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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.
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In order to reach the subarachnoid compartment, insertion of a needle that penetrates the dura undoubtedly has also to perforate the arachnoid membrane. It follows that intradural lesions can occur even after the slightest of trauma to the spinal cord or nerve roots (paraesthesiae) thereby initiating an inflammatory reaction in this trabecular membrane, followed by the appearance of some features common to ARC.42 These include some cases of syringomyelia subsequent to a traumatic puncture of the spinal cord43,44 or when pseudomeningoceles45 appear after spinal operations. Cases of multiple invasive interventions with injections of chemically irritant substances such as depo-medrol46 and methrotraxate,47 by repeatedly producing inflammatory responses of the arachnoid and the adjacent dural wall, may eventually result in arachnoiditis ossificans,48 arachnoid cysts,49 or pachymeningitis,50 all of which are extreme features of ARC .

In addition, cases of cauda equina syndrome and transient nerve root irritation that are usually thought to be only functional, temporary complications, are shown—through non-invasive diagnostic tests (coronal views in MRI images, nerve conduction studies and EMG)—to be quite the opposite by identifying definite lesions within the cauda equina. In the author’s opinion, for most of these cases, the inflammatory phase51,52 behaves, clinically and functionally, as ARC and eventually progresses to permanent neurological deficits.53

Interpretation of Symptoms

Although the presence of signs and symptoms that do not conform with the representation of typical radiculopathy may cast some skepticism about the patient’s veracity and credibility, physicians must realize that, in arachnoiditis, there are desynchronized reflex responses to random production of hyperesthesia that result in axonal injury.54 Burning sensations which appeared in over 90% of our patients with arachnoiditis (see Table 2) are usually evoked by sustained pressure during nociceptor sensitization (noticed after long standing or walking), but always outlast the period of stimulation. These pain signals are most likely transmitted by fast-conducting primary afferents, as when severe burning pain is seen after repetitive stimulation or ectopic firing.55 On the other hand, sensory deficit manifestations such as tingling, “pins and needles," formication, and even pruritus seen in some of our patients (see Table 2) may represent ectopically-generated nerve impulses to certain maneuvers such as stretching or flexing the lower extremities, turning from the supine to the lateral position, both of which induce excitation of deep tissue afferents.56,57

Hyperesthesia (see Table 2) appearing weeks after surgery may herald Wallerian degeneration accompanied by an increase of endoneurial fluid pressure58,59 extending to the distal root ganglia which, in turn, generates a mechanical stimulus to evoke abnormal activity in sensory neurons.60 Another mechanism, occurring 4 to 6 months after laminectomy, may have a role in the production of areas of hyperesthesia alternating with areas of sensory diminution. This mechanism involves considerable constrictive scarring and fibrosis surrounding a nerve root (extradurally) and thus compromising the intraneural blood flow sufficiently enough to result in localized ischemia.

Further, traumatic lesions of the nerve roots or the spinal cord by either traumatic punctures, spinal fractures, forceful surgical retraction,61 or dissection, etc., may eventually affect some portions of the Lissauer’s tract and the substancia gelatinosa which are thought to participate in some of the mechanisms of pain suppression.62,63 This finding suggests that at least some of the deafferentation type of pain may be due to an indirect dis-inhibition of the dorsal horn’s transmission cells. In these instances the pain-related symptoms will be evident in the immediate postoperative period.

Another mechanism for the production of ARC is the accumulation that may occur outside of the dural sac after surgical operations. Though is recognized that the blood, itself, does not usually cross the dural barrier, substances such as leukotrienes and cytokins resulting from the degradation of blood cells may do so.64

A recently identified source of discomfort, previously ignored, is the presence in post-lumbar spine laminectomy patients in whom fibrosis and scar tissue proliferates at the site of the operation constricting the dural sac and dilating it distally.65 This complication appears three to six months following surgery and results in a gradual enlargement of the diameter of the sac, accompanied by markedly altered circulation of the cerebrospinal fluid from brain-to-spine and vice versa. Moreover, the function of the arachnoid villi, that allow unidirectional exit of the CSF toward the venous circulation is markedly reduced, if not obliterated, by this proliferative process. This condition manifests as a continuous gnawing and uncomfortable sensation of pressure in the lumbosacral spine and is usually not relieved by anti-inflammatory or narcotic analgesics.

Mechanical irritation (walking, pedaling, and gardening) may be associated with an erithematous discoloration (rubor) and a warming sensation of the feet that appears to initiate, by stimulation, a sympathetic mediated pain (see Table 2). The occurrence of antidromic vasodilatation, as well as mechanical and thermal hyperalgesia may be interpreted as a recruitment of the sympathetic nervous system into reflex action contributing, by default, to an unorganized vasomotor symptomatology. This would explain the complex mechanism of the neuropathic pain phenomenon experienced by patients with ARC that includes sympathetic-mediated symptoms and signs.66

The feasibility of having different mechanisms for different types of pain appears plausible, as allodynia, hyperalgesia, and burning sensations are subtypes of neuropathic pain.60 This sympathetic-parasympathetic imbalance may be responsible for the frequent diaphoresis, heat intolerance, and nocturnal hyperactivity of the sweat glands seen in ARC. This also suggests participation of an autoimmune reaction, as some patients appear to be more susceptible to develop more scarring and adhesions in the healing process than others (see Table 3). This variant is perhaps an exaggerated response generated by an antigen-antibody reaction in a hypersensitive patient.66 These neurotoxic responses may repeatedly generate endogenous pirogens resulting in an intermittent low-grade fever, similar to that seen in patients with lupus erythematosus, polyarteritis nodosa, Reiter’s syndrome, etc. Though, there is no specific pattern, low-grade fever implies an active autoimmune process67 with its usual periodicity and is a concept supported by the findings of abnormal activity of gamma-glutamyl transferase in CSF,68 defective fibronolysis,69 and in some cases of arachnoiditis and failed back surgery syndrome.

Last updated on: April 13, 2017