Arachnoiditis is a broad term denoting inflammation of the meninges and subarachnoid space. It is characterized by thickening of the arachnoid membrane and dura matter adhesions that result in chronic lower back pain. Complications include cranial neuropathies, myelopathy, and radiculopathy. 
Arachnoiditis has many causes, including infectious, inflammatory, and neoplastic processes. Infectious causes include bacterial, viral, fungal, and parasitic agents. Noninfectious inflammatory etiologies include surgery, intrathecal hemorrhage, and the administration of intrathecal agents, such as myelographic contrast media, anesthetics, and steroids. [1, 2, 3, 4, 5]
The most severe type of arachnoiditis is adhesive arachnoiditis, with scar tissue compressing the nerve roots and ultimately disrupting both blood supply and flow of cerebrospinal fluid. Adhesive arachnoiditis can progress to arachnoiditis ossificans, or ossification of the spinal arachnoid. [1, 2, 3, 4, 5]
Neoplasia includes the hematogenous spread of systemic tumors, such as breast and lung carcinoma, melanoma, and non-Hodgkin lymphoma. Neoplasia also includes direct seeding of the cerebrospinal fluid (CSF) from primary central nervous system (CNS) tumors, such as glioblastoma multiforme, medulloblastoma, ependymoma, and choroid plexus carcinoma. 
Because of its noninvasive nature, multiplanar capabilities, and superb soft-tissue characterization, magnetic resonance imaging (MRI) is the study of choice for the diagnostic evaluation of arachnoiditis. [7, 8] For patients in whom MRI is contraindicated, computed tomography (CT) myelography is an acceptable alternative. [9, 10, 11, 12, 13, 14]
Neural effects of arachnoiditis are demonstrated in the images below.
The spinal cord and nerve roots cannot be evaluated with routine plain radiographs. However, myelography with the intrathecal administration of iodinated contrast material is useful in evaluating the contents of the thecal sac. In adults, the conus medullaris normally terminates between the T12-L1 and L1-L2 levels. Below these levels, the nerve roots normally float freely within the thecal sac. Meningeal inflammation leads to thickened or clumped nerve roots (as in the images below), blockage of CSF flow, and the formation of CSF loculations. With radiographic findings, the degree of confidence is high.
MRI is far superior to conventional CT scanning in the evaluation of arachnoiditis because of the poor contrast resolution in CT scans between the spinal cord and nerve roots and CSF. However, CT myelography is effective in demonstrating the classic imaging findings of arachnoiditis. These include narrowing or blockage of the subarachnoid space, irregular collections of contrast material, thickened or matted nerve roots, and absent filling of nerve root sleeves.  With conventional CT scanning, the degree of confidence in findings is low. With myelography, the degree of confidence is high. (See the image below.)
Magnetic Resonance Imaging
As previously stated, MRI is the study of choice for the diagnostic evaluation of arachnoiditis. [15, 16, 9, 10] T1-weighted MRI scans, as demonstrated in the images below, may reveal an indistinct or absent cord outline due to the increase in the signal intensity of the surrounding CSF. This may be the result of an elevation in CSF protein content, the presence of inflammatory exudate, or the formation of adhesions along the surface of the spinal cord.
T2-weighted MRI scans may demonstrate CSF loculation and obliteration of the subarachnoid space or irregularly thickened, clumped nerve roots (as in the first 2 images below), which occasionally may be misinterpreted as a tethered cord or a thickened filum terminale. With more severe arachnoiditis, progression of nerve root clumping and leptomeningeal adhesions may lead to angular defects in the dural sac. Peripheral adherence of the nerve roots to the walls of the thecal sac produces the so-called featureless, or empty, sac, as seen in the third image below.
Contrast enhancement is an inconstant finding. When it does occur, enhancement may be the result of a vascular network within the fibrous stroma that develops in the subarachnoid space. Three patterns of enhancement have been described:
The most common pattern of enhancement (seen in the image below) is a smooth, linear layer of enhancement outlining the surface of the cord and nerve roots.T1-weighted sagittal fat-suppressed contrast-enhanced MRI of the lumbar spine in tuberculous arachnoiditis and meningitis shows thin, linear leptomeningeal enhancement of the conus medullaris and cauda equina.
The second-most common pattern is a nodular pattern (seen in the image below) with discrete foci of enhancement seen along the surface of the cord and nerve roots.T1-weighted sagittal MRI of the cervical spine in tuberculous arachnoiditis shows nodular pockets of enhancement in the subarachnoid space after the administration of contrast material.
The least common pattern consists of diffuse intradural enhancement that completely fills the subarachnoid space (as demonstrated in the images below).T1-weighted sagittal nonenhanced MRI of the lumbar spine shows signal intensity throughout the subarachnoid space that is diffusely increased, compared with that of the spinal cord (arrow), in tuberculous arachnoiditis.T1-weighted sagittal contrast-enhanced MRI of a lumbar-spine tuberculous arachnoiditis reveals diffuse enhancement that fills the entire subarachnoid space. Tuberculosis (TB) bacilli were isolated from the CSF.
No pattern of enhancement has been found to be characteristic of any specific infectious agent or pathologic process. In general, benign arachnoiditis enhances less avidly than does carcinomatous meningitis; however, MRI findings alone cannot be used to differentiate infection from neoplasm. 
In one report, arachnoiditis could not be excluded on routine postoperative intravenous-enhanced MRI in a patient with progressive paraparesis and sphincter incontinence. Arachnoiditis was differentiated from postoperative changes with intrathecal-enhanced MRI. Doses ranging from 0.8 to 2 ml of gadolinium mixed with 3 to 5 ml of the patients' CSF under sterile conditions have been injected into the subarachnoid space. MRI was performed utilizing T1-weighted, fat-suppressed sequences in 2-3 orthogonal planes.
Purported advantages of gadolinium-enhanced intrathecal MR imaging include an absence of ionizing radiation, the capability of direct multiplanar imaging, an absence of bony artifact, and high spatial and contrast resolution. It should be noted that although a cooperative multicenter study of 95 patients failed to demonstrate behavioral changes, neurologic alteration, or seizure activity with intrathecal gadolinium, the administration of intrathecal gadolinium is not approved for use by the FDA and has been used off-label.
Gadolinium-based contrast agents have been linked to the development of nephrogenic systemic fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). The disease has occurred in patients with moderate to end-stage renal disease after being given a gadolinium-based contrast agent to enhance MRI or MRA scans. NSF/NFD is a debilitating and sometimes fatal disease. Characteristics include red or dark patches on the skin; burning, itching, swelling, hardening, and tightening of the skin; yellow spots on the whites of the eyes; joint stiffness with trouble moving or straightening the arms, hands, legs, or feet; pain deep in the hip bones or ribs; and muscle weakness. For more information, see Medscape.
With MRI findings, the degree of confidence is high. Sarcoidosis and spinal anesthesia may cause false results.