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Progressive neurologic deterioration following spinal cord injury unrelated
to anatomical compression of the spinal cord or spinal instability has become more widely recognized.
Cystic myelopathy or posttraumatic syringomyelia as a cause of progressive
neurologic deterioration has been well described. One sees a spinal cord
cyst develop at the injury site, which may progressively ascend and/or
descend with time. Clinically, progressive loss of sensation and strength,
as well as worsening spasticity, pain, hyperhidrosis, autonomic dysreflexia,
and a Horner’s Syndrome, may occur.
Introduction. Progressive neurologic deterioration following spinal cord
injury unrelated to anatomical compression of the spinal cord or spinal
instability has become more widely recognized. Cystic myelopathy or
posttraumatic syringomyelia as a cause of progressive neurologic
deterioration has been well described.1,2 One sees a spinal cord cyst
develop at the injury site, which may progressively ascend and/or descend
with time (Figure 1). Clinically, progressive loss of sensation and
strength, as well as worsening spasticity, pain, hyperhidrosis, autonomic
dysreflexia, and a Horner’s Syndrome, may occur. More recently, the
noncystic posttraumatic tethered cord has been associated with identical
progressive neurologic deterioration.1-3, 6 With this entity, scar tissue
which forms around the spinal cord at the time of injury, fixes or tethers
the cord to the dura, thereby inhibiting the normal motion of the spinal
cord within the dura sac, as well as normal spinal fluid flow. (Figure 2)
Fig 1.
This cervical MRI of a patient with spinal cord injury shows a cyst
ascending from the injury site at C3-4 and a second cyst descending to the
C5-6 level.
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Fig 2.
This cervical MRI of a patient with spinal cord injury shows the spinal cord
tethered to the posterior spinal canal at the C6-7 level. There is no cyst.
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Fig 3.
This cervical MRI shows the spinal cord in Figure 2 after it was surgically
untethered. Note the reconstituted posterior subarachnoid space.
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Fig 4.
This cervical MRI shows the spinal cord in Figure 1 after it was surgically
untethered and after the cysts were shunted. Note the reconstituted
posterior subarachnoid space and collapse of the cysts.
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It has been suggested that posttraumatic tethering from arachnoidal scar is
a necessary precursor to cyst formation, and that both cystic and noncystic
entities share similar pathophysiologic mechanisms with cyst formation being
an end point of a process.
Surgical treatment for both cystic and noncystic entities involves releasing
the scar tissue around the spinal cord. That is, untethering the spinal
cord, restoring more normal spinal fluid flow past the injury site, and
adding a graft of dura to expand the subarachnoid space and minimize the
chance of rescarring. If a cyst exists, a shunt tube must be placed into the
cyst cavity to allow the release of cyst fluid. (Figures 3 & 4)
Surgical treatment is primarily reserved for significant and progressive
loss of neurologic function. In certain cases, surgery is performed to
relieve pain, spasticity, autonomic dysreflexia and hyperhidrosis, but only
if these symptoms are poorly controlled with medications. Because of the
medical complexity of the spinal cord injured population, surgery should be
performed with the support of physiatrists, nurses, and therapists
experienced with the spinal cord injured population. In experienced hands,
one can expect corrective surgery for posttraumatic spinal cord cysts and
tethered cords to halt the progressive loss of function, and allow for some
return of lost function.1-3
Research is being performed with
The Craig Center for Spinal Injury and
The Karolinska Institute to find ways to permanently obliterate
posttraumatic cyst cavities with biologic tissue, eliminating the need for
shunt tubes. The first obliteration of a posttraumatic spinal cord cyst
using a vascularized graft of omentum was performed in 1994.4 The first
obliteration of a posttraumatic spinal cord cyst using human embryonic nerve
cells was performed in January, 1997.5
In the later case, human embryonic nerve cells successfully grew to fill and
obliterate a posttraumatic cyst cavity in a patient and halted its progress.
Additional patients have since been operated on and are presently being
followed in this pilot study.
Conclusion. In summary, posttraumatic cystic and tethered spinal cords can
result in clinically significant neurologic deterioration months to years
after a spinal cord injury. Treatment requires a surgical release of scar
tissue around the spinal cord (untethering) to restore more normal motion to
the cord as well as restore more normal CSF flow dynamic. Cyst cavities may
require definitive shunting. The goal is primarily to halt progressive
neurologic loss, but some return of lost function is often achieved.
Research is underway using embryonic cellular therapy which may provide an
improved treatment strategy in the future.
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References
1. Edgar R, Quail P. Progressive posttraumatic cystic
and non-cystic myelopathy. Brit J Neurosurg. 1994;8:7-22.
2. Falci S, Best L, Froelich J, Lammertse D. Surgical, imaging and evoked
potential correlates of spinal cord and rootlet tethering in progressive
post-traumatic myelopathies. J Spinal Cord Med. 1995;18:154. Abstract.
3. Lee T, Arias J, Andrus H, Quencer R, Falcone S, Green B. Progressive
posttraumatic myelomalacic myelopathy; treatment with untethering and
expansive duraplasty.
J Neurosurg. 1997;86:624-628.
4. Falci S, Zwiebel P. Treatment of refractory progressive post-traumatic
cystic myelopathy with a new technique: Myelocyst-omental grafting
J of Spinal Cord Med. 1995;18:154. Abstract.
5. Falci S, Holtz A, Akesson F, et al. Obliteration
of a post-traumatic
spinal cord cyst with human embryonic spinal cord grafts: First clinical
attempt. J of Neurotrauma. Submitted for publication.
6. Froelich J, Falci S, Lammertse D, Best L. Assessment of cord tethering by
phase contrast MR CSF/flow analysis. J Spinal Cord Med. 1995;18:127.
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