Background and Objectives:While academic centers have traditionally valued faculty research and educational accomplishments, clinical excellence is often assumed or underappreciated. Accordingly, neurology residency programs frequently offer structured pathways for aspiring clinician-scientists or educators, but few offer dedicated training to launch residents into academic careers focused on clinical mastery. Guided by self-regulated learning principles and the Master Adaptive Learner framework, the aim of this curriculum was to equip neurology postgraduate year (PGY)-4 residents with the foundational skills of the master clinician by advancing the following: (1) clinical acumen and diagnostic reasoning; (2) a scholarly and evidence-informed approach to their work; (3) outstanding communication, professionalism, and humanism; and (4) effective navigation and leadership within complex health care systems. Methods:Using the Kern six-step curriculum design framework, we developed a 6-month Master Clinician track that included didactics, customized clinical rotations, reflective patient portfolios, and a scholarly project. Didactics addressed topics such as cognitive bias, adaptive expertise, communication, and clinical uncertainty. Clinical rotations were learning-focused experiences tailored to resident interests. Track residents maintained 2 patient portfolios: one for in-depth case analysis ("depth" portfolio) and another to track diagnostic accuracy ("breadth" portfolio). The scholarly project reinforced a reflective approach to patient care and promoted academic inquiry skills. Assessments of the track included an exit survey on completion, patient portfolio audits, and post-track surveys for 3 years after graduation from residency. Results:Five residents completed the track in the first 5 years (2017-2022). Baseline residency milestone ratings were similar between participants and nonparticipants. Track components received high ratings (≥4.6 on a 5-point scale), with didactics on cognitive bias and teaching skills rated highest. Portfolios averaged 32 cases (breadth) and 8 cases (depth). Residents highlighted clinical uncertainty, communication, and cognitive bias as the most relevant sessions for patient care. Over 3 years of follow-up, high satisfaction with the track persisted and most enrollees elected academic clinical or clinician-educator careers. Discussion:A residency track that used didactics, customized clinical experiences, case-tracking, and reflective practices to foster clinical excellence was well received by residents. Neurology programs should consider similar tracks to develop academic clinicians focused on excellence in patient care.

Delirium is a neurologic syndrome characterized by inattention and cognitive impairment frequently encountered in the medically ill. Peripheral inflammation is a key trigger of delirium, but the patient-specific immune responses associated with delirium development and resolution are unknown. This retrospective cohort study of prospectively collected biospecimens examines RNA sequencing from peripheral blood mononuclear cells of adults hospitalized for COVID-19 to better understand patient-specific factors associated with delirium (n = 64). Longitudinal transcriptomic analyses highlight persistent immune dysregulation in delirium, marked by increasing expression trajectories of genes linked to innate immune pathways, including complement activation, cytokine production, and monocyte/macrophage recruitment. Genes involved adaptive immunity showed a declining trajectory over time in patients with delirium. Although corticosteroid treatment suppressed some aspects of immune hyperactivation, aberrant responses contributing to delirium were exacerbated. Delirium resolution was characterized by normalization of key transcripts such as CCL2 and innate immune markers. Novel associations with delirium were found in genes related to stress granule assembly and DUSP2 and KLF10 , which mediate T-cell responses. These findings provide insights into the peripheral immune responses accompanying delirium and their modulation by corticosteroids. Future trials targeting aberrant inflammatory responses may mitigate the severe outcomes associated with delirium due to COVID19.

Background and Objectives:Electronic health record documentation burden negatively affects physician satisfaction and patient care. Although well-constructed notes are important for care quality and safety, most note templates are created and maintained by individual physicians, leading to inefficiency and variable note quality. This study aimed to assess whether standardized, condition-specific note templates could enhance the efficiency and quality of notes written by neurology residents in the outpatient setting. Methods:In a quality improvement study with a randomized, nonblinded design from July 2021 to June 2022, neurology residents were assigned standardized templates for epilepsy, headache, and Parkinson disease (PD) in 2 outpatient clinics. The standardized templates were created with input from specialists in these disorders. Efficiency was gauged based on the time and characters involved in note writing while quality was assessed by adherence to American Academy of Neurology quality metrics for each condition through chart review. A qualitative survey gathered resident opinions on the templates. Linear regression models were used in the efficiency and quality analyses. Results:The study included 23 of 34 neurology residents. Templates were used in 36% of eligible encounters over the first 6 months of the study and 65% over the last 6 months. No significant difference in time spent on note writing was observed between the template and nontemplate groups. While both groups showed similar quality measures across most domains, the template group documented quality measures more consistently for driving status in epilepsy (92% vs 53%, p = 0.002), medication-related motor symptoms in PD (95% vs 50%, p = 0.01), and lifestyle changes in headache management (77% vs 21%, p = 0.005). Resident feedback suggested that the templates facilitated clinic workflows and prompted more thorough patient inquiry. Discussion:Standardized, condition-specific templates improved documentation of quality metrics without increasing time spent. Despite initial low uptake of template use, an increase was observed over time, indicating potential for wider acceptance with implementation efforts. These templates, updated and maintained by subject matter experts, serve as an opportunity to incorporate quality care checklists and knowledge into a clinician's workflow. This warrants further research into template implementation and its effects on care quality and education for neurologists and generalists.

Delirium is a neurologic syndrome characterized by inattention and cognitive impairment frequently encountered in medically ill older adults. As a hallmark of age-related brain vulnerability, delirium offers a clinical model to investigate how peripheral immune responses contribute to acute brain dysfunction. Peripheral inflammation is a key trigger of delirium, but the patient-specific immune responses that drive delirium onset and recovery remain poorly understood. This retrospective cohort study of prospectively collected biospecimens examines RNA sequencing from peripheral blood mononuclear cells of adults hospitalized for COVID-19 to better understand patient-specific factors associated with delirium (n = 64). Longitudinal transcriptomic analyses highlight persistent immune dysregulation in delirium, marked by increasing expression trajectories of genes linked to innate immune pathways, including complement activation, cytokine production, and monocyte/macrophage recruitment. Genes involved adaptive immunity showed a declining trajectory over time in patients with delirium. Although corticosteroid treatment suppressed some aspects of immune hyperactivation, aberrant responses contributing to delirium were exacerbated. Delirium resolution was characterized by normalization of key transcripts such as CCL2 and innate immune markers. Novel associations with delirium included transcripts related to stress granule assembly and the T cell regulators DUSP2 and KLF10. Delirium in COVID-19 is associated with distinct and dynamic peripheral immune trajectories that are modulated by corticosteroids. Further understanding these mechanisms has important implications for preventing delirium in older adults. These findings provide novel mechanistic insights with translational relevance for immunomodulatory strategies targeting maladaptive immune responses to prevent or treat delirium in medically ill populations.

GLP-1 agonists have been a welcome addition to the armamentarium in the treatment of diabetes and obesity. While this class of medications is generally considered safe and effective, potentially severe neurological complications may be associated with rapid weight loss and nutritional deficiencies following GLP-1 agonist use. We present a 37-year-old woman who was prescribed semaglutide for diabetes and weight loss who subsequently experienced significant weight reduction and rapid glycemic control over three months. Thereafter, she developed progressive right leg numbness and weakness, followed by similar symptoms in the left leg, and blurred vision. Initially diagnosed with B12 deficiency, her symptoms worsened despite supplementation, leading to acute encephalopathy and transfer to a tertiary center. Neurological examination revealed disorientation, ocular abnormalities, weakness, sensory deficits, and preserved ankle jerks. Diagnostic workup was notable for thiamine deficiency, NCS/EMG showing a severe, axonal polyneuropathy, and nerve biopsy redemonstrating severe axonal neuropathy. After extensive diagnostic workup, the most likely etiology of her clinical presentation was favored to be non-alcoholic Wernicke's encephalopathy (NAWE) and treatment-induced neuropathy of diabetes (TIND). This case suggests that vulnerable individuals may experience significant adverse neurological complications from the metabolic effects of GLP-1 agonist use. As a class effect, the benefits of these medications outweigh the risks, but their use warrants consideration of their potential sequelae.

Background Ataxia is a hallmark of the anti-GQ1b antibody syndrome, though it is unclear whether this symptom arises primarily from sensory nerve injury or from cerebellar involvement. We report a case of a patient with a clinically isolated post-infectious pancerebellar syndrome with anti-GQ1b antibody positivity. Case Presentation A 22-year-old previously healthy woman presented with acute-onset, progressive imbalance, limb ataxia, and dysarthria following an upper respiratory tract infection. She had no paresthesias, numbness, or diplopia. Neurological examination revealed an isolated pancerebellar syndrome including ocular and limb dysmetria, intention tremor, and gait ataxia. All sensory modalities were unaffected, reflex testing was normal, and there was no ophthalmoplegia. In-hospital serum and CSF testing was unremarkable, and brain magnetic resonance imaging was normal. The patient was empirically treated with intravenous immunoglobulin. Her symptoms were moderately improved by discharge (hospital day 5), and fully resolved several months later. Serological testing sent during the hospitalization subsequently revealed anti-GQ1b IgG positivity. Conclusions This case expands the spectrum of anti-GQ1b syndrome to include isolated cerebellar ataxia, suggesting that ataxia in this syndrome can have cerebellar origin. Clinicians should consider anti-GQ1b testing in cases of acute cerebellar ataxia following infection.

Vitamin B12 is critical for hematopoiesis and myelination. Deficiency can cause neurologic deficits including loss of coordination and cognitive decline. However, diagnosis relies on measurement of vitamin B12 in the blood, which may not accurately reflect the concentration in the brain. Using programmable phage display, we identified an autoantibody targeting the transcobalamin receptor (CD320) in a patient with progressive tremor, ataxia, and scanning speech. Anti-CD320 impaired cellular uptake of cobalamin (B12) in vitro by depleting its target from the cell surface. Despite a normal serum concentration, B12 was nearly undetectable in her cerebrospinal fluid (CSF). Immunosuppressive treatment and high-dose systemic B12 supplementation were associated with increased B12 in the CSF and clinical improvement. Optofluidic screening enabled isolation of a patient-derived monoclonal antibody that impaired B12 transport across an in vitro model of the blood-brain barrier (BBB). Autoantibodies targeting the same epitope of CD320 were identified in seven other patients with neurologic deficits of unknown etiology, 6% of healthy controls, and 21.4% of a cohort of patients with neuropsychiatric lupus. In 132 paired serum and CSF samples, detection of anti-CD320 in the blood predicted B12 deficiency in the brain. However, these individuals did not display any hematologic signs of B12 deficiency despite systemic CD320 impairment. Using a genome-wide CRISPR screen, we found that the low-density lipoprotein receptor serves as an alternative B12 uptake pathway in hematopoietic cells. These findings dissect the tissue specificity of B12 transport and elucidate an autoimmune neurologic condition that may be amenable to immunomodulatory treatment and nutritional supplementation.

The Neurohospitalist Core Competencies comprise a set of competency-based learning objectives that encapsulate the knowledge, skills, and attitudes of neurohospitalitists who specialize in the care of hospitalized patients with neurologic conditions. These competencies serve to characterize the rapidly expanding field of neurohospitalist medicine. The 27 chapters are divided into 3 sections entitled: neurological conditions, clinical interventions and interpretation of ancillary studies, and neurohospitalist role in the healthcare system. Each individual learning objective in the chapters describes a specific concept with an action verb to illustrate the behavior that the neurohospitalist exhibits. The individual neurohospitalist may not exhibit mastery in each of the topics included as individual practices vary in scope and practice pattern. A few examples of how the complete set of competencies may be used include in the creation of curricula for neurohospitalist fellowships, to assist in defining the scope of practice of neurohospitalists for administrative leaders of hospitals and departments, and in influencing the direction of further research and quality improvement in the field.

Introduction Interhospital transfer is an important mechanism for improving access to specialized neurologic care but there are large gaps in our understanding of interhospital transfer for the management of non-stroke-related neurologic disease. Methods This observational study included consecutive patients admitted to an adult academic general neurology service via interhospital transfer from July 1, 2015 to July 1, 2017. Characteristics of the referring hospital and transferred patients were obtained through the American Hospital Association Directory, a hospital transfer database maintained by the accepting hospital, and the electronic medical record. The analyses used descriptive statistics to examine the cohort overall and compare characteristics of patients transferred from an emergency department and inpatient service. Results 504 patients were admitted via interhospital transfer during the study period. Of these, 395 patients (78.4%) were transferred because the referring hospital lacked capability, and 139 patients (27.6%) were transferred from an emergency department as opposed to inpatient service. Seizures was the most common diagnosis (23.8%). Patients who were transferred from an emergency department had a higher proportion covered by Medicaid (44.6%) than those transferred from an inpatient service (28.8%) and had a shorter median length of stay (3 days; IQR 2-7 vs 7 days; IQR 4-12). Conclusions The majority of observed interhospital non-stroke neurologic transfers occurred to improve access to specialized neurological care for patients, though patients transferred from the ED, as opposed to an inpatient service, had lower health care utilization, and this will be important to consider when developing systems of care and in future research.

To investigate the association between preoperative delirium and plasma neuropathology biomarkers.

Adults with Parkinson disease (PD) are hospitalized at higher rates than age-matched controls, and these hospitalizations are associated with significant morbidity. However, little is known about the consequences of critical illness requiring intensive care unit (ICU)-level care in patients with PD. The aim of this study was to define the characteristics and outcomes of adults with PD admitted to the ICU. We performed a retrospective nested case–control study using the Medical Information Mart for Intensive Care IV data set. Adults with PD were identified, and the index ICU admission for these subjects was matched 1:4 with index ICU admissions without a PD diagnosis based on age, sex, comorbidities, illness severity, ICU type, and need for mechanical ventilation. Primary outcomes were in-hospital mortality and discharge location. Secondary outcomes were length of stay and prespecified complications. A total of 630 adults with PD were identified. Patients with PD were older and were more likely to be male, have more comorbidities, and have higher illness severity at presentation. A matched analysis revealed adults with PD did not have a significant difference in in-hospital mortality but were more likely to be discharged to a higher level of care. Adults with PD had longer hospital lengths of stay and increased odds of delirium, pressure ulcers, and ileus. During critical illness, patients with PD are at increased risk for longer hospital lengths of stay and complications and require a higher level of care at discharge than matched controls. These findings reveal targets for interventions to improve outcomes for patients with PD and may inform discussions about goals of care in this population.

Background: Susac syndrome is a vasculopathy, resulting in the classic triad of branch retinal artery occlusion (BRAO), inner ear ischemia, and brain ischemia. In this retrospective chart review, we characterize fluorescein angiography (FA) findings and other ancillary studies in Susac syndrome, including the appearance of persistent disease activity and the occurrence of new subclinical disease on FA. Methods: This multicenter, retrospective case series was institutional review board–approved and included patients with the complete triad of Susac syndrome evaluated with FA, contrasted MRI of the brain, and audiometry from 2010 to 2020. The medical records were reviewed for these ancillary tests, along with demographics, symptoms, visual acuity, visual field defects, and findings on fundoscopy. Clinical relapse was defined as any objective evidence of disease activity during the follow-up period after initial induction of clinical quiescence. The main outcome measure was the sensitivity of ancillary testing, including FA, MRI, and audiometry, to detect relapse. Results: Twenty of the 31 (64%) patients had the complete triad of brain, retinal, and vestibulocochlear involvement from Susac syndrome and were included. Median age at diagnosis was 43.5 years (range 21–63), and 14 (70%) were women. Hearing loss occurred in 20 (100%), encephalopathy in 13 (65%), vertigo in 15 (75%), and headaches in 19 (95%) throughout the course of follow-up. Median visual acuity at both onset and final visit was 20/20 in both eyes. Seventeen (85%) had BRAO at baseline, and 10 (50%) experienced subsequent BRAO during follow-up. FA revealed nonspecific leakage from previous arteriolar damage in 20 (100%), including in patients who were otherwise in remission. Of the 11 episodes of disease activity in which all testing modalities were performed, visual field testing/fundoscopy was abnormal in 4 (36.4%), MRI brain in 2 (18.2%), audiogram in 8 (72.7%), and FA in 9 (81.8%). Conclusions: New leakage on FA is the most sensitive marker of active disease. Persistent leakage represents previous damage, whereas new areas of leakage suggest ongoing disease activity that requires consideration of modifying immunosuppressive therapy.

OBJECTIVE:To assess the prevalence and clinical implications of variant sciatic nerve anatomy in relation to the piriformis muscle on magnetic resonance neurography (MRN), in patients with lumbosacral neuropathic symptoms.MATERIALS AND METHODS:In this retrospective single-center study, 254 sciatic nerves, from 127 patients with clinical and imaging findings compatible with extra-spinal sciatica on MRN between 2003 and 2013, were evaluated for the presence and type of variant sciatic nerves, split sciatic nerve, abnormal T2-signal hyperintensity, asymmetric piriformis size and increased nerve caliber, and summarized using descriptive statistics. Two-tailed chi-square tests were performed to compare the anatomical variant type and clinical symptoms between imaging and clinical characteristics.RESULTS:Sixty-four variant sciatic nerves were identified with an equal number of right and left variants. Bilateral variants were noted in 15 cases. Abnormal T2-signal hyperintensity was seen significantly more often in variant compared to conventional anatomy (40/64 vs. 82/190; p = 0.01). A sciatic nerve split was seen significantly more often in variant compared to conventional anatomy (56/64 vs. 20/190; p < 0.0001). Increased nerve caliber, abnormal T2-signal hyperintensity, and asymmetric piriformis size were significantly associated with the clinically symptomatic side compared to the asymptomatic side (98:2, 98:2, and 97:3, respectively; p < 0.0001 for all). Clinical symptoms were correlated with variant compared to conventional sciatic nerve anatomy (64% vs. 46%; p = 0.01).CONCLUSION:Variant sciatic nerve anatomy, in relation to the piriformis muscle, is frequently identified with MRN and is more likely to be associated with nerve signal changes and symptomatology.

Importance:Despite discrete etiologies leading to delirium, it is treated as a common end point in hospital and in clinical trials, and delirium research may be hampered by the attempt to treat all instances of delirium similarly, leaving delirium management as an unmet need. An individualized approach based on unique patterns of delirium pathophysiology, as reflected in predisposing factors and precipitants, may be necessary, but there exists no accepted method of grouping delirium into distinct etiologic subgroups. Objective:To conduct a systematic review to identify potential predisposing and precipitating factors associated with delirium in adult patients agnostic to setting. Evidence Review:A literature search was performed of PubMed, Embase, Web of Science, and PsycINFO from database inception to December 2021 using search Medical Subject Headings (MeSH) terms consciousness disorders, confusion, causality, and disease susceptibility, with constraints of cohort or case-control studies. Two reviewers selected studies that met the following criteria for inclusion: published in English, prospective cohort or case-control study, at least 50 participants, delirium assessment in person by a physician or trained research personnel using a reference standard, and results including a multivariable model to identify independent factors associated with delirium. Findings:A total of 315 studies were included with a mean (SD) Newcastle-Ottawa Scale score of 8.3 (0.8) out of 9. Across 101 144 patients (50 006 [50.0%] male and 49 766 [49.1%] female patients) represented (24 015 with delirium), studies reported 33 predisposing and 112 precipitating factors associated with delirium. There was a diversity of factors associated with delirium, with substantial physiological heterogeneity. Conclusions and Relevance:In this systematic review, a comprehensive list of potential predisposing and precipitating factors associated with delirium was found across all clinical settings. These findings may be used to inform more precise study of delirium's heterogeneous pathophysiology and treatment.

Background Gadolinium enhancement of spinal nerve roots on magnetic resonance imaging (MRI) has rarely been reported in spinal dural arteriovenous fistula (SDAVF). Nerve root enhancement and cerebrospinal fluid (CSF) pleocytosis can be deceptive and lead to a misdiagnosis of myeloradiculitis. We report a patient who was initially diagnosed with neurosarcoid myeloradiculitis due to spinal nerve root enhancement, mildly inflammatory cerebrospinal fluid, and pulmonary granulomas, who ultimately was found to have an extensive symptomatic SDAVF. Case presentation A 52-year-old woman presented with a longitudinally extensive spinal cord lesion with associated gadolinium enhancement of the cord and cauda equina nerve roots, and mild lymphocytic pleocytosis. Pulmonary lymph node biopsy revealed non-caseating granulomas and neurosarcoid myeloradiculitis was suspected. She had rapid and profound clinical deterioration after a single dose of steroids. Further work-up with spinal angiography revealed a thoracic SDAVF, which was surgically ligated leading to clinical improvement. Conclusions This case highlights an unexpected presentation of SDAVF with nerve root enhancement and concurrent pulmonary non-caseating granulomas, leading to an initial misdiagnosis with neurosarcoidosis. Nerve root enhancement has only rarely been described in cases of SDAVF; however, as this case highlights, it is an important consideration in the differential diagnosis of non-inflammatory causes of longitudinally extensive myeloradiculopathy with nerve root enhancement. This point is highly salient due to the importance of avoiding misdiagnosis of SDAVF, as interventions such as steroids or epidural injections used to treat inflammatory or infiltrative mimics may worsen symptoms in SDAVF. We review the presentation, diagnosis, and management of SDAVF as well as a proposed diagnostic approach to differentiating SDAVF from inflammatory myeloradiculitis.

Importance Despite discrete etiologies leading to delirium, it is treated as a common end point in hospital and in clinical trials, and delirium research may be hampered by the attempt to treat all instances of delirium similarly, leaving delirium management as an unmet need. An individualized approach based on unique patterns of delirium pathophysiology, as reflected in predisposing factors and precipitants, may be necessary, but there exists no accepted method of grouping delirium into distinct etiologic subgroups. Objective To conduct a systematic review to identify potential predisposing and precipitating factors associated with delirium in adult patients agnostic to setting. Evidence Review A literature search was performed of PubMed, Embase, Web of Science, and PsycINFO from database inception to December 2021 using search Medical Subject Headings (MeSH) terms consciousness disorders , confusion , causality , and disease susceptibility , with constraints of cohort or case-control studies. Two reviewers selected studies that met the following criteria for inclusion: published in English, prospective cohort or case-control study, at least 50 participants, delirium assessment in person by a physician or trained research personnel using a reference standard, and results including a multivariable model to identify independent factors associated with delirium. Findings A total of 315 studies were included with a mean (SD) Newcastle-Ottawa Scale score of 8.3 (0.8) out of 9. Across 101 144 patients (50 006 [50.0%] male and 49 766 [49.1%] female patients) represented (24 015 with delirium), studies reported 33 predisposing and 112 precipitating factors associated with delirium. There was a diversity of factors associated with delirium, with substantial physiological heterogeneity. Conclusions and Relevance In this systematic review, a comprehensive list of potential predisposing and precipitating factors associated with delirium was found across all clinical settings. These findings may be used to inform more precise study of delirium’s heterogeneous pathophysiology and treatment.

Background Accurate, pragmatic risk stratification for postoperative delirium (POD) is necessary to target preventative resources toward high-risk patients. Machine learning (ML) offers a novel approach to leveraging electronic health record (EHR) data for POD prediction. We sought to develop and internally validate a ML-derived POD risk prediction model using preoperative risk features, and to compare its performance to models developed with traditional logistic regression. Methods This was a retrospective analysis of preoperative EHR data from 24,885 adults undergoing a procedure requiring anesthesia care, recovering in the main post-anesthesia care unit, and staying in the hospital at least overnight between December 2016 and December 2019 at either of two hospitals in a tertiary care health system. One hundred fifteen preoperative risk features including demographics, comorbidities, nursing assessments, surgery type, and other preoperative EHR data were used to predict postoperative delirium (POD), defined as any instance of Nursing Delirium Screening Scale ≥2 or positive Confusion Assessment Method for the Intensive Care Unit within the first 7 postoperative days. Two ML models (Neural Network and XGBoost), two traditional logistic regression models (“clinician-guided” and “ML hybrid”), and a previously described delirium risk stratification tool (AWOL-S) were evaluated using the area under the receiver operating characteristic curve (AUC-ROC), sensitivity, specificity, positive likelihood ratio, and positive predictive value. Model calibration was assessed with a calibration curve. Patients with no POD assessments charted or at least 20% of input variables missing were excluded. Results POD incidence was 5.3%. The AUC-ROC for Neural Net was 0.841 [95% CI 0. 816–0.863] and for XGBoost was 0.851 [95% CI 0.827–0.874], which was significantly better than the clinician-guided (AUC-ROC 0.763 [0.734–0.793], p < 0.001) and ML hybrid (AUC-ROC 0.824 [0.800–0.849], p < 0.001) regression models and AWOL-S (AUC-ROC 0.762 [95% CI 0.713–0.812], p < 0.001). Neural Net, XGBoost, and ML hybrid models demonstrated excellent calibration, while calibration of the clinician-guided and AWOL-S models was moderate; they tended to overestimate delirium risk in those already at highest risk. Conclusion Using pragmatically collected EHR data, two ML models predicted POD in a broad perioperative population with high discrimination. Optimal application of the models would provide automated, real-time delirium risk stratification to improve perioperative management of surgical patients at risk for POD.