A 60-year-old woman presented to the spine clinic for a complaint of progressive severe pain in her lower back of approximately 2.5 years’ duration. She previously underwent an L4-S1 TLIF for mobile spondylolisthesis and radiculopathy 3 years earlier at an outside institution. The patient reported significant improvement in her preoperative symptoms at that time, to the point where she was participating in physical therapy with minimal pain. At 6 months after the index surgery, she fell and reported hearing a distinct “pop” in her back. Since the fall, she remained bedridden with shooting, “shock-like” pain down her left leg associated with a progressively worsening left-sided foot drop (muscle strength 2/5) but with intact genitourinary function and perineal sensation. She was seen in our clinic 2.5 years after the index surgery for the progression of these symptoms. Radiological workup with radiographs and magnetic resonance imaging of the lumbar spine were notable for retropulsion of the L5-S1 interbody cage into the spinal canal, otherwise excellent positioning of the L4-5 interbody, and pedicle screws with posterolateral bridging bone [Figure and ]. These findings were stable over the previous 2.5 years based on radiographic studies obtained after her fall. The patient's original surgeon suggested revision surgery with the high risk of cerebrospinal fluid (CSF) leak and neurological deficit and the patient deferred a surgical option at that time. However, because of the her progression of her symptoms, she sought a second surgical opinion.\nConsidering the prolonged interval between the index surgery and the time of presentation to our clinic and the exact central position of the retropulsed interbody [], we were concerned that significant scar tissue and osteophytic ridge formation would hinder visualization of the graft and place the surrounding neural tissue at risk due to the retraction that would be necessary if the interbody were accessed via the original surgical corridor. In addition, the patient had adjacent segment degeneration and stenosis at the L3-4 segmental level, which explained her progression of symptoms. Our recommendation was a more direct transdural approach that would represent virgin territory, obviating scar tissue while providing adequate visualization with minimal retraction of neurological tissue during retrieval of the interbody. An anterior approach via anterior lumbar interbody fusions was also considered, but a posterior-only approach was recommended because of the presence of additional pathology at L3-4 that required treatment. After risks, benefits, and alternatives to intradural and transdural approaches were explained, the patient agreed to proceed with transdural removal of the retropulsed L5-S1 interbody, along with an L3-4 laminectomy and extension of her fixation from L3 to S1.\nThe prior surgical incision was opened, and surgical dissection was carried down to the existing instrumentation at L4-5 and L5-S1. After the locking caps on all six screwswere removed, the titanium rods were removed, and each screw was inspected for pseudarthrosis. Bilateral L4 and L5 screws were notably loose and promptly replaced with screws of larger diameter. An L3-4 laminectomy was performed, and L3 pedicle screws were placed. After this, we turned our attention toward the L5-S1 interspace, where the surgical corridor for the original TLIF was unidentifiable secondary to several large osteophytic ridges and extensive scar tissue. Residual lamina at this interspace was identified and removed easily with punch Kerrison rongeurs (Integra LifeSciences, Plainsboro, NJ) until normal midline dura was identified. The surgical microscope was brought in for the transdural portion of the operation. The thecal sac was opened with a number 11 blade in a linear fashion [], and after the egress of CSF, the dura was tacked to the muscle margins. With the retraction of intradural sacral roots [], the herniated interbody was easily visible and palpable through the ventral dura; it was compressing the left-sided exiting sacral rootlets. A Penfield number 2 was used to gently retract the nerve rootlets to either side, and a number 11 blade was once again used to open the ventral dura in a linear fashion directly over the herniated interbody [Figure and ]. Once open, the ventral dura was retracted to either side of the herniated interbody, and a graft inserter was threaded into the interbody []. Using repetitive rocking motions medially/laterally to disrupt any bridging osteophytes attached to the interbody, wecarefully shimmied the cage out through the ventral dura, traversing the thecal sac, and finally out through the opening in the dorsal dura []. The intradural nerve rootlets were inspected for any damage. The dura was closed in sequential fashion, ventrally then dorsally, using 5-0 Prolene sutures (Ethicon Endo-Surgery, Inc., Blue Ash, OH) and buttressed with DuraSeal (Covidien, Mansfield, MA) sealant []. Segmental fixation was completed with titanium rods locked in place from L3 to S1, along with autograft/allograft bone placed posterolaterally []. A lumbar drain was not placed, and the patient was kept flat for 24 h. A few hours postoperatively, the patient noted immediate improvement in her pain but had no improvement in her foot drop. She was up and mobilizing on postoperative day (POD) 2 with the physical therapy team, off all narcotics on POD 3, and discharged to rehabilitation on POD 4. At her 12-month follow-up visit, she was self-ambulatory, performing her normal activities of daily living, and had a complete resolution of pain and some improvement in foot drop (to muscle strength 3/5).
A 48-year-old female was admitted with a 6-month history of progressive decrease in the vision. At admission, the neurological examination showed bitemporal hemianopsia and a decreased pupillary reaction to light in both eyes. Fundus oculi examination showed a light papilla bilaterally. The patient did not complain of pituitary dysfunction.\nBrain magnetic resonance imaging (MRI) showed a 2 cm hypointense lesion on T2-weighted images inside the optic chiasm in the suprasellar region. On T1-weighted images, the lesion appeared as an intraaxial lesion inside the optic chiasm without contrast enhancement after gadolinium administration []. The patient underwent cerebral angiography that did not reveal any vascular malformation.\nSurgery was performed via a right pterional approach. The lesion was dissected out from arachnoid adherences and coagulated by using a quantum molecular resonance-based bipolar coagulation (Vesalius®). This device uses a relatively low temperature that does not exceed 45–50°C, having minimum effect on nervous tissues, nerves, and blood vessels. The cavernoma was shrunk and dissected out from the chiasma []. The postoperative course was uneventful. On the 5th day following surgery, the patient underwent ophthalmological examination that revealed improvement in vision on the left eye without changes in the visual field. The histopathological analysis of the resected lesion confirmed the preoperative diagnosis of CM. Five months following the operation, MRI showed complete removal of the vascular lesion [].