Atlas Section

10.1055/b-0039-167999

9 Lumbar Injection Therapy

Pain in the lumbar spine primarily arises in the two inferior lumbar vertebral motor segments, i.e., L4/L5 and L5/S1. One reason why the most marked disorders of form and function are found here is because of the exceptional loading placed on the inferior lumbar spine. Another reason is that spinal nerves and their efferent branches are found in the immediate vicinity. The sacroiliac joints (SIJs) also usually contribute to this painful situation. They belong functionally to the inferior lumbar vertebral motor segments, and the dorsal ramus of the spinal nerve connects them with the S1 nerve root. The special topographical relationship between the musculoskeletal system and the nervous system in this region is of particular importance not only to pain therapists, but also to surgeons.

9.1 Specialized Lumbar Neuroanatomy

The vertebral body and the intervertebral disk form the anterior border of the lumbar spinal canal, and the ligamentum flavum and the vertebral arch form the posterior border. The pedicles and the intervertebral foramina are found laterally. The lumbar vertebral canal is a cylindrical cavity that changes its shape and volume with every movement of the trunk: trunk flexion increases its volume, and trunk extension causes it to narrow.

The contents of the lumbar vertebral canal include the dural sac, nerve roots, and peridural tissue. The peridural tissue consists of veins and fatty tissue and encases the nerve root, ensuring that it is protected from the bony borders of the vertebral canal even during extreme movements of the lumbar spine.

The displacement of spinal cord segments in relation to their corresponding motor segment in the vertebral column is at its most extreme in the lumbar spine. The inferior end of the spinal cord extends only to the first or second lumbar vertebra. The spinal nerves exit the vertebral canal through their corresponding intervertebral foramina inferior to this, and travel for a long distance in the subarachnoid space, where they are usually found laterally. There is thus no need to worry about nerve injuries when conducting medial lumbar punctures and myelography, or during transdural disk punctures.

Paramedian protrusions and prolapses can cause the intrathecal compression of spinal nerves and more deeply situated nerve root syndromes. The entire length of the long inferior spinal nerves and the filum terminale, the final fibers of the spinal cord that extend down to the second coccygeal vertebra, is called the cauda equina.

After leaving the dural sac, the nerve root travels in a direction dictated by the segmental level. The more inferior the nerve root is, the more acutely angled it is as it exits the dural sac. This explains why different topographical relationships are observable between each nerve root and intervertebral disk in the lumbar vertebral motor segments. The exit point for the L4 nerve root is found at the same level as the L3 vertebral body, the L5 nerve root exits the dural sac at the height of the inferior edge of the L4 vertebral body, and the S1 nerve root exits at the inferior edge of the L5 vertebral body (Fig. 9‑1).

An L4/L5 intervertebral disk prolapse (Fig. 9‑1, arrows) exerts pressure primarily on the L5 nerve root. The L4 nerve root is affected only when the prolapse is very large and is displaced in a lateral or superior direction, as a result of the L4 nerve root passing superior to the L4/L5 intervertebral disk. The S1 and L5 nerve roots can be affected at the same time at the L5/S1 intervertebral segment, even by a small lateral prolapse (Fig. 9‑1, arrows). The L5 spinal nerve root lies in the upper section of the intervertebral foramen, directly on the outer lamellae of the intervertebral disk. The L5 nerve root has only a very small amount of free space within the L5/S1 intervertebral foramen. The lumbar nerve roots are affected by intervertebral disks only in the two inferior segments: it is here that there is the most danger of compression arising from an intervertebral disk.

The foraminal articular region, with the spinal nerves exiting the intervertebral foramen and the efferent nerve branches, is of particular interest. Directly after its exit from the intervertebral foramen, the spinal nerve divides into a thicker ventral ramus, a somewhat thinner dorsal ramus, and a tiny sinuvertebral nerve. The dorsal ramus divides into a lateral branch that runs to the facets and a medial branch that runs to the spinous process (Fig. 9‑2). The recurrent branch (meningeal branch, sinuvertebral nerve; see Fig. 9‑3) passes through the intervertebral foramen, back into the spinal canal, and innervates the rear section of the anulus fibrosus, the posterior longitudinal ligament, and the dura.

Fig. 9‑3 (second spinal nerve) demonstrates how close the spinal nerves and their branches are to the muscles and joints, and also to the sympathetic trunk via the ramus communicans connection in the foraminal articular region of the inferior lumbar vertebral motor segments. Nociceptors in the joint capsule, the posterior longitudinal ligament, and the periosteum of the vertebral body are located in close proximity to the afferent fibers of various nerves. Disorders of form and function in the musculoskeletal system cause reactive changes in the joint capsule and outer edges of the vertebral body as a result of intervertebral disk degeneration. At the same time, this causes irritation of the nociceptors found there, leading to neuralgia when afferent fibers are irritated over a longer period of time. The autonomic reaction is directly and indirectly involved as a result of the irritation of the ramus communicans from the meningeal branch to the sympathetic trunk and via the spinal nociceptive reflex arc (see Chapter 1, “Moving from Acute to Chronic Pain: Nociceptor Sensitization”).

Fig. 9.1 Nerve roots that traverse and exit in the inferior lumbar vertebral canal. The traversing nerve roots run vertically in the vertebral canal, intrathecally and extrathecally, and pass over the intervertebral disk. The spinal nerve roots lateral to the medial pedicle border are labeled as exiting nerve roots and have an oblique to horizontal course. The S1 nerve root is a traversing nerve root up to its exit point from the sacral canal.

Fig. 9.2 Lumbar spinal nerve with ventral ramus and dorsal ramus. Reproduced with permission from Bogduk 1997.

Fig. 9.3 The spinal nerve with its branches. Reproduced with permission from Bogduk 1997

The foraminal articular region of the lower lumbar vertebral motor segments is particularly important in the development and treatment of chronic back pain and sciatica. Obviously, the nociceptive neuralgic structures, located so close to each other, are suited for local treatment, e.g., infiltration.

9.2 Basic Therapy for Lumbar Pain

General therapeutic measures, such as bed rest, heat treatment, massage, electrotherapy, and analgesics, act in some way on the vicious circle of pain–tense muscles–pain, resulting in freedom from pain in mild cases. The lumbar intervertebral disks experience the least amount of loading when the patient is positioned horizontally with the lumbar lordosis flattened out and the hip and knee joints flexed. For this reason, the use of the so-called Fowler position is recommended as the first treatment measure (Fig. 9‑4 a, b).

Fig. 9.4 **(a, b)** The Fowler position: hip and knee joints are placed at right angles, in a step-like manner. The sciatic nerve is maximally relaxed in this position. The lumbar lordosis is flattened, which in turn widens the intervertebral foramina and the lumbar vertebral canal. The zygapophyseal joint capsules are relieved of loading. **Caution**: When mobilization is difficult, always think of **thrombosis prophylaxis**, using low-dose heparin and antithrombotic stockings.

Heat, in the form of mud packs, heat pads, or infrared treatment, acts to relieve pain and muscle tension. Analgesics and anti-inflammatories are additionally administered when pain is very severe (see Chapter 4, “Multimodal Medication Concomitant Therapy”).

Massage and electrotherapy are first administered in acute lumbar syndromes after the acute symptoms have been largely relieved by positioning, heat treatment, and analgesics. Electrotherapy is administered using high frequency, low frequency, and interferential currents (see Chapter 4, “Electrotherapy”).

Ultrasound relaxes ligamentous and insertional tendinopathies, especially in the region of the interspinous ligaments and the short back muscles. Diadynamic currents have a deep analgesic effect at the nerve roots and their branches. Deeper-lying spinal structures can also be reached by the use of short-wave radiation.

Manual therapy is indicated in the treatment of lumbar spinal pain when acute local zygapophyseal joint or SIJ symptoms are present, or when another functional disorder is the focus of attention. This is precisely ascertained using manual assessment techniques (see Chapter 2.2). Manual therapy should be used with caution when intradiscal mass displacement, protrusions, and prolapses are present, as manipulation can sometimes increase the degree of protrusion.

If the anulus fibrosus is intact, the use of traction enables displaced intervertebral disk tissue to return to the center of the disk. Several options are available for traction in the lumbar spine region, including self-traction, permanent traction devices positioned on the iliac crest, or traction belts (Krämer 1997). Traction on an inclined bed or traction table, or using Perl’s apparatus, has now been replaced by the more manageable flexion cube, which repositions lumbar intervertebral disk protrusions in the same way, combined with heat treatment.

The physician fits these orthopedic aids individually according to how treatment is progressing, on the basis of clinical neurological signs that must be reassessed at regular intervals.

The supportive and corrective function of flexion orthoses is useful in the treatment of acute and chronic pain in the lumbar spine that is caused by the displacement of intradiscal mass and a hyperlordotic position of the zygapophyseal joints. Their use is indicated in postsurgical segmental instability, e.g., following discotomy, percutaneous nucleotomy, or chemonucleolysis. Degenerative instability with height reduction in the posterior section of the vertebral motor segment is also an indication for the use of orthoses, which should reduce loading on the vertebral motor segment by increasing intra-abdominal pressure and flattening out the lumbar lordosis. This flattening leads to widening of the intervertebral foramina and the spinal canal (Fig. 9‑5a–d).

During physical therapy, pain is relieved by using traction in a neutral position. This is usually conducted in a relaxed position with the legs raised in the Fowler position (Fig. 9‑6). When acute pain is present, this is in fact the only possible starting position. The patient is placed in this initial position and attempts to move normally and to stabilize the affected spinal region at the same time. As the symptoms start to diminish, other starting positions can be used until the lordosis is normal again.

Fig. 9.5 Flexion orthosis used in the treatment of acute and chronic pain in the lumbar spine caused by a narrowing of the posterior intervertebral disk height and compression of the zygapophyseal joint. The effect is obtained by using an orthosis with a suprapubic abdominal pad **(a, b)**, which pushes the abdomen in. The straight back section flattens the lumbar lordosis **(c, d)**. The increase in intra-abdominal pressure lowers the intradiscal pressure by approximately 30%.

Fig. 9.6 Proprioceptive neuromuscular facilitation (PNF) treatment in a pain-relieving position (treatment cube).

9.2.1 Movement Program (MIPFR) for the Lumbar Spine

The first rule of back school is “keep moving.” With this in mind, all types of movement that do not provoke back pain are appropriate, based on the movement in pain-free range of motion (MIPFR; see Chapter 3.5) principle. Central to the movement program for chronic back pain are back-friendly sports that use linear movements, e.g., swimming, jogging, and cycling. Other patterns of movement are also appropriate as long as the patient does not adapt an excessively lordotic posture or thoracic kyphosis combined with rotary movements. The sports or types of exercise recommended in the individual treatment program should be ones the patient mentioned as favorites in their initial assessment, so that exercises are conducted daily and regularly.

9.3 Special Therapy for Lumbar Pain

9.3.1 Local Pain Syndromes in the Lumbar Spine (Local Lumbar Syndrome, Nonspecific Back Pain)

By definition, the pain caused by local lumbar syndromes is restricted to the lumbosacral region, i.e., there is no radiation into the lower limbs. The back pain is felt at its point of origin, so we are dealing with a nociceptively governed clinical picture.

The pain arises in the nociceptors of the zygapophyseal joint capsules, the posterior longitudinal ligament, and the interspinous ligaments. The nociceptors found in the muscle attachments and the long and short back muscles themselves are secondarily affected. The sensitive fibers of the meningeal branch and the dorsal ramus of the spinal nerve are predominantly affected. The permanent reflex tension in the back extensor muscles is perceived as unpleasant and painful. These patients suffer from position-dependent back pain, muscle tension, and restricted mobility of the lumbar spine. The different symptoms found in the local lumbar syndrome are often summarized in the term “nonspecific back pain,” especially when the examiner is unable to assess precisely where the pain is originating from.

In order to target the local treatment of back pain, it is important to know where the pain originates, i.e., the zygapophyseal joint, back muscles, or SIJs. Important information is gained from the medical history and the results of the manual therapy assessment. Many investigators have indicated the importance of the zygapophyseal joints in the development of back pain (Ghormley 1933; Badley 1941; Mooney and Robertson 1976; McCall et al 1979; Carrera 1980; Young and King 1983; Lau et al 1985; Moran et al 1988).

The symptoms can begin suddenly, for instance, when the trunk is abruptly rotated, or may arise gradually without any special reason. During the subjective assessment, patients often mention exposure to cold or remaining in the same posture for some time among the precipitating factors. During the examination, the patient can quite clearly localize where the pain is coming from, in the initial stages. Pain is usually felt more on one side in the region of the SIJs and the lumbar back extensors. This is in the area supplied by the posterior branch of the L5 and S1 nerve roots. Permanent irritation of the dorsal ramus results in the development of a neuralgia-governed component, where pain spreads into the proximal sections of the lower limb and cannot be allocated to a specific segment, such as in the buttock region. Patients present with the typical tender points at the spinous processes and along the posterior section of the SIJs. In addition, the back extensors are distinctly under a certain amount of tension and the mobility of the lumbar spine is restricted. When acute pain syndromes are present, a motor reaction causes the patient to immediately adopt a posture of slight trunk flexion and, in some cases, lateral flexion (Fig. 9‑7a, b). This posture should not be altered, as it represents a protective reflex which aims to prevent further irritation of the nociceptors in the zygapophyseal joint capsule and the posterior longitudinal ligament.

Fig. 9.7 **(a, b)** The adaptive posture seen in an acute lumbar syndrome (lumbago) with the trunk slightly bent forward and laterally flexed.

9.3.2 Treatment of Acute Low Back Pain

The main aim of treatment in acute local lumbar syndromes is the immediate elimination of pain, interrupting the chronification process right from the start. Peripherally acting analgesics (see Chapter 4, “Multimodal Medication Concomitant Therapy”) block nociception and the distribution of pain signals at their point of origin. The simultaneous administration of local infiltrations at the source of pain is recommended. The source of pain is ascertained during the manual therapy assessment and by trial injections. The interspinous ligament insertions, usually between L4/L5 and L5/S1, as well as the zygapophyseal joint capsules, are suspected when acute arthroligamentous back pain is present. When pain is felt more on one side, the back extensors tense up asymmetrically and one SIJ is also often included in the primary painful event. Immediate mobilization (manual therapy), with the support of local infiltration with local anesthetics and concurrent electrotherapy, prevents a permanent blockage in the affected zygapophyseal joint and SIJ.

In this phase, patients immediately accept the rules of back school, as incorrect posture and behavioral patterns immediately cause severe pain. Patients should be familiarized with these rules from the very beginning to prevent recurrence of pain and the evolution of chronic pain. As long as they do not attempt heavy physical labor, even patients with acute low back pain can pursue their accustomed lifestyle with only slight restrictions if they follow the postural and behavioral guidelines learned from back school. They can continue to walk, sit, stand, and carry out tasks involving light to moderate physical labor.

Controlled studies into acute low back pain (Coomes 1961; Gilbert et al 1985; Postacchini et al 1988; Deyo et al 1991; Szpalski and Hayez 1992; Malmivaara et al 1995; Wilkinson 1995) have demonstrated that bed rest and immobilization impede the healing process rather than helping it. Therapeutic approaches that use centrally depressing medication are therefore obviously inappropriate. The emphasis should be on interventions that affect the nociceptive region locally. Treating physicians should choose the method that they are most familiar and comfortable with from the range of therapies that conform to this concept.

Pain therapy for acute low back pain:

Analgesics.
Pain-relieving position.
Cryotherapy (heat therapy).
Local infiltrations (trigger points, facets, SIJ).
Manual therapy (traction).

9.3.3 Treatment of Chronic Low Back Pain

Pain that endures for weeks or months is at risk of becoming chronic. Patients find it more difficult to retain their accustomed lifestyle, and psychological disturbances are inevitable. The pain changes in character and is permanently present, sometimes even during the night.

Initially, the pain is selectively located at a zygapophyseal joint or in the area surrounding an SIJ. This develops into a diffuse pain in the lower back that spreads over the entire lumbosacral region. It can spread into one or both limbs as a pseudoradicular form of pain. The permanent tension in the back extensors and the proximal limb muscles causes insertional tendinopathies at the pelvis, the spinous processes, and eventually also in the upper sections of the trunk.

Interdisciplinary treatment programs in the context of “multimodal pain management” are becoming more important for treating chronic back pain (see Chapter 11.3, “Multimodal Program”).

The goal of multimodal pain management is functional restoration at the physical, psychological, and social level. For the patient in question, this may involve restoring the ability to work, enabling better understanding of chronic pain, learning to deal rationally with pain medication, or increasing self-esteem.

In individual cases, injection therapy may be performed if it is indicated under careful consideration.

Pain therapy for the chronic lumbar syndrome:

Heat.
Local injections.
Movement therapy.
Back school.
Psychotherapy.
Progressive muscle relaxation.

9.3.4 Pain Therapy for the Lumbar Nerve Root Syndrome

Dermatomal spread of pain into the leg indicates the irritation of a spinal nerve, with the involvement, in particular, of the ventral ramus. This is a neuralgia-governed clinical picture. Generally speaking, the spinal nerves belonging to the two most inferior lumbar vertebral motor segments are affected and patients present with symptoms of sciatica.

Lumbar nerve root syndromes are caused by intervertebral disk protrusions or prolapses and/or bony impingement in the lateral recess and in the intervertebral foramen. The clinical symptoms associated with discogenic sciatica arise suddenly in most cases and quickly adopt neuralgic characteristics. The afferent fibers in the spinal nerve are rapidly converted to nociceptors. Pain that is position-dependent and is accompanied by a feeling of numbness or ants crawling along the dermatome is characteristic of this disorder (Fig. 9‑8). The neuralgia can be accentuated by external factors such as axial loading, sudden changes in posture, and bending the trunk.

Fig. 9.8 The typical adaptive posture for acute sciatica on the right-hand side.

In the lumbar nerve root syndrome, pain chronification is predetermined because of the neuralgia. The lumbar nerve root syndrome is a primary chronic disorder: the conversion of a primary conducting nerve to a nerve with a nociceptor function already signifies chronicity. The longer the condition remains, the less chance there is that simple forms of intervention, such as manipulation, traction, or a nerve root block, can rapidly improve the pain. The constant irritation of the spinal nerve root leads to secondary symptoms with motor and autonomic reactions. Over time, central changes occur in the perception and processing of pain. In some cases, characteristics such as different positions affecting pain levels and the day–night pattern can no longer be observed: pain is felt permanently, and associated psychological symptoms appear. The constant maladaptive postures cause muscle tension and insertional tendinopathies not only in the lumbar region, but also in the upper sections of the trunk.

Pain therapy for the lumbar nerve root syndrome targets not only the peripheral nociception, but also primarily the transmission and processing of pain signals; local injections using lumbar spinal nerve analgesia (LSPA) and epidural injections are the main focus. In both acute and chronic lumbar nerve root syndromes, it is advisable to tackle the point of nerve root compression directly (see Chapter 11, “Multimodal Spinal Therapy”).

9.3.5 Pain Therapy for Lumbar Spinal Canal Stenosis

The characteristic pain arising from a lumbar spinal canal stenosis varies according to the amount of weight-bearing when walking and standing, and is reduced by all postures involving trunk flexion (flattening out the lordosis). This differs from the ischemic pain caused by circulatory disorders. Leg pain is the main symptom. It presents as bilateral pain that is found especially along the anterior side of the thigh in the case of central spinal canal stenosis and as an ipsilateral dermatomal spread in the case of lateral spinal canal stenosis. The leg pain often develops after walking only a few steps, and is therefore also described as intermittent spinal claudication.

Possible causes for the constriction in the lumbar vertebral canal include bony involvement (vertebral arch, vertebral body) as well as the involvement of soft tissue structures (intervertebral disk, connective tissue). Spinal canal stenosis can occur in one segment or in several segments, depending on the cause. In most cases, the epidural space is characteristically narrowed by the ligamentum flavum protruding from the posterior side and the degenerative changes found in the intervertebral disk from the anterior side (Fig. 9‑9). Both of these protrusions develop as part of the degenerative narrowing of the intervertebral section. Hyperlordosis amplifies these phenomena. These deformations are initially symptom-free and are described as compensated spinal canal stenosis. An increase in the lumbar lordosis due to age-related abdominal muscle weakness, small amounts of intradiscal mass displacement with the amplification of one or more intervertebral disk protrusions, and postural and behavioral changes with an associated increase in the lumbar lordosis additionally narrow the space available for the neural elements in the lumbar vertebral canal. This continues until there is no more space available and leads to the development of compression-related pain (Krämer et al 2012).

Fig. 9.9 Sagittal MRI section of the lumbar spine; spinal canal stenosis at two levels with protrusion of the intervertebral disks from anterior (a) and the ligamentum flavum from posterior (p).

9.3.6 Decompensated Spinal Canal Stenosis

Compression-related nerve root edema and congested epidural veins lead to the rapid development of spinal canal syndrome, which is accompanied by severe pain in both legs (Krämer et al 2004). This can occur in one segment or several. As it is mainly spinal nerves that are being compromised, the pain is dominated by neuralgia. According to Porter (1985), the neurogenic intermittent claudication associated with spinal canal stenosis never exceeds a certain level and does not result in paraplegia.

Because of the neuralgic character of the pain, centrally acting analgesics are administered as part of the symptomatic pain therapy for lumbar spinal canal stenosis with the aim of maintaining the mobility of the (mainly older) patients. The disorder of venous drainage in the spinal canal should be treated with agents that stimulate blood flow. The spinal nerve roots that are compromised in the vertebral canal are best reached by the use of epidural injections. In the case of a central spinal canal stenosis involving several segments, the use of a posterior epidural injection is appropriate as several segments can be reached at the same time. When patients present with a lateral spinal canal stenosis with compression of a single spinal nerve in the lateral recess or in the intervertebral foramen, an epidural perineural injection is indicated. Spinal nerve analgesia and facet infiltration are administered to complement the treatment, addressing the hyperlordosis and the tense lumbar muscles (Theodoridis 2012).

Causal pain therapy aims to flatten out the lumbar lordosis and thus significantly widen the lumbar vertebral canal. This additionally flattens intervertebral disk protrusions on the anterior side of the spinal canal and the protruding ligamentum flavum on the posterior side. The lumbar lordosis immediately flattens out when the patient is placed in the Fowler position and wears a flexion orthosis while standing and walking. Physical therapy focuses mainly on strengthening the abdominal muscles. Twice-daily stationary cycling (mornings and afternoons for 30 minutes) complements the physical therapy program when conducted as MIPFR (Table 9‑1).

Table 9.1 Pain therapy for spinal canal stenosis
Symptomatic	Causal
Psychological pain therapy Central analgesia	Fowler position
Stimulation of venous blood flow	Physical therapy from the pain-relieving position
Epidural injection	Stationary cycling (MIPFR)
Spinal nerve analgesia	Flexion orthosis
Facet infiltrations	Decompression surgery
Abbreviation: MIPFR, movement in pain-free range of motion.

Surgical widening of the lumbar spinal canal is an option when the disorder is resistant to treatment. It was common in the past to widen the spinal canal using a laminectomy over several levels. Nowadays, surgical intervention is limited to microdecompression at the affected segment. This is based on the knowledge that spinal canal stenosis is caused only by intervertebral disk involvement or the narrowing of a recessed area.

9.3.7 Pain Therapy for Problem Patients Who Have Undergone Spinal Surgery

These patients still have back and leg pain even after one or several intervertebral disk operations or surgical fusions. Chronic pain arises both from the peripheral nociception in the vertebral motor segment and in the neurologically modified nerve fibers. There is therefore a mixture of nociceptive and neuralgia-governed pain symptoms. The particular characteristic of pain chronification in postsurgical patients is that the actual operation on the spine (either open intervertebral disk surgery or spinal fusion surgery) involved nociceptors that were already sensitized and nerve fibers that were already modified into nociceptors. Direct intraoperative trauma to the nociceptors and the neurologically modified nerves in the area of the wound has led to further permanent damage. Postsurgical scar tissue is formed, with the involvement of neural structures that have previously been neuropathically damaged (Fig. 9‑10). These neuropathically modified nerves and sensitized nociceptors, which are repeatedly irritated by tension in the scar tissue, form the pathological and anatomical substrate for chronic pain in patients who have already undergone spinal surgery.

Fig. 9.10 MRI scan of a patient suffering from a postdiscotomy syndrome following an open lumbar intervertebral disk operation at the L4/L5 segment. A surgical scar can be seen on the right-hand side. It extends continually from the skin, via the subcutaneous tissue and the back extensors, into the inner space of the lumbar vertebral canal. The scar tissue then extends further, passing between the dura and the vertebral canal, affecting the traversing and exiting nerve roots, and extends as far as the intervertebral disk. Movement of the (degenerative or surgically) unstable intervertebral segment is transferred anteriorly directly to the scar and the entrapped neuropathically modified nerve root. Likewise, movement in the back muscles is transferred posteriorly to the nerve root by the pull on the scar.

Character and Severity of Pain

The pain in these cases is characterized by a bilateral, mixed pseudoradicular/radicular set of symptoms. Frequently, several nerve roots are involved. Neurological deficits may also be the result of previous operations and should not always be attributed to the current clinical picture. Severe neurological disorders are quite rare: although the nerve root is strangulated by the scar tissue, it is not completely severed. Pseudoradicular components and nociceptively amplified pain are the result of segmental instability with irritation of the zygapophyseal joint capsule and the nociception in the posterior longitudinal ligament. These patients have only a small pain-free range of motion because spinal nerve roots and their branches, now partly fixated by scar tissue, have been partially severed during surgery, leaving free nerve endings.

Note

The strands of connective tissue along the dura and nerve root can be compared to wind chimes that are stirred into action by any kind of careless movement.

Nociceptors and afferent fibers are in a permanently irritated state. Inflammatory and edematous processes cause swelling in the spinal nerves and further narrow the space that is left in the vertebral canal. A vicious circle begins. The mobility of the sciatic nerve root during trunk flexion is most affected. This is noticeable when the leg is extended and raised, or when the patient sits with straightened legs. In severe postsurgical pain syndromes, the Lasègue test is bilaterally positive after only 10 to 20 degrees of movement. The mobility of dura and nerve roots in the vertebral canal is often so limited that even flexing the neck aggravates the typical range of symptoms (Fig. 9‑11).

Fig. 9.11 The slightest change in the volume and consistency of the intervertebral disk causes a reaction in the disk and the nerve root because these two structures are connected by scar tissue.

Symptoms of postdiscotomy syndrome:

Bilateral, mixed pseudoradicular/radicular symptoms.
Double-sided positive Lasègue’s test.
Inability to flex trunk or sit with legs extended.
Epidural scarring seen on MRI and CT.

Patients with a pronounced postdiscotomy syndrome following one or several intervertebral disk operations are considerably impaired: they are unable to sit, stand, or lie down normally (Fig. 9‑12). As they have no serious neurological deficits, these patients are often labeled as “pension neurotics” or categorized as suffering from psychological overlay.

Fig. 9.12 A patient with a pronounced postdiscotomy syndrome following several intervertebral disk operations, who has considerable functional limitations in daily life and can walk only with the use of walking aids.

The severity of a postdiscotomy syndrome is primarily determined by the subjective level of impairment. Objective criteria, such as neurological deficits, scarring, and instability, are not always an accurate measure of severity. Several consultations with the patient with different people observing may be necessary to define their amount of suffering. The straight-leg-raise test in lying and sitting is relatively reliable, as is observing the patient when they sit with their legs extended, take off and put on their shoes and socks, and flex the trunk during other activities (Table 9‑2).

Table 9.2 Level of severity of postdiscotomy syndrome
Level	Pain	Lasègue’s test	Medication	Functional capabilities	Expert opinion	DD in %
I	No resting pain, mild pain on loading	Negative	Occasionally	Restrictions for heavy physical labor and competitive sports	Able to work, but no heavy physical labor	<20
II	Mild resting pain, severe pain on loading	Positive	Regularly weak, occasionally strong	No work that places load on the spine, no sports	Often unable to work, occupational disability for work that loads the spine	30–80
III	Severe permanent pain	<30 degrees	Constantly severe	Walking aids, requires assistance from others	General disability	100
Abbreviation: DD, degree of disability. Source: Adapted from Krämer et al 2014.

Therapy Approaches

The pain therapy approach for problem patients who have previously undergone back surgery is multifaceted. It corresponds to the patient’s mixture of nociceptive and neuralgic symptoms and the associated significant changes in pain transmission and perception. Either peripherally or centrally acting analgesics are administered, depending on whether the nociceptive or neuralgic component is more prominent. As the centralization process is usually quite advanced, most patients report that only centrally acting analgesics bring relief (Theodoridis et al 2004).

Local injection therapy is used to directly influence the nociception and neuralgia in the previously operated vertebral motor segment. The use of epidural injections and spinal nerve analgesia at the affected segments is well established. When administering interlaminar epidural injections using the loss-of-resistance technique, injections must be placed one or two segments higher or access obtained via the sacral canal (as an epidural sacral injection). This is necessary because of the adhesions found in the epidural space at the surgical site. The epidural perineural injection technique is the best way of directly influencing the entrapped, edematously swollen nerve root. Intradiscal injections may be considered if the postsurgical MRI or CT still shows a broad-based indentation caused by an intervertebral disk protrusion.

Chronic pain conditions originate mainly in the dorsal ramus and are treated with facet infiltrations and scar infiltrations.

To treat instability, the second pathogenetic component in the postdiscotomy syndrome, it is worth trialing the use of a trunk orthosis. Flexion orthoses that relieve loading on the posterior section of the vertebral motor segment seem to be appropriate. Concurrent physical therapy with isometric stabilizing exercises starting in a pain-relieving position is essential. The trunk muscles are trained using intensive exercises. The ultimate aim is for these muscles to take over the function of the orthosis and contribute to the stabilization of the previously operated vertebral motor segments.

Multifaceted pain therapy is justified in the treatment of the postdiscotomy syndrome because of the syndrome’s multifaceted etiology and pathogenesis and its equally multifaceted set of symptoms. All types of intervention that do not cause additional damage to the patient are important. The body’s own pain-inhibiting mechanisms should be activated as much as possible. This includes all of the psychological measures available to cope with and reduce the pain, as well as the use of an individually tailored movement program (MIPFR; Table 9‑3).

Table 9.3 Pain therapy for problem patients who have previously undergone spinal surgery
Symptomatic	Causal
Analgesics (central and peripheral)	Stabilization of the trunk muscles, physical therapy
Psychological pain therapy	Psychological pain therapy
Local injections	Back school
Alternative medicine	Orthosis (temporary)
Movement therapy	Spondylodesis

9.3.8 Pain following Lumbar Spondylodesis

A posterior, anterior, or posteroanterior spondylodesis at the affected vertebral motor segment is a surgical treatment option when all conservative measures that aim to stabilize the surgically unstable segment have failed. This operation is also performed when posttraumatic instabilities and deformations (e.g., spondylolisthesis) are present. The main indication worldwide is nevertheless the problem patient who has previously undergone one or more intervertebral disk operations. By eliminating the instability component, it is usually possible to relieve a large proportion of the pain in postdiscotomy syndromes. However, new pain symptoms often develop, originating in the neighboring segments or the SIJs. This pain complex is called the postfusion syndrome (Krämer 1997). The pain arising from the segment instability near the fusion site, the SIJs, and the new scar tissue is then combined with the residual pain coming from the postdiscotomy syndrome.

The pain therapy approach for this particularly problematic group of postsurgical patients is largely the same as for the postdiscotomy syndrome. The predominant set of local symptoms has to be identified using clinical neurological examinations and, in particular, trial local infiltrations. The psychological care of these patients is particularly important. After undergoing repeated and sometimes very complicated operations, they are very skeptical about any type of medical intervention and tend to prefer long-term medication with centrally acting analgesics.

9.4 Exercise Program

The exercise program aims to make use of the limited pain-free range available. Back surgery patients with severe pain can once again exercise without running the risk of their pain increasing during or following activity—mainly swimming, cycling, and some suitable exercises. The sports instructor should focus on expanding the patient’s possible movement spectrum by introducing him or her to other patterns of movement, such as:

Jogging under minimal loading.
Aqua-jogging.
Thera-Band exercises in a lying position.

For many patients, it is a positive experience, in general, to be able to move more frequently without experiencing pain.

9.5 Lumbar Injection Therapy

9.5.1 Lumbar Spinal Nerve Analgesia

Principle

Posterolateral injection of a local anesthetic (mixed with steroids as off-label use, when necessary) into the foraminal articular region of the vertebral motor segment.

Topographical and anatomical palpation points determine the injection angle and needle path. The LSPA differs from the Reischauer (1953) and Macnab and Dall (1971) techniques in that the needle is placed at an angle rather than in a sagittal direction. The injection site is 8 to 10 cm lateral to the midline and the needle is inserted at an angle of approximately 60 degrees. Using this method, bony contact is always established with the posterolateral section of the lumbar vertebra.

Indication

All acute and chronic local and radicular lumbar syndromes are indications for LSPA. However, other forms of lumbar vertebral motor segment irritation caused by osteoporotic fracture, spondylolyses, tumor-related pain, spinal canal stenoses, and inflammatory pathological changes, particularly in the area of the vertebral joint capsule, also respond well to this method of treatment.

Indications for LSPA:

Local lumbar syndrome.
Lumbar nerve root syndrome.
Osteoporosis.
Spondylolysis, spondylolisthesis.
Tumor.
Spinal canal stenosis.
Rheumatic inflammatory changes to the vertebral column.
Postdiscotomy syndrome.

Technique

The needle is 10 to 15 cm long (usually 12 cm), depending on the soft tissue depth. The intervertebral foramina of the inferior lumbar spine are best reached by inserting the needle 8 cm lateral to the midline at the same level as the iliac crests. The needle is placed at a 60-degree angle in the horizontal plane and at different angles in the vertical plane depending on which nerve root is affected. To infiltrate the L3 nerve root, the needle is inserted at an angle of 0 degrees (Fig. 9‑51 , Fig. 9‑52 , Fig. 9‑53).

To infiltrate the L4 nerve root, the needle is inserted at an angle of 30 degrees (Fig. 9‑40 , Fig. 9‑41 , Fig. 9‑42 , Fig. 9‑43 , Fig. 9‑44 , Fig. 9‑45 , Fig. 9‑46 , Fig. 9‑47 , Fig. 9‑48 , Fig. 9‑49 , Fig. 9‑50).

The needle is inserted superior to the L5 transverse process for 1 to 2 cm until bony contact is made. The tip of the needle is then positioned on the lateral facet, immediately next to the intervertebral foramen, or along the side wall of the vertebral body. It is here that the ventral ramus, the efferent branches of the dorsal ramus, the meningeal branch, and the ramus communicans run down to the sympathetic trunk.

To infiltrate the L5 nerve root when it exits the L5/S1 intervertebral foramen, the needle tip is further lowered underneath the L5 transverse process, corresponding to an angle of approximately 50 to 60 degrees in the vertical plane. The needle is inserted until bony contact is made with the lateral vertebral body or the lateral facet (Fig. 9‑14 , Fig. 9‑15 , Fig. 9‑16 , Fig. 9‑17 , Fig. 9‑18 , Fig. 9‑19 , Fig. 9‑20 , Fig. 9‑21 , Fig. 9‑22 , Fig. 9‑23 , Fig. 9‑24 , Fig. 9‑25 , Fig. 9‑26 , Fig. 9‑27 , Fig. 9‑28 , Fig. 9‑29 , Fig. 9‑30 , Fig. 9‑31 , Fig. 9‑32 , Fig. 9‑33 , Fig. 9‑34 , Fig. 9‑35 , Fig. 9‑36 , Fig. 9‑37 , Fig. 9‑38 , Fig. 9‑39).

CT-monitored spinal nerve analgesia (Fig. 9‑13a–c) has demonstrated that the injected solution disperses through the intervertebral foramen, additionally reaching the traversing S1 nerve root at the exact point where the L5/S1 intervertebral disk applies pressure onto the nerve.

It is possible for a root sheath to be punctured in the intervertebral foramen. For this reason, constant attempts to aspirate are made while the needle is being inserted, particularly during the final phase of the procedure. When contact is made with the nerve root, the patient indicates the presence of a sudden sharp pain radiating into the leg. This pain phenomenon can be largely prevented by proceeding slowly with continual preinjection and aspiration. It is therefore recommended that a total of 10 mL of a dilute local anesthetic solution be used for the injection, as in the end usually only 4 to 5 mL are available for the actual injection at the target site. Once the final position of the needle has been correctly established, it is possible to add a longer-lasting local anesthetic (e.g., bupivacaine) and/or a glucocorticoid (off-label use, e.g., 10 mg triamcinolone) depending on the presenting clinical situation.