12 Evaluation of Epidural Pathology and Epiduroscopic Images

12.1 Introduction

Among the most exacting and difficult tasks for any pain therapist are the diagnosis of and treatment for neuraxial pain syndromes For carrying out invasive–interventional pain medicine procedures in the vicinity of the spinal column, knowledge of the topographic anatomy of the neuraxial region is an absolutely indispensable prerequisite ( Fig. 12.1). This is especially true for spinal endoscopy. Knowledge of endoscopic anatomy is the basis for a proper professional evaluation of the endoscopic neuraxial anatomical findings. Epiduroscopy (EDS) is carried out percutaneously through the sacral hiatus or sacrococcygeal ligament anywhere from the sacral to the cervical region of the spinal column of the patient depending on the location of the pathologic anatomical findings and utilizing a professional investigative technique.^1,2

A review of the literature for endoscopic investigations of the spinal column, makes clear that these are primarily investigations of the epidural space of the dorsal sacral or dorsal lumbar regions of the spinal canal. The cause for this, among other things, is that a majority of pathologic processes occur in the lumbar section of the spinal column. Some epiduroscopes that are used, on the basis of their technical construction and outfitting, allow only very limited endoscopic investigations, maximally in the lumber spinal column region and often with restricted image quality.

In most published clinical reports of the findings and therapeutic results of epiduroscopies with flexible endoscopes,, the images that identify, verify, or clarify the normal or pathologic anatomical findings are not included. Only isolated reports and very few useful endoscopic images exist about normal endoscopic anatomy and its pathologic alterations. The sporadically published endoscopic images did not include comparative images of similar pathologic findings from different patients either. The Epiduroscopy DVD (2006) by Schütze³ was an attempt to make the first visual epiduroscopic atlas and to promote a unified nomenclature for pathologic anatomical findings in the neuraxial region.

In this chapter the pathologic anatomical findings from patients with pain syndromes, observed exclusively via a percutaneous flexible endoscopic investigation technique (spinal endoscopy [epiduroscopy]) are presented from a systematic, topographic, clinical, and practical point of view.

Neuraxial endoscopic investigation technique makes it possible to visualize the pathologic anatomical structures accessible to the epiduroscope in the sacral, lumbar, thoracic, and cervical regions of the spinal column of a patient with a pain syndrome. Epiduroscopy also conveys the dynamics of the epidural space as well as a visual understanding for this topographic region so important for pain medicine. For patients with neuraxial pain syndromes, spinal endoscopy is an excellent minimally invasive endoscopic procedure for diagnosis of pathologic structural changes.

12.2 Pathogenesis of Neuraxial Pathologic Findings

Fig. 12.1 Illustration of simplified orientation and documentation of spinal topography and endoscopic navigation. The epidural space is shown in red, and the intracanthal space in black. DM, dorsal medial epidural space; DL, dorsal left lateral epidural space; DR, dorsal right lateral epidural space; VR, ventral right lateral epidural space; VL, ventral left lateral epidural space; VM, ventral medial epidural space. (Reproduced with permission of Schütze 2008.6)

Fig. 12.2 Common pathologic changes in the epidural space in patients with neuraxial pain syndromes: (a) adhesions, (b) fibroses, and (c) chronic inflammation.

Neuraxial pain syndromes are characterized by pathomorphological changes in the spinal canal both for patients with pain syndromes who have been operatively treated and those who have been nonoperatively treated ( Fig. 12.2).

Via endoscopic investigation, epidural pathologic anatomical structures such as adhesions, fibroses, radiculopathies, ischemias, perineural edemas, congested veins, chronic inflammatory processes (arachnoiditis, epiduritis, and radiculitis), sequestration and nerve root compressions, or cysts and tumors can be diagnosed.^4,5,6 Pathologies such as ependymomas, schwannomas, or chordomas of the sacrum, and tethered cord syndrome in the neuraxial section of the cauda equina, filum terminale, and conus medullaris are difficult to diagnose, above all in the initial stage these diseases, but can be identified early endoscopically. Also, through spinal endoscopy the possibility exists of taking out adequate tissue samples for fine tissue pathologic diagnostics on site.⁶

In the future, technological advances such as virtual chromoendoscopy, an endomicroscopic technique, will also be available with spinal endoscopy. Endomicroscopy can endoscopically visualize and distinguish cellular, vascular, and connective tissue structures, for example through laser-supported and confocal fluorescence technology or special visualization tools. Thereby, histologic evaluation of pathologic anatomical structures becomes possible in real time during the endoscopy (see Chapter 14).

It is known that no single mechanism underlies the origin and maintenance of pain. Not only pathologic structural changes but also biochemical processes in the neuraxial region are responsible for the generation of pain. Inflammatory and immunologic processes exist, with activation of nociceptors, in which mechanical influences are involved more or less predominantly in the generation of pain.^7,8,9

With the help of immunohistochemical investigation techniques it has been determined that, for example, autologous intervertebral disk material, if it comes in contact locally or diffusely epidurally with nerve tissue, provokes immunologic inflammatory processes in the adjacent nerve root.¹⁰ Tissue of the nucleus pulposus, when it protrudes into the epidural space from a herniated intervertebral disk, can trigger chemically induced inflammatory processes. These processes are immunocompetent cellular reactions against expressed intervertebral disk material. The evidence of monoclonal antibodies against Tlymphocytes and macrophages supports this interpretation.¹¹ The results confirm the conjecture that even with radicular symptoms of pain, the pain is not due purely to mechanical changes (such as pressure) on the nerve root.¹² Also in clinical studies it has been shown that only with irritated or inflammatorially changed nerve roots is compression or traction perceived as painful.

These pathologic changes, combined with impeded cerebrospinal fluid (CSF) circulation and insufficient fibrinolysis, lead to, for example, impaired nutrition of the affected nerve root, which subsequently leads to changes in the CSF and cell body. The nerve root can become compromised, deformed, or stretched through pathologic changes in the intervertebral disk, facet joints, or intervertebral foramina.¹³ These deformations of the nerve root or the dorsal spinal ganglion lead to impairment of the local microcirculation, with wide-ranging clinical consequences.^14,15,16

12.3 Pathologic Findings in the Epidural Space: Adhesions, Fibroses, and Chronic Inflammatory Processes

On the basis of our clinic’s long-running experiences with more than 2,000 spinal epiduroscopic investigations in patients suffering from pain, I will attempt, in what follows, to classify and evaluate the common pathologic anatomical findings ( Fig. 12.3).

Fig. 12.3 Schematic transverse section through the spinal canal with ventral positioning of the epiduroscope for orientation. (Reproduced with permission of Schütze 2008.6)

Fig. 12.4 Blood vessel in the postoperative cervical epidural space with beginning adhesive encasement (picture-in-picture technique).

12.3.1 Adhesions

The formation of adhesions can be explained pathophysiologically on the basis of special healing mechanisms in the neuraxial space and on an imbalance, arising from injury, between fibrinogenesis and fibrinolysis ( Fig. 12.4).^11,17

Epidural adhesions or adhesive regions occur very frequently in our patient population. Richardson et al diagnosed epidural adhesions as the cause of pain in all endoscopically investigated patients with chronic radicular back pain.¹⁸

Fig. 12.5 Epiduroscopic view of an intervertebral disk herniation (left) in the cervical epidural section with formation of an adhesion between the spinal dura mater (right) and the posterior longitudinal ligament (left).

As an example of the special pathogenesis of epidural adhesions, material from a herniated intervertebral disk can escape into the epidural space through a ruptured anulus fibrosus. In response to the proteoglycans from nucleus pulposus in the epidural cavity, serotonin, histamine, bradykinin, prostaglandin, and phospholipase A2 are released. This initiates inflammatory reactions, which in turn lead to epidural adhesions ( Fig. 12.5). This example demonstrates that epidural adhesions can arise even without a preceding operative neuraxial intervention or inflammatory process.

Fig. 12.6 (a,b) Inclusion of epidural vessels in developing fine connective tissue adhesion strands.

The extent of epidural adhesion formation depends decisively on the presence of local ischemia, inflammation-reaction hematomas, foreign body particles, mechanical and thermal irritation, dehydration, and allergic reactions ( Fig. 12.6).^19,20,21,22

On that basis, marked to excessive epidural adhesions, which are bound fast to the spinal dura mater, can provoke quite considerable pain in response to mechanical stress even after proper endoscopic observation that does not disturb the structures in any way to cause pain.

Endoscopic Identification

In the endoscopic image, easily identifiable, diversely structured epidural adhesions appear as irregular, often bizarre, delicate to strong, white or white-gray connective tissue structures.

Roughly simplified, soft adhesions can be distinguished from stiff ones by contact with the endoscope itself or microsurgical instruments.

Epidural adhesions can be observed to cover up blood vessels, nervous structures, and foreign bodies (sequestration, implanted catheters, electrodes) with thick connective tissue structures or else to occupy space, filling up the epidural cavity ( Fig. 12.7).

Nervous structures (nerves and nerve roots) completely enclosed by adhesions react, often with a pain reaction, on contact.

Topographic Aspects

Sacral and lumbar regions

In most endoscopic investigations on frequent failed back surgery syndrome (FBSS) cases, postoperative adhesions of varying degrees occur mainly in the lumbar region operated on. The adhesions are frequently associated with marked fibrosis. Often they can be overcome to expand the endoscopic region of investigation only with the use of microsurgical instruments or modified access techniques.

Fig. 12.7 Space-occupying epidural adhesions (left) in contact with spinal dura mater (right).

Adhesions and areas of adhesions in the thoracic and cervical regions of the spinal column have special clinical significance ( Fig. 12.8).

Especially in topographic spinal column regions of intervertebral disk prolapse and herniation, after standard interventional microsurgical operative procedures marked cervical and thoracic epidural adhesions are frequently diagnosed endoscopically.

Our experience verifies that increased adhesions are endoscopically encountered especially in the ventral thoracic and cervical pain regions. The adhesions are frequently in loose connection with the posterior longitudinal ligament. Highly marked or space-filling adhesions occurred in our investigations in the ventral T4 and T10 segments. The cervical adhesions were diagnosed endoscopically in our patient population primarily in the cervical spine segments with vertebral bodies C5–C6 and C6–C7, and less often with C7–T1 and C4–C5.

12.3.2 Fibroses

Endoscopically visible epidural fibroses are very often diagnosed in connection with spinal stenoses, spinal column instabilities, and intervertebral disk prolapse and herniation ( Fig. 12.9). According to Laus et al, excessive fibrosis is also frequently a consequence of an insufficient intraoperative hemostasis.²³

Adiffuse increase in connective tissue in the epidural space leads to fibrosis (wound healing), which is also easily identified endoscopically. If the increased collagen production leads to a pathologic hardening (induration), an epidural sclerosis occurs ( Fig. 12.10).¹¹

Fig. 12.8 (a,b) Cervical space-occupying epidural adhesions (picture-in-picture technique).

Fig. 12.9 (a,b) Pain-relevant, ribbon-shaped lumbar epidural fibrosis that is connected with the spinal dura mater and the ligamentum flavum.

The clinical phenomena of an atypical spread of regional anesthesia (missed segments) in classical epidural anesthesia may also be explained by epiduroscopically visible pathologic structures such as marked adhesions and fibroses. The unfavorable result in patients can be explained by the neuraxial pathologic anatomical changes such as inflammatory processes, adhesions, and/or fibroses that alter resorption relationships.24

Special Pathogenesis

Epidural fibrosis possesses central significance in pain medicine ( Fig. 12.11).

Fibroses observed endoscopically along the dural sac and the nerve roots are often a cause for postoperative pain syndromes such as FBSS. A regional inflammatory reaction with edema formation in neurogenous structures, local circulatory disturbances, as well as adhesions can explain the emergence of an epidural fibrosis.

Fig. 12.10 (a,b) Strand-shaped collagen fibers without recognizable vascularization organize into an epidural fibrosis.

Fig. 12.11 (a,b) Marked space-occupying and stenosing epidural scars.

Osteophytes (bony outgrowths) and protrusions or sequestrations of the nucleus pulposus due to intervertebral disk prolapse and herniation, respectively, can stretch the posterior longitudinal ligament. This compression, in connection with inflammatory changes and changes in the permeability or in the transmural pressure of the endoneural capillaries, can result in edema.

Finally, further pathologic processes lead to disturbance of the epidural blood flow. According to Brown’s investigations, the venous blood flow can already be impaired by 5 to 10 mm Hg in the affected segment and the arterial supply reduced by 20 to 30%.9 Through the disturbance in perfusion due to an applied pressure of 10 mm Hg, nutrient transport to the nerve root can be reduced about 20 to 30%. The inflammatory reaction favors the emergence of an epidural fibrosis.^11,25

A significant increase of collagen fibers is observed with chronic inflammation, long-standing edema, and the filling of tissue wounds. Pathologic tissue alterations are recognized not only by the growth of collagen fibers but by the abnormal structure of various collagen fiber types. The structural proteins fibrillin or elastin can likewise be pathologically changed.¹¹

It should be part of everyday clinical life to apply exclusively preservative-free solutions epidurally or spinally, because preservatives also can induce epidural fibroses and even neurotoxic reactions in the vicinity of the spinal cord.

Epidural scars

A pathologic increase in connective tissue in the epidural space is designated as an epidural fibrosis or epidural scar. (The terms “epidural sclerosis”, “callus”, and “induration” are also used as synonyms for epidural fibrosis.) Epidural scars play an extraordinarily important role in pain medicine.

The formation of an epidural scar proceeds through the following stages.

1. The first stage, of healing by first intention, is the normally running healing process ending with formation of small amount of granulation tissue.

2. The second stage, of healing by second intention, from the end of the first stage runs until massive granulation tissue formation, by which strong scarring occurs.

3. Scar formation concludes with the stage of wound healing, or repair.

Epidural wound healing is indicated by a strong loss of locally specific cells and can be compensated for by a corresponding scar formation, leading to functional impairment of the tissue.¹¹

Wound healing, in which connective tissue encloses nervous structures followed by subsequent scar formation, leads to clinically significant nerve root compression sign and localized back pain as well as diminution of conduction. Krämer correctly compares the connective tissue strands on the spinal dura mater and nerve roots to bell ropes that are actuated by every unthinking movement.¹⁵

Epidural wound healing is not always a harmless reaction to a reparative inflammatory process; rather, it is often harmful resulting in a specific chronic neuraxial pain syndrome.

Endoscopic Identification

In the endoscopic image, epidural proliferations of connective tissue appear as fibroses, depending on the degree of collagen markedness, in a clear white or gray-white color, and they present themselves as avascular, as a rule. Epidural fibroses range in appearance from strandlike, to space-occupying and in consistency from flexible to stone-hard. Fibroses that are strandlike can be confused with an epidural peripheral nerve. Epidural vessels or nervous structures can also be enclosed in fibroses.

In the pathologic process of epidural space-occupying fibroses, parts of the spinal dura mater and posterior longitudinal ligament or ligamentum flavum are often firmly included. Fibroses in the form of clamplike connective tissue strands can also be seen to pull around the nervous structures and nerve roots and put pressure on them mechanically. The connective tissue strands can also hinder the slippage of the nerve root in the intervertebral foramen.

Epidural fibroses can also be identified as broad flat malformations between the affected nerve root and the osseous environment in the lateral recess.

Along with the epidural fibroses, local chronic inflammatory processes (epiduritis, radiculitis, and arachnoiditis) or a perineural fibrosis, as in FBSS, can also be diagnosed endoscopically in the epidural cavity.

Topographic Aspects

Sacral and lumbar regions

As with adhesions, fibroses are found in the sacral and lumbar regions in most endoscopic investigations. On the basis of a large number of endoscopic investigations of our patients with FBSS, postoperatively arising fibroses, or scars, of varying extent are very frequently encountered. Lumbosacral fibroses often form the basis for spinal stenosis ( Fig. 12.12).

To perform successful spinal endoscopies, obstructing fibroses in the sacral or lumbar regions of the epidural space must occasionally be removed by means of microsurgical instruments or the use of a laser.

Thoracic and cervical regions

Fibroses in the thoracic and cervical regions are very frequently clinically relevant to pain. In contrast to the situation in the cervical and lumbar regions, only 0.75% of all intervertebral disk prolapses are diagnosed in the thoracic region, due to lesser biomechanical loading.^8,26

Our investigations show that fibroses are endoscopically observed in target regions of pathologic processes (regions operated on, with implants, where polymethylmethacrylate [PMMA] bone cement was used, etc.), especially in the ventral cervical and thoracic pain regions ( Fig. 12.13).

Marked local to completely stenosing fibroses (in which parts of the longitudinal posterior ligament and/or the spinal dura mater are often firmly included) occur, according to our experience, in the ventral thoracic segments T4–T10( Fig. 12.14). Fibroses occur mainly in the ventral cervical epidural C5–C6, C6–C7 segments.

Fig. 12.12 (a,b) Epidural fibrosis in lumbosacral region being investigated.

Fig. 12.13 Accidental distribution of polymethylmethacrylate (PMMA) for a vertebroplasty into the epidural space, epiduroscope in the dorsal epidural space presentation of fibrosis between the ligamentum flavum and the spinal dura mater (picture-in-picture technique).

After long periods of time, epidural fibroses develop in the region of implanted spinal cord stimulation (SCS) electrodes for neuromodulation ( Fig. 12.15).

Over the course of time through a strengthened epidural scar formation or marked fibrous enclosure of the tip of an SCS electrode, the electrode can become ineffective. Cicuendez et al reported on spinal cord compression due to epidural scar tissue formation around an SCS electrode.^27,28 In these patients, SCS neuromodulation was ineffective and paraparesis was encountered a year after SCS electrode implantation. After operative decompression, histologic investigation of the epidural tissue around the SCS electrode confirmed an epidural fibrosis from which microbiological investigation excluded a chronic infection ( Fig. 12.16).

Epiduroscopy opens the possibility of detecting increased production of fibrous connective tissue or granuloma formation in the region of an SCS electrode tip and intervening microsurgically as necessary in order to restore the effectiveness of neuromodulation after long use, above all without operative electrode replacement.

Case presentation

In two patients with long-standing implanted SCS electrodes (Medtronic, Inc., Minneapolis, MN, USA; St. Jude Medical Inc., St. Paul, MN, USA) in which electrostimulation was no longer effective, an endoscopic investigation with subsequent microsurgical adhesiolysis was performed because of the suspicion of epidural fibrosis of the SCS electrode tip ( Fig. 12.17).

Using the FLEX-X²⁹ flexible epiduroscope (Karl Storz, Tuttlingen, Germany) introduced percutaneously via the sacral access to the dorsal catheter location at levels T9–T10, a white, avascular fibrosis strand embedded in the surrounding fatty tissue was observed. The structure of the endoscopically identified strand corresponded to one of the nerves that passes through the cavity. Via fluoroscopic C-arm imaging in the lateral beam direction, it was confirmed that the SCS electrode tip was contained in the epidural fibrosis.

With the help of special microsurgical instruments advanced through the working channel of the epiduroscope, the SCS electrode tip was laboriously freed from the epidural fibrosis, restoring the epidural electrostimulation and the accompanying pain reduction.

Fig. 12.14 (a,b) Epidural ventral strand-shaped, avascular, connective tissue fibroses in segment L1–L2.

Fig. 12.15 Thoracic epidural fibrosis after spinal cord stimulation electrode implantation (figure-in-figure technique)

Along with normal catheter positioning, sling and loop formations of the catheter, and folding back of the catheter tip through fibrosis or adhesions could also be observed under endoscopic view in our patients ( Fig. 12.18).

It is practically impossible under endoscopic view for a rollup or a knot or sling formation to occur in placement of a stylet-guided catheter through the working channel of the endoscope. With catheters not placed under endoscopic view, injections in the region of a nerve root can come out in a vein or in a ligament in our experience ( Fig. 12.19).

After a long epidural residence period for an implanted catheter, fibroses form along its course. Aldrete¹⁹ found clinical signs of epidural fibrosis between 21 days and 320 days after an epidural catheter was placed.

From our experience, after a residence period of 1 month after placement of a polyurethane catheter, because of marked adhesions and the beginning local fibrosis the catheter was endoscopically recognizable only with effort.

During an epiduroscopic control investigation, we found signs of a nonbacterial inflammatory reaction already after a catheter implantation period of 5 to 7 days ( Fig. 12.20).

We confirmed that even epidural catheters placed under endoscopic view or epidurographic control with their tips in the pain-relevant region (a locale with highly developed fibrotic material), after epidural application of local anesthesia, attained a negative analgesia result.

Endoscopic identification and handling for catheter placement or removal can be made easier by strong catheter coloration and corresponding marking aids.

Catheter shear-off

Depending on the catheter implantation technique, the possibility of shearing the catheter off exists, for example, in installation, withdrawal, or removal of the catheter (e.g., through the Tuohy needle). In fact, there are no hints about serious neurologic sequelae of a sheared-off catheter as a foreign body, but some authors advocate surgical removal of it.

To reach the target region for catheter extraction, fibrotic changes around long-implanted catheters in the epidural cavity must be loosened microsurgically. However, the discovery of the catheter after a long residence period in the epidural space can be laborious. On the basis of fibrinous jacketing of the catheter, it is often difficult to distinguish it endoscopically from the remaining epidural fibroses and nerves. We found it necessary to break up the catheter jacketing microsurgically by means of miniature grasping forceps in order to explant the sheared-off catheter part from the epidural cavity or intrathecal space ( Fig. 12.21). Because of the catheter material (polyurethane), it is advisable to forgo the use of a laser-supported adhesiolysis.

Fig. 12.16 (a–c) Epidural adhesions and fibroses are seen forming around an implanted spinal cord stimulation electrode (picture-in-picture technique).

Fig. 12.17 (a) Implanted spinal cord stimulation electrode in dorsal thoracic epidural space. (b) Grasping forceps plus spinal cord stimulation electrode in the epidural space for mechanical adhesiolysis.

12.3.3 Inflammatory Processes

Fig. 12.18 (a) Folding back of a conventionally placed spinal catheter, lumbar to caudal. (b) Exact thoracic site of the catheter after correction.

Fig. 12.19 Anteroposterior (AP) epidurogram with a radiopaque catheter following injection of contrast into the lower vena cava.

Chronic neuraxial inflammatory processes are frequently associated with extensive destruction of the original tissue structures and finally with wound healing. Macrophages, lymphocytes, plasma cells, and eosinophilic granulocytes play an important role in chronic inflammation. The cytokines secreted by these cells lead to marked and long-lasting changes of the affected tissue.11,15,30,31

Epiduritis

Epiduritis is a partial or space-occupying inflammatory process of structures in the epidural space. In an endoscopic image epiduritis presents with the cardinal signs of redness, swelling, and edema and test positive on a pain provocation test.

Choi et al reported on 24 patients who underwent epiduroscopy because of chronic back pains. In all of these patients, endoscopopy revealed inflammation characteristic of epiduritis.⁵

In most cases of patients with chronic inflammatory neuraxial diseases, such as spondylitis, diskitis, spondylodiskitis, radiculitis, or epiduritis, the ventral sections of the spinal canal are involved ( Fig. 12.22).

In our more than 2,000 epiduroscopic investigations, we comparatively diagnosed some 42% of patients with chronic inflammatory processes in the sense of a locally limited chronic inflammatory process, with the signs of radiculitis and/or epiduritis ( Fig. 12.23).

Laboratory chemical signs of an inflammation, such as an elevated red blood cell sedimentation rate, an elevated level of C-reactive protein or an elevated leukocyte count, cannot be regularly detected in patients in whom a chronic inflammatory process (arachnoiditis, epiduritis, or radiculitis) has been diagnosed.

Endoscopic identification

Chronic inflammatory processes in the epidural space, such as epiduritis, radiculitis, or arachnoiditis, present in endoscopic images as significantly hyperemic, edematous bloated tissue structures.

The often regionally limited epiduritis is diagnosed as a local inflammaory reaction with the cardinal signs of redness, swelling, and edema. The affected epidural structures are strongly hyperemic (reddish to dark red) and edematously bloated. Epiduritis is delimited very significantly from the other healthy epidural tissue by color.

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