Internal Disc Disruption (IDD) is a common cause of disabling low back pain in a substantial number of young, healthy adults. Crock described this painful entity and reported annular fissures that distort the internal architecture of the disc.40 Externally the disc appears relatively intact and is not deformed. Its etiology has been speculative but emerging circumstantial evidence favors a traumatic etiology.

Symptoms
IDD is often found in young adults with a history of trauma. They present with severe pain that is predominantly axial in nature (either low back pain or neck pain), the symptoms are of chronic duration and typically worse with any loading of the disc and/or activities that increase the intradiscal pressure. Such activities often include bending, lifting, sitting and, sometimes changes in posture. Unlike disc herniations however, this pain is not the result of disc compression upon the nerve root.

In most IDD patients the pain does not usually radiate into either extremity past the knee to the foot. Typically, these patients have no "hard/classic" neurological findings. Generally there is no motor loss, or (dermatomal) sensory loss, no loss of deep tendon reflexes or root tension signs.

Pathology and Biochemistry of Internal Disc Disruption

IDD is thought to be the result of a structurally incompetent and internally painful intervertebral disc. Farfan speculated that IDD was initiated by an endplate fracture following compression injury to the disc.

He portrayed IDD as the consequence of an un-arrested repair response that consumed the disc. The emerging picture is that IDD is the result of fatigue failure under compression which results in an endplate fracture that imposes abnormal stresses on the posterior annulus and which initiates an internal degradation of the nuclear matrix material.

Severe axial loading of the spine may produce end-plate disruption rather than damage to the annulus fibrosis. This is due to the fact that the load-bearing capabilities of the annulus are different than the end-plate and vertebral body. It has been demonstrated that, as force is rapidly applied, the end-plate and vertebral body are deformed at a greater rate than the disc, thus producing disruption in the end-plate 41.

The region of the vertebral end-plate is innervated by divisions ofthe gray rami of the sympathetics and sinuvertebral nerve.42 These nerves travel with blood vessels and have been noted in all anatomical locations within the vertebral body except in the deeper zones of the annulus or in the nucleus pulposus.

Disc material has also been implicated as a causative agent for chemically induced low back pain due to the irritating nature of the nucleus pulposus when it comes in contact with other structures. 43, 44

Diagnosis of Internal Disc Disruption

A clinical diagnosis of IDD, in the absence of objective clinical findings, may be difficult. This is because there are many spinal problems, which can result in nearly the exact same symptoms. Because of this, clinicians must rely on diagnostic testing to arrive at and confirm this diagnosis. Occasionally, a simple MRI is diagnostic for this process if there is a visible High Intensity Zone (HIZ), but most of the time it is non-specific and further testing is needed.

The standard diagnostic test is provocative discography. This test may show both the structural abnormality of the disc and may demonstrate reproduction of concordant pain that is the hallmark of this disorder. This is performed when surgical treatment is contemplated. VAX-D is a non-invasive procedure and the treatment may be undertaken with a diagnosis based upon history, clinical findings and MRI studies.

In these patients, the annulus appears to be extremely painful, although there is no herniation. They often reveal circumferential and radial tears radiographically. 45 This is a significant diagnostic factor because the usual diagnostic tests will appear normal. Not only is it important to identify the disc level exhibiting IDD, it is also essential for the discogram to identify adjacent normal discs if surgical treatment is to be entertained.

Plain film radiographs are essentially normal, as are CT examinations and myelography. MRI examination of these patients may reveal the presence of focal marrow conversion adjacent to the end-plates of the involved segments. This may be the result of local stress to the end-plate region, ischemia, or an inflammatory process.46, 47

Current Treatments of Internal Disc Disruption

Since the symptoms of discogenic pain are often related to increases in intradiscal loading, currently conservative treatment programs have been aimed at increasing global trunk strength in an effort to "unload" the disc and thus decrease the pain, and activity modification.

 Many IDD patients do not achieve satisfactory results with current non-invasive programs so they often consider surgery.

VAX-D –Treatment For Internal Disc Disruption & Diagnostic Indicators

Proteoglycans are an essential component of the nucleus responsible for retention of water content necessary for metabolic functions of the nucleus. Therefore loss of proteoglycans accounts for the loss of signal intensity with darkening of the MRI in T2 weighted images without concomitant loss in disc height as is seen in the early stages of degenerative disc disease. This and/or the presence of a High Intensity Zone (HIZ) on the MRI are indicative of IDD.

Certain tissue inhibitors of the metalloproteinases normally keep reparative and destructive activities in balance. If the balance is disturbed Stromelysin in particular can outstrip the ability of cells to repair the annulus and either prevent repair or even create a necrotic environment where degradation predominates.

While there may be various factors that might contribute to an imbalance of cellular function it is known that cell viability depends on a very narrow range of pH between 6.9 and 7.1. Cellular function in the disc is dampened by slight decreases in pH to the extent that only minimal cell function exists if the pH drops below 6.4, a decrease of only 0.6. In this context we have postulated that a persistent anaerobic state coupled with accumulation of lactic acid could lead to loss of cell viability and necrotizing discopathy. Others have postulated that IDD follows trauma resulting in rupture of the end plate.

Cases of IDD that present with an HIZ, on MRI, are thought to be a form of necrotizing discopathy with heightened apoptosis of cellular elements of the disc. This is especially relevant where the patient manifests constitutional disturbances consistent with the systemic circulation of protein degradation catabolites observed in necrotizing lesions.

In his textbook on the subject Bogduk commented that necrosis could be part of the syndrome afflicting some pathologic processes involving discs.

In considering the mechanisms prevalent in IDD, basic biochemical investigations are needed to elucidate the role of

matrix metalloproteinase (MMP) inhibitors. There are three principle MMP enzymes involved in disc degradation, Collagenase, Gelatinase and Stromelysin. These enzymes are released in an inactive form and are activated by certain agents such as plasmin. Collagenase and Gelatinase act together to cleave Type II collagen primarily found in the nuclear matrix. Stromelysin is the most destructive, cleaving various types of collagen found in the nucleus and annulus as well as aggressively attacking proteoglycans that constitute the matrix of the nucleus.

Mettaloproteinase degradation, in particular that of Stromelysin, releases catabolites from collagen and proteoglycan breakdown which not only can cause low back pain due to chemical irritation but also can elicit systemic symptomatology through permeation via a disrupted annulus into the venous plexus.

Provision of an aerobic medium in the disc necessary for reparative cell activity could facilitate reversal of the imbalance of repair vs enzymatic degradation. While this may be adequate in some cases it can be expected to fail where enzymatic activity continues uninhibited by natural biological factors and/or where cell viability has been damaged beyond recovery.

Many patients diagnosed with IDD will attain temporary relief of their symptoms with vertebral axial decompression during a session but they often relapse after a period of remission. It is thought that they exhibit an on-going inflammation in the intervertebral disc associated with degradation. Therefore, for these patients a definitive VAX-D protocol has been developed and has proven to be very effective.

Metalloprotienase inhibitors might be directly injected into the disc. However the ability to create a positive diffusion gradient through decompression of the disc might enhance the transfer of orally ingested agents from the serum into the disc.

Preliminary studies report promise in cases of IDD with the administration of Methylprednisolone 4-8 mg, given orally one to two hours before VAX-D. This combined treatment is recommended each day for the first week of treatment and continued on Monday, Wednesday and Friday of the second week. The shortness of this regimen should not pose any problems with steroid dosage.

Sequential treatment with Doxycycline 200 mg orally may be given one to two hours before VAX-D. This dosage should be started on Tuesday and Thursday of the second week and continued daily for the duration of the VAX-D therapy.

This compound is utilized here for its activity as a metalloprotienase inhibitor not as an antibiotic. Doxycycline was approved as a metalloprotienase inhibitor by the FDA in 1999.

Summary of VAX-D Protocol for Internal Disc Disruption

1. Methylprednisolone - 4 to 8 mg taken orally one to two hours before each VAX-D session.

	First week of VAX-D treatment - One dose each day
	Second week of treatment - one dose Monday, Wednesday and Friday

2. *Doxycycline (Vibromycin) - 200 mg. Taken orally one or two hours before each VAX-D session

	Second week of treatment- Tuesday and Thursday Thereafter each day for the duration of VAX-D sessions.
	For optimum absorption the above medications should be ingested on an empty stomach, and *Doxycycline should not be administered to patients who are allergic to tetracyclines.