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Endoscopic endonasal skull base surgery is associated with a low level of patient-reported post-operative nasal morbidity. There is no significant difference in frequency of crusting, blockage, pain or discharge between pituitary and other anterior skull base pathology groups. However, anterior skull base surgery would appear to be associated with an increased rate of anosmia post-operatively.

Patients with intracranial HPC-SFT require periodic, long term monitoring for extra-cranial metastases. Metastases occur in any age group and can occur early and late. They vary in location and are typically diagnosed following symptomatic presentation. There is no suggested imaging modality for surveillance. Higher grade primary tumors have a greater risk of metastasis. Regular clinical review is essential with early imaging for symptoms of recurrence/metastasis with imaging modality dependent on clinical concern. Quality evidence for an imaging surveillance protocol in this heterogeneous group of patients is lacking. A multicenter study on appropriate surveillance may be of benefit.

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Background/ObjectivesWe recently developed techniques to monitor intraspinal pressure (ISP) and spinal cord perfusion pressure (SCPP) from the injury site to compute the optimum SCPP (SCPPopt) in patients with acute traumatic spinal cord injury (TSCI). We hypothesized that ISP and SCPPopt can be predicted using clinical factors instead of ISP monitoring.MethodsSixty-four TSCI patients, grades A–C (American spinal injuries association Impairment Scale, AIS), were analyzed. For 24 h after surgery, we monitored ISP and SCPP and computed SCPPopt (SCPP that optimizes pressure reactivity). We studied how well 28 factors correlate with mean ISP or SCPPopt including 7 patient-related, 3 injury-related, 6 management-related, and 12 preoperative MRI-related factors.ResultsAll patients underwent surgery to restore normal spinal alignment within 72 h of injury. Fifty-one percentage had U-shaped sPRx versus SCPP curves, thus allowing SCPPopt to be computed. Thirteen percentage, all AIS grade A or B, had no U-shaped sPRx versus SCPP curves. Thirty-six percentage (22/64) had U-shaped sPRx versus SCPP curves, but the SCPP did not reach the minimum of the curve, and thus, an exact SCPPopt could not be calculated. In total 5/28 factors were associated with lower ISP: older age, excess alcohol consumption, nonconus medullaris injury, expansion duroplasty, and less intraoperative bleeding. In a multivariate logistic regression model, these 5 factors predicted ISP as normal or high with 73% accuracy. Only 2/28 factors correlated with lower SCPPopt: higher mean ISP and conus medullaris injury. In an ordinal multivariate logistic regression model, these 2 factors predicted SCPPopt as low, medium–low, medium–high, or high with only 42% accuracy. No MRI factors correlated with ISP or SCPPopt.ConclusionsElevated ISP can be predicted by clinical factors. Modifiable factors that may lower ISP are: reducing surgical bleeding and performing expansion duroplasty. No factors accurately predict SCPPopt; thus, invasive monitoring remains the only way to estimate SCPPopt.Electronic supplementary materialThe online version of this article (10.1007/s12028-018-0616-7) contains supplementary material, which is available to authorized users.

In some centers, monitoring the lumbar cerebrospinal fluid (CSF) is used to guide management of patients with acute traumatic spinal cord injuries (TSCI) and draining lumbar CSF to improve spinal cord perfusion. Here, we investigate whether the lumbar CSF provides accurate information about the injury site and the effect of draining lumbar CSF on injury site perfusion. In 13 TSCI patients, we simultaneously monitored lumbar CSF pressure (CSFP) and intraspinal pressure (ISP) from the injury site. Using CSFP or ISP, we computed spinal cord perfusion pressure (SCPP), vascular pressure reactivity index (sPRx) and optimum SCPP (SCPP opt ). We also assessed the effect on ISP of draining 10mL CSF. Metabolites at the injury site were compared with metabolites in the lumbar CSF. We found that ISP was pulsatile, but CSFP had low pulse pressure and was non-pulsatile 21% of the time. There was weak or no correlation between CSFP versus ISP (R=-0.11), SCPP (csf) versus SCPP (ISP) (R=0.39) and sPRx (csf) versus sPRx (ISP) (R=0.45). CSF drainage caused no significant change in ISP in 7/12 patients, a significant drop by <5mmHg in 4/12 patients and by ~8mmHg in 1/12 patient. Metabolite concentrations in the CSF versus injury site did not correlate for lactate (R=0.00), pyruvate (R=-0.12) or lactate-to-pyruvate ratio (R=-0.05) with weak correlations noted for glucose (R=0.31), glutamate (R=0.61) and glycerol (R=0.56). We conclude that, after a severe TSCI, monitoring from the lumbar CSF provides only limited information about the injury site and that lumbar CSF drainage does not effectively reduce ISP in most patients.

Early after spinal cord injury, fever is associated with more deranged injury site metabolism than normothermia and worse prognosis.

In five patients with acute, severe thoracic traumatic spinal cord injuries (TSCIs), American spinal injuries association Impairment Scale (AIS) grades A-C, we induced cord hypothermia (33 °C) then rewarming (37 °C). A pressure probe and a microdialysis catheter were placed intradurally at the injury site to monitor intraspinal pressure (ISP), spinal cord perfusion pressure (SCPP), tissue metabolism and inflammation. Cord hypothermia-rewarming, applied to awake patients, did not cause discomfort or neurological deterioration. Cooling did not affect cord physiology (ISP, SCPP), but markedly altered cord metabolism (increased glucose, lactate, lactate/pyruvate ratio (LPR), glutamate; decreased glycerol) and markedly reduced cord inflammation (reduced IL1β, IL8, MCP, MIP1α, MIP1β). Compared with pre-cooling baseline, rewarming was associated with significantly worse cord physiology (increased ICP, decreased SCPP), cord metabolism (increased lactate, LPR; decreased glucose, glycerol) and cord inflammation (increased IL1β, IL8, IL4, IL10, MCP, MIP1α). The study was terminated because three patients developed delayed wound infections. At 18-months, two patients improved and three stayed the same. We conclude that, after TSCI, hypothermia is potentially beneficial by reducing cord inflammation, though after rewarming these benefits are lost due to increases in cord swelling, ischemia and inflammation. We thus urge caution when using hypothermia-rewarming therapeutically in TSCI. Hypothermia is being investigated as a potential therapy for traumatic brain injury (TBI) 1 and traumatic spinal cord injury (TSCI) 2 based on compelling evidence from several laboratories and animal species that hypothermia is neuroprotective. In animal models of TBI, hypothermia has been shown to target many pathological processes including reducing the metabolic rate, inflammation, edema, oxidative stress, excitotoxicity, electrolyte imbalance as well as apoptotic and necrotic cell death in vulnerable tissue 3-8. Despite the encouraging findings of animal studies, randomized controlled human trials have failed to show functional benefit of hypothermia in TBI patients 1,9,10. Therapeutic hypothermia is also beneficial in animal models of TSCI: rodent models of TSCI show improved histological and functional outcomes after hypothermia 11,12. Small, non-randomized studies of TSCI patients also suggest improved functional outcomes after local 13,14 or systemic hypothermia 2,15. To date, there are no published randomized controlled trials of hypothermia for TSCI. Despite the wide interest in therapeutic hypothermia for CNS injuries, there is paucity of mechanistic data from humans regarding the effect of hypothermia on the injury site. In TSCI patients, the effect of cooling and rewarming on cord swelling, metabolism and inflammation are unknown. It is thus unclear if hypothermia and