Treatment of Low-Back Pain with Oxygen-Ozone Therapy

Abstract

Oxygen-ozone therapy for the treatment of low back pain was introduced for the first time in 1985. Over the years, numerous case studies have been presented in the literature reporting positive results ranging from 75% up to almost 90% in the treatment of low back pain, whether or not complicated by sciatica due to disc-radicular impingement caused by disc herniation. The authors have been carrying out these treatments for over 25 years, and in this chapter, they report their experience in the treatment with oxygen-ozone therapy, first examining the biochemical bases and the mechanisms of action of the gaseous mixture of oxygen and ozone, the various infiltrative techniques, then moving on to evaluate the therapeutic results obtained in the treatment of patients suffering from both discogenic and non-discogenic low back pains caused by pathology of the posterior compartment (facet synovitis, Baastrup syndrome, spondylolysis and spondylolisthesis, facet degeneration).

1. Introduction

Low back pain—with or without sciatic nerve involvement—affects roughly 80% of the population at least once in a lifetime and is the leading cause of lost working days, with a major impact on national health organization and cost.

The treatment of choice for LBP sciatica, up to 20 years ago, was surgery, but conservative measures are now preferred in the wake of unsatisfactory surgical outcomes in around 15–20% of the cases. Among the techniques adopted in the last decade for the treatment of pain in the sciatic nerve caused by disc herniation or non-discal spine diseases (osteophytosis, spondylolysis, facet joint syndrome, etc.), the use of the treatment of back pain with targeted infiltration of O₂-O₃ has increasingly gained a foothold in many countries.

In recent years, several studies have demonstrated the utility of oxygen-ozone therapy in the treatment of herniated disc-related sciatica with its reduction in size on follow-up imaging examination (Figure 1a-b).

Figure 1.

a-b: (a) Large L4-L5 disc herniation (arrow), (b) completely resolved by oxygen-ozone therapy.

Oxygen-ozone therapy for the treatment of herniated discs was introduced for the first time in 1985. Over the years numerous cases have been presented in the literature reporting positive results ranging from 75% to almost 90% in the treatment of low back pain, also complicated by sciatica due to disc-radicular impingement, determined by the presence of a herniated intervertebral disc [1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16].

Low back pain and sciatica are pathologies, which can be identified as highly disabling, increasingly widespread in every social category. In recent years, they have also constantly manifested themselves at an earlier age, in the population. They arise acutely, following unusual effort or movement, or slowly, often with progressive aggravation.

They can be sustained by numerous and different vertebral pathologies, often concomitant: discopathies, facet joints, spondylolysis (with or without listhesis), somatic and interapophyseal arthrosis, spinal canal stenosis, root and synovial cysts, meningiomas, primary or metastatic neoplastic pathology, etc.

To choose the best therapy, in cases of low back pain and/or sciatica, a precise diagnosis—formulated after a careful objective clinical examination supported by adequate diagnostic tools—is therefore essential. It is very important to exclude the presence of a motor neurological deficit, which may represent an indication for surgical treatment. In particular, in addition to standard radiograms of the spine, computed tomography (CT) and/or magnetic resonance imaging (MRI) offer important information about the nature and etiology of the clinical situation associated with the symptoms encountered.

2. Pharmacological mechanisms of action of oxygen-ozone therapy for herniated disc

An analysis of pain caused by nerve root compression is a prerequisite for understanding the mechanisms underlying the effect of ozone on pain in patients with herniated discs [16]. Root pain is commonly related to nerve compression (disc root impingement or spinal impingement). However, there is a lot of evidence in clinical practice that the cause-and-effect relationship of radicular pain is not as simple as generally thought. For example, we know that many people are asymptomatic despite an incidental disc herniation during spinal neuroimaging for reasons other than disc disease. In two well-known published articles, only 3% of 98 and 116 asymptomatic patients showed a normal MRI finding. Furthermore, patients with known disc herniation live with the lesion between pain attacks, even though the morphology of the disc lesion and subsequent nerve root compression remain unchanged on CT and MRI scans.

Successful medical management of medical management or micro-invasive surgery such as intramuscular or intradiscal injection of oxygen-ozone is commonly found in a fair number of patients, in resolution pain without altering the morphology of the hernia, i.e., without changing the structure of the disc lesion.

Lastly, even though disc compression is surgically corrected, many patients continue to experience pain, relieved or even exacerbated, regardless of the herniated disc structural changes seen on neuroimaging scans after surgery, related to inflammation of neural structures and perineural. These results led us to investigate the mechanisms responsible for radicular pain related to pharmacological mechanisms of ozone action on herniated disc.

3. Pathogenesis of root pain

Reviewing the state of the art, we can distinguish two broad categories of pathogenetic mechanisms: mechanical and inflammatory, to which pain exacerbation linked to chronic illness should be added pain exacerbation linked to chronic illness [17, 18].

1. Pathogenetic components of root pain:

Mechanical pressure

The mechanical factors responsible for pain are related to the mass effect of the herniated disc material.

In turn, these can be divided into:

• Direct mechanical factors: considering the absence of nociceptors located in the nerve bundle, these factors are associated, in order of importance, to:

  • Compression of the spinal ganglion, possible intraforaminal and extraforaminal herniation;

  • Deformation and flattening of the ligaments and annulus, location of the afferent nociceptors to Luschka’s nerve of the posterior root of the spinal nerve;

  • Deformation and flattening of nerve fibers disrupting the myelin nerve sheath with possible major conduction abnormalities.

• Indirect mechanical factors I (also known as “vasculomediated”):

  • “Ischemic” vasculomediated factors. Characterized by trophic nerve impairment caused by compression of the arterial afferents and microcirculation of the nerve bundle and secondary anoxic demyelination of the nerve fibers;

  • Vasculomediated factors due to venous stasis with edema and trophic nerve impairment caused by partial or total blockage of venous reflux (especially in intraforaminal herniations). This factor appears to be the most important mechanical factor responsible for root pain because of its effects on the spinal ganglion (considering the anatomical relations between the intraforaminal vessels and spinal ganglion).

1. Pathogenetic components of root pain:

Inflammation

A major role in the origin of root pain is to be found in neural and perineural inflammation [19, 20]. Some evidence, though speculative, concerning the importance of inflammatory factors suggests that higher levels of antibodies anti-pso P27 (markers for inflammatory process, particularly of autoimmune origin) can be found in CSF from patients with low back pain and sciatica [21].

They include:

• Immune-mediated inflammatory reaction: evidence demonstrates that disc protrusion can be the cause of immune inflammatory events.

The hypothesis (even if not universally accepted) regarded as most likely to account for this behavior may be the fact that the adult intervertebral disc, from a humoral standpoint, is segregated with respect to the immune system as long as it is confined within the fibrocartilaginous structure of the annulus. Once herniated, the disc is recognized as “non-self” by the immunocompetent system, and this factor triggers a cell-mediated reaction in other tissues. The presence of peridiscal inflammatory tissue is confirmed by the CT and MR finding of peripheral enhancement of the disc fragment after i.v. contrast administration [22].

Additional experimental findings of the autoimmune component of peridiscal inflammation underline the action macrophages with expression of the IL 1β gene—characteristic of autoimmune reactions—and the reduction of mechanical hyperalgesia following drug-induced leucopenia under experimental conditions [23].

• Inflammatory reaction due to biohumoral factors linked to disc tissue. Experimental evidence in this field includes the following:

  • Phospholipase A2 (PLA2): The herniated disc material contains increased levels of PLA2 enzyme activity. PLA2 plays the role of powerful inducer of the inflammatory reaction for its enzymatic activation to arachidonic acid causes to the production of major chemical mediators of inflammation, like prostaglandins and leukotrienes. Moreover, PLA2 may damage nerve fibers by attacking perineural and neural membrane phospholipids [24];

  • Matrix metalloproteinases (MMPs): There is a significant production of this enzyme that enhances the inflammatory reaction by attacking disc tissue;

  • Prostaglandin E2 (PGE2): The disc tissue and the enzymatic intervention of PLA2 (a powerful inducer of inflammation) produce PGE2. The same factors are applied to interleukin 6 (IL6) [25];

  • Evidence investigating a recently identified glycoprotein, YKL-40, is undergoing, at the moment. This glycoprotein is produced in abundance following joint lesions, including degenerative disease, which could be one of the main mediators of the inflammatory reaction in disc disease [26].

1. Pathogenetic components of root pain: Symptoms exacerbated by chronic pain:

By exacerbation of symptoms caused by chronic pain we mean the mechanism by which the chronic mechanical and inflammatory stimulation of the nerve root stimulates the ganglionic and periganglionic nociceptors (mainly polymodal type C) responsible for hyperalgesia, a condition presenting allodynia, i.e., a lowering of the pain threshold and an increase in pain intensity also following subliminal stimuli, in some cases also activating spontaneous pain discharges [20].

3.1 Pharmacological mechanisms underlying the effect of ozone on the various components of root pain

1. Effect of ozone on direct mechanical pressure

The effect ozone is thought to have on the herniated disc as such is based on biochemistry composition of the intervertebral disc, mainly composed of proteoglycans and collagen [26, 27]. Cartilage proteoglycans [28] comprise a series of copolymers consisting of a protein core, called the “core protein,” bound to about 100 unbranched side chains of chondroitin sulfate and up to 50 keratan sulfate chains. Chondroitin sulfate chains are strongly polyanionic and bind large amounts of water, while keratan sulfate chains are less so.

Collagen forms a solid fibrous armor that supports and neutralizes traction and shear forces due to joint movement. Of the 14 known collagen types, the outermost part of the annulus fibrosus mainly belongs to type I. Type II collagen predominates in the innermost part of the annulus, and type IV is mainly found in the “nucleus pulposus” [29].

Thus, the nucleus pulposus and herniated disc are complex macromolecular structures containing water bound to various hydrophilic matrices.

How does ozone attenuate direct mechanical compression?

Due to its solubility and pressure, once injected into the disc, ozone dissolves into the intradiscal water and decomposes immediately generating a cascade of reactive oxygen species (ROS) [25]. Because intradiscal water contains a minimal amount of fatty acids, lipoperoxides are unlikely to form. The oxidation of the various substrates present in the disc, in particular glucose, galactose, N-acetylglycosamine, glucuronic acid, glycine, and 4-hydroxyproline, breaks the intra- and intermolecular ligands leading to the collapse of its three-dimensional structure. These events can occur in both the nucleus pulposus and disc herniation and are thought to lead to fluid reabsorption and fibrosis [30, 31, 32].

1. Effect of ozone on the indirect mechanical factors

Indirect mechanical factors are largely mediated by vessels. In this case, oxygen-ozone exerts one of its best-known pharmacological effects, namely the increase of intra- and trans-tissue oxygenation, thus improving hypoxia and venous and lymphatic stasis.

1. Effect of ozone on the cell-mediated inflammatory response

Ozone influences the cell-mediated inflammatory response to hernia by two main pharmacological mechanisms [25]:

• inhibition of proteinase release by macrophages and polymorphonuclear neutrophils;

• enhance the release of immunosuppressive cytokines (interleukin 10, TGF beta 10) which inhibit any cytotoxic clones [33].

1. Effect of ozone on the biohumoral inflammatory response

The possible effect of ozone on the biohumoral component of the inflammatory response is more complex. Taking into account the biohumoral factors involved in the inflammatory response, ozone could carry out its action as follows:

• inhibiting the synthesis of pro-inflammatory prostaglandins;

• inhibiting the release of bradykinin or pain-inducing compounds;

• neutralizing the endogenous ROS and stimulating the local production of antioxidant enzymes;

• increasing the release of antagonists and the pro-inflammatories cytokines such as interleukin 1, 2, 8, and 15 [33].

1. Effect of ozone on symptoms exacerbated by chronic pain

Ozone is thought to relieve symptoms exacerbated by chronic pain as a type of “chemical acupuncture” or “reflex therapy.” This depends on the counter-irritant effect of the needle-gas combination, which would have a bending action on the antinociceptor system. The insertion of the needle and the subsequent injection of positive pressure ozone stimulate the nociceptors of the paravertebral muscles. This in turn can inhibit nociceptive neurons in the spinal cord by releasing opioid peptides. In other words, stimulation by pressure and chemoreceptors and muscle spindle fibers at the site of disc disease can give rise to a kind of local lateral inhibition. Last but not least, any direct nociceptive stimulation is known to relieve pain through the mechanism of diffuse noxious inhibitory control [25].

3.2 Conclusive remarks

In light of current knowledge, radicular pain from nerve root compression is to be considered a symptom of multifactorial origin in which the neural and perineural inflammatory reaction and its biohumoral mediators play a preponderant role, flanked by venous stasis from mass effect on the circulation perineural. Nerve compression seems to play an adjuvant role by generating nerve conduction abnormalities due to demyelination of the fibers with a direct or indirect anoxic-ischemic mechanism.

Since pain is multifactorial, ozone can also have a multifactorial pharmacological effect by relieving disc compression through narrowing and triggering pro-fibrous mechanisms in disc herniation, thus counteracting the inflammatory cascade of biohumoral and cell-mediated components and improving the hypoxic state related to artery compression and venous stasis. Finally, ozone can have a reflexotherapy effect (“chemical acupuncture”) by breaking the chain of chronic pain that stimulates the anti-nociceptor analgesic mechanisms [32, 33].

4. Application methods

4.1 Ozone therapy in the paravertebral muscle bundles: “Classic” technique

The patient is placed on the bed in the prone position. The disc space to be treated is identified through anatomical cutaneous landmarks: line of the spinous process with recognition of the spinous process of L4 at the level of the trans-iliac line and then positioned 2÷2.5 cm bilaterally to the interspinous spaces (Figure 2). Thorough skin disinfection is carried out in the area to be infiltrated, skin anesthesia with ethyl chloride spray, needle insertion, generally 23G (Gauge) for lumbar treatment, and 25G for the cervical.

Figure 2.

Paravertebral intramuscular infiltration of O₂-O₃.

Following the correct insertion of the needles into the muscles, aspiration occurs, and we proceed with the injection of the oxygen-ozone mixture with an optimal therapeutic window using doses at a concentration of 20/25 μg/ml. and volume: 5 ml. by injection, the entire therapeutic cycle consists on average of 8–10 infiltrations, 2 infiltrations every week.

4.2 CT-guided intraforaminal technique

The treatment is carried out in day hospital and the infiltration technique is the same that is used for discographies; in fact, a preliminary CT examination is foreseen to establish the infiltration point at the skin level and subsequently, the distance of this is measured last from the conjugation foramen. Local anesthesia with ethyl chloride spray is performed. The needle used is always a 22G needle of variable length, and usually, we use 9-cm Terumo needles. Proper needle placement is then verified using CT scans. The tip of the needle must be approximately 4–5 mm from the foraminal region; 3 cc of oxygen-ozone mixture at 25 μg/ml are injected. After that, the needle is withdrawn a few mm and another 5–6 cc. of gaseous mixture are injected into the mass of the joint. We then proceed by carrying out a CT check of the correct distribution of the oxygen-ozone mixture (Figure 3). The patient remains under clinical supervision for about 30 minutes before being discharged. The clinical benefit of the treatment is almost immediate. The patient is then clinically re-evaluated after 10 days, and if the result has not been satisfactory a second treatment is carried out, this operation can be repeated once or twice. Three months after the end of treatment, a CT scan of the treated disc herniation is performed in all treated patients. There are no contraindications, and no side effects have ever been reported.

Figure 3.

Correct positioning of the needle under CT guidance.

The intraforaminal administration of ozone CT guided with the proposed modality combines the precision in the control of the needle path with the curative possibility of all the O₂-O₃ infiltration techniques used up to now. Improvement of local circulation with eutrophic effect in the both vicinity of the compressed and suffering nerve root and at the level of muscle spasm; the normalization of the level of cytokines and prostanglandins with anti-inflammatory and pain-relieving effect; the increase in the production of superoxide dismutase (SOD) with minimization of oxidizing reagents (ROS); and finally the close proximity to the herniated material that determines accelerated dehydration or destruction of a non-vascularized tissue that justifies the good final result.

The rapid resolution of painful symptoms with no complications, the ease of execution of the method, and complete control of the infiltration via CT allow, today, to propose oxygen ozone therapy with CT-guided intraforaminal technique as a valid alternative to surgical treatment of herniated disc if the latter is not considered essential and therefore a method of choice among conservative therapies.

4.3 Intradiscal technique

Percutaneous treatment of discolysis with oxygen-ozone (O₂-O₃) can be performed subcutaneously fluoroscopically or under CT guidance. In both cases the oxygen-ozone mixture is injected into the intervertebral disc, along the postero-lateral, extra-articular route.

The procedure can be performed in Day Hospital or One Day Surgery.

4.4 Fluoroscopic guide

It is necessary to observe some pretreatment recommendations also concerning the X-ray room for the surgery.

The X-ray room must in fact have instruments suitable for anesthesiological assistance. Compliance with asepsis must be guaranteed, a fluoroscopic apparatus must be available (preferably isocentric) with a “C” arm that allows direct scopic control, and, finally, peripheral venous access to the patient must be guaranteed.

Thorough skin disinfection and a sterile field must be carried out before the puncture.

The patient lies on the X-ray bed in lateral decubitus (access is ipsilateral to the site of the symptoms). Under fluoroscopic guidance, the puncture of the intervertebral disc is performed with a 22 G needle.

The intradiscal position (the needle tip must be in the center of the interbody space) is documented by acquiring radiographic images in the A-P and L-L projections (Figure 4a-b). After placing a millipore filter on the syringe, proceed with the injection of 7–8 cc of O₂-O₃ mixture at a concentration of 25 μg/ml, of which 3–4 ml intradiscally and, once the needle has been withdrawn with the apex projecting at the interapophyseal joint, another 4 cc is injected in the periradicular and paravertebral soft tissues.

Figure 4.

a-b. (a) Latero-lateral view, (b) antero-posterior view. Correct needle placement.

For higher interbody spaces, disc access is more direct than the L5-S1 space. Once the patient has been placed in lateral decubitus position and the nucleus pulposus has been positioned in the center of the interbody space, a lateral rotation of the arc of about 35° is performed, which allows recognition of the ipsilateral joint at the level of the posterior third of the interbody space. The needle is inserted in the middle third of the interbody space, and its path must be followed in the lateral projection. During the procedure under fluoroscopic guidance, radiographic documentation of the final position of the needle in the main radiological projections is performed.

As mentioned, the approach to the L5-S1 space under fluoroscopic guidance differs from that of the higher disc spaces: Once the patient is positioned in lateral decubitus position and the nucleus pulposus of L5-S1 in the center of the radiographic image, rotation is performed of the arc of about 35°, which allows recognition of the intervertebral joint thus projected at the level of the posterior third of the disc space.

Access to the disc, masked by the ipsilateral iliac wing, is possible, at this level, only with a further inclination of the arch in the cranio-caudal direction. An area of access to the disc is thus obtained, delimited inferiorly by the superior somatic limiter of S1, posteriorly by the anterior profile of the superior articular process of S1 and anteriorly by the superior profile of the ipsilateral iliac wing. At the end of the procedure, the patient must maintain the lateral decubitus position for about 30 minutes; bed rest on the first day after treatment and chair rest on the second day are also indicated. For the following period, a gradual resumption of activities without loading the lumbosacral region should be recommended.

4.5 CT guide

The patient must be positioned in prone decubitus with devices that reduce the physiological lumbar lordosis. A targeted CT examination is carried out on the level to be treated and the distance from the spinous process to the cutaneous entry point of the needle is calculated, which allows an easy puncture of the central part of the disc (preferably the nucleus pulposus) with an angle of 45°.

Metal landmarks are placed on the skin and, once the entry point has been identified, it is traced with a demographic pencil.

Once you reach the level of the disc you will feel the sensation of yielding of a tense structure due to the entry of the needle into the disc itself (Figure 5).

Figure 5.

Correct positioning of the needle in the heart of the disc.

This is followed by the intradiscal injection of the O₂-O₃ mixture in quantities of 3–4 ml at a concentration of about 25 μg/ml.

Finally, a CT control of the distribution of the mixture is performed. At the end of the treatment, the patient will have to switch from prone to supine position and keep the latter for about 2 hours.

5. What to treat

5.1 Disc herniation

Several studies have demonstrated the utility of oxygen-ozone therapy in the treatment of herniated discs with the result of herniated discs reduced in size [1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 34, 35, 36].

In our experience, which dates back to 1993, we carry out treatments of both lumbar and cervical disc herniation with CT-guided intraforaminal technique with therapeutic results in complete agreement with what is reported in the international literature, ranging from 75% up to almost 90% of success therapeutic in the treatment of low back pain complicated or not by sciatica due to disc-radicular impingement due to disc herniation (Figure 6a-b).

Figure 6.

a-b: (a) L4-L5 paramedian left preforaminal disc herniation (arrow). (b) Complete dehydration after treatment with oxygen-ozone.

6. Infiltration technique: Our experience

Treatments are performed under CT guidance, using the deep intraforaminal-paravertebral infiltration technique. Based on the neuroradiological documentation and the patient’s clinical symptoms, it is decided to treat the patient and at what level. After being informed about the procedure and possible complications, the patient signs the informed consent. Preliminary CT scans are performed in the prone patient to confirm the pathology and level to be treated. At this point, the skin is disinfected using special preparations for general skin antisepsis (Citro jod 100 registration n° 1805 of the Ministry of Health based on polyvinylpyrrolidone iodine). A preliminary CT scan is performed to locate the skin approach point. Local anesthesia is carried out with ethyl chloride spray and subsequently, always using the CT guide, the spinal needle is positioned; normally, needles of variable caliber between 22 and 25 G are used. The perfect positioning of the needle is checked with a CT scan. Fill a 10-ml syringe in polyethylene with the gas mixture at a concentration of 25 μg/ml. The gaseous mixture is then injected. Generally injecting a variable volume from 3 to 5 cc of O₂-O₃ gaseous mixture in relation to the pathology to be treated. After the infiltration, further CT scans are performed to document the correct distribution of the gaseous mixture. All materials used must be sterile and disposable.

In recent years, especially thanks to the introduction of MR sequences with Fat Saturation and gadolinium in patients with degenerative disease of the lumbar spine and low back pain, diagnostic imaging has become even more helpful to the clinician in making diagnoses to decide the best therapeutic strategy to adopt based on the pathology to be treated.

In particular, in patients with non-radicular low back pain, this syndrome may arise from changes of the posterior elements of the lumbar spine (the “posterior vertebral compartment”).

In fact, in most cases, good patient selection allows striking clinical results; with reference to our case studies in all the different applications selected we have found optimal therapeutic results in a percentage of about 75% of the cases treated considering the various pathologies overall.

The rapid resolution of pain, with no complications, the ease of performing the method and complete control of infiltration under TC control allow today to propose the CT-guided oxygen ozone therapy as a viable alternative to the various treatments currently being proposed for the various pathologies of the posterior compartment so much that it can be proposed as a method of choice between conservative therapies.

Emphasizing how this type of therapy does not contraindicate other infiltrative or surgical therapies.

It is also possible to treat selected frameworks with oxygen-ozone such as:

Facet synovitis

Intra and/or interapophyseal synovitis is an inflammatory disease of the synovial membrane, at the base there is usually a micro- or macro-traumatic event, sometimes it can also arise in young adults as a result of excessive stress on the spine, a typical finding in sportsmen who practice extreme sports with considerable spinal stresses.

The onset, in most cases, is acute with low back pain, and the symptoms can be unilateral if only one joint is involved or “bar” in case of involvement of both massive joints [37].

Diagnosis is often not easy and it is essential to perform an MR with contrast media injection to have a clear diagnosis ([38, 39, 40, 41, 42]; Figures 7 and 8).

Figure 7.

Axial lumbosacral MRI after gadolinium administration: Bilateral post-traumatic apophyseal synovitis (arrows).

Figure 8.

In the treatment of interapophyseal synovitis, the needle is positioned under CT guidance at the level of the joint.

Baastrup syndrome

Baastrup syndrome, described by the Danish radiologist Christian Baastrup in 1933 and also known by the Anglo-Saxon term of “kissing spines,” is characterized by the presence of arthrosis between the spinous apophyses of the vertebral column, which leads to the formation of real “neo-joints” and is often the cause of low back pain that is refractory to common treatments with anti-inflammatory and pain-relieving drugs. It predominantly affects the female sex with an F:M = 4:1 ratio and is usually diagnosed in the third decade of age.

The diagnosis is radiological: The standard Rx shows an extreme hyperlordosis of the lumbar tract up to the mutual contact of the spinous processes and a degeneration of the same.

The course of the disease is progressive and in the face of an accentuation of the low back pain, it is indicated to complete the investigations with an MRI with Fat/Sat sequences and possible administration of gadolinium in order to highlight any inflammatory focal points in the acute phase ([43, 44, 45, 46, 47, 48, 49]; Figures 9 and 10a-b).

Figure 9.

Sagittal MRI after contrast medium administration: Pathological impregnation at the interspinous ligament at L3-L4.

Figure 10.

a-b: (a) axial MRI intense and homogeneous impregnation of the interspinous ligament at L3-L4 (Baastrup syndrome) (arrows), (b) resolution of the picture after infiltration with oxygen-ozone.

Spondylolysis and spondylolisthesis

Spondylolysis is a bony defect of the neural arch. If the bony defect results in a forward shift of one vertebral body on another, this is called spondylolisthesis (a term coined by Kilian in 1854).

Spondylolisthesis is classified according to the Meyerding classification in relation to the degree of sliding of the overlying vertebral body compared to the underlying one (Figure 11).

Figure 11.

Meyerding’s classification uses as a criterion the degree of sliding of the overlying vertebra (b) with respect to the underlying one (a).

7. Meyerding’s classification

The degree of forward shift of one vertebral body on another is measured as a percentage according to Meyerding’s classification:

Grade I 0-33%

Grade II 34-66%

Grade III 67-99%

Grade IV 100% and spondyloptosis

First-degree spondylolisthesis is asymptomatic in most cases and is often an occasional finding; however, in a small percentage of patients it can manifest itself with back pain complicated or not by sciatica.

Most patients with symptomatic grade I spondylolisthesis and spondylolysis do not require surgery and the treatment approach is physiokinesitherapy in nature, but when symptoms do not resolve with physical therapy, they may require spinal stabilization surgery.

Based on our experience, we carry out treatments in patients with first-degree spondylolisthesis (less than 33% anthelisthesis), bilateral isthmic lysis, and associated discopathy (disc herniation or protrusion).

All patients are treated by CT-guided bilateral periganglionic infiltration of O₂-O₃ and O₂-O₃ injection into the lysis points in the neural arch ([12]; Figures 12 and 13a-b).

Figure 12.

Positioning of the spinal needle in the lysis point. CT check.

Figure 13.

a-b. (a) Placement of the spinal needle at the intraforaminal level. (b) Control of the distribution of the post-infiltration gaseous mixture.

8. Facet degeneration

Twenty-five to 45% of chronic low back pain is due to facet joint syndrome. Obviously, this syndrome can be accompanied by other problems contributing, mainly or partially, to pain and disability. Facet degeneration commonly occurs in the elderly. There are many conditions capable of generating facet symptoms, and among these, osteoarthritis is the most frequently encountered. This condition results in the reduction or disappearance of articular cartilage, erosion of the adjacent bone margin, abnormal bone growth of the facet and articular processes, and ultimately joint instability, which can lead to vertebral subluxation. The sensitive nerve endings of the facet joints and surrounding tissues undergo irritation resulting in the sensation of spinal pain. The selection of patients eligible for interventional treatment makes use of both clinical-anamnestic data and data derived from the use of Diagnostic Imaging. Conventional radiographic examination and computed tomography are used to highlight joint relationships, anomalous growths of the joint bone component, and the reduction of joint spaces, an indirect index of cartilage remodeling; but MRI is mainly used, in particular in T2-weighted fast spin echo with fat suppression and T1-weighted fast spin echo with fat suppression and administration of paramagnetic contrast medium, to identify the active inflammatory process within or surrounding the facet joint.

Several types of treatment have been proposed for the pain of facet syndrome: intra-articular injection, nerve blocks, and radiofrequency thermos-neurolysis [12].

At a clinical level, to select patients afflicted by this pathology, we use a series of now well-codified criteria. The diagnosis is suspected from the description of the pain and by making the patient practice both passively and actively movements that set the facets in motion:

• Deep low back pain, often more on one side than the other;

• Pain referred to the groin, thigh, buttock, and iliac crest;

• Pain on acupressure of the facets themselves;

• Increased pain with movement of extension (bending back) of the spine;

• Pain on rotation of the trunk toward the affected side;

• Aggravation of pain after prolonged standing and sitting position;

• Improvement with bed rest;

• Stiffness of the column;

• Absence of lower limb neurological deficits in sensation and movement;

• X-ray picture on plain X-ray, CT scan, and typical MRI.

All patients are treated with CT-guided technique, positioning the 22G spinal needle near or inside the facet joint and injecting 2–3 cc of O₂-O₃ gas mixture at 25 μg/ml (Figure 14).

Figure 14.

CT check of the correct positioning of the needles at the level of the massive joints.