Surgery for arachnoiditis?

When I was in for my visit yesterday I was explaining the pain and symptoms I have to the nurse practitioner, she had not seen me before, and we got on a quick discussion about arachnoiditis and possible treatments. She has a friend who was diagnosed with arachnoiditis and saw an orthopedic (not sure why though) surgeon who performed surgery to try and fix the arachnoiditis.

Now several things popped into my mind at once, the foremost being why would someone see an orthopedic surgeon for an obvious neurological defect? The second was how did they perform surgery to correct arachnoiditis as I have been told that in most cases it cannot be done and in the ones where it can be done, very few are successful.

I did some quick searching this morning and did find some information on surgical procedures for arachnoiditis. As I suspected there are some cases where surgery is tried but it is not so successful that I would even consider it as an option right now. I can only imagine how advanced some of those cases may have been for them to even consider an attempt at surgery.

Article here

Arachnoiditis and Syringomyelia

Arachnoiditis

Posterior Approach
Posterior Approach is inflammation of the tissues surrounding the spinal cord or the nerve roots. Its is somewhat of a misnomer as it implies pathology of only the arachnoid mater. In reality the aura mater, the arachnoid mater, the pia mater and the surrounding vasculature are involved to varying degrees.

Scarring may then ensue to varying degrees. This scarring was originally reported as 2 types, "arachnoiditis adhesive circumscripta spinalis" the localized form and "arachnoiditis adhesive diffuse spinalis" the generalized form. Currently 3 types of arachnoiditis are recognized in the lumbar spine radiographically. Type I is focal nerve root adhesion which obliterates the nerve root sheath and may mimic a herniated disc on myelography. Type II is circumferential adhesions of the nerve roots with an open central canal. It may be localized or diffuse. Type III is complete obliteration of the subarachnoid space.

Arachnoiditis may result from infectious meningitis; subarachnoid bleeding from trauma, arteriovenous malformations, or iatrogenic puncture; intrathecally administered oil based contrast agents; intrathecal corticosteroids; surgery within or about the thecal sac and nerve roots; lumbar disc disease; spinal stenosis; segmental instability; herniated disc; as a familial disorder; or it may arise spontaneously. The exact etiology of the fibrosis is unclear, as is the explanation for its varied distribution.

Arachnoiditis was first described in the mid to late 1800's as an autopsy finding. It was seen more frequently after the advent of myelographic contrast agents. The diagnosis is made radiographically, most often on myelogram but also on MRI and occasionally on newer generation CT scanners.

Most cases of arachnoiditis are asymptomatic. Those that are symptomatic may cause burning pain in the back and or legs, altered strength and sensation in the lower extremities, limited ROM of the lumbar spine and impotence. Symptoms are probably produced by mechanical constriction or limitation of motion of the lumbar nerve roots. There may be some contribution by the altered flow of nutrients to the affected nerves due to diminished blood flow and restricted CSF flow in the affected area. Clinically the disorder develops and progresses over a course of 6 to 18 months. Wilkinson feels that progression beyond 24 months is unlikely to be due to arachnoiditis alone.

If symptoms are attributable to arachnoiditis, are progressive and occur within 1 year of the surgical procedure consideration may be given to microsurgical lysis of the subarachnoid adhesions. The results are varied and successes frequently are less than 50% in different series. Wilkinson reported a series of 17 patients treated with microsurgical lysis of adhesions. Despite an initial good outcome of 75%, less than 50% maintained their improvement at one year, and almost 20% developed new and permanent neurologic deficits after the procedure.

Other treatment options include intrathecal corticosteroid administration, selective intrathecal phenol sensory rhizotomy, dorsal column stimulator implantation and dorsal column rhizotomy. The success rates of these treatments are generally in the 50% range in different series, with some patients made worse by the treatment.

In addition to the above arachnoiditis at higher levels may lead to the development of syringomyelia.

Syringomyelia
The etiology of syringomyelia is unclear. Several theories exist, all of which may play some role in the development of the syrinx. Gardner proposed that obstruction of the outlets of the 4th ventricle led to increased pressure within the ventricles. This increased pressure, further increased by postural changes, valsalva maneuvers and the normal pulse wave associated with the heart beat cause extravasation of CSF through the obex and into the central canal of the spine, causing the syrinx.

Bering in 1955 demonstrated that the choroid plexus transmits arterial pulsations to the CSF. He showed that with systolic pulsation the pressure increases in the ventricle and the CSF is forced out of the foramina into the subarachnoid space. This has confirmed recently with sonography in humans.

Williams examined pressure differentials between the brain and the spinal canal in patients with hindbrain abnormalities (ArnoldChiari malformation). He found that valsalva maneuvers caused epidural venous engorgement which caused a rise in intraspinal pressure. This rise in intraspinal pressure sent a pressure wave cephalad and caudad. As the wave traveled cranially, it would pass the herniated hindbrain and enter the cranium. When the valsalva stopped and the pressure returned to normal the hindbrain would act as a one way valve producing postvalsalva pressure gradients of 100mm of Hg. The relative negative pressure within the spinal cord/column could "suck" CSF into the syrinxes. He also theorized that the water hammer effect of the pulsations of the epidural veins could act to enlarge the syrinxes.

Ball and Dayan, and Aboulker hypothesize that CSF may be forced into the parenchyma of the cord along perivascular channels (VirchowRobin spaces), or along nerve roots.

Pillay et al recently unified the above theories into one. They felt that some or all may play a role in the development of syringomyelia in different situations. In cases of 4th ventricle outlet obstruction both Gardner's and Williams' theories probably contribute. In syrinxes associated with trauma or focal arachnoiditis there is probably a contribution as proposed by Ball and Dayan, and Aboulker.