Faculty Bibliography

BACKGROUND/UNASSIGNED:Although vertebral hemangiomas (VH) are relatively common, aggressive symptomatic VH are rarely reported (i.e. in up to 11% of cases). Multiple other benign and malignant primary bone tumors must be considered in the differential diagnosis. Here, we review the clinical diagnosis and surgical management for aggressive hemangiomas, while also presenting 2 patients with thoracic lesions requiring posterior surgical decompression/fusion, with/without vertebroplasty, embolization, and/or CyberKnife radiosurgery. METHODS/UNASSIGNED:The classification system for these tumors ranges from Types I-IV; I Occupy < 50% of a vertebral body (VB), II-Occupy > 50% VB (IIb Thoracolumbar - Symptomatic), III-Occupy 100% VB, and IV-Occupy 100% VB involved plus extension into the pedicles, laminae, spinous process, and epidural space. RESULTS/UNASSIGNED:Radiographically (i.e. X-rays, MR, CT) these lesions originate in the vertebral bodies, but aggressive VH extend into the pedicles, laminae, spinous processes, and epidural space causing both spinal cord/root (i.e., myelopathy/radiculopathy)) compression. Surgical options include anterior, posterior, or circumferential decompressions with/without fusions, percutaneous vertebroplasty, embolization, radiation, and/or chemotherapy. Early treatment maximizes neurological recovery and limits/avoids permanent injury. CONCLUSION/UNASSIGNED:Aggressive VH are rare lesions that most frequently occur in the thoracic spine. Notably, the subset of Type IV lesions that extend into the pedicles, laminae, spinous processes, and epidural space may cause symptomatic myelopathy/radiculopathy warranting early surgical intervention to optimize neurological outcomes.

Deep neural networks (DNNs) are promising computational models for understanding visual object recognition. Yet, whether DNNs use similar visual cues for object recognition as humans do remains unknown. We created an image set that systematically untangles global shape, internal parts, and texture information, and compared human recognition behavior against >200 DNNs spanning diverse architectures, training diets, and training objectives. No DNNs replicated humans' cue-reliance profile, including those with recurrence or specialized training. Fine-tuned text-image contrastive-trained models, regardless of architecture, were most human-like overall, but lost their human-alignment when the global shape was disrupted. Strikingly, all DNNs substantially underperformed humans when the global shape cue alone was critical to object recognition. Furthermore, alignment with ventral stream neural recordings in an existing database did not predict alignment to human behavior, and model performance does not always predict its human-alignment. Together, these findings reveal systematic and persistent differences between human and machine vision.

<p>Background: Salvador Dalí (1904-1989), the great Surrealist painter, developed a progressive parkinsonian syndrome during the last decade of his life that ended his artistic career and reduced him to near-total dependence. Multiple physicians documented tremor, rigidity, and progressive disability, yet no clinical account has been published in the neurological literature. Summary: Drawing on contemporaneous press reports, biographies based on primary sources, sworn medical testimony, and a published quantitative analysis of his paintings, this review compiles the chronological evolution of Dalí's neurological symptoms. Non-motor features (including nocturia without urological explanation and erectile dysfunction from at least 1974) were documented years before the onset of visible motor symptoms, a sequence consistent with, but not diagnostic of, prodromal synucleinopathy. The motor phase, beginning around 1980, was characterized by asymmetric resting tremor affecting the right upper extremity, rigidity, gait impairment, and progressive akinesia. Despite examinations by prominent neurologists including Lluís Barraquer Bordas and François Lhermitte, the diagnosis remained contested throughout Dalí's life. Drug-induced parkinsonism was implicated in the initial crisis, but the continued deterioration after drug withdrawal argues against a purely iatrogenic etiology. No autopsy was performed. Key Messages: This case illustrates a problem familiar to practicing neurologists: the difficulty of diagnosing parkinsonism in patients with complex premorbid personalities, where emerging neuropsychiatric symptoms are absorbed into longstanding behavioral patterns. Today, biomarkers detecting α-synuclein aggregates in peripheral tissues would greatly reduce such diagnostic uncertainty; these tools were not available in Dalí's lifetime. </p>.

Home-based transcranial direct current stimulation (tDCS) for major depressive disorder (MDD) has progressed from early feasibility studies to an approved clinical treatment, highlighted by the US Food and Drug Administration's 2025 premarket approval of the Flow FL-100 device. This milestone shifts the field from asking whether home-based tDCS can be delivered safely and effectively to defining how it should be implemented in routine clinical practice. This review synthesizes the current evidence on treatment outcomes, adherence, and safety, with an emphasis on factors that determine successful real-world implementation. Randomized controlled trials support the efficacy of home-based tDCS when delivered using adequate cumulative dosing, structured treatment protocols, and appropriate supervision or adherence monitoring. In contrast, shorter-duration and fully unsupervised protocols have generally shown less favorable outcomes, although the independent contributions of dose, treatment duration, and supervision remain difficult to disentangle. High adherence has been reported with user-centered device design, standardized training, remote monitoring, and scalable supervision models that maintain treatment fidelity while supporting broad clinical deployment. Home-based tDCS has demonstrated an excellent safety profile when delivered using standardized equipment, structured protocols, and active monitoring, exemplified by more than 30,000 supervised home-based sessions delivered through a large academic clinical program without reported skin lesions or serious adverse events attributable to tDCS. Remaining priorities include optimizing acute and maintenance dosing strategies, identifying predictors and biomarkers of response, defining the role of paired behavioral interventions, personalizing treatment for special populations - including perinatal patients, older adults, and adolescents - and integrating home-based tDCS within interventional psychiatry care pathways. The evidence supports a transition from proof-of-concept to clinical implementation, with future research focused on optimizing delivery, personalizing treatment, and expanding access to evidence-based neuromodulation for depression.

This manuscript presents the perspective of the International Society of Cartilage Repair of the Ankle (ICCRA) regarding a recent English High Court ruling that challenges established principles of evidence-based sports orthopaedic care. Following a legal case involving a professional footballer and the surgical management of an ankle fracture with concomitant arthroscopy, the authors highlight significant discrepancies between the legal conclusions and the current scientific literature. The ruling suggests that arthroscopic intervention contributed to the development of ankle arthritis and premature termination of the athlete's career. However, substantial evidence demonstrates that posttraumatic ankle arthritis is a well-recognised sequela of ankle fractures, particularly in the presence of prior injury and syndesmotic instability. Arthroscopy at the time of fracture fixation is widely regarded as the standard of care for identifying and managing intraarticular pathology. The judgement is critiqued for disregarding expert orthopaedic testimony, misinterpreting scientific evidence and endorsing unsupported theoretical mechanisms linking routine arthroscopic procedures to accelerated joint degeneration. The authors emphasise that such conclusions contradict accepted surgical practice and risk establishing harmful precedents that may deter appropriate management of similar injuries. This ICCRA statement highlights the need for alignment between medico-legal reasoning and scientific evidence to safeguard patient care and uphold the integrity of orthopaedic decision-making. LEVEL OF EVIDENCE: NA.

BACKGROUND:Autonomic dysfunction is associated with adverse cardiovascular outcomes, increased symptom burden, and impaired quality of life. Although it is increasingly recognized in patients with breast cancer, its prevalence has not been well established. METHODS:A systematic review and meta-analysis were conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 recommendations. Databases used were Embase, PubMed/MEDLINE, Scopus, Web of Science, and LILACS (Latin American and Caribbean Health Sciences Literature). Studies were included if they assessed autonomic function in patients with breast cancer and reported or provided sufficient data to estimate the prevalence of autonomic dysfunction, published in English or Spanish from 1954 to February 2026. The quality of the studies was assessed using the Newcastle-Ottawa Quality Assessment Scale and the NIH Quality Assessment Tool. RESULTS: = 90.8%). CONCLUSIONS:Autonomic dysfunction affects nearly one in two patients with breast cancer, highlighting dysautonomia as a prevalent, often subclinical, and underrecognized complication with potential implications for cardiovascular health, symptom burden, and quality of life. PROSPERO registration number CRD420251253332.

BACKGROUND AND PURPOSE/OBJECTIVE: MATERIALS AND METHODS/METHODS: RESULTS: CONCLUSIONS:The dynamics of the CVR response can reveal differential and previously occult temporal signatures in the pharmacologic response of white matter to ACZ, suggesting potential interactions between macrovascular and microvascular hemodynamic impairment.

Basal forebrain cholinergic neurons play a key role in cognition. This neuronal system is highly dependent on nerve growth factor (NGF) for its synaptic integrity and the phenotypic maintenance of its cell bodies. Basal forebrain cholinergic neurons progressively degenerate in Alzheimer's disease and Down's syndrome, and their atrophy contributes to the manifestation of dementia. Paradoxically, in Alzheimer's disease brains, the synthesis of NGF is not affected and there is abundance of the NGF precursor (proNGF). We have shown that this phenomenon is due to a deficit in NGF's extracellular metabolism which compromises proNGF maturation and exacerbates its subsequent degradation. We hypothesized that a similar imbalance should be present in Down's syndrome. Using a combination of quantitative reverse transcription-polymerase chain reaction, enzyme-linked immunosorbent assay, western blotting and zymography, we have investigated signs of NGF metabolic dysfunction in post-mortem brains from the temporal (n = 14), frontal (n = 34) and parietal (n = 20) cortex obtained from Down's syndrome subjects and age-matched controls (age range 31-68 years). We further examined primary cultures of human fetal Down's syndrome cortex (17-21 gestational age weeks). We report a significant increase in proNGF levels in human Down's syndrome brains, with a concomitant reduction in the levels of plasminogen and tissue plasminogen activator mRNA as well as an increment in neuroserpin expression; enzymes that partake in proNGF maturation. Down's syndrome brains also exhibited elevated zymogenic activity of MMP9, the major NGF-degrading protease. Our results indicate a failure in proNGF maturation in Down's syndrome brains and a likely enhanced proteolytic degradation of NGF, changes which can compromise the trophic support of basal forebrain cholinergic neurons. The alterations in proNGF and MMP9 were also present in cultures of Down's syndrome fetal cortex; suggesting that this trophic compromise may be amenable to rescue, before frank dementia onset. Our study thus provides a novel paradigm for cholinergic neuroprotection in Alzheimer's disease and Down's syndrome.

BACKGROUND AND OBJECTIVES/OBJECTIVE:The most effective treatment strategy to prevent relapses after a first myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) event remains unclear. Our objective was to evaluate the comparative effectiveness of maintenance therapies in preventing relapses in pediatric-onset MOGAD. METHODS:We analyzed prospectively collected data from November 2011 to August 2023 across 13 US pediatric neuroimmunology centers. Eligible patients had demyelinating disease onset before age 18 years, confirmed MOG-IgG positivity through cell-based assay, and negative aquaporin-4 IgG. Maintenance therapies were defined as ≥90 consecutive days of treatment and included IV immunoglobulin (IVIG), anti-CD20 therapy, oral corticosteroids, and other immunosuppressants. Two complementary approaches were used: (1) a primary full-course analysis using time-varying Cox proportional hazards models, adjusted for a priori-selected confounders, accounting for treatment changes throughout the disease course, and (2) a secondary early-course analysis using 1:1 propensity score-matched Cox models for the first qualifying treatment initiated within 90 days of onset, applying an intention-to-treat framework to minimize immortal time bias. RESULTS:< 0.001), and prior relapse count was a strong predictor of future relapse risk. DISCUSSION/CONCLUSIONS:In this large, prospective, multicenter pediatric MOGAD cohort, IVIG was the only treatment consistently associated with reduced relapse risk across both analytical approaches, supporting its potential role as first-line maintenance therapy. Anti-CD20 therapy showed directional trends warranting further investigation. Key limitations include potential residual confounding by indication and small sample sizes in certain treatment categories. Randomized controlled trials are needed to confirm these findings.

Sensory processing is fundamentally shaped by stimulation history. For example, in visual cortex, neural responses are reduced for repeated or sustained stimuli (adaptation). These phenomena are well characterized and effectively modeled by divisive normalization. We asked whether these same computational principles govern somatosensory processing. We used fMRI (6 participants, all female) and intracranial electroencephalography (iEEG, 2 participants, both male) to measure responses to time-varying vibrotactile stimuli in human somatosensory cortex. Stimuli consisted of single- and paired-pulses with durations and interstimulus intervals ranging from 0.05 to 1.2 s. We extracted BOLD time courses to capture neural response amplitudes, and high-frequency iEEG broadband envelopes to capture fast neural dynamics. In both experiments, we observed pronounced sub-additive temporal summation. Responses to longer or repeated stimuli were consistently lower than predicted by linear integration. Computational modeling revealed that divisive normalization models outperformed linear models in cross-validated accuracy across both datasets. These results demonstrate that somatosensory temporal dynamics closely mirror those in the visual system. Our findings suggest that the nervous system employs similar computational principles across modalities to encode sensory information across time.Significance statement How the brain integrates sensory information over time is a fundamental question in neuroscience. While nonlinear temporal integration is well documented in visual cortex, it has not been extensively mapped in the human somatosensory system. By combining fMRI with intracranial EEG in humans, we demonstrate that somatosensory responses to tactile stimulation exhibit subadditive temporal summation. This nonlinearity is accurately captured by a divisive normalization model, matching observations in the visual system. Our results suggest that normalization is a canonical computation shared across different modalities to manage temporal dynamics, providing a unified framework for understanding how the brain encodes dynamic sensory stimuli.