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Spine surgery has significantly progressed due to innovations in surgical techniques, technology, and a deeper understanding of spinal pathology. However, numerous challenges persist, complicating successful outcomes. Anatomical intricacies at transitional junctions demand precise surgical expertise to avoid complications. Technical challenges, such as underestimation of the density of fixed vertebrae, individual vertebral characteristics, and the angle of pedicle inclination, pose additional risks during surgery. Patient anatomical variability and prior surgeries add layers of difficulty, often necessitating thorough pre- and intraoperative planning. Technological challenges involve the integration of artificial intelligence (AI) and advanced visualization systems. AI offers predictive capabilities but is limited by the need for large, high-quality datasets and the "black box" nature of machine learning models, which complicates clinical decision making. Visualization technologies like augmented reality and robotic surgery enhance precision but come with operational and cost-related hurdles. Patient-specific challenges include managing postoperative complications such as adjacent segment disease, hardware failure, and neurological deficits. Effective patient outcome measurement is critical, yet existing metrics often fail to capture the full scope of patient experiences. Proper patient selection for procedures is essential to minimize risks and improve outcomes, but criteria can be inconsistent and complex. There is the need for continued technological innovation, improved patient-specific outcome measures, and enhanced surgical education through simulation-based training. Integrating AI in preoperative planning and developing comprehensive databases for spinal pathologies can aid in creating more accurate, generalizable models. A holistic approach that combines technological advancements with personalized patient care and ongoing education is essential for addressing these challenges and improving spine surgery outcomes. [ABSTRACT FROM AUTHOR]

Spinal serotonin enables neuro‐motor recovery (i.e., plasticity) in patients with debilitating paralysis. While there exists time of day fluctuations in serotonin‐dependent spinal plasticity, it is unknown, in humans, whether this is due to dynamic changes in spinal serotonin levels or downstream signaling processes. The primary objective of this study was to determine if time of day variations in spinal serotonin levels exists in humans. To assess this, intrathecal drains were placed in seven adults with cerebrospinal fluid (CSF) collected at diurnal (05:00 to 07:00) and nocturnal (17:00 to 19:00) intervals. High performance liquid chromatography with mass spectrometry was used to quantify CSF serotonin levels with comparisons being made using univariate analysis. From the 7 adult patients, 21 distinct CSF samples were collected: 9 during the diurnal interval and 12 during nocturnal. Diurnal CSF samples demonstrated an average serotonin level of 216.6 ±$ \pm $ 67.7 nM. Nocturnal CSF samples demonstrated an average serotonin level of 206.7 ±$ \pm $ 75.8 nM. There was no significant difference between diurnal and nocturnal CSF serotonin levels (p =.762). Within this small cohort of spine healthy adults, there were no differences in diurnal versus nocturnal spinal serotonin levels. These observations exclude spinal serotonin levels as the etiology for time of day fluctuations in serotonin‐dependent spinal plasticity expression. [ABSTRACT FROM AUTHOR]

A 48-year-old male with progressive congestive myelopathy had a craniocvervical DAVF treated with surgical clipping using ICG to confirm solitary inflow. [ABSTRACT FROM AUTHOR]

Movement is executed through the balanced action of excitatory and inhibitory neurotransmission in motor circuits of the spinal cord. Short-term perturbations in one of the two types of transmission are counteracted by homeostatic changes of the opposing type. Prolonged failure to balance excitatory and inhibitory drive results in dysfunction at the single neuron, as well as neuronal network levels. However, whether dysfunction in one or both types of neurotransmission leads to pathogenicity in neurodegenerative diseases characterized by select synaptic deficits is not known. Here, we used mouse genetics, functional assays, morphological methods, and viral-mediated approaches to uncover the pathogenic contribution of unbalanced excitation-inhibition neurotransmission in a mouse model of spinal muscular atrophy (SMA). We show that vulnerable motor circuits in the SMA spinal cord fail to respond homeostatically to the reduction of excitatory drive and instead increase inhibition. This imposes an excessive burden on motor neurons and further restricts their recruitment to activate muscle contraction. Importantly, genetic or pharmacological reduction of inhibitory synaptic drive improves neuronal function and provides behavioural benefit in SMA mice. Our findings identify the lack of excitation-inhibition homeostasis as a major maladaptive mechanism in SMA, by which the combined effects of reduced excitation and increased inhibition diminish the capacity of premotor commands to recruit motor neurons and elicit muscle contractions.

Background and Objectives: Aneurysms in the cavernous segment of the internal carotid artery (ICA) often present in an indolent fashion with limited morbidity. However, their growth progression and possible rupture over time remains poorly defined, thereby limiting optimization of serial follow-up. Thus, we aim to describe the progression of cavernous ICA aneurysms over time, as well as the patient and aneurysm characteristics associated with possible growth and rupture status., Methods: We identified a consecutive cohort of 157 patients from 2007 to 2021 with cavernous ICA aneurysms. Patient demographic data, possible risk factors, presenting symptoms, radiographic features of aneurysms, size progression, rupture status, and concomitant noncavernous aneurysm rupture data were manually extracted., Results: One hundred and fifty-seven patients (mean age at diagnosis 57.2 ± 15.6 years; 85.4% females) with 174 cavernous carotid aneurysms (CCAs) were followed for an average of 7.1 ± 4.8 years. 76.4% of aneurysms were identified incidentally, with predominantly ocular palsies as the presenting symptoms in remaining primary cases. Most aneurysms were small, and of the 168 aneurysms that were followed, 98.2% did not demonstrate appreciable growth. Of the aneurysms that grew, it took an average of 6.0 years to grow 1.6 ± 0.2 mm. Demographic data, hypertension, and smoking status were not associated with aneurysm growth. Most radiographic features also were not associated with growth, except long-axis diameter, which had an odds ratio of 1.4 (CI: 1.2, 1.8) on multivariable analysis. Presenting clinical symptoms were not associated with growth. No CCAs ruptured during follow-up., Conclusion: Cavernous ICA aneurysms in our series demonstrate no rupture and limited growth over years of clinical follow-up. No radiographic or patient risk factors were associated with growth except initial aneurysm size. Hence, small CCAs may not require close follow-up over time., (Copyright © Congress of Neurological Surgeons 2024. All rights reserved.)

Background Suboccipital craniectomy (SOC) in conjunction with dura opening and duraplasty for posterior fossa decompression is an effective treatment for symptomatic Chiari 1 malformations (CM1), primarily carried out in the pediatric population. However, dural opening and reconstruction are associated with an increased risk of complications, and their necessity in the adult population has not yet been robustly demonstrated. Given differences in clinical presentation and disease severity between the pediatric and adult patients, we aimed to identify if SOC alone with intraoperative ultrasound confirmation of adequate restoration of pulsatile motion of cerebellar tonsil is sufficient to treat symptomatic CM1 while mitigating surgical risks. Methods We identified a retrospective, institutional cohort of adult patients who underwent SOC for Chiari decompression between 2014 and 2023. Demographic, clinical, and radiographic features were extracted for each patient. Clinical outcomes were assessed using the Chicago Chiari Outcome Scale (CCOS) and Motor-Sensory-Sphincter signs score (Clinical Sign Score (CSS)). Radiographic outcomes assessed cerebellar ectopia and associated syrinx characteristics. Results A total of 15 patients were identified, with an average follow-up period of three years. Eight patients underwent SOC with duraplasty, whereas seven patients underwent SOC only without duraplasty. Both groups of patients were of similar age at surgery and had similar nature and duration of symptoms prior to surgery. On pre-operative radiographic evaluation, both groups of patients had similar lengths of cerebellar ectopia (9.9±11.0 mm to 11.1±5.7 mm, p=0.591), and associated syrinxes (75% vs. 42.9%, p=0.205). Intraoperatively, both groups had similar estimated blood losses, though the length of surgery was significantly shorter when durotomy was spared (202±58.3 minutes to 116.3±47.8 minutes, p=0.011). The length of ICU stay was also significantly longer in the durotomy group (1.1±0.6 days to 0.0 days, p<0.001). Neither group reported any post-operative complications. On follow-up, both groups demonstrated similar reductions in cerebellar ectopia and syrinx characteristics. Clinically, the CCOS and CSS scores were similar between the two cohorts at follow-up, with no repeat surgery required in either group. Conclusion Our cohort suggests that for adult CM1 patients, SOC decompression alone without dural reconstruction might lead to comparable clinical and radiographic outcomes to SOC decompression with durotomy/duraplasty, especially if intraoperative ultrasound confirms good cerebrospinal fluid (CSF) flow after SOC. Notably, sparing durotomy and duraplasty is also associated with decreased operative time and decreased ICU stay., Competing Interests: The authors have declared that no competing interests exist., (Copyright © 2024, Jha et al.)

Antibiotics have revolutionized survival from central nervous system (CNS) infections. Sixty years after the death of Sir Hugh Cairns, we present archive material of historical interest from the Radcliffe Infirmary in Oxford from the time of his first trials of penicillin for CNS infection. We discuss Cairns' important wartime and subsequent contributions to antibiosis in CNS infection and include drawings by Audrey Arnott illustrating the surgical techniques used to treat abscesses at the time.