The Anatomy of 
Adhesive Arachnoiditis


This illustration (
from Noback CR: The Human Nervous System, McGraw-Hill, Inc., 1967) illustrates the human subarachnoid space surrounding the brain and spinal cord.  60% of spinal fluid is produced within the brain and 40% from the spinal subarachnoid space.  It flows, as shown, and is absorbed by the venous arachnoid granulations.  This spinal fluid is produced at the rate of 0.35cc/min, or 500-750cc/day.  Turnover rate is 3-5 times/day.  A normal adult has a ventricular volume of about 30cc and about 100+cc in the surrounding subarachnoid space.  The subarachnoid space serves to be a hydraulic cushion for the floating brain, a source of nutrition as well neurotransmitters.  This space is the most fragile and sensitive area of the human body.

When the subarachnoid space is subject to insult or inflammatory change damage and scarring occur.  One of the primary difficulties in addressing the subject of neuropathologic change, particularly that of adhesive arachnoiditis is the great amount of confusion regarding nomenclature.  Adhesive arachnoiditis is an advanced form of arachnoiditis and is most often confused with the latter.  Some of the other terms by adhesive arachnoiditis has been referred to have been:


Serosa Circumscripta Spinalis
Intraspinal Granulomatosis
Obliterative Arachnoiditis
Chronic Arachnoiditis
Spinal Meningitis
Chronic Spinal Meningitis
Chemical Meningitis
Sterile Meningitis
Granulomatous Meningitis

There has been a "Tower of Babel" in regard to the terminology used to define the normal anatomy of the lumbar spinal column, the dural membranes, and the subarachnoid space. In the image, to the left, the nerve rootlets of the cauda equina, which are in motor and sensory pairs (shown as single nerves for simplification).  If a lumbar puncture were to be performed the needle would simply push the nerve roots, floating in cerebrospinal fluid, out of the way.  If a similar procedure were attempted in a patient with Class III Adhesive Arachnoiditis, where the nerve roots were fixed to each other and to the dura mater, the needle could easily injure or sever the nerves.

Adhesive Arachnoiditis comes about as a progression of inflammatory change secondary to insult or injury occurring over a period of time.  This progression involves:


Acute Inflammatory Phase (Class I)
Beginning of Chronic Phase (Class II)
Chronic Scar Phase (Class III)
Arachnoiditis Ossificans

            
Adhesive Arachnoiditis: Acute Inflammatory Phase (Class I)
In the illustrations of the first, or acute inflammatory phase, shown above, the nerve roots are swollen and hyperemic (vascular dilatation).  Pathologic specimens show acute inflammatory cells predominating.


Adhesive Arachnoiditis: Beginning of Chronic Phase (Class II)
In the illustrations of the second phase, shown above, the nerve root swelling has progressively decreased (the nerves are beginning to be encased in collagenous scar tissue). Pathologic specimens show a mix of acute and chronic inflammatory cells.


Adhesive Arachnoiditis: Chronic Scar Phase (Class III)
By the time the process has reached the chronic phase there is prominent collagenous scar deposition.  The nerve roots are adherent to each other and to the meninges.  Surgically opening the dura often shows what appears to be an empty sac because the nerves are now actually part of the dural membrane.  By the Class III stage the inflammatory cells seen document a chronic process.  The nerves themselves have been progressively deprived of nourishment as the nutrient blood vessels have atrophied and the "percolating" nourishment derived from the cerebrospinal fluid has markedly decreased.  It is, in fact, a tribute to the human nervous system that in the face of such adversity, in can, in the great majority of cases, continue to maintain "normal" function.  The only way this can happen is if the adverse process occurs slowly enough to allow the system to adapt and acclimate. The acclimization is, however, fragile.  Because function is maintained precariously any additional insult (i.e. trauma, surgery, myelography, etc.) can tip the balance and cause onset of clinical disability and incapacitation.

By far the greatest number of cases of adhesive arachnoiditis which have occurred throughout the world during the 20th century resulted from oil myelography with either Pantopaque® or Myodil®.  Because these substances are hyperbaric once they were placed in the subarachnoid space they would migrate to the distal portion, where they remained, producing progressive scarring. 

 
The patterns of adhesive arachnoiditis scar are typically quite variable in their patterns.  Sown above are drawings of variable scar patterns in three actual cases.  These are patterns reflecting diffuse, multi-level involvement, characteristic of the introduction of a toxic foreign body substance into the sub-arachnoid space.  The last illustrations to the right shows how residual droplets of foreign body substance (in this case Pantopaque®)  are surrounded by encapsulating scar reflecting the body's defense against foreign body substances.
The illustrations to the left demonstrate an example of focal adhesive arachnoiditis.  In this case it is due to the local inflammatory effect of a hypertrophic facet joint intruding into the central spinal canal.  Focal inflammation is also typical following segmental spinal trauma or focal spinal surgery.
Adhesive Arachnoiditis: Arachnoiditis Ossificans
The image to the left is a year 2000 CT scan performed on a 71 year old woman who developed clinically significant adhesive arachnoiditis following a 1971 Pantopaque® myelogram.  Control of her constant pain required implantation of a spinal cord neurostimulator which provided good pain control allowing the patient return to normal function.  In 1990 she began to experience progressive bowel and bladder dysfunction.  The CT scan shows classic arachnoiditis ossificans where the scar tissue has calcified.
The red dots represent the spaces occupied by the nerve roots.  These nerves are being progressively strangled by the progression of scar calcification.