Verdoorn, Jared T.

Tolosa–Hunt syndrome is characterized by unilateral retro-orbital headaches and cranial nerve palsies, usually involving cranial nerves III–VI. It is rare for other cranial nerves to be involved, although this has previously been reported. We report a 19-year-old woman presenting with typical features of Tolosa–Hunt syndrome but ultimately developing bilateral facial nerve palsies and enhancement of both facial nerves on magnetic resonance imaging. The patient presented with unilateral retro-orbital headaches and palsies of cranial nerves III–VI. She was diagnosed with Tolosa–Hunt syndrome but was non-compliant with her corticosteroid treatment due to side effects. She returned with progressive left followed by right facial nerve palsy. Her corresponding follow-up magnetic resonance imaging scans showed sequential enhancement of the left and right facial nerves. She ultimately had clinical improvement with IV methylprednisolone. To our knowledge, Tolosa–Hunt syndrome associated with bilateral facial nerve palsy and corroborative facial nerve enhancement on magnetic resonance imaging has not previously been described. Moreover, our patient’s clinical course is instructive, as it demonstrates that this atypical presentation of Tolosa–Hunt syndrome can indeed respond to corticosteroid treatment and should not be mistaken for other entities such as Bell’s palsy.

The nasoseptal flap is a well‐recognized “work‐horse” flap for anterior skull base reconstruction. The sphenopalatine artery (SPA), which accounts for a large portion of the arterial supply in the nasal cavity, forms a basis for the flap pedicle. In addition, the identification of the SPA as it emerges from the pterygopalatine fossa into the nasal cavity via the sphenopalatine foramen (SPF) is useful during the transpterygoidal approach to the infratemporal fossa. This identification is also useful for treatment of epistaxis in the nasal cavity, and aids in the prevention of vascular complications in a surgical setting. Previous studies have shown the relationship of the sphenopalatine foramen to the floor of the nasal cavity, choanal arch, and maxillary line. To enhance endoscopic visualization this study set out to identify the relationship of the anteroinferior bony border of the sphenoid sinus, the superior nasal concha, and the middle nasal concha as anatomical landmarks to the SPF. A total of n = 33 cadaveric hemisections were studied. In addition, the SPF was identified in coronal computerized tomography (CT) scans of the dissected cadavers acquired from the Anatomical Bequest Program at the Mayo Clinic (IRB approval #19‐010471), n = 8. Nasal mucosa was reflected from the lateral nasal wall where the SPF was located. The exit of the SPA’s main arterial trunk at the SPF was measured in relation to the sphenoid sinus, superior nasal concha, and middle nasal concha and the number of branches was recorded. Measurements on CT imaging were taken posterior to the ostiomeatal unit and maxillary sinus at initial visualization of the sphenoid sinus. Measurements of the SPF in relation to the inferior bony boundary of the sphenoid sinus were recorded (mm). All radiologic images were collected, and measurements were taken using Association for Quality Imaging (AQI) software. Images were analyzed and processed using Fiji ImageJ software. Results of this study showed the immediate surgical relationship of the sphenoid sinus, superior nasal concha, and middle nasal concha to the SPA as it traverses the SPF into the nasal cavity. Average distance from the SPF to the anterior‐inferior bony boundary of the sphenoid sinus was 2.5mm, the superior nasal concha was 4.12mm, and the middle nasal concha was 2.86mm. Radiological measurements taken in coronal CT images from the inferior bony boundary of the SPF to the inferior bony boundary of the sphenoid sinus was on average 4.94mm. Number of primary branches off of the SPA arterial trunk, and branching patterns varied between 2–3 with instances of a single long SPA arterial trunk traveling more than 3 mm followed by two small branches inferiorly. These relationships can be used to safely identify the SPA as it exits the SPF during surgery to prevent vascular complications due to occluded visualization of the region. Support or Funding Information American Association of Anatomists Short‐Term Visiting Scholarship Award

Study Design. Retrospective matched cohort study. Objective. To determine if low-pressure lumbar provocation discography (PD) results in long-term accelerated disc degeneration, internal disc disruption, or disc herniation in patients with symptomatic low back pain (LBP). Summary of Background Data. Study of subjects without clinically-significant LBP suggests that high-pressure PD may accelerate disc degeneration. Methods. Consecutive patients with symptomatic LBP who underwent magnetic resonance imaging (MRI), PD, and repeat MRI more than 7 years later, but did not undergo subsequent spinal fusion surgery, were included. Punctured discs were matched (1:2 to 1:4) to corresponding discs in a control cohort by age, BMI, Pfirrmann score (±2), and presence of disc herniation; control cohort inclusion required MRIs for symptomatic LBP, separated by more than 7 years. The primary outcome of the study was a progression in Pfirrmann score category (I–II, III–IV, V). MRI disc-to-CSF T2 signal-intensity ratio, disc height, disc herniations, high intensity zones (HIZs), and Modic changes were assessed. Results. Baseline and follow-up MRIs were available for 77 discs exposed to PD, and for 260 discs in the matched control cohort. There was no difference in the proportion of punctured discs that advanced in Pfirrmann score category in the PD group (17%, 95% CI 9–27%) compared with corresponding discs in the Control group (21%, 95% CI 17–27%), P = 0.3578, or in non-punctured discs in the PD group (35%, 95% CI 21–51%) compared with corresponding discs in the Control group (34%, 95% CI 27–42%), P = 0.1169. There were no differences in disc-to-CSF T2 signal-intensity ratio, presence of disc herniations, HIZs, or Modic changes following puncture in the PD versus matched cohort discs or in the non-punctured PD cohort discs versus corresponding control cohort discs (P > 0.05). Conclusion. Patients with symptomatic LBP who underwent low-pressure PD, but who did not undergo a subsequent spinal fusion surgery, developed disc degeneration and new disc herniations at a similar rate to corresponding discs in matched control patients. Level of Evidence: 3