Subscription is FREE for qualified healthcare professionals in the US.

Suspecting and Diagnosing Arachnoiditis

A review of the symptoms noted in a group of patients with arachnoiditis presents an analysis of clinical observations of this disease.
Page 1 of 8

Arachnoiditis (ARC) is a nonspecific inflammatory process usually caused by an invasion into the dural sac—whether by bacteria, blood, or injections of various irritant substances that produce a spectrum of pathological changes originating on the arachnoid membrane. The resulting inflammatory response eventually proliferates to other intrathecal neural elements leading to fibrosis and adhesions that involve the nerve roots, the arachnoid, the spinal cord, and the dura mater. This progression culminates in permanent disability characterized by severe intractable pain, neurological deficit, and other related symptoms.1 Although this process may involve any site where the arachnoid membrane and neural structures are found, the most common presentation occurs in the lumbosacral region affecting not only the distal spinal cord, but also the cauda equina’s nerve root and the sympathetic nerve fibers connected to them.,2 In addition to pain sensory alteration and motor deficits, it may also be accompanied by other symptoms such as low-grade fever, profuse diaphoresis, heat intolerance, nausea, bladder and/or bowel dysfunction, and sexual impairment. Evidently, this syndrome is, by far, more complex than the involvement of the meningeal layers. Whereas the main clinical features represent a physical injury producing functional damage or alteration, the ensuing devastating disease is always associated with unrelenting chronic pain and major psychological and social impacts.

Due to the scarcity of objective data regarding the correct diagnosis of arachnoiditis, the author and a group of collaborators (see acknowledgements) associated with the author’s clinical facilities have, over a period sixteen years, tabulated comprehensive data on arachnoiditis patients. The data was obtained from the clinical history from all the medical records available, patient physical and neurological exams, and a review all the available films in 489 patients in whom the diagnosis of arachnoiditis had been suspected or affirmed by other clinicians. All patients were seen personally by the author from 1989 to 2006. A good number of patients were refer to the author’s pain management facilities for diagnosis and treatment, with most patients coming from distant states or from other countries. Many other patients came of their own accord after they developed symptoms resembling arachnoiditis following a medically-related event that included incidental invasion of the vertebral canal. In the last decade, by far, the largest number of patients have also received, at one time, the diagnosis of Failed Back Syndrome (FBS). As a matter of clarification, it is important to note that not all the patients having arachnoiditis had FBS and not all the patients with FBS had ARC.

Historical Background

After Charcot and Joffroy3 first described a syndrome resembling ARC in 1869, other series of cases caused by infectious diseases such as tuberculosis,4 syphilis,5 parasitic,6 or fungal organisms7 appeared in the medical literature nearly 150 years ago. In 1909, the british neurosurgeon Victor Horseley8 wrote a classic description of the clinical symptoms, together with operative and postmortem findings in patients with arachnoradiculitis. This classical description was followed by Foix and Alajouanine9 who, in 1926, correlated the symptoms with the location in the spinal cord and nerve root pathological findings. In 1930, Vincent et al.10 described the first non-infective cases of ARC related to the introduction and increased popularity of myelography as a diagnostic test in the 1930’s. However, it was not until two decades later11 that the alarm was sounded about the possibility of pantopaque and other oil-soluble contrast media12,13 producing permanent neurological deficit. This feasibility was initially doubted since many of the patients having myelograms either had an ongoing neurological disease14 or had spinal operations15 soon thereafter, so it was therefore difficult to discern the origin of subsequent neurological deterioration or to define the onset of new symptoms. This dilemma was aggravated by the fact that the only diagnostic procedure available to confirm the presence of ARC, at that time, was to perform another myelogram. Even when tomography became available, intradural sac pathology could only be defined when oil-soluble or some of the early water-soluble contrast media were injected intrathecally.16 Although the use of oil-based dyes had been discontinued in Scandinavian countries in 1965, and despite multiple reports of severe arachnoiditis following the intrathecal injection of iophendylate and other oil-soluble dyes, the FDA did not stop its sale in the USA until 1986.

Possible Etiology of Arachnoiditis

Recognizing that arachnoiditis of the lumbosacral spine can also occasionally be caused by infections like meningitis, viruses like HIV, and parasites like echinococcus, readers are referred to a review on that subject.2 This series include a group of patients that apparently acquired this disease while under going diagnostic or therapeutic procedures of the spine. Efforts to identify the possible causative factor(s) were made by reviewing all the pertinent medical records and correlating the radiological findings from the time of appearance of the low back pain. All subsequent procedures and interventions were reviewed. Since many of these patients were not evaluated until months or years after the apparent event that might have caused ARC, a retrospective assessment of the events related to spinal diseases, injuries, operations or any other invasive procedure performed in or near the spine were evaluated to identify any possibly related event in the available documentation. The precise probable cause was identified in 472 cases (96.5%); in the remaining 17 cases (3.5%), probable cause was deduced from sudden changes in the intensity and frequency in symptoms that coincided with a considerable change documented in the neurological exam, together with definite radiological findings reported at about that time. Previously, only a portion of the total number of patients included in this series was published.1 This series encompasses all the patients seen from 1989 to 2006, making this the most current report.

As shown in Table 1, this updated series includes 489 patients (233 men and 256 women ranging from 24 to 94 years old). Most of the patients were middle-aged, with an average of 53.4 years (from 27 to 86 years of age) for men and 48.4 years for women (from 22 to 92 years old). Twenty six cases, in whom some of their medical records and some of their radiographs were reviewed but not examined directly by the author, were excluded from this series.

Last updated on: May 19, 2015
First published on: January 1, 2006