Keywords arachnoid cysts - spinal cord injuries - spinal cord compression
Introduction
Arachnoid cysts are rare; these injuries can occur at all levels of the dural sac,
and can have congenital, traumatic, iatrogenic or inflammatory origin.[1 ]
[2 ] Cysts are believed to form due to herniation of the arachnoid membrane through a
dura-mater defect. Traumatic cysts are even rarer, and are caused by penetrating trauma,
spinal fractures associated with dural lesions by bone fragments, and intraoperative
iatrogenic dural injuries.[3 ] The most common sites for the cyst ostium are the entry point of the dorsal root
into the dural sac and the dural midline.[1 ] The clinical presentation ranges from asymptomatic cases to pain, weakness, paresthesia
and paralysis due to neural compression. The imaging evaluation includes computed
tomography (CT), myelography and magnetic resonance imaging (MRI). The surgical intervention,
when required, consists of primary closure of the dural defect through a posterior
approach, accompanied by laminectomy and/or costotransversectomy.[1 ]
Although rare, arachnoid cysts can be a complication of spinal fractures, which are
commonly seen by orthopedists and neurosurgeons; as such, all physicians must be aware
of these lesions.
In the present article, we report a case of a patient presenting compressive thoracic
myelopathy due to an unusual intradural arachnoid cyst with posttraumatic manifestation,
its resolution, and a literature review on the subject.
Case Report
A 46-year-old female patient had been in a car accident in the previous 7 months,
and suffered a compressive fracture of the tenth thoracic vertebra, type B (A1) according
to the Arbeitsgemainchaft für Osteosynthesefragen (Working Community for Osteosynthesis
Issues, AO) group classification.[4 ] Back then, emergency care was performed at another hospital, with conservative treatment
of the fracture using a thoracolumbar orthosis. After three months, the patient was
walking with increasing difficulty and developed severe spastic paraparesis and an
inability to walk in the last month. When the patient came to our outpatient service,
she had grade-III motor strength in the left lower limb and hypoesthesia distal to
the L1 dermatome. In addition, she presented exacerbation of the deep-tendon reflexes,
a positive Babinski sign, and inexhaustible clonus. The results of the routine laboratory
tests were within normal range. Thoracic spine radiographs showed no acute osteoarticular
changes or fracture sequelae. The MRI showed: an old fracture of the T10 vertebral
body sparing the anatomy; widening of the space between the T9 and T10 spinous processes,
suggesting chronic ligament rupture; alteration of the spinal cord signal at the T9,
T10 and T11 levels, consistent with myelomalacia; and posterior adhesion of the spinal
cord at the T7-T9 level and anterior adhesion at the T9-T12 level, associated with
adhesive arachnoiditis and a ventral arachnoid cyst at the vertebral canal in these
levels, posteriorly dislocating the cord ([Figure 1 ]). In the same week, the patient underwent a surgical decompressive treatment through
a posterior approach, accompanied by laminectomy and left costotransversectomy in
T9 and T10 for the anterior approach to the vertebral canal. An anterolateral durotomy
was then performed with a direct approach to the arachnoid cyst for drainage and repair
with 5-0 nylon suture, followed by stabilization and arthrodesis with pedicle screws
and pins from T8 to T11 ([Figures 2 ], [3 ] and [4 ]). No orthosis was required, and rehabilitation began on the first postoperative
day. The neurological deficit gradually improved in about a week, with recovery of
the strength of the lower limbs and sensitivity. Six months later, there was residual
ataxia, but the patient walked with no assistance or orthosis. There were no complications
related to the surgical site. The follow-up tests showed adequate position and alignment
of the fused segment, as well as bone healing ([Figure 5 ]).
Fig. 1 Sagittal T2-weighted magnetic resonance imaging showing an old fracture at the T10
vertebral body; space widening between the T9-T10 spinous processes, suggesting chronic
ligament rupture; alteration of the spinal-cord signal at the T9, T10 and T11 levels,
consistent with myelomalacia; posterior adhesion of the spinal cord at the T7-T9 level,
and anterior adhesion at the T9-T12 level, associated with adhesive arachnoiditis
and an arachnoid cyst at these levels. The white arrows show the boundaries of the
cyst and posterior spinal adherence.
Fig. 2 Laminectomy and costotransversectomy (white arrows) after the insertion of the pedicle
screws at the T8 and T11 levels to approach the arachnoid cyst and perform the subsequent
stabilization.
Fig. 3 Microscope image showing durotomy and cyst drainage at the T9 and T10 levels.
Fig. 4 Repair of arachnoid cyst using primary, 5-0 non-absorbable nylon suture. The arrows
highlight the edge of the durotomy to approach the cyst.
Fig. 5 Posterolateral and lateral radiographs of the thoracic spine at the end of the procedure,
showing adequate position and alignment of the pedicle screws.
Discussion
While arachnoid cysts are rare, concomitant compressive myelopathy is even rarer.[2 ]
[5 ]
[6 ] The frequent use of MRI scans increased the reports of these injuries.[6 ] Most cases have an idiopathic origin and are asymptomatic.[5 ] Among the potential causes, posttraumatic injuries, as presented here, are rare.
Their prevalence is not yet available in the literature, probably due to the fact
that asymptomatic cases are not interesting enough to be published, and only cases
with concomitant myelopathy are reported.[7 ] Most arachnoid cysts are located in the thoracic spine, followed by the lumbar,
lumbosacral and thoracolumbar spines.[8 ] Posttraumatic cysts are caused by a defect in the inner dural layer.[5 ] Ventral cysts can cause weakness and myelopathy, while dorsal cysts present with
neuropathic pain and paresthesia.[7 ] The symptomatology differs because ventral lesions can compress the territory of
the anterior spinal artery, leading to weakness or myelopathy, while dorsal lesions
locally compress the spinal tracts, resulting in radiculopathy and pain.[9 ] Failure in treating the cause of the cyst can lead to recurrences, whose frequency
is still unknown.[3 ] Myelography and CT scans reveal compression of the structures adjacent to the cyst
and the site of communication between the lesion and the dural sac. The MRI shows
a mass effect on the adjacent structures, revealing a hypersignal on the cerebrospinal
fluid in T2-weighted images.[1 ] Radical cyst removal is the treatment of choice; if not feasible due to technical
limitations, the cyst must be drained.[4 ]
[6 ]
[7 ]
[8 ]
[9 ]
[10 ] Hemilaminectomy sparing the posterior-ligament complex was performed in most cases
reported in the literature; it is sufficient to approach the cyst, avoiding complications
such as deformity and instability, as well as the need for additional stabilization.
In this case, laminectomy was associated with a two-level costotransversectomy due
to the ventral location of the cyst and the need to approach it without dislocating
the spinal cord. Non-absorbable wires can be used, and, in cases of major failures,
complemented by covering with fat tissue, fascia, dural substitute or fibrin sealant.[1 ]
[2 ]
[5 ] In most published reports, the patients evolved with total improvement in the neurological
deficit and the myelopathy after surgery.[1 ]
[3 ]
[7 ]
[9 ] Since this is a rare condition, with few publications and a low level of evidence,
the reproducibility in the clinical practice and the discussion regarding treatment
options are limited.
Arachnoid cysts are rare lesions that can produce neurological deficit through a mass
effect on the spinal cord. In case of myelopathy, the treatment of choice is cyst
resection or drainage, which must be performed immediately.
