Ankylosing spondylitis in the neck, also known as cervical ankylosing spondylitis, is a potentially serious autoimmune disease that affects the spinal joints. Patients are frequently functionally disabled by the disease and might even become completely incapacitated. Many patients cannot turn their heads, nor move their heads up or down to any large degree. Diagnosis and treatment of AS is one of the practice specialties of rheumatologists. These physicians focus on the joints and connective tissues of the human anatomy, so they are well qualified to provide expert guidance on spondylitis conditions.
This essay details ankylosing spondylitis disorders that affect the anatomy of the neck. We will investigate the symptoms, causes and treatments of the disease, as well as its relationship to the HLA-B27 genetic marker.
What is Ankylosing Spondylitis in the Neck?
AS is an autoimmune disease and is closely related to rheumatoid arthritis. The disorder occurs because parts of the immune system target the body’s healthy tissues, instead of protecting the anatomy from foreign invaders. In the case of cervical AS, the body attacks the spinal joints in the neck, often causing visible damage and functional impairment.
The spinal symptoms of AS usually include inflammation and fusion of the vertebral bones. This process can sometimes be seen externally, as swelling and disfigurement in the affected region. Typically, patients will have a rigid posture, since their spine no longer bends or flexes, as designed. The head is often pushed forward and can not be straightened, regardless of the effort applied. The greater the region that is fused, the more predisposed patients become to spinal trauma. Pain is usually present, although not in every case. Neurological symptoms might also result, including compressive neuropathy conditions caused by foraminal stenosis or spinal stenosis.
The disease has varying severities, ranging from insignificant to extreme. Furthermore, some cases never progress past a certain degree, while others continue to degenerate with time, leading to ever-worsening symptomatic and visual expressions.
There are few universal attributes of ankylosing spondylitis and each case should always be evaluated on an individual basis. This is especially important because the condition is often misdiagnosed as rheumatoid arthritis, gout, lupus or some other type of autoimmune disorder. Likewise, these other conditions can also mistakenly be diagnosed as AS. This is why it is vital to see a diagnostic specialist when any autoimmune disease is suspected.
Ankylosing Spondylitis in the Neck and HLA-B27
Human gene HLA-B27 is found in over 90% of ankylosing spondylitis sufferers. However, the gene is also found in people who do not have AS, nor will they ever develop the disorder. Various theories have been proposed about why some people with this genetic marker will develop AS and others will not. Some of the leading possible explanations include:
The HLA-B27 gene may need to interact with some form of bacterial or viral contaminant in order to activate the autoimmune process that causes AS. Various specific contaminants have been proposed, but none are universally accepted, even among doctors who embrace this particular causative theory.
The gene might be activated to begin the autoimmune reaction through mindbody interactions. Organic chemicals might act upon the gene, causing it to become pathological in some people, but not others.
The HLA-B27 gene might require other specific combinations of genes to create AS, although these genes have not yet been identified.
It should also be noted that a minority of people who have conclusively been diagnosed with ankylosing spondylitis do not possess the HLA-B27 gene at all.
Ankylosing Spondylitis in the Neck Considerations
Autoimmune disorders are very difficult to deal with, both medically and psychologically for the patient. Doctors have a difficult time trying to ascertain why normal immune responses go awry and attack healthy bodily tissues. These doctors have an uphill battle treating these diseases, without seriously compromising the overall wellness of the individual. Meanwhile, affected patients must live with the idea that their bodies are causing terrible harm to themselves. There is no contaminant to blame and no injury. This can be a horrific emotional burden to bear.
Treatment for AS usually revolves around the application of potentially dangerous pharmaceutical products, including pain management, anti-inflammatory, immune-suppressing and DMARD drugs.
Physical and occupational therapy helps many patients to preserve functionality and some measure of flexibility.
Surgery is used in certain cases where neurological consequences result. These procedures usually entail decompression of spinal nerves or the spinal cord in the neck. In some extreme instances, surgery must be done to free-up compressed circulatory structures, glands, lymph tissue and other structures that may be harmed from the progressive deformity of the neck anatomy.
There have only been anecdotal accounts of mindbody therapies being used successfully to treat AS, but since there are no risks to consider, there is certainly no harm in trying these alternative approaches to care.
Analysis of Ankylosing Spondylitis in the Neck
AS can be a truly sinister disease, but it does not have to become so. Some patients are utterly disabled by the disease, while others are basically spared. A minority of patients only show the beginning signs of AS, but the condition never progresses. A great number of diagnosed cases will progress through an active phase of growth, then the condition will naturally plateau out, slow down or stop worsening altogether. The most extreme cases will deteriorate year by year, until the patient is frozen solid into an unbending and fragile figure. Unfortunately, there is no way to determine how a given case will progress, except by observing and treating it day to day.
As a final note, patients are advised to thoroughly discuss the risk/benefit ratio of certain pharmaceutical products, before considering their use. Many of the most dangerous drugs show little proof of holding the disease in check, but demonstrate known and significant risk factors. We have spoken to several patients who found the treatments to be worse than the condition. Being that the condition might slow down or become inactive by itself, some varieties of pharmaceutical therapy should be contemplated carefully.