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).
History and examination\nA 42-year-old male with a history of right eye visual field abnormalities presented with recent visual disturbances of the right eye and intermittent headaches. The visual disturbances were described as intermittent spots of blurriness. Initial MRI with contrast showed an oval-shaped lesion within or abutting the right optic chiasm. The lesion demonstrated intrinsic T1 hyperintensity (Figure ), as well as susceptibility and increased T2 and fluid-attenuated inversion recovery (FLAIR) signal. In the subsequent months, the patient complained of worsening visual changes that included the left eye as well. Visual acuity was graded 20/30 OD, 20/20 OS, and visual field testing revealed a very small scotoma in the left lower quadrant of the right eye. Pupils were equal, round, and reactive to light. Color vision was within normal limits with 14 out of 14 color plates correctly named in each eye. A dilated funduscopic exam revealed the discs to be sharp and pink with a cup to disc ratio of 0.1 OD, 0.2 OS and no optic nerve pallor on either side. Extra-ocular motility was intact bilaterally. At this time, the patient was referred to our services and was diagnosed as a possible CM, with a differential diagnosis, including craniopharyngioma, meningioma, and arteriovenous malformation (AVM). Due to the eloquent location of the lesion and the risk of visual loss, observation was chosen over surgery. Two months after presentation to the clinic, the patient visited the emergency department due to headaches and further visual changes in the inferior fields of both eyes, citing increased blurriness specifically. Visual acuity worsened to 20/40 OD, with no visual field cuts and no papilledema bilaterally. The patient was started on corticosteroids. Repeat MRI showed an expansion of the right optic chiasm/nerve lesion with increased T1 hyperintensity compatible with acute hemorrhage (Figure ). The lesion extended posteriorly and laterally to abut the right uncus and right cerebral peduncle. Visual field deficits were present in about three-quarters of his vision in both eyes, including the left temporal field and the right inferior nasal field (Figure ). After discussing therapeutic strategies with the patient, the decision was made to operate because subsequent bleeding could have caused irreversible blindness in both eyes.\nOperation\nUnder general anesthesia, the senior author (EMD) performed a right pterional craniotomy for the resection of the right optic nerve and chiasm CM. Brain relaxation was performed by draining cerebrospinal fluid from the cisterns, making the opening of the Sylvian fissure unnecessary. The right optic nerve was identified microscopically and followed back to the chiasm, which showed purplish discoloration with hemosiderin staining. Discoloration was distributed along the superomedial aspect of the optic nerve on the right side and the posterior aspect of the optic chiasm. The CM was microdissected from the surface of the optic nerve without incising the nerve itself. The middle portion of the CM was densely adherent to the vasculature of the optic chiasm and nerve. Cauterization of the residual portion of the CM was completed, preserving the vasculature in order to reduce the likelihood of an ischemic event. Frozen and permanent specimens were sent to pathology. The frozen section returned as abnormal vessel and hematoma. Surgically, there was GTR; however, subsequent radiographic imaging provided evidence that the resection may have been subtotal (see discussion). Craniotomy closure occurred by the replacement of the bone flap and the reapproximation of the myocutaneous flap.\nPostoperative course\nThere were no immediate complications following the procedure. The permanent specimen returned as CM and three weeks postoperatively, the patient had regained approximately half of the vision that was lost and continued to improve (Figure ). MRI 12 months postoperatively showed no sign of recurrence (Figure ). Over two years after surgery, the patient had resumed all preoperative activities and reported significant visual recovery, with headaches occurring only once weekly. Thirty-two months after resection, MRI showed a small slightly lobulated area of T1 hyperintense material within the postoperative cavity along the right aspect of the optic chiasm (Figure ). This finding was new as compared to prior imaging and suggested that minimal recurrence in this location should be considered. Upon follow-up with ophthalmology, visual field deficits were stable. MRI at 39 months postresection showed previously seen small amounts of T1 hyperintensity in the central and right aspect of the optic chiasm with significantly decreased conspicuity (Figure ). Only a trace amount of T1 hyperintensity remained at the right aspect of the optic chiasm, suggesting the 32-month postop scan may have demonstrated a trace amount of subacute hemorrhage in the area suspected of being residual CM. During ophthalmological follow-up at three years, the patient mentioned having difficulty reading and more consistently occurring headaches since his office visit six months prior. Headaches were reported to be different than past migraines. When compared to older visual field testing, there was a worsening of deficits in the left eye but within the standard deviation. Visual acuity remained stable at 20/30 OD, 20/20 OS. The suspected residual CM will be followed with serial imaging and visual field tests with the possibility of additional surgical resection in the case of visual deterioration.