Spinal Diseases: Bacterial Causes

[Linda]

Richard,
Please don't take offense...I think many of us are convinced by the articles and research you have done. I think at this point, what would be most helpful for the community is some research and a list of U.S. physicians for U.S. patients who will do testing for mycoplasmas because I live in one of the bigger metro areas and I have not been able to find a doctor that will even write a prescription to send my blood off for testing for mycoplasmas. It is so frustrating as I am facing a life-threatening revision surgery now and my spine is getting worse and worse as the days go by. Please a list of doctors that will write or do the testing even if it is really small. Names, locations and contact information would be so appreciated. Again, please don't take offense and know I, for one, really do appreciate the time you have put into your research for us.
Thanks,

[Toebin]

Hey Linda,

When your docs turned down your request to have mycoplasma tests done what did they say ? I'm trying to decide which of my numerous physicians to discuss this with right now and plan on having tests done soon. I would be interested in the excuse any MD can give for a simple blood test that could change the outcome of the chronic pain we have.. and need to develop my response to them should my docs try to stop me ....

Right now I think three of my medical team would be more than happy to write for the tests.. but I may be sadly mistaken once I give it a go...

I'll let you know how it turns out !!

I'm awaiting results of a whole battery of new tests that we just concluded.. once I get those , if there is no clear cut cause of my continued pain I'm gonna hit the trail with my mycoplasm requests...

[Harrison]

Effect of MALP-2, a Lipopeptide from Mycoplasma fermentans,on Bone Resorption In Vitro

GRAZYNA PIEC,1† JELENA MIRKOVITCH,1 SILVIA PALACIO,1 PETER F. MU¨HLRADT,2
AND ROLF FELIX1*

Department of Clinical Research, Bone Biology, University of Bern, CH-3010 Bern, Switzerland,1 and Immunobiology Research Group, Gesellschaft fu¨r Biotechnologische Forschung,D-38124-Braunschweig, Germany2
Received 8 June 1999/Returned for modification 7 July 1999/Accepted 9 September 1999

Mycoplasmas may be associated with rheumatoid arthritis in various animal hosts. In humans, mycoplasma arthritis has been recorded in association with hypogammaglobulinemia.

Mycoplasma fermentans is one mycoplasma species considered to be involved in causing arthritis. To clarify which mycoplasmal compounds contribute to the inflammatory, bone-destructive processes in arthritis, we used a well-defined lipopeptide, 2-kDa macrophage-activating lipopeptide (MALP-2) from M. fermentans, as an example of a class of macrophageactivating compounds ubiquitous in mycoplasmas, to study its effects on bone resorption. MALP-2 stimulated osteoclast-mediated bone resorption in murine calvaria cultures, with a maximal effect at around 2 nM. Antiinflammatory drugs inhibited MALP-2-mediated bone resorption by about 30%. This finding suggests that MALP-2 stimulates bone resorption partially by stimulating the formation of prostaglandins. Since interleukin-6 (IL-6) stimulates bone resorption, we investigated IL-6 production in cultured calvaria. MALP-2 stimulated the liberation of IL-6, while no tumor necrosis factor was detectable.

Additionally, MALP-2 stimulated low levels of NO in calvaria cultures, an effect which was strongly increased in the presence of gamma interferon, causing an inhibition of bone resorption. MALP-2 stimulated the bone-resorbing activity of osteoclasts isolated from long bones of newborn rats and cultured on dentine slices without affecting their number. In bone marrow cultures, MALP-2 inhibited the formation of osteoclasts. It appears that MALP-2 has two opposing effects: it increases the bone resorption in bone tissue by stimulation of mature osteoclasts but inhibits the formation of new ones.

Full article: http://iai.asm.org/cgi/reprint/67/12/6281.pdf

[Harrison]

A recently published book addresses many of these unanswered questions – it’s called "Cure Unknown," written by Pamela Weintraub. Though it focuses on Lyme disease, it also explains:

- Why accurate blood tests for Lyme (and co-infections like mycoplasma) are unavailable;
- Why many Lyme treatment doctors have been targeted and literally run out of town (addressing Linda’s question);
- Why there are so few doctors practicing medicine that can help the hundreds of thousands of people with these kinds of chronic, degenerative infections;
- Why so many people continue to be undiagnosed and untreated.

There is so much information packed into this book, yet written in such a concise manner, you’ll start and finish all 354 pages in a week! I highly recommend it for a long list of reasons.

See the author’s site at http://www.cureunknown.com/ Also note the many links and descriptions on the bottom of that page.

[Harrison]

J Lab Clin Med. 2005 Aug;146(2):55-63.

Mycoplasma pneumoniae and central nervous system complications: a review.Guleria R, Nisar N, Chawla TC, Biswas NR.

Department of Medicine, All India Institute of Medical Sciences, Ansari Nagar, New Delhi, India.

Mycoplasma pneumoniae is a common cause of community-acquired pneumonia. Little is known about the extrapulmonary manifestations of this organism. Numerous central nervous system (CNS) manifestations have been described with M. pneumoniae. CNS involvement is probably the most common site of involvement in addition to the respiratory system.

Up to 7% of patients hospitalized with M. pneumoniae may have CNS symptoms. Common CNS presentations include encephalitis, aseptic meningitis, polyradiculitis, cerebellar ataxia, and myelitis. The mechanism behind these CNS manifestations remains unclear. Direct invasion, neurotoxin production, or an immune-mediated mechanism has been proposed. Newer diagnostic techniques for the direct detection of the antigen and the microorganism are proving useful for the detection of extrapulmonary disease. This review comprehensively reviews the CNS complications that have been reported with M. pneumoniae.

PMID: 16099235 [PubMed - indexed for MEDLINE]

Conn Med. 2002 Jul;66(7):387-9.

Atypical mycobacterial osteomyelitis in a non-AIDS patient.

Niazi S, Batra V, Zangrilli JG.
Department of Medicine, Division on Critical Care, Pulmonary, Allergic, and Immunologic Diseases, Thomas Jefferson University, Philadelphia, Pennsylvania, USA.

Disseminated Mycobacterium avium intercellulare (MAI) infection is rare in non-AIDS patients. We report a 60-year-old woman with chronic lung disease who developed vertebral osteomyelitis due to MAI. She was treated successfully with combined therapy consisting of rifampin, ethambutol, and clarithromycin.

[Maddie]

Originally Posted by Harrison

Once again, the US medical system is being outdone by countries who focus on the cause of disease. Most of these "diagnostic" studies are published from overseas. It really gets me mad!

Harrison, does this mean that the other countries are taking this seriously, and that their citizens are getting proper treatment, taking this into consideration?

Over this long trek to get treatment, I have often thought about the logistics of moving to Germany or some other country that seems to be miles ahead in terms of medical treatment.

Has anyone tried to do this?

[Harrison]

And the article below is evidence of this unfortunate fact. However, though this is a shocking admission by the CDC, it does represent progress, albeit a few decades late. I believe the outfall from statements like this will have some rather dramatic repercussions -- at least this is my hope.

Just to clarify, these mycobacterial bugs in question are intracellular. They are so small, and so sophisticated, that they literally tunnel into blood cells and live (and love!) there. Their insidious ways make them hard to detect, but also make them tougher for the immune system (and diagnostic technology) to identify. As they "live and love," they compromise the immune system, or disease tissue that tends to be less vascular (e.g., damaged tissue, cartilage, ligaments, joints).

As a sidenote, this spine patient community has a significant number of patients from Michigan, Minnesota and other states with a disproportionate number of tick-reported diseases. Frankly, I am very surprised that the CDC would release this report based on "strong presumptive evidence," as they have maintained a decidedly cautious position on TBDs (tick-borne diseases).

Note: If this is the first time you read this lengthy topic, please start from the beginning and carefully read the whole thing. Go to Thread Tools > Show Printable Version to print the topic.
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CDC WeeklyOctober 24, 2008 / 57(42);1145-1148

Anaplasma phagocytophilum Transmitted Through Blood Transfusion --- Minnesota, 2007

Anaplasma phagocytophilum, a gram-negative, obligate intracellular bacterium of neutrophils, causes human anaplasmosis, a tickborne rickettsial disease formerly known as human granulocytic ehrlichiosis (1). In November 2007, the Minnesota Department of Health was contacted about A. phagocytophilum infection in a hospitalized Minnesota resident who had recently undergone multiple blood transfusions. Subsequent investigation indicated the infection likely was acquired through a transfusion of red blood cells. This report describes the patient's clinical history and the epidemiologic and laboratory investigations. Although a previous case of transfusion-transmitted anaplasmosis was reported (2), this is the first published report in which transfusion transmission of A. phagocytophilum was confirmed by testing of the recipient and a donor.

Although polymerase chain reaction (PCR) assays provided reliable evidence of transmission in this case, no cost-effective method for screening blood donors for A. phagocytophilum exists. Screening donors for a recent history of tick bite is not likely to be sensitive or specific because such exposures are common and often not recalled by persons with anaplasmosis (3). Physicians should consider the possibility of anaplasmosis in patients who develop posttransfusion acute thrombocytopenia, especially if accompanied by fever, and should report suspected transfusion-associated cases to health authorities.

Case Report

The patient, a male aged 68 years with a medical history of chronic renal insufficiency, psoriatic arthritis, ankylosing spondylitis, and corticosteroid therapy, underwent elective knee arthroplasty and synovectomy on October 12, 2007. Three weeks before his hospitalization, the patient had traveled to an area where blacklegged ticks (Ixodes spp.) were endemic, but he did not spend time outdoors and had no known tick bites. Several hours after the procedure, the patient developed bleeding at the surgical site and associated coagulopathy, indicated by elevated international normalized ratio (INR) and partial thromboplastin time (PTT) and by decreased fibrinogen and platelet counts.

The extensive hemorrhage required two surgical evacuations of hematoma from the knee, popliteal artery embolization, and transfusion of multiple blood components. During October 12--21, the patient received 34 units of nonleukoreduced red blood cells (RBC), 4 units of leukocyte-reduced apheresis platelets, 14 units of fresh frozen plasma (FFP), and 7 units of cryoprecipitate. The components came from 59 individual blood donors; all donations were collected by Memorial Blood Centers (St. Paul, Minnesota). On October 19, the patient developed sepsis and multisystem failure. He was treated empirically with antibiotics (cefazolin, piperacillin/tazobactam, vancomycin, and levofloxacin). Blood cultures were negative on October 18, 20, and 31, and urine cultures were negative on October 19 and 25.

On October 31, the patient was found to have worsening thrombocytopenia. His platelet count declined from 178,000/mm3 on October 31 to 54,000/mm3 on November 5. On November 1, he developed hypotension and fever attributed to urinary tract infection. He was treated with levofloxacin and sulfamethoxazole/trimethoprim and was afebrile by November 3. On November 3, 22 days after admission, a peripheral blood smear from the patient demonstrated inclusions compatible with A. phagocytophilum morulae in neutrophils.

Retrospective review of an October 15 blood smear from the patient showed no evidence of intracellular morulae. Whole blood specimens from November 3--5 were positive for A. phagocytophilum DNA by PCR assays conducted at the Mayo Medical Laboratory, Minnesota Department of Health, and CDC. Serum from November 3--5 was tested at CDC and found to be weakly positive by indirect immunofluorescence assay (IFA) (titer 1:64) for immunoglobulin G (IgG) antibodies to A. phagocytophilum. Doxycycline treatment was begun on November 5. The patient's platelet count steadily improved and returned to a normal level of 163,000/mm3 on November 10. Pretransfusion blood samples and serum from the patient's convalescence period were not available for further testing. The patient improved clinically and was transferred to a rehabilitation unit on November 13. After rehabilitation, the patient was discharged on December 3, 2007.

Epidemiologic and Laboratory Investigation

In early November, Memorial Blood Centers began an investigation to identify whether any of the 59 blood donors associated with the 34 RBC, 4 platelet, 14 FFP, and 7 cryoprecipitate units had evidence of A. phagocytophilum infection. Paired whole blood specimens from the original donations had been retained from all 34 RBC donors and eight of 14 FFP donors and were available for PCR testing. During November 2007--March 2008, Memorial Blood Centers also collected postdonation blood samples for serologic testing and information on recent illness history and potential tick exposure from 53 of the 59 donors. In addition, plasma components from two FFP donors and two cryoprecipitate donors who donated again during December 2007--January 2008 were retained for serologic testing. The whole blood specimens retained from initial donation were tested by PCR, followed by sequencing of the PCR amplicons at CDC. Serum and plasma specimens were tested by IFA for IgG antibodies to A. phagocytophilum.

PCR and IFA tests on samples from a female RBC donor aged 64 years were positive for A. phagocytophilum infection (Table). A. phagocytophilum DNA was found in an RBC product donated by this woman on September 28 and transfused to the patient on October 13. IgG IFA titers to A. phagocytophilum were 1:512 and 1:256, respectively, in subsequent sera collected November 17 and December 18. The donor did not recall being bitten by a tick, but had spent time in wooded areas of northeast Minnesota where anaplasmosis is endemic within the month before her donation. She reported no history of fever during the month before or after her donation. No other patients received blood components from her donation.

No whole blood samples from other tested donors were PCR positive for A. phagocytophilum. Sera from two RBC donors were weakly positive by IFA (titer 1:64), but their respective whole blood samples from the original transfused units were PCR negative. These two donors did not live on wooded property and reported they had no tick exposure or illness during the 2 months before donation. Available postdonation serum samples from other donors were negative for A. phagocytophilum by IFA (titer <1:32).

Reported by:

M Kemperman, MPH, D Neitzel, MS, Minnesota Dept of Health; K Jensen, J Gorlin, MD, E Perry, MD, MemorialBloodCenters, Saint Paul; T Myers, MD, T Miley, MD, ParkNicolletMethodistHospital, Saint Louis Park, Minnesota. J McQuiston, DVM, ME Eremeeva, MD, PhD, ScD, W Nicholson, PhD, J Singleton, National Center for Zoonotic, Vector-Borne, and Enteric Diseases; J Adjemian, PhD, EIS Officer, CDC.

Editorial Note:

A. phagocytophilum, the causative agent of anaplasmosis, typically is transmitted to humans by infected Ixodes spp. ticks. In wooded areas of the United States, A. phagocytophilum is transmitted by the blacklegged tick (Ixodes scapularis) in the Northeast and upper Midwest and by the western blacklegged tick(Ixodes pacificus) on the West Coast. In infected persons who are symptomatic, illness onset occurs 5--21 days after a bite from an infected tick. Initial presentation typically includes sudden onset of fever, headache, malaise, and myalgia, often accompanied by thrombocytopenia, leukopenia, and elevated liver transaminases. Severe infections can include prolonged fever, shock, confusion, seizures, pneumonitis, renal failure, hemorrhages, opportunistic infections, and death (1). Anaplasmosis and other tickborne diseases, including human ehrlichiosis, Rocky Mountain spotted fever, and babesiosis, caused by Ehrlichia chaffeensis or Ehrlichia ewingii, Rickettsia rickettsii, and Babesia spp., respectively, represent a potential risk for transmission via blood transfusion in the United States (2--6).

The case described in this report provides strong presumptive evidence that A. phagocytophilum infection in this patient was acquired through blood transfusion. Pretransfusion blood samples and convalescent serum from the transfusion recipient were not available for PCR or serologic testing to demonstrate conclusively that the patient was free of A. phagocytophilum infection before his hospitalization on October 12.

However, the patient reported limited outdoor exposure that might include potential tick contact during the 3 weeks before hospitalization, and a blood smear collected 3 days after hospital admission showed no evidence of intracellular morulae. The timing of events and the expected incubation period for anaplasmosis (5--21 days) suggest that the patient's exposure most likely occurred during hospitalization. A. phagocytophilum DNA was found in a retained sample from the implicated RBC product that was transfused to the recipient, providing strong evidence that this was the likely route of disease transmission to the blood transfusion recipient. Some blood transfusion recipients (i.e., those who are immune compromised) likely are at increased risk for developing severe complications associated with tickborne diseases.

Both A. phagocytophilum and E. chaffeensis can survive in refrigerated RBCs, and possible transfusion-transmission cases have been reported for anaplasmosis (Minnesota Department of Health, unpublished data, 1998) (2,3,5,6). However, because of the rarity of transfusion-associated cases, concerns regarding the specificity of available tests, (none of which are approved by the Food and Drug Administration), and the economic costs associated with implementation, the U.S. blood supply is not routinely screened for tickborne disease using laboratory methods (7).

As a method to reduce the risk for certain pathogens in blood products, blood banks often defer donations if the potential donor is ill at the time of donation. However, persons infected with tickborne disease might experience mild illness or have asymptomatic infection, as was the case with the implicated donor in this report (1,3). Screening donors for a recent history of tick bite is unlikely to identify high-risk donors, because this type of exposure frequently is not recalled by persons with anaplasmosis (3). In this case, the implicated donor did not recall a tick bite, although she did report contact with wooded habitat in an anaplasmosis-endemic area. Nearly 75% of the other blood donors in this investigation reported similar outdoor contact, making the screening of blood donors for tick-related exposures poorly predictive for possible infection. Because Ehrlichia and Anaplasma are associated with white blood cells, leukoreduction techniques would be expected to reduce the risk for Ehrlichia and Anaplasma transfusion-transmission through RBC components (5,8). In the absence of effective screening tools to identify donors or products infected with the organisms, physicians should weigh the benefits of using leukoreduced blood components, to potentially reduce the risk for Ehrlichia and Anaplasma transmissions.

Although transfusion-associated transmission of A. phagocytophilum appears to be rare, reported incidences of anaplasmosis and other tickborne diseases are increasing in the United States (1). A record 322 cases of anaplasmosis were reported in Minnesota in 2007 (6.2 cases per 100,000 population) (9). As the incidence of tickborne diseases increases, physician vigilance for possible transmission of these agents via transfusions also should increase. In addition to other more common etiologies, physicians should suspect possible rickettsial infection if transfusion recipients develop acute thrombocytopenia posttransfusion, especially if accompanied by fever. Such signs should lead to rapid assessment for rickettsial agents and empiric treatment with doxycycline (1). Although insensitive, blood smear can provide timely support for a presumptive diagnosis of anaplasmosis, followed by IFA or PCR to confirm the diagnosis (1). Similarly, babesiosis should be suspected in patients who develop hemolytic anemia and fever posttransfusion (3,4).

Anaplasmosis and ehrliciosis are nationally notifiable diseases. Suspected cases of tickborne rickettsial diseases should be reported promptly to the state or local health department, and suspected transfusion-associated transmission should be reported to the supplying blood center and appropriate public health authorities.

Acknowledgments

The findings in this report are based, in part, on contributions by G Liu, PhD, and K Smith, DVM, PhD, Minnesota Dept of Health; M Kuehnert, MD, National Center for Preparedness, Detection, and Control of Infectious Diseases, and S Holzbauer, DVM, Coordinating Office for Terrorism Preparedness and Emergency Response, CDC.


References

1. CDC. Diagnosis and management of tickborne rickettsial diseases: Rocky Mountain spotted fever, ehrlichiosis, and anaplasmosis---United States. MMWR 2006;55 No.RR-4).
2. Eastlund T, Persing D, Mathiesen D, et al. Human granulocytic ehrlichiosis after red cell transfusion. Transfusion 1999;39:117S.
3. McQuiston JH, Childs JE, Chamberland ME, Tabor E. Transmission of tickborne agents of disease by blood transfusion: a review of known and potential risks in the United States. Transfusion 2000;40:274--84.
4. Herwaldt BL, Neitzel DF, Gorlin JB, et al. Transmission of Babesia microti in Minnesota through four blood donations from the same donor over a 6-month period. Transfusion 2002;42:1154--8.
5. McKechnie DB, Slater KS, Childs JE, Massung RF, Paddock CD. Survial of Ehrlichia chaffeensis in refrigerated, ADSOL-treated RBCs. Transfusion 2000;40:1041--7.
6. Kalantarpour F, Chowdhury I, Wormser GP, Aguero-Rosenfeld ME. Survival of the human granulocytic ehrlichiosis agent under refrigeration conditions. J Clin Microbiol 2000;38:2398--9.
7. AuBuchon JP. Meeting transfusion safety expectations. Ann Intern Med 2005;143:537--8.
8. Mettille FC, Salata KF, Belanger KJ, Casleton BG, Kelly DJ. Reducing the risk of transfusion-transmitted rickettsial disease by WBC filtration, using Orientia tsutsugamushi in a model system. Transfusion 2000;40:290--6.
9. CDC. Final 2007 reports of nationally notifiable infectious diseases. MMWR 2008;57:901, 903--13.

Article at http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5742a1.htm

[Harrison]

Naturally, the NIH does not fund this kind of useful research. I hope this changes!
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Grading of degenerative disk disease and functional impairment: imaging versus patho-anatomical findings.

Quint U, Wilke HJ.
Orthopaedic and Trauma Center, Spine Unit, St Marien-Hospital Hamm, Nassauerstr. 13-19, 59065, Hamm, Germany, ulrich.quint@marienhospital-hamm.de.

Degenerative instability affecting the functional spinal unit is discussed as a cause of symptoms. The value of imaging signs for assessing the resulting functional impairment is still unclear. To determine the relationship between slight degrees of degeneration and function, we performed a biomechanical study with 18 multisegmental (L2-S2) human lumbar cadaveric specimens. The multidirectional spinal deformation was measured during the continuous application of pure moments of flexion/extension, bilateral bending and rotation in a spine tester.

The three flexibility parameters neutral zone, range of motion and neutral zone ratio were evaluated. Different grading systems were used: (1) antero-posterior and lateral radiographs (degenerative disk disease) (2) oblique radiographs (facet joint degeneration) (3) macroscopic and (4) microscopic evaluation. The most reliable correlation was between the grading of microscopic findings and the flexibility parameters; the imaging evaluation was not as informative.

[Harrison]

One of the things I try to do as an advocate is to connect with patients, medical researchers and experts in the field(s) of degenerative disease. A few months ago, I personally met a woman who is a patient, researcher, expert, writer…and more.

Pam Weintraub is the author of Cure Unknown, an up-to-date book on Lyme disease (mentioned in my 8-19-08 post). Her amazing body of work will be reviewed on Channel 5 Boston tonight on the Chronicle magazine at 7:30 PM. I believe she is a real “mover and shaker” and agent of change; which explains in part why this enlightening special on Lyme disease(s) will be aired. If you are in New England, do tune in to watch what may be the media’s first in-depth look at this terrible epidemic.

[Harrison]

While doing some research, I found the following page was expired...but I found an archived (cached) page. There is some useful diagnostic information herein. It's also (er, was) one of the few places on the Internet where you will find a doctor admitting that Lyme disease (et al pathogens) can directly cause a cervical spine disorder! Does anyone else find it significant that a rheumatologist is admitting this?!

Some of the formatting was funky, so I'll attach a PDF of this content too. I am guessing this was written in 2003. It was published the GWU web site in 2004 and removed in 2005.
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Management of Neck Pain: A Primary Care Approach
DAVID G. BORENSTEIN, George Washington University

Among the many disorders that cause neck pain, biomechanical stress is the most common. Nonoperative therapies offer relief in most patients within three months. Those with chronic or radicular pain require additional evaluation and multiple therapies for effective relief. Systemic illness and spinal compression require prompt intervention to prevent serious complications.

Dr. Borenstein is Clinical Professor of Medicine, The George Washington University Medical Center, Washington, D.C.

A common complaint evaluated by primary care physicians, neck pain affects about 10% of the population of the United States every year. Although cervical spine disorders have a diverse etiology (Table 1), biomechanical disorders that occur secondary to overuse, trauma, or deformity are the most common cause of neck pain. Typically, these disorders are characterized by correlating exacerbation or alleviation of symptoms with certain physical activities.

Table 1. Causes of Cervical Spine Disorders

Biomechanical
Neck strain
Herniated disk
Spondylosis
Myelopathy
Myelopathy

Infectious
Osteomyelitis
Diskitis
Meningitis
Herpes zoster
Lyme disease

Referred
Thoracic outlet syndrome
Pancoast's tumor
Esophagitis
Angina
Vascular dissection

Neurologic
Brachial plexitis
Peripheral entrapment
Neuropathies
Reflex sympathetic dystrophy

Rheumatologic
Rheumatoid arthritis
Ankylosing spondylitis
Psoriatic arthritis
Reiter's syndrome
MyelopathyEnteropathic arthritis
Polymyalgia rheumatica
Fibromyalgia
Myofascial pain
Diffuse idiopathic skeletal hypertrophy
Microcrystalline disease

Neoplastic
Osteoblastoma
Osteochondroma
Giant cell tumor
Hemangioma
Metastases
Multiple myeloma
Chondrosarcoma
Chordoma
Gliomas
Syringomyelia
Neurofibroma

Miscellaneous
Paget's disease
Sarcoidosis

Most biomechanical disorders of the cervical spine have a natural history of improvement. More than 50% of patients will have decreased pain in two to four weeks; 80% will be asymptomatic in two to three months, and most will improve without requiring diagnostic x-rays or laboratory tests. Such studies are reserved for patients with histories or physical findings that suggest cord or nerve root compression or systemic illness. These disorders are uncommon causes of neck pain but require thorough evaluation and immediate treatment.

Spinal Compression

Cervical myelopathy occurs secondary to compression of the spinal cord or nerve roots in the spinal canal. Only one third of patients complain of neck pain. Although cervical myelopathy is rare, one form, spondylitic myelopathy, is the most common cause of spinal cord dysfunction in patients older than age 55. The location, duration, and size of lesions influence the severity and distribution of symptoms. Compression usually results from a combination of osteophyte growth and degenerative disk disease. Symptoms may involve all limbs and include difficulty in walking and urinary or fecal incontinence.

The most frequent presentation is arm and leg dysfunction. Older patients may describe leg stiffness, foot shuffling, and a fear of falling. Common findings include weakness of the appendages, spasticity, fasciculations, and hyperreflexia, clonus, and Babinski's reflex in the lower extremities.

Many imaging techniques can be used for diagnosis. Plain x-rays reveal advanced degenerative disease with narrowed disk spaces, facet joint sclerosis, and osteophytes; computed tomographic (CT) myelograms can distinguish osteophytes from protruding disks, and magnetic resonance imaging (MRI) can detect the extent of spinal cord compression (Figure 1). Plain x-rays are the most convenient test to use but do not reveal nerve compression. CT myelograms are used presurgically to identify bone, disks, and canal space.

Cervical spondylitic myelopathy has a gradual progression; severe myelopathy seldom develops in patients who do not exhibit signs at presentation. Although some patients improve with conservative therapy, those with progressive myelopathy require surgery to prevent further cord compression, vascular compromise, and myelomalacia. Obviously, surgery is most effective when performed before severe neurologic deficits develop.

Systemic Illness

Positive responses to one or more questions about systemic symptoms accompanying neck pain necessitate additional evaluations.

Tumors. Pain with fever or weight loss suggests the presence of a tumor or infection. Pain that is greatest at night or with recumbency is associated with infiltration of the spinal cord and tumors of the vertebral column. Patients with neurologic signs should undergo MRI of the central nervous system. A spinal cord tumor appears as a single mass; in contrast, demyelinating disease produces multiple lesions.

Patients who have nocturnal pain without neurologic signs may have a bone tumor. Benign tumors tend to affect the posterior elements of vertebral bodies. If plain x-rays are unable to detect alterations in vertebral architecture, bone scans are sensitive alternatives for revealing lesions over the entire axial skeleton. CT scans can locate suspected tumors not detected with other imaging methods. All tumors should be biopsied and treated; surgical excision is preferred for accessible tumors.

Spondyloarthropathies and Other Rheumatic Diseases produce early-morning neck stiffness that lasts for hours. Patients usually have extensive disease in other articular locations. Flexion-extension views reveal the presence of C1-C2 subluxation. Women with spondyloarthropathy may have neck disease without low back pain. A Ferguson view of the pelvis is a useful test to detect sacroiliitis if neck x-rays do not reveal syndesmophytes or squaring of vertebral bodies. Patients with polyarthritis can be identified with bone scans and erythrocyte sedimentation rate (ESR) measurement; treatment requires maximum doses of nonsterodial anti-inflammatory drugs (NSAIDs). Joint instability warrants bracing or surgical fusion if neural dysfunction is documented.

Polymyalgia rheumatica occurs predominantly in women older than 60 years. In such patients, pain is often localized to the proximal muscles of the shoulders and thighs. An elevated ESR is the most common laboratory finding. Treatment with daily low-dose corticosteroids is often effective.

Visceral Source of Pain. Patients may have neck pain secondary to cardiovascular, gastrointestinal, or neurologic disorders. Vascular lesions in the neck (carotodynia) can cause localized pain. Esophageal disorders should be considered if neck pain occurs when patients are eating; posterior esophageal lesions may affect the prevertebral space to produce pain. An esophagram can identify abnormalities of peristalsis or structure; endoscopy may detect intrinsic esophageal lesions. Neurologic disorders may involve cranial nerve lesions that cause cervical spine and facial pain.

Nonoperative Therapies
Patients without systemic disorders should be treated with nonoperative therapy for three to six weeks. Among the available therapies, NSAIDs can decrease the pain and inflammation that is associated with localized disease. Although agents with rapid onset and good analgesic effect are preferred, those with sustained-release properties may offer better relief with fewer tablets per day. Muscle relaxants do not affect peripheral muscles but do offer additional relief for patients with increased paracervical muscle contractions; physicians should in- form patients of these drugs' potential sedative effect. Temperature modalities may also be useful. Ice massage for 10 minutes provides additional analgesia in some cases, whereas application of heat may decrease muscle tightness and improve range of motion in others. Injection of a mixture of 1 mL of semisoluble corticosteroid and 3 to 5 mL of lidocaine into the area of maximum tenderness in the paravertebral musculature or trapezii may be another way to decrease pain.

Patients should understand that the eventual goal of therapy is a return to normal neck motion. This may be difficult to accomplish. Patients often prefer to wear a cervical collar and limit motion. Short-term immobilization is useful--particularly at night, when movement during sleep causes pain. A soft collar that supports but does not extend the neck is an appropriate treatment; however, its use should decrease as neck pain diminishes. The use of a collar with cervical hyperextension should be severely limited; in contrast, patients with disk herniations will require full-time collar immobilization to limit radicular pain for longer periods.

Most patients, including those with cervical radiculopathy, improve and return to normal activity within two months. Patients who are still symptomatic after six weeks of nonoperative treatment are separated into two groups--those with neck pain and those with arm pain as the major complaint.

Neck Pain as the Major Complaint

Patients with pain only in the cervical area, trapezii, and shoulders may have one of many disorders. The different types of relevant biomechanical neck pain may be differentiated by characteristics summarized in Table 2.

Table 2. Selected Characteristics of Biomechanical Neck Pain (See PDF)

Strain causes pain in the middle or lower portion of the posterior neck. The pain may be diffuse or localized to both sides of the spine. Physical examination reveals local tenderness in the paracervical muscles, decreased range of motion, and loss of cervical lordosis. No abnormalities are found with neurologic or shoulder examinations. X-rays of the spine may be normal or reveal a loss of lordosis. Laboratory test results are normal.

Therapy for chronic cervical strain includes NSAIDs, muscle relaxants, local injections, and exercises (including strengthening and range-of-motion). The choice and dosage of NSAIDs may be modified for patients with severe chronic pain.

Cervical Spondylosis (Osteoarthritis) is associated with disk degeneration and approximation of articular surfaces. Instability causes osteophyte formation in the uncovertebral and zygapophyseal joints, and diffuse pain may radiate from the neck to the shoulders, occipital area, or the interscapular muscles. Physical examination may reveal midline tenderness and pain at the limit of motion with extension and lateral flexion.

Radiographic findings are significant only if they correlate with the patient's clinical signs and symptoms. Plain x-rays of the cervical spine typically demonstrate intervertebral narrowing and facet joint sclerosis. MRI reveals degenerative cervical disk disease in more than 50% of patients 40 years of age or older. Scans are indicated in patients who have persistent pain that radiates to the shoulders; imaging serves to locate nerve impingement for subsequent treatment.

Patient education is essential for pain management. Most patients have a relapsing course with recurrent exacerbations of acute neck pain; hence, therapy requires a balance between stability and maintenance of motion. Range-of-motion exercises maximize neck flexibility; cervical collars decrease pain by restricting neck movement. NSAIDs and local injections may help to diminish neck and referred pain.

Cervical Hyperextension (Whiplash) is an acceleration-deceleration injury to the soft tissue structures in the neck. Common causes include rear-impact motor vehicle accidents, falls, and diving accidents and other sports injuries. Paracervical muscles are stretched or torn, and the sympathetic ganglia may be damaged, resulting in Horner's syndrome, nausea, hoarseness, or dizziness; intervertebral disk injuries occur with severe trauma.

The first symptoms occur 12 to 24 hours after trauma. Patients experience stiffness and pain with motion; they may also have difficulty in swallowing or chewing. Physical examination reveals soreness, paracervical muscle contraction, and decreased range of motion. Neurologic examination is often unremarkable, but radiographs can reveal loss of cervical lordosis. In severely injured patients, structural damage identified on x-rays mandates immediate stabilization.

Nonnarcotic analgesics, NSAIDs, and muscle relaxants reduce pain and facilitate neck movement. Treatment of most whiplash injuries includes use of a cervical collar for a minimal period of time. The collar is removed as soon as pain relief is obtained. Longer use of collars has resulted in delayed recovery. The Quebec Task Force on whiplash-associated disorders showed that prolonged use of cervical collars resulted in increased pain, decreased range of motion, and a longer recovery. Patients whose symptoms last for more than six months usually have a zygapophyseal joint injury and rarely experience significant improvement.

When fever or weight loss develops during nonoperative management, patients should undergo x-ray evaluation to assess bone integrity. If x-rays are negative, MRI or CT scans may locate the lesion and guide placement of biopsy needles.
Elevated ESR or C-reactive protein values identify patients with inflammatory lesions. The ESR may also be monitored during therapy to document improvement. Antibiotics are the treatment of choice for osteomyelitis and diskitis in the absence of neural compromise or paracervical abscess.

Fractures. Pain directly over the bony structures (vertebral arch or body) of the cervical spine is usually a sign of fracture or expansion of bone; physical examination can locate the point of maximum tenderness. Conditions that replace bone with abnormal cells or increase mineral loss from trabeculae predispose patients to fractures that occur spontaneously or with minimal trauma and result in localized pain.
Imaging techniques can identify the location of fractures if the physical examination is equivocal. Bone scans are helpful when x-rays of the neck are normal. MRI can identify the presence of malignant cells that do not stimulate osteoblast activity (e.g., myeloma). Biochemical and hematologic tests may detect perturbations of calcium meta- bolism or the presence of hemo- globinopathies; as noted, an elevated ESR is common with inflammation.

Fibromyalgia. Patients without systemic disorders should be examined for tender or trigger points. Such patients will have normal ESRs but experience localized pain with pressure (tender point) or radiation of muscle pain distal to the area of pressure (trigger point). Tender points are associated with a generalized pain syndrome, fibromyalgia; trigger points are associated with myofascial pain syndrome.
Patients with fibromyalgia benefit from aerobic exercise and antidepressants; those with myofascial disorders improve with injections of combined anesthetic and semisoluble corticosteroid. If patients do not have muscle tenderness, they should undergo a complete psychosocial evaluation. In patients with psychiatric disturbances, conversion reactions or substance dependence often are the cause of neck pain.

Arm Pain as the Major Complaint

Disk Herniation. In patients with arm pain refractory to nonoperative management, the underlying cause often is pressure from a herniated disk or hypertrophic bone and secondary inflammation of the nerve roots. Herniation can result from sudden exertion, as in heavy lifting. Neck pain is minimal or absent, and the injury causes pain that spreads from the shoulder to the forearm and hand and is sometimes severe enough to limit arm use.

Physical examination will detect increased radicular pain with any maneuver that narrows the intervertebral foramen and places tension on the affected nerve, such as compression, extension, or lateral flexion of the cervical spine (Spurling's sign).
Neurologic examination will reveal sensory abnormalities, reflex asymmetry, or motor weakness correlated with the affected spinal nerve root and degree of impingement. The characteristics of radicular pain caused by nerve root compression are summarized in Table 3.

Table 3. Characteristics of Radicular Pain Caused by Cervical Nerve Root Compression

Nerve Root
Area of Pain
Sensory Loss
Motor Loss
Reflex Loss
C5
Neck to outer shoulder, arm
Shoulder
Deltoid
Biceps, supinator
C6
Outer arm to thumb, index finger
Index finger, thumb
Biceps
Biceps, supinator
C7
Outer arm to middle finger
Index, middle fingers
Triceps
Triceps
C8
Inner arm to ring and little finger
Ring, little fingers
Hand muscles
None

MRI is the best technique to locate disk herniation and nerve root impingement; electromyography and nerve conduction tests will document nerve dysfunction and differentiate peripheral entrapment syndromes (e.g., carpal tunnel syndrome) from spinal nerve impingement.

Therapy includes controlled physical activity, firm cervical collars, NSAIDs, and traction. Patients may require full-time collar immobilization to limit radicular pain for weeks at a time. Those with recalcitrant pain may also obtain relief from epidural corticosteroid injections at the level of nerve impingement documented by MRI. Low-dose oral corticosteroids (10 mg to 15 mg/day) may be considered for patients who refuse epidural injections. Corticosteroids should be used for a limited period; dosage is tapered slowly once radicular symptoms have resolved. Many patients' arm symptoms resolve within three months.

When there is unequivocal evidence of nerve root compression (i.e., physical findings corroborated by MRI or CT findings), surgical decompression should be considered. Some studies suggest that patients who undergo such surgery do better than those who do not. Although nonoperative management of patients with radicular pain may prevent progression to cervical myelopathy, some patients nevertheless experience persistent arm pain. When performed in selected patients with good technique, surgery is successful for more than 90% of cases. In one study, for example, anterior diskectomy with fusion achieved excellent outcomes in 94% of patients.

Other Causes. Patients with arm pain that occurs with exertion should undergo a vascular evaluation. If chest pain occurs in conjunction with arm pain, coronary artery disease (CAD) should be investigated with an electrocardiogram and a stress test; positive stress test results (reproduction of arm pain) confirm the presence of CAD. Exertional pain limited to the arm suggests thoracic outlet syndrome. Adson's test can detect the impingement. The test is performed by taking the patient's pulse at the wrist. While the pulse is continuously palpated, the arm is then abducted, extended, and externally rotated. The patient takes a deep breath and turns the head toward the arm being tested. Compression of the subclavian artery results in a marked diminution of the radial pulse. Patients with thoracic outlet syndrome may benefit from isometric shoulder girdle exercises, improved posture, and restriction of arm movement above the head. Surgery is helpful in a minority of patients who do not respond to other therapy.

Patients with persistent arm pain, numbness, and weakness require an apical view chest x-ray to rule out Pancoast's tumor, which invades the inferior portions of the brachial plexus and causes pain by compression of local neural tissues. Such patients require palliative radiation therapy.

Chronic Neck Pain

Patients without a specific diagnosis are considered to have chronic neck pain. Education, patience, and encouragement are important components of therapy. Chronic pain management requires convincing the patient that the goal of therapy is to maximize physical function. A combination of therapies is necessary to reach this goal. Exercise programs that improve aerobic conditioning and range of motion are helpful. Patients may benefit from an increased NSAID dosage or switching to a different NSAID. Tricyclic antidepressants offer additional pain relief mediated through the central nervous system. Narcotic analgesics are generally discouraged but may be used at a specified effective dose to treat patients who experience an acute exacerbation of pain. The goal for these patients is gradual decrease of dosage and eventual discontinuance of narcotic analgesics.

Patients with chronic pain should be encouraged to return to some form of work. Movement aids the adaptive process by improving function and countering the inactivity that can exacerbate pain. The appearance of new symptoms or marked exacerbation of preexisting complaints are indications for reevaluation.

Conclusion

Many disorders are implicated in neck pain, but biomechanical problems of the cervical spine are the most common cause. Diseases affecting the cervical spine are rare but important causes of pain; certain symptoms and signs help to identify the more serious clinical conditions. Most patients improve with nonoperative therapy within three months; only about 10% of patients require surgical intervention.
Selected Reading

Aker PD et al: Conservative management of mechanical neck pain: Systemic overview and meta-analysis. BMJ 313:1291, 1996
Bell GR, Ross JS: The accuracy of imaging studies of the degenerative cervical spine: Myelography, myelo-computed tomography, and magnetic resonance imaging. Semin Spine Surg 7:9, 1995
Bernhardt M et al: Cervical spondylitic myelopathy. J Bone Joint Surg 75A:119, 1993
Borenstein DG, Wiesel SW, Boden SD: Neck Pain: Medical Diagnosis and Comprehensive Management, WB Saunders, Philadelphia, 1996, pp 161-437
Brodsky AE: Cervical angina: A correlative study with emphasis on the use of coronary arteriography. Spine 10:699, 1985
Ferrante FM et al: Clinical classification as a predictor of therapeutic outcome after cervical epidural steroid injection. Spine 18:730, 1993
Herkowitz HN, Kurz LT, Overholt DP: Surgical management of cervical soft disc herniation: A comparison between the anterior and posterior approach. Spine 15:1026, 1990
Lehto IJ et al: Age-related MRI changes at 0.1 T in cervical discs in asymptomatic subjects. Neuroradiol 36:49, 1994
Lindgren K, Oksala I: Long-term outcome of surgery for thoracic outlet syndrome. Am J Surg 169:358, 1995
Martel W: The occipito-atlanto-axial joints in rheumatoid and ankylosing spondylitis Am J Roentgenol 86:223, 1961
Praemer A, Furner S, Rice DP: Musculoskeletal Conditions in the United States. American Academy of Orthopaedic Surgeons, Park Ridge, Ill., 1992, pp 23-33.
Redford JB, Patel AT: Orthotic devices in the management of spinal disorders. Phys Med Rehabil 9:709, 1995
Spitzer WO et al: Scientific monograph of the Quebec Task Force on whiplash-associated disorders: Redefining "whiplash" and its management. Spine 20(suppl 8):1S, 1995
Watt I, Cummins B: Management of rheumatoid neck. Ann Rheum Dis 49:805,1990


Was originally published here: http://www.uphs.upenn.edu/medicine/Medicine/Jaeger_Archive/neck_pain.htm