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Percutaneous Disk Interventions


Low back pain (LBP) and radicular pain due to spinal disease are very common symptoms, resulting in long absences from work or daily activities. Roughly 80% of adults suffer from back pain or LBP during a lifetime and of these, 44% experience pain in the cervical region, 15% in the thoracic, and 66% at the lumbar level. Most symptoms revolve spontaneously within a few days or weeks with conservative medical therapy, but about one-third of patients progress to chronic pain. The most common cause of LBP with classical irradiation along the nerve root course is intervertebral disk herniation revealed by computed tomography (CT) or magnetic resonance within 8 to 9 months after the beginning of back pain. The other causes include facet joint syndrome, spinal stenosis, spondylosis, and nerve entrapment syndrome.

In recent years, a wide range of minimally invasive percutaneous techniques have been developed as “alternative” treatments to surgery for patients with LBP due to a small or contained herniated disk, when conservative therapy has been unsuccessful. Surgical intervention is still considered the treatment of choice for extruded, migrated, and free-fragment herniated disk or neurological motor deficit.

The percutaneous intervertebral disk techniques can be classified in two main categories:

  • Mechanical, thermal, or chemical decompression:

    • Automated percutaneous lumbar diskectomy (APLD)

    • Percutaneous laser disk decompression

    • Percutaneous coblation nucleoplasty

    • Intradiskal electrothermal therapy (IDET)

    • Percutaneous intradiskal radiofrequency thermocoagulation

    • Chemodiskolysis with O 2 -O 3 mixture

    • Radiopaque gelified ethanol (RGE) (DiscoGel)

  • Biomaterials implantation (hydrogel)/disk cell therapies

The rationale of decompression treatments is to reduce the intradiskal pressure by removing a small nuclear volume in different ways, with subsequent inward imploding of the herniation. Others such as thermal decompression rely on fibrosis of the disk to decrease nerve root compression and disruption the pain receptors in the annulus area. The mean success rates for all decompression techniques range from 75% to 94%. , , The outcomes depend on the characteristics of herniation itself and on the chosen technique.

All techniques can be performed under CT or fluoroscopy guidance under local anesthesia. They offer effective results with long-term stable effects, low costs, and low rate of complications. They can be performed in outpatient surgery, resulting in minimum discomfort of the patient and, in the case of failed treatment, all treatments can be repeated once. All procedures can be applied to either cervical or lumbar levels.

Alternatively, promising techniques of biomaterial implantation therapies in intervertebral disk regeneration aim to restore normal biomechanical function. However, safety and long-term efficacy are still to be proved with these techniques.

Pathogenesis of low Back Pain

In the presentation of LBP, intervertebral disk degeneration and its secondary herniation play a decisive role. The pathogenesis of diskogenic pain appears to be multifactorial, including both mechanical mechanisms and inflammatory reaction.

Mechanical Causes

Direct mechanical effects are due to direct compression from the herniated disk on spinal nerve roots (intra- and extraforaminal herniation) and mechanical deformation of the posterior longitudinal ligament and annulus with nociceptor stimulation of the recurrent nerve of Luschka. Indirect mechanical factors are ischemia caused by pressure upon afferent arterioles and nerve bundle microcirculation with consequent anoxic demyelination of nerve fibers and venous stasis.

Inflammatory Factors

Degenerative disorder of the disk is characterized generally as enhanced extracellular matrix degradation, neovascularization, nerve ingrowth, and increased expression of catabolic cytokines, resulting in anatomic and biochemical disk changes and loss in structural integrity.

If a disk ruptures, exposing nucleus pulposus (formed by proteoglycans immunologically segregated after birth) to the vascular system, this may trigger an inflammatory process, with autoimmune cell-mediated response. Once activated, macrophages invade disk tissue, secrete proinflammatory cytokines (interleukin 1, tumor necrosis factor alpha) and matrix metalloproteinase 1 and 3, which degrade diskal tissue and increase the inflammatory reaction. However, the inflammatory cascade involves growth of blood vessels and nerves into the inner layers of annulus and nucleus. In addition, biohumoral immune response is activated, producing prostaglandin E2 and leukotriene from arachidonic acid, leading to the firing of nerve roots, with consequent inflammation and pain.

Indication and Contraindications

General Inclusion Criteria

  • Clinical criteria: LBP and sciatica not responsive to conservative medical therapy, physiotherapy, and other manipulations for a period not less than 4 to 6 weeks.

  • Neurological criteria: paresthesia or hypoesthesia over the dermatome involved, mild muscle weakness, and signs of root-ganglion irritation.

  • Neuroradiology (CT, magnetic resonance imaging):

    • Symptomatic contained small and medium-sized herniated disk complicated or not by degenerative disk-vertebra disease

    • Pain evoked by low-pressure contrast injection in the compromised disk during diskography for APLD, IDET, and nucleoplasty techniques

    • Residue of surgical (micro-) diskectomy, with herniation recurrence and/or hypertrophic fibrous scarring

  • Psychological criteria: Patient capable of providing informed consent to the treatment with a commitment to cooperate and undergo subsequent checks and rehabilitative physiotherapy.

The best results are reported for small and medium-sized herniations with a normal spinal canal, without disk calcifications.

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