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Arachnoiditis Part 1: Clinical Description

Arachnoiditis is a rare, but extremely debilitating, chronic pain condition caused by injury to the arachnoid layer of the spinal cord. The goal of treatment is to improve a patient’s function and quality of life by alleviating (but not eliminating) symptoms, especially pain.
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The Pathologic Process

Cascade of Events and Symptoms

Clinical management of the AA patient demands an understanding of the cascade of events and symptoms. The first event in the pathologic process of AA is one of inflammation, followed by nerve root entrapment, bundling, and adhesion formation (Figure 1). In addition to nerve roots, the other spinal layers—the pia and dura—may be encompassed in the scarred, adhesive, affected area. As noted, the scarred area interferes with the normal flow of CSF and electric currents. Since the cause of the scarring is inflammation, the process may be progressive. Severe pain develops rapidly in the process because nerve roots become entrapped and adhesions form. Both localized pain and radiating pain are present.



Centralized Pain Symptoms

The second event is centralization of pain and its attendant overstimulation of the sympathetic nervous and hormonal systems. AA produces centralization of pain rather early in its course. All the sequelae of centralized pain can be present, including fibromyalgia-type distribution, depression, fatigue, insomnia, hypertension, tachycardia, hyperhidrosis, and vasoconstriction manifested by cold hands and feet. There will be overstimulation of the hypothalamic-pituitary-adrenal-
thyroid-gonadal hormone system. The severe pain of AA can cause exhaustion of the hormonal system.7,8

Autoimmune Sequelae

The third event in the cascade is the development of autoimmunity, which causes intermittent, inflammatory attacks on tissue, joints, and lymph nodes (Table 2). Patients with AA may develop symptoms and signs of a typical autoimmune disorder, such as systemic lupus erythematosus. These symptoms include intermittent fever, lymphadenopathy, malaise, joint pain, skin rashes, dry eyes, allergies, and hypersensitivity to medications.1 Inflammatory biomarkers, such as erythrocyte sedimentation rate and C-reactive protein can be elevated in patients with AA. In addition, AA has autoimmune sequelae similar to those seen following traumatic brain injury (TBI).7-9 Brain and spinal cord tissue is antigenic if it enters the general circulation.6 As with TBI, AA may cause enough tissue damage that cord particles can reach the general circulation and cause an autoimmune, inflammatory disorder.


Making the Diagnosis

The use of imaging devices may cause some confusion. In some severe AA cases, MRI shows typical evidence of AA. Unfortunately, in other cases, MRI in not diagnostic. Consequently, the diagnosis of AA might have to be made on a history of trauma, infection, or penetration of the dural layer, along with the signs and symptoms described.


Most cases of AA occur in the lumbar spine, although it can also occur in the cervical and thoracic areas. Patients with lumbar AA describe their pain as excruciating, radiating into the buttock, groin, and/or legs. Headache occurs almost universally in patients with AA, perhaps due to obstruction of normal spinal fluid flow. A hallmark sign of AA is an inability to sit for long periods of time, if at all. Patients may request to lie on your exam room floor because they cannot sit in a chair or on an exam table. In severe cases, patients say they must stand to eat and lay down in a car or on a plane.

When the injury includes the lower spine, nerve roots that connect to the bladder, bowel, or genitalia can become entrapped. Consequently, bladder and bowel dysfunction almost always are present to some degree. Incomplete bladder emptying and constipation are the usual problems, and they usually require medical treatment. Sexual function can be severely impaired.

Patients frequently describe pain that appears to move or migrate around the upper torso. These pains may be described as tingling, burning, creeping, or pruritic.

Physical examination of the patient is variable. There can be increased pain with pressure over the primary pain site. In severe cases, there almost always will be some weakness of the lower extremities, as well as decreased reflexes. The weakness can affect walking, and many patients will require a cane and snug shoes to safely ambulate. Muscle wasting of the lower extremities can be evident.

Trapping of Electricity

It is my personal observation and intuitive reasoning that the AA site traps or collects electricity because normal nerve conduction is blocked by scarring and adhesions. Patients often describe themselves as harboring a lot of electricity and some report they “burn out” wrist watches and computer mice.

When I have attempted to use an electric current or electromagnetic device over an AA pain site, I sometimes have caused excruciating pain. The same device usually relieves pain in the usual spine patient who has simple arthritic degeneration or stenosis. I even have observed severe pain develop in some patients when a magnet is placed over the AA pain site.

Treatment Strategies

Early Treatment

As noted, clinical management of the AA patient demands an understanding of the cascade of events and symptoms. Pain practitioners should suspect AA is in the early, developing stage in any patient with severe back pain and a history of possible entry of a foreign substance into the subdural or subarachnoid spaces. This is important because it may be possible to prevent the progression of inflammation to adhesion formation.

When I suspect a case, I vigorously attempt to use systemic, not local or epidural, methylprednisolone or other corticosteroid plus anti-inflammatory agents in an attempt to prevent formation of adhesions. Acetazolamide should be attempted because, just as in glaucoma, it decreases the volume of lymph-related fluids, including spinal fluid. Pain relief with acetazolamide essentially is diagnostic of AA. My clinical experience is limited with minocycline (Minocin, Solodyn, others), but I believe this agent might suppress glial cell activation and inflammation in the spinal cord, as has been reported in animal studies.

Treating Established Cases

Once AA is established, treatment must be aggressive and comprehensive. Both peripheral and central pain components will have to be managed. There are no clinical guidelines for the treatment of AA, but it is prudent to follow established practices for treating other chronic pain conditions. Standard pharmacologic agents should be quickly and vigorously pursued; otherwise, a patient with AA will become disabled by pain, becoming bed-ridden and possibly suicidal.

Last updated on: March 27, 2017
Continue Reading:
Arachnoiditis Part 2—Case Reports