Abstract
Arachnoiditis is the development of chronic inflammation and progressive fibrosis of the arachnoid and pia layers of the meninges from physical or chemical irritation. As arachnoiditis progresses, inflammation can lead to fibrosis. In severe cases, the arachnoid fibrosis can cause compressive nerve root and spinal cord adherence and ischemia, resulting in progressive pain and neurologic deficits. Typically, arachnoiditis develops slowly during the period of months after the initial insult, although it may continue to develop for years. While the symptoms associated with arachnoiditis are heterogeneous and often difficult to distinguish from other disease processes, patients most frequently report burning pain or paresthesias; weakness may also occur. The diagnosis of arachnoiditis is most often made through the use of magnetic resonance imaging. Treatment of arachnoiditis is palliative. Conservative measures include medications aimed at treating neuropathic pain; anti-inflammatories and opiates are also used. Physical rehabilitation is sometimes limited by pain, but remains an important part of treatment. To date, corticosteroid injections and surgical treatments have shown little benefit for arachnoiditis symptoms. Neuromodulation is a growing field that shows promise in future arachnoiditis treatment. Traditional dorsal column stimulation has had some limited success. In the past few years, the field of neuromodulation has expanded to include dorsal root ganglion stimulation, high-frequency stimulation, and burst stimulation modalities. These technologies may give arachnoiditis sufferers more relief than previous therapies.
Definition
The meninges are a system of three protective membranes that surround the central nervous system and consist of the pia mater, arachnoid mater, and dura mater layers. Arachnoiditis is the development of chronic inflammation and progressive fibrosis of the arachnoid and pia layers of the meninges. This is thought to be from an original insult, such as chemical irritation or physical manipulation, which leads to an inflammatory cascade. It can occur subsequent to a variety of conditions, although it is most commonly a sequela of spinal surgery or the result of intrathecal injection of radiographic dyes and chemicals with neurotoxic preservatives. Some of the etiologic factors linked to the development of arachnoiditis are listed in Table 96.1 . Because arachnoiditis is rare, specific incidence and prevalence are uncertain.
| Agents injected into the subarachnoid space |
|
|
|
|
| Spinal surgery or trauma |
|
| Intradural surgeries |
|
|
|
|
|
| Infection |
|
|
|
|
When microtrauma to the vasculature of the arachnoid membrane and pia mater occurs, it can impair the normal mechanisms for control of meningeal fibrosis. This may result in the deposition of fibrous collagen bands in the arachnoid-pia membranes and cause the nerve roots to adhere to each other as well as to the dural sac. The pathophysiologic mechanism of arachnoiditis involves a progression from root inflammation (radiculitis) to root adherence (fibrosis). In severe cases, the arachnoid fibrosis can cause compressive root ischemia, and progressive neurologic deficits may ensue. When this condition occurs in the meninges of the cervical and thoracic regions, the spinal cord can become enmeshed and constricted as well. Pain is the result of dural adherence with nerve root traction and nerve ischemia. Typically, arachnoiditis develops slowly during the period of months after the initial insult, although it may continue to develop for years, resulting in worsening pain and paresthesias or progressive neurologic injury.
Symptoms
The symptoms associated with arachnoiditis are heterogeneous and often difficult to distinguish from other disease processes, such as radiculopathy, spinal stenosis, cauda equina syndrome, and neuropathies. Also, because arachnoiditis is often acquired iatrogenically during the course of evaluation and treatment of spinal disorders, patients often have concomitant symptoms of mechanical back pain or myofascial pain in addition to the arachnoiditis symptom complex.
Patients with arachnoiditis principally report burning pain or paresthesias. However, these symptoms often do not follow typical radicular patterns. Pain is usually constant but exacerbated by movement. Some patients experience secondary muscle spasms. Weakness and muscle atrophy may also occur, and bowel or bladder sphincter dysfunction is not uncommon. Onset is insidious, and symptoms may first be manifested years after the inciting event. Symptoms can range from mild (such as slight tingling of the extremities) to severe (such as excruciating pain with progressive neurologic deterioration). The condition may also be asymptomatic and discovered only incidentally on magnetic resonance imaging (MRI).
Physical Examination
Neurologic examination typically reveals a patchy distribution of lower motor neuron deficits. Examination findings may include loss of reflexes, muscle weakness, muscle atrophy, anesthesia, gait instability, and reduced rectal tone. Less commonly, arachnoiditis may involve the spinal cord; in these instances, upper motor neuron findings (hyperreflexia, spasticity, presence of Babinski response) can be found on examination.
A complete neurologic examination should be performed at the time of initial diagnosis. In the event that symptoms worsen, this examination may then be used as a benchmark to ascertain whether neurologic deterioration is occurring. In the setting of progressive neurologic decline, it is incumbent upon the treating physician to rule out other pathologic processes (such as a new disc herniation) before neurologic deterioration is attributed solely to progressive arachnoid fibrosis.
Functional Limitations
Patients with arachnoiditis may exhibit a variety of functional limitations, the degree of which corresponds to the extent of the neurologic impairments and the severity of the pain. Gait instability, reduced ambulatory capacity, and impairment in activities of daily living are not uncommon. As time goes by, patients tend to suffer secondary effects of immobilization and deconditioning, causing further functional impairment. The severe pain and impaired mobility tend to isolate patients socially and to limit their ability to work. Because the pain associated with arachnoiditis is usually present even at rest, sedentary work or light duty does not always improve a patient’s symptoms enough to facilitate employment despite activity restrictions.
Diagnostic Studies
Presently, the diagnosis of arachnoiditis is most often made through the use of MRI. Historically, myelography was used routinely for diagnosis of arachnoiditis; characteristic findings included the observance of prominent nerve roots as well as various patterns of filling defects. The advent of computed tomography (CT) and MRI has made diagnosis easier.
MRI is preferred to CT myelography because of its noninvasive nature. Typical findings include adherent roots located centrally in the thecal sac (considered mild arachnoiditis), an “empty sac” (where roots are adherent to the wall of the thecal sac), and a mass of soft tissue replacing the subarachnoid space (severe disease). These findings are well seen on T2-weighted axial images ( Figs. 96.1 and 96.2 ). Although the administration of contrast material with MRI may help rule out other diseases in the differential diagnosis, such as tumors and infection, contrast enhancement is not necessary to visualize the characteristic appearance of arachnoiditis.
Related posts:
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
