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.
Bibliography
Bleasel, A., Clouston, P., et al. Posttraumatic Syringomyelia Following
Uncomplicated spinal Fracture. J. Neurol. Neurosurg. Psych. 1991 Feb;54(6)
5513
Caplan, L.R., Norohna, A.B., et al. Syringomyelia and Arachnoiditis
J. Neurol. Neurosurg. Psych. 1990 Feb;53(2) 106113
Hoyland, J.A., Freemont, A.J., et al. Retained Surgical Swab Debris
in Postlaminectomy Arachnoiditis and Peridural Fibrosis. JBJS 70B,
659662. 1988
Johnson, A., Ryan, M.D., et al. DepoMedrol and Myelographic Arachnoiditis.
Med. J. Aust. 1991 Jul 1;155(1):1820
Pillay, P.K., Awad, I.A., Hahn, J.F. Gardner's Hydrodynamic Theory
of Syringomyelia Revisited. Clev. Clin. J. Med. 59:4, 373380. 1992
Wilkinson, H.A. Alternative Therapies for the Failed Back Syndrome.
in THE ADULT SPINE. J. W. Frymoyer ed. 1991. Patient.20692092
A sketch of a lumbar spinal nerve, its roots and meningeal coverings.
The nerve roots are invested by pie mater, and covered by arachnoid and
aura as far as the spinal nerve. The aura of the aural sac is prolonged
around the roots as their aural sleeve, which blends with the epineunum
of the spinal nerve.
Theories of syringomyelia. A, normal cerebrospinal fluid dynamics, with
small arrows showing free flow of cerebrospinal fluid through outlets of
the fourth ventricle, and large arrows indicating free flow around the craniocervical junction. B. Gardner's hydrodynamic theory, in which obstruction of the fourth ventricular outlet channels the cerebrospinal fluid pulse wave through the obex into the central canal of the spinal cord, creating a syrinx. C, Williams' theory, in which foremen magnum obstruction leads to development
of a craniospinal pressure gradient, causing hindbrain impaction and syrinx
formation. D, the theories of Ball and Dayan and Aboulker, in which foremen
magnum pathology leads to increased inmspinal pressure, forcing fluid into
the spinal cord through the VirchowRobin spaces or nerve roots.
Proposed unified theory of syringomyelia includes Gardner' hydrodynamic
forces magnified in the setting of foremen magnum obstruction as suggested
by Williams. Transparenchymal fluid migrations (as advocated by Ball and
Dayan and by Aboulker) might act count for coalescence and propagation of
syringes, as well as for focal post. traumatic syringomyelia not associated
with hindbrain pathology.
Diagram of arterial supply of cord. Border zone in the centre zone of
the cord is depicted in broken lines.
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