Pain is a complex neurophysiologic phenomenon, initiated peripherally, appreciated centrally, and in between modified by a complex relationship of fiber tracts (18). Chronic pain carries with it the burden of past experiences and emotional and socioeconomic reactions (18). Is it any wonder that scientists have not solved the puzzle of pain? Add to that the fact that patients cannot describe pain, and we have a foundation of quicksand on which to construct an understanding and treatment of one of the most common presenting complaints in medicine: low back pain.

Let us try to follow pain from its origin to a patient’s response to the painful stimulus.

From the original work of Kellgren (12) to the more recent work of Mooney and Robertson (17), the concept of referred pain has enjoyed wide support among spine surgeons. Whether this support is correct remains to be seen in light of new work that must be done in this field. The most confusing position has been stated by Bogduk and Twomey (3), which states that if pain traveling down the leg is not associated with neurologic symptoms or signs, it is not true radicular pain. This is obviously incorrect, because many patients with sciatica, especially those in the younger age group, present exclusively with leg pain and marked reduction of straight leg raising (SLR), with little in the way of neurologic symptoms or signs. On investigation, they are found to have a disc herniation; when the disc herniation is treated, these symptoms abate. To conclude that these patients had referred sclerotomal or myotomal pain rather than true radicular pain is obviously an error.

At the other end of the spectrum, there are those in the field who state that any pain that does not go below the knee is referred pain and that any pain that travels below the knee is radicular pain. This also is incorrect because there are many young patients who present with a disc herniation manifested only by high iliac crest or buttock discomfort. On investigation, they are found to have a disc rupture; when the disc rupture is treated, their pain disappears.

Finally, there are patients who have radiating pain down the leg, full SLR, and no neurologic changes and who are also thought to have referred extremity pain. Some of these patients are in the older age group and, on computed tomography (CT) scanning and magnetic resonance imaging (MRI), are found to have various degrees of encroachment in the lateral zone. When these encroachment phenomena are relieved microsurgically, the pain disappears and, obviously, they have had radicular rather than referred discomfort.

For all of these reasons, it is time to repeat the work of Kellgren (12) and Mooney and Robertson (17), knowing exactly the pathology that lies at each segment as documented on CT scan and MRI. It is predicted that many of the patients who have previously been tagged with the label “referred pain” will, in fact, have radicular pain due to the direct involvement of a nerve root.

Many experts would accept patients as having referred pain when they present with a very diffuse sensation in their legs, which is bilateral in nature and not associated either with any radicular pattern or any root tension irritation or compression findings. Provided that those patients do not have spinal stenosis on CT scan or MRI, they probably have referred pain.

The concept of referred pain is one of two types of discomfort. Either it is a deep discomfort felt in a sclerotomal or myotomal distribution or it may be superficial in nature and felt within the skin dermatomes. The fact that gallbladder pain can be felt in the shoulder obviously supports the fact that referred pain is a phenomenon that does occur.

In theory, somewhere in the nervous system is a convergence and summation of nerve impulses from the primary painful area. This is probably lamina 5 in the dorsal horn. The stimulation of this lamina opens a gate and allows central dispatch of the pain message and distal referral of other sensations that indicate referred pain. The essential feature of the relationship between the site of the pain and the distal referral is the common segmental origin of the sensory innervation for both the origin and the distal referral site. Some of that commonality may occur in the complicated ascending pathways in the spinal cord. You can increase the painful sensation by touching the sites of referred pain. These areas are known as trigger zones, and, through various methods of stimulation and anesthetization, referred pain can be altered.

In summary, the concepts of referred pain are likely to be alerted with today’s sophisticated investigations in the form of CT scanning and MRI. With these tools in hand, it is time to go back and repeat the outstanding work of Kellgren (12) and Mooney and Robertson (17) in an attempt to further understand the concept of referred pain.

Partial tears of the attachment of muscles may occur, giving rise to local tenderness and pain of short duration. There is always a history of specific injury. The pain and tenderness are always away from the midline. This is a young person’s injury occurring in strong muscles that are guarding a healthy spine. A similar injury sustained by an older man, with weaker muscles and degenerated disc, is much more likely to result in a posterior joint strain.

The lesions heal quickly with the passage of time despite, rather than because of treatment. Injections of local anesthetic (with or without the addition of local steroids) into the areas of maximal tenderness certainly afford temporary relief of varying duration, but it is doubtful whether they speed the resolution of the underlying pathology.

The symptoms may persist for approximately 3 weeks, during which time the patient is well advised to avoid provocative activity. If symptoms persist beyond this period of time, the problem should be carefully reassessed lest some more significant underlying lesion has been overlooked.

The name “fibrositis” was first introduced by Sir William Gowers (7) in 1904, when he coined the word to denote nonspecific inflammatory changes in fibrous tissue that he felt were responsible for the clinical syndrome of “lumbago.” Fibrositis is now the most common cause of chronic, widespread, nonarticular, musculoskeletal pain in general practice. To date, the underlying pathologic lesion has never been demonstrated histologically and probably does not exist. The so-called fibrositic nodules, or tender points, which are palpable over the iliac crest, are usually localized nodules of fat. These “trigger points” are considered to be one of the hallmarks of fibrositis. Never mind that the examiner forgot to test the skin overlying these trigger points for tenderness or that the point locations have not been submitted to rigid scientific testing to determine validity.

The tender points are situated in an area that is a common site of referred tenderness derived from an underlying spinal lesion and they, along with the overlying skin, may be tender on pressure. The demonstration of a tender nodule associated with back pain and the occasional relief of
symptoms by the injection of local anesthetic has lent weight to this clinical concept. Surgical exploration of the nodules has revealed their questionable anatomic nature.

The concept of fibrositis becoming the most common cause of back pain in general practice for nearly half of a century is a classic example of how the phenomenon of referred pain and tenderness have clouded the recognition of the pathologic basis of low back pain derived from soft tissue disorders. There is no reason why the term should not be retained to describe the clinical syndrome: “low back pain of undetermined origin associated with tender points.” However, it must be remembered that the term does not denote a specific pathologic process. Rather, it describes a perfectionist or anxiety-laden personality, with diffuse chronic pain, in whom the bones, joints, bursae, and nerves are normal. These patients complain of musculoskeletal pain; nothing can be found on physical examination or investigation (except the tender points), so these patients are lumped into the nebulous category of fibrositis. If their syndrome is localized to one area of the body, such as the low back, there is a tendency to label the entity “myofascial pain syndrome” rather than fibrositis. This hair splitting does little to help us understand the problem.

Much of what we are describing throughout this text conforms to the traditional medical model of disease:

Fibrositis does not fit this model. Although it is a recognizable collection of symptoms (with few signs) (Table 4-1), it fails the remaining tests of the traditional medical model. By the time the diagnosis is made, you have a despondent patient and a frustrated primary care physician.

There is little question that the syndrome can be modified by psychosocial and economic factors (20).

Treatment of fibromyalgia patients is less than gratifying because the syndrome cannot be cured. Those clinicians with the patience of Job can do a great deal to ameliorate symptoms and lead patients to a better quality of life.

Effective methods of treatment have included some or all of the following:

All too often, the doctor-patient relationship follows two extremes concerning fibrositis: (a) “The condition doesn’t exist; all of the patients are crazy and I will not care for them” and (b) “The patients are sick and require extensive investigation and treatment,” which some clinicians would describe as overservicing. The best road to follow with these patients is the middle road, helping the patient to understand the psychosomatic nature, placing them in a vigorous self-supervised exercise program and, on occasion, providing low doses of amitriptyline (Elavil) to help with the sleep disorder.