement.4

Impingement may occur as a result of loss of competency of the rotator cuff. Pain from any cause, such as overuse or injury, may lead to disuse or weakness of the cuff. The weakness results in cephalad migration of the humeral head due to loss of depressors. This superior migration of the humeral head increases the impingement, thus reinforcing the cycle.

Classification of the Impingement Syndrome

Several classification systems are used with the impingement syndrome. Neer5 divided impingement syndrome into three stages. Stage I involves edema and/or hemorrhage. This stage generally occurs in patients less than 25 years of age and is frequently associated with an overuse injury. Generally, at this stage the syndrome is reversible. Stage II is more advanced and tends to occur in patients 25 to 40 years of age. The pathologic changes that are now evident show fibrosis as well as irreversible tendon changes. Stage III generally occurs in patients over 50 years of age and frequently involves a tendon rupture or tear. Stage III is largely a process of attrition and the culmination of fibrosis and tendinosis that have been present for many years.

In testing for impingement, the physician moves the patient's shoulder passively while placing downward pressure on the acromion.

FIGURE 2. Lateral view of scapula, showing the three types of acromion.

History and Physical Examination

Pain, weakness and loss of motion are the most common symptoms reported. Pain is exacerbated by overhead or above-the-shoulder activities. A frequent complaint is night pain, often disturbing sleep, particularly when the patient lies on the affected shoulder. The onset of symptoms may be acute, following an injury, or insidious, particularly in older patients, where no specific injury occurs.

The key feature of the physical examination is an assessment for signs of impingement. All the impingement tests involve moving the shoulder passively (through forward flexion, internal and external rotation with the arm abducted 90 degrees, and adducted) with approximately 5 to 10 lb of force directed inferiorally on the acromion, thus narrowing the subacromial space. The examiner tests to see if pain appears with these maneuvers and disappears when the examiner removes the downward acromial push.6

The shoulder assessment in Figure 3 is a modification of a form developed by the Research Committee of the American Shoulder and Elbow Surgeons.7,8 Since the development of this form, studies on rotator cuff muscles show that the supraspinatus is more effectively tested with the thumb-up position (i.e., "full can") rather than the thumb-down position as shown in the form and that Gerber's lift-off test recruits the subscapularis better than forceful internal rotation does.9 (In Gerber's lift-off test [not depicted], the patient places the hand over the spine posteriorally at the belt line with the palm facing posteriorly. The patient is then instructed to "lift off" the hand in a posterior direction against resistance and this movement is compared with the contralateral arm.)

Range of motion

Impingement signs

Strength

1. Forward elevation (maximum arm-trunk angle)

6. Impingement I (passive forward elevation in slight internal rotation)

10. Forward flexion

2. Abduction (note classic painful arc)

7. Impingement II (passive abduction 90 degree external rotation)

11. External rotation (arm comfortably at side--teres minor/infraspinatus)

3. External rotation (arm comfortably at side)

8. Impingement III (passive abduction 90 degree internal rotation)

12. Internal rotation (arm comfortably at side--subscapularis)

4. External rotation (arm at 90 degree abduction)

9. Impingement IV (passive adduction: crossover)

13. Abduction--supraspinatus

5. Internal rotation (highest posterior anatomy reached with thumb)

FIGURE 3. Illustrations showing elements of a shoulder assessment. Also included on a shoulder assessment would be determination of acromioclavicular joint tenderness, supraspinatus/greater tuberosity tenderness, biceps tendon tenderness (using Speed's test), atrophy and crepitus. (In Speed's test, the arm is fully extended anteriorly, palm facing up. The examiner pushes down on the hand as the patient resists. Pain in the anterior shoulder is a positive test for biceps tendinitis.)

Diagnostic Testing

Plain radiographs can be useful in depicting anatomic variants or calcific deposits. They are specifically useful in ruling out calcific tendonitis and predisposing factors such as type III acromions or acromioclavicular joint arthritis. The three recommended views are the anteroposterior view with the arm at 30 degrees external rotation, the outlet Y view and the axillary view.10

Plain radiographs of the shoulder can be useful in depicting anatomic variations or calcific deposits.

The outlet Y view is useful because it shows the subacromial space and can differentiate the acromion processes. The axillary view is helpful in visualizing the acromion and the coracoid process, as well as coracoacromial ligament calcifications. The anteroposterior view is also excellent for assessing the glenohumeral joint, subacromial osteophytes and sclerosis of the greater tuberosity.

Ultrasonography and arthrography have been used when rotator cuff tears are suspected. However, arthrography is invasive and expensive. Magnetic resonance imaging, although expensive, provides the best imaging mode for rotator cuff pathology but, ultimately, arthroscopy is the best diagnostic modality.11

Differential Diagnosis

Many conditions can mimic impingement. Calcific tendinitis may occur in patients 30 to 50 years of age. The calcific deposit is usually in the supraspinatus tendon and can be very painful. Acromioclavicular arthritis can be a source of pain by itself, in addition to causing impingement. Radiographs show the degenerative changes. A subluxing or dislocating shoulder can be painful and cause impingement. Impingement or an injury can lead to adhesive capsulitis (frozen shoulder), a complication arising from pain and disuse. In this condition, the capsule of the joint becomes fibrosed. These disorders may present as shoulder pain and may also be associated with impingement. Table 2 presents a more complete synopsis of the differential diagnosis.

Treatment

In patients with stage I impingement, conservative treatment is often sufficient. Conservative treatment involves resting and stopping the offending activity. It may also involve prolonged physical therapy. Sport and job modifications may be beneficial. Nonsteroidal anti-inflammatory drugs (NSAIDS) and ice treatments can relieve pain. Ice packs applied for 20 minutes three times a day may help. A sling is never used, because adhesive capsulitis can result from immobilization.

TABLE 2

Causes of Shoulder Pain

Problem

Presentation

Laboratory/radiographic findings

Treatment

Impingement

Positive impingement signs, painful motion, night pain

Radiographs may be normal or may show outlet obstruction (spurs, type 2 or type 3 acromion), aided with lidocaine injection

NSAIDs, rehabilitation, subacromial steroid injection, subacromial decompression

Rotator cuff tear

Weakness, atrophy; end result of chronic impingement, frequently precipitated by injury

Radiographs may show decreased subacromial space, osteophytes; MRI shows tears

Rehabilitation, especially in older patients; surgery in younger patients

Biceps tendon rupture

Bulge in the distal humerus ("Popeye" muscle), usually precipitated by injury; weakness in the supinators (20% loss), weakness in the elbow flexors (8% loss)

Radiographs normal or same as in impingement

NSAIDs, rehabilitation, repair in younger patients for both strength and cosmesis (competitive body builders)

Acute calcific tendinitis

Severe acute shoulder pain, very painful, restricted motion, tenderness on greater tuberosity

Radiographs show calcific deposits

NSAIDs and analgesics, rehabilitation and analgesics, steroid injection (usually), arthroscopic decompression (sometimes)

Adhesive capsulitis (frozen shoulder)

Loss of active and passive range of motion, pain at extremes of patient's motion; usually secondary to pain from a previous shoulder problem

Same as in impingement, tears

NSAIDs, rehabilitation modalities; if no improvement after 18 months, manipulation under anesthesia; most patients respond to a dedicated rehabilitation program

AC arthritis

Pain, swelling at AC joint, usually associated with impingement

AC joint narrowing, hypertrophy, spurs

Ice, NSAIDs, steroid injections in AC joint (difficult injection); resect distal clavicle if conservative treatment does not work

Glenohumeral arthritis

Chronic pain, loss of motion, crepitus, disuse atrophy

Joint space narrowing, changes in humeral head

NSAIDs, physical therapy, total shoulder arthroplasty in advanced cases

Septic arthritis

Acute painful limited motion, fever, chills

Elevated white blood cell count, erythrocyte sedimentation rate, synovial fluid white blood cell count >100,000 per mm3 (10.0 3 10< per L), positive culture and Gram stain; early radiographs normal, later radiographs show erosive changes

Intravenous antibiotics, surgical irrigation

Rheumatoid arthritis

Usually multiple, small-joint, symmetric

Radiograph shows joint space narrowing, osteoporosis; rheumatoid factor, erythrocyte sedimentation rate

NSAIDs, DMARDs, steroid injection

Gout

Podagra, monoarthritis

Serum uric acid, crystals in joint fluid

Colchicine, NSAIDs, allopurinol (Purinol, Zyloprim), probenecid (Benemid, Benuryl)

Lyme disease

Tick bite, erythema migrans

Lyme titer, characteristic rash

Antibiotics

Lupus erythematosus

Multiple joints affected

Antinuclear antibody, erythrocyte sedimentation rate

NSAIDs, antimetabolites

Spondylo-arthropathy

Sacroiliac joint

HLA B27

NSAIDs

Avascular necrosis

Predisposing factors such as steroid use, trauma, alcoholism; frequently idiopathic; painful motion

Early radiographs normal; later radiographs show humeral head flattening; proceeds to degenerative arthritis

NSAIDs, physical therapy, hemi- or total shoulder arthroplasty

Cervical radiculopathy

Radiating pain below shoulder or to upper back, decreased and painful range of motion in neck, positive Spurling's test,* neurologic changes in arms, normal shoulder examination

Radiographs show degenerative changes in cervical spine; MRI may show compressive radiculopathy

NSAIDs, physical therapy, traction, surgical decompression

Tumor

Mass, history of smoking

Chest radiograph may show Pancoast's tumor

Surgery, chemotherapy

Thoracic outlet

Decreased pulses with provocative maneuvers

May require angiography

Surgery

NSAIDs=nonsteroidal anti-inflammatory drugs; AC=acromioclavicular; DMARDs=disease modifying antirheumatic drugs (including immunosupressants); MRI=magnetic resonance imaging.

*--Radicular pain reproduced with head compression.

Once the acute pain resolves, a specific strengthening program for the rotator cuff is recommended for prevention of future injuries. The motions of the rotator cuff that are emphasized for strengthening are internal rotation, external rotation and abduction. It is important to remember that the function of the rotator cuff, in addition to generating torque, is to stabilize the glenohumeral joint; thus, stronger rotator cuff muscles result in better glenohumeral joint stabilization and less impingement. A typical initial exercise program involves the use of 4 to 8 oz weights, with 10 to 40 repetitions performed three to five times a week.

Patients with stage II impingement may require a formal physical therapy program. Isometric stretches are useful in restoring range of motion. Isotonic (fixed-weight) exercises are preferable to variable weight exercises. Thus, the shoulder exercises should be done with a fixed weight rather than a variable weight such as a rubber band. Repetitions are emphasized, and a relatively light weight is used. Sometimes, sports-specific techniques are useful, particularly when strengthening the throwing motion, the serving motion or swimming motions. In addition, physical therapy modalities such as electrogalvanic stimulation, ultrasound treatment and transverse friction massages can also be helpful.

Therapeutic Injections
Therapeutic injections (lidocaine plus a corticosteroid) are useful both because they are therapeutic and also because they can help the physician differentiate impingement from other problems. Indications for therapeutic injections include the following:

Shoulder strengthening exercises should emphasize internal rotation, external rotation and abduction.

•Rotator cuff impingement that does not improve with conservative treatment, including NSAIDs and physical therapy.

•Older patients with clearly operable lesions, such as subacromial spurs, who are not good surgical candidates. Frequently, older, poor surgical candidates can be helped with periodic injections.

•As a diagnostic technique. If a patient fails to improve following a subacromial space injection and has normal radiographs with an ambiguous physical examination, the rotator cuff may not be the problem. Thus, after the injection, repeat impingement testing will verify the diagnosis if the pain is ameliorated.12-14

•For temporary pain relief in a patient with an operable lesion.

Although there are several entry points for shoulder injections, the posterior subacromial approach is perhaps the easiest (Figure 4). Furthermore, by angling the needle to the underside of the acromion, the physician can easily verify that the needle is properly positioned and, since the humeral head lies more anteriorally, there is no danger of hitting it. It is important not to inject directly into the tendon and, if resistance to flow is encountered, the needle should be directed away from the site. Some potential weakening of the tendon can occur with injection directly into the rotator cuff. We recommend using 8 to 9 mL of lidocaine (Xylocaine), 1 percent, mixed with 20 mg of triamcinolone (20 mg per mL) or a similar amount of methylprednisolone (Depo-Medrol), 20 mg per mL, or betamethasone (Celestone), 6 mg per mL. The large volume floods the rotator cuff surface. A 1.5-in, 22-gauge needle usually works well.

FIGURE 4. Injection technique, posterior subacromial approach.

Operative Treatment
Not all cuff tears diagnosed clinically, or by arthography or MRI require surgical repair. A rotator cuff tear is not, in itself, an indication for surgery.15,16 In fact, survey studies using MRI have shown a high incidence of unsuspected full or partial tears of the rotator cuff in asymptomatic adults.17,18 Most older patients with impingement and rotator cuff tears actually do well without surgery. However, surgery might be considered in a patient who has failed to improve after six months of conservative treatment or in a patient less than 60 years of age with a debilitating tear that impairs function.

Before the advent of arthroscopy, many of these procedures were done using the standard Neer procedure, which decompressed the rotator cuff by shaving the anterior 2 cm of the underside of the acromion through an open incision. The rotator cuff was entered through a deltoid incision, which disrupted the deltoid attachment and left a scar of up to 5 cm in length. In the appropriate patient, arthroscopic acromioplasty has advantages because the deltoid is not disrupted as much, and the glenohumeral joint can also be examined.2,10,11

Figure 3 was developed by HealthPartners, 1996, with assistance from Jon Burns, and photographs by Ann Lazor and Charlie Straw.

THE AUTHORS

ALLEN E. FONGEMIE, M.D.,
is head of the Primary Care Orthopedic Clinic for HealthPartners in Minneapolis, and provides orthopedic training to residents and primary care physicians. He is also associate professor of family practice on the clinical faculty at the University of Minnesota Medical School--Minneapolis. Dr. Fongemie is a graduate of the University of Vermont College of Medicine, Burlington, and completed a residency in family practice at the University of Minnesota. He has a certificate of qualification in sports medicine.

DANIEL D. BUSS, M.D.,
serves as assistant professor of orthopedic surgery at the University of Minnesota and is director of the shoulder service there. A graduate of the University of Minnesota Medical School--Minneapolis, he also serves as a consultant in orthopedics for the Minnesota Twins.

SHARON J. ROLNICK, PH.D.,
serves as program director for clinical research for Group Health Foundation, the research subsidiary of HealthPartners. She obtained her doctorate from the University of Minnesota.

Address correspondence to Allen Fongemie, M.D., Como Medical Center, 2500 Como Ave., St. Paul, MN 55108. Reprints are not available from the authors.

REFERENCES

1.Poppen NK, Walker PS. Normal and abnormal motion of the shoulder. J Bone Joint Surg [Am] 1976;58:195-201.

2.Iannotti JP, ed. Rotator cuff disorders: evaluation and treatment. Park Ridge, Ill.: American Academy of Orthopaedic Surgeons monograph series 1991:5.

3.Bigliani LU, Morrison DS, April EW. The morphology of the acromion and its relationship to rotator cuff tears. Orthop Trans 1986;10:228.

4.Swain RA, Wilson FD, Harsha DM. The os acromiale: another cause of impingement. Med Sci Sports Exerc 1996;28:1459-62.

5.Neer CS 2d. Anterior acromioplasty for the chronic impingement syndrome in the shoulder: a preliminary report. J Bone Joint Surg [Am] 1972;54:41-50.

6.Buss D. Shoulder assessment form. Minneapolis: The Minneapolis Sports Medicine Center, 1994.

7.Richards RR, An KN, Bigliani LU, Friedman RJ, Gartsman GM, Gristina AG, et al. A standardized method for the assessment of shoulder function. J Shoulder Elbow Surg 1994;3:347-52.

8.Kelly BT, Kadrmas WR, Speer KP. The manual muscle examination for rotator cuff strength. An electromyographic investigation. Am J Sports Med 1996;24:581-8.

9.Magee DJ. Orthopedic physical assessment. 2d ed. Philadelphia: Saunders, 1992.

10.Hawkins RJ, Mohtadi N. Rotator cuff problems in athletes. In: DeLee J, Drez D, Stanitski CL, eds. Orthopaedic sports medicine: principles and practice. Philadelphia: Saunders, 1994.

11.Iannotti JP, Zlatkin MB, Esterhai JL, Kressel HY, Dalinka MK, Spindler KP. Magnetic resonance imaging of the shoulder. Sensitivity, specificity and predictive value. J Bone Joint Surg [Am] 1991;73: 17-29.

12.Larson HM, O'Connor FG, Nirschl RP. Shoulder pain: the role of diagnostic injections. Am Fam Physician 1996;53:1637-43.

13.Warner JP. Pathophysiology and findings in impingement and rotator cuff teams. Presentation at the annual AMSSM (American Medical Society for Sports Medicine) meeting. Hilton Head Island, S.C.: April 1995.

14.Hawkins RJ, Kennedy JC. Impingement syndrome in athletes. Am J Sports Med 1980;8:151-8.

15.DePalma AF. Surgery of the shoulder. 3d ed. Philadelphia: Lippincott, 1983.

16.Bartolozzi A, Andreychik D, Ahmad S. Determinants of outcome in the treatment of rotator cuff disease. Clin Orthop 1994;308:90-7.

17.Miniaci A, Dowdy PA, Willits KR, Vellet AD. Magnetic resonance imaging evaluation of the rotator cuff tendons in the asymptomatic shoulder. Am J Sports Med 1995;23:142-5.

18.Sher JS, Uribe JW, Posada A, Murphy BJ, Zlatkin MB. Abnormal findings on magnetic resonance images of asymptomatic shoulders. J Bone Joint Surg [Am] 1995;77:10-5.

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Dorsal Scapular nerve some  C4 & mostly C5 innervation.  See Brachial Plexus  below

Prevalence of annular tears and disc herniations on MR images of

the cervical spine in symptom free volunteers

C.W. Ernst∗, T.W. Stadnik, E. Peeters, C. Breucq, M.J.C. Osteaux

Department of Radiology and Medical Imaging, University Hospital V.U.B., Laarbeeklaan 101, 1090 Brussels, Belgium

European Journal of Radiology 55 (2005) 409–414

1. Introduction

The cervical and lumbar spine are among the first areas

of the human body to show demonstrable imaging evidence

of degenerative joint disease [1] but the relation between abnormalities

in the cervical (and lumbar) spine and neck pain

(or low back pain) is frequently controversial.

Annular tears are frequently identified on magnetic resonance

(MR) images in patients with neck pain or brachialgia.

The annulus fibrosis is innervated by the recurrent meningeal

nerve and by the small branches from the ventral ramus of thesomatic nerve [2]. Annular tear, therefore, can be responsible

for neck pain or brachialgia.

A history of neckpain or brachialgia can also be related

to discogenic pain produced by disc herniation. On

the other hand, the high prevalence of disc protrusions in

symptom-free populations has been reported in lumbar spine

studies (e.g., Stadnik et al. [5], Jensen et al. [3]). The relation

between the discovered disk herniation and trauma

remains one of the most important problems in insurance

claims.

Previous studies [1,4] already reported the prevalence of

asymptomatic degenerative disc disease of the cervical spine,

however, no attempt was made to categorize the discovered

disc herniations. The prevalence of annular tears in the cervical

spine of asymptomatic subjects was never reported.