2022 American Neuropsychiatric Association Annual Meeting Abstracts

Background: The prevalence of suicide among Veterans with TBI is high. It is unclear what mediates the association between TBI and suicidal ideation (SI) though it is known that a. impulsivity is a risk factor for suicide b. having had a TBI is associated with developing impulsivity and c. mental illness such as depression and PTSD are further risk factors for SI and commonly co-occur with TBI. What is unknown is whether impulsivity plays a role in SI in the TBI population. Objective: This study aimed to explore the relationship between TBI and SI and whether or not impulsivity mediates that association while controlling for psychiatric comorbidities through retrospective chart review. Methods: Charts of 164 Veterans from three sites were reviewed. 95 Veterans had mild to severe TBI (60 mild, 20 moderate, 25 severe) and 69 had no TBI history. Presence/absence of suicidality was determined by any affirmative mention of SI in the chart. Data was analyzed using multiple logistic regression models. Results: In unadjusted analyses, TBI was significantly associated with SI (p<0.001). On controlling for covariates (impulsivity, mental illness history, etc.) TBI was no longer associated with of SI, but impulsivity (OR=15.35, p=0.004) was, suggesting impulsivity mediates the relationship between TBI and SI. Conclusion: The disappearance of a relationship between TBI and suicidality when we controlled for impulsivity suggests the presence of impulsivity plays a significant role in development of suicidality among Vets with TBI.

Background: Depression and anxiety are prevalent among people living with epilepsy (PWE), and are associated with poor quality of life, non-adherence to treatment, increased risk of seizures, and suicide. Routine screening allows for early diagnosis, referral, and treatment, thus improving health outcomes for PWE. Screening feasibility concerns emerged in busy clinical practices during COVID-19. Objective: To examine the feasibility of depression and anxiety screening using a e-questionnaires in a tertiary epilepsy clinic. Methods: As part of a Quality Improvement program, adult PWE were offered e-questionnaires in clinic from January 2019 to March 2020 (pre-COVID era), shifting to patient-portal from May 2020 to December 2021(during COVID). E-questionnaires included validated screening instruments for depression and anxiety; PHQ-9 (Patient Health Questionnaire-9) and GAD-7 (Generalized Anxiety Disorder Questionnaire). E-questionnaire scores were abstracted manually, then entered in a local database. We report overall completion proportions during the pre- and COVID eras, and severity of depression and anxiety among those who completed the screening. Results: A total of 416 patients completed both e-questionnaires during 2019–2021 with mean age of 56.1 (SD=16.5); 33% female. 60% and 37% patients completed both e-questionnaires during pre-COVID and COVID, respectively. Out of 211 patients who completed PHQ-9, 67% (N=144/211) had no-reported depression, 16%,7.5%, 6%, and 1.8% had mild, moderate, moderate-severe, and severe depression, respectively. Out of 159 patients who completed GAD-7, 68% patients had no-reported anxiety, 14.8%, 7%, 8.7% had mild, moderate, and severe anxiety, respectively. Conclusion: Through virtual care, mental health screening was feasible during COVID-19, in a busy tertiary epilepsy clinic.

Background: Relapsing polychondritis (RP) is a rare autoimmune disorder characterized by inflammation of cartilage and other connective tissues. Neuropsychiatric manifestations of RP, while considered to be infrequent, have been described in case reports without consistent cerebrospinal fluid (CSF) investigations for other autoimmune conditions. We present a case of RP-associated N-methyl-D-aspartate receptor (NMDAR) encephalitis that calls attention to the utility of CSF testing. Case History: A 44-year-old male with RP was referred for neuropsychiatric evaluation of inconsistent memory loss, episodic aggression, and functional decline originally attributed to alcohol use. Examination was notable for stereotypies, perseveration, apathy, and no sensorimotor deficits. Brain magnetic resonance imaging with and without contrast demonstrated generalized atrophy. The initial electroencephalogram was normal. CSF studies were notable for mildly elevated protein (62 mg/dl) and anti-NMDAR NR1 antibodies. Despite aggressive immunosuppressive therapies and empiric treatments for possible catatonia, his cognitive and functional status did not improve. Conclusion: To our knowledge, our patient represents the first published case in which antibodies to the NR1 subunit of the NMDAR were found in a patient with RP and subacute cognitive decline. Literature review yielded 22 cases of RP with CSF and/or serum autoimmune antibody testing. In three cases, one or more antibodies were detected: 1) anti-GFAP in CSF, 2) GluR-N2B and GluRδ2 in CSF but not found in serum, and 3) GluRε2(NR2B) in serum and CSF. These cases argue for investigation for autoimmune encephalitides in patients with RP presenting with neuropsychiatric symptoms and cognitive decline.

Background: Capgras Syndrome (also known as Imposter Syndrome) is a rare delusional disorder where the patient believes someone they know has been replaced by an imposter. This case provides a unique etiology with trauma and the extended length of time since diagnosis. Case History: Capgras Syndrome has primarily been noted in patients with a history of Schizophrenia, Neurodegenerative disorders, and Cerebrovascular Accidents, particularly right hemisphere Frontal and Parietal subcortical white-matter leading to the loss of facial recognition. Our patient is an 87-year-old male. In 2017, he had a fall resulting in two subdural hematomas, which required hospitalization and rehabilitation. 3 days after the injury, the patient began to have episodes (lasting several days) of being unable to recognize his wife. During the episodes he sees her as an ex-wife, an estranged sister, his mother, and a friend. MRI revealed bilateral frontal lobe encephalomalacia and a benign meningioma. The meningioma was partially removed in 2018 due to concerns for potential invasion but yielded little effect on his delusion. Medications currently include Quetiapine and Rivastigmine. His partner reports that the Rivastigmine initially decreased the frequency of episodes. Four months later he began to have delusions again. Since that time, the length of the episodes has increased. Conclusion: Rivastigmine initially reduced the frequency of the delusion; however, the delusion has continued to progress. Over the past 5 years, the episodes have progressed in their frequency and length. This may shed light on expected courses for future patients with similar presentations.

Background: In mid-2020, the Stephen Jackson lab published intriguing results showing that rhythmic—but not arrhythmic—stimulation of the median nerve (MNS) entrained EEG power at the same frequency. Rhythmic MNS reduced tic severity in Tourette syndrome (TS). However, no control condition was tested and stimulation blocks lasted only 1 minute. Objective: This study tests the hypotheses that tic improvement is specific to rhythmic stimulation, which alone entrained cortical activity, and that it lasts after MNS ends. Methods: Detailed methods were registered at DOI 10.17605/OSF.IO/8JTEP. People aged 15–64 with TS have two study visits, one for rhythmic and one for arrhythmic MNS, in random order. Subjects and staff are blind to order, and video raters are additionally blind to block order and to stimulation on versus off. Results: Twenty-four participants have completed both visits, and two more have completed one visit. Enrollment and blinded ratings continue. On 43 of 50 visits, discomfort was rated as none or minimal. 19 of 26 participants had at least one visit rated “very much” or “much improved,” whether by self or investigator ratings. Nine of 26 participants rated at least one visit as “complete or nearly complete remission of symptoms” and 14 more rated at least one visit as “decided improvement, partial remission.” Urge severity decreased during stimulation blocks, but non-significantly more so on arrhythmic stimulation days. Conclusion: MNS appears to be well tolerated and some participants had remarkable symptom improvement, but rhythmic stimulation does not outperform arrhythmic stimulation for self-reported urge to tic.

Background: During the COVID-19 pandemic, complementary and integrative therapies delivered via mHealth technologies have become more popular due to their accessibility. As more users are downloading apps to address health concerns, it is important to analyze the ever-growing marketplace’s features and limitations. Objective: We aimed to assess the characteristics of the pain application (app) marketplace and determine improvements to mobile health (mHealth) that could assist patients with pain disorders in obtaining more accessible care. Methods: After searching the iOS and Google Play Stores for commercially available pain apps that met pre-specified search criteria, trained app raters entered 47 apps into the Mobile-Health Index and Navigation Database (MIND) published by the Division of Digital Psychiatry at BIDMC. Through a 105-question objective rating framework, each app was evaluated for its accessibility, privacy, cost, functionalities, features, and clinical foundations. The data was compared with a control group of non-pain apps—matched for platform and cost—to examine the traits of pain apps in contrast with the rest of the marketplace. Results: The top features were 44.7% (21/47) offered symptom tracking, 34.0% (16/47) offered medication tracking, and 42.6% (20/47) offered physical health exercises. Just 2.13% (1/47) of apps offered HIPAA privacy protections or had a crisis management feature. Additionally, only 10.64% (5/47) of pain apps were supported by efficacy studies. Conclusion: Commercially available pain apps are typically used to record pain episodes or document medications. However, the lack of privacy, crisis management, and efficacy studies may be preventing their clinical implementation.

Background: Cognitive trajectories and the affected cognitive domains can be highly variable in Parkinson’s disease (PD). Given this heterogeneity, important risk factors contributing to cognitive decline in PD subpopulations may be overlooked in larger PD populations. Objective: Explore risk factors contributing to heterogenous trajectories in specific cognitive domains in PD. Methods: Data were obtained from the Parkinson’s Progression Markers Initiative. We used latent class mixed modeling to identify classes on longitudinal performance of six individual neuropsychological tests (outcomes) measuring five cognitive domains with 14 dichotomous predicted risk factors (categorical indicator variables). Using backwards selection, we determined the predicted risk factors with significant influence on neuropsychological score change over time. Lastly, we used multinomial regression analysis to determine which risk factors predict class assignment for the six outcomes. Results: 421 de novo PD participants were included in the 5-year longitudinal analysis. All six outcomes produced three similar latent classes with class 1 (highest baseline) and class 2 (intermediate baseline) showing improvement or slight decline and class 3 (lowest baseline) showing steepest decline. The significant baseline variables common to all six models include non-White/Hispanic race/ethnicity and low screening MoCA score. There are no common baseline risk factors predicting assignment to class 3 for all six outcomes, however potentially modifiable risk factors contributing to at least two class 3 assignments include sedentary/light physical activity, depression, possible REM sleep behavior disorder, and vascular risk factors. Conclusions: Further defining risks associated with specific PD endophenotypes may aid in developing clinically relevant cognitive decline predictor tools.

Background: Deep brain stimulation (DBS) is an effective treatment to manage motor symptoms in Parkinson’s disease (PD). Subthalamic nucleus (STN) versus globus pallidus internus (GPi) DBS is regarded as the more efficacious brain target site depending on patient clinical characteristics (e.g., cognitive status, motor symptom profile). Despite DBS being equally effective for men and women, women undergo DBS less than men, possibly due to differences in clinical presentation. Objective: We explored whether gender also influences the likelihood of STN versus GPi DBS. Methods: Sixty-four people living with Parkinson’s disease referred from the community to a hospital-based movement disorders clinic for comprehensive DBS pre-surgical evaluation. Measures of global cognition, mood, fatigue, apathy, and disease severity were collected. Demographic information was also captured. Chi square analyses examined gender differences by brain target site (STN or GPi). Independent samples t tests examined differences in clinical and demographic characteristics by gender. Results: Men underwent STN (vs. GPi) significantly more than women (χ²[2, N=64]=6.13, p=0.01). Independent-samples t tests determined no significant differences between men and women in global cognition (p=0.08), mood (p=0.06), fatigue (p=0.18), apathy (p=0.14), age (p=0.32), disease severity (p=0.25), or disease duration (p=0.23). Conclusion: The current study is the first to examine gender differences by DBS brain target site. Results suggest that men undergo STN (vs. GPi) DBS surgery more than women despite no significant clinical or demographic differences between groups in the variables explored. Other potential explanatory factors, including pre-surgical dopamine load, motor presentation, and neurocognitive variables, will be examined.

Background: Effort mobilization is critical for goal directed behaviour across the human lifespan. Effort discounting is the process of reducing the subjective value of a reward as increasing effort that is required to obtain that reward. However, the neurobehavioral substrates of processes within effort-reward decision-making in older adults are poorly understood. Objective: To identify related brain regions associated with effort discounting to help us better understand factors affecting normal cognitive aging. Methods: We examined the effect of effort discounting on functional brain connectivity in 19 cognitively normal older adults (10 males; mean age=66±6 years). Participants completed a computerized cognitive task, the Effort Expenditure for Rewards Task, capturing decision making to expend effort for monetary rewards through binary choices between high-reward-high-effort or low-reward-low-effort options. We modelled subjective value to assess the k parameter, as a proxy of effort discounting, and then examined the association to brain functional connectivity. Regions associated to the salience network—right/left anterior insula (AI) and anterior cingulate cortex (ACC)—were selected in seed-to-voxel analyses with age, sex, and Bayesian information criterion as covariates. Results: Increased willingness to exert effort for reward was associated with enhanced functional connectivity between ACC and right lateral occipital cortex, and between the left AI, cerebellum and precuneus cortex (voxel p<0.001, cluster p<0.05 FDR corrected). The effect size of effort discounting was greater for ACC (r²=0.737 for ACC; r²=0.718 for left AI). Conclusions: Effort discounting is associated with functional connectivity changes involving the anterior cingulate cortex and left anterior insula in cognitively healthy older adults.

Background: Catatonia is a neuropsychiatric syndrome characterized by motor and behavioral signs that can manifest due to neurologic, psychiatric, and/or general medical conditions. Studies found the prevalence of catatonia to be 5%–18% on inpatient psychiatric units and 1.6%–1.8% on psychiatry consultation-liaison services. When catatonia occurs during pregnancy, swift recognition and treatment is necessary for the safety of the pregnant woman and the fetus. Here we present a case of a woman who developed catatonia during labor. Case History: A 28-year-old G1P0 woman without known psychiatric or medical history presented at full-term to the hospital following membrane rupture. Psychiatry was consulted immediately when the obstetrics team found the patient unresponsive and not following commands. She had mild tachycardia, with vitals and laboratory studies otherwise unremarkable. On examination, she displayed withdrawal, mutism, immobility/stupor, and staring, without noted rigidity or catalepsy. She received lorazepam 1 mg IV twice, after which she spoke one-word answers. The following morning, the patient was alert and had a safe forceps-assisted vaginal delivery, receiving lorazepam 3 mg IV total in divided doses throughout delivery. She continued to display flat affect and reported delusion of another baby still inside her. Once medically stable, the patient was admitted to inpatient psychiatry for further stabilization. Conclusion: Although literature exists on peripartum catatonia, to our knowledge, this is the first reported case of initial presentation of catatonia during labor. This case highlights the importance of rapid recognition and treatment of catatonia, with the goal of the mother’s active participation for safe delivery.

Background: In recent years, there has been increasing interest in heritable/genetic causes of mental health problems. New techniques with gene sequencing and screening have allowed case reports to be written about a variety of genes, though there have been no definitive candidate genes isolated. Case Summary: In this poster, we present a case report of a patient with a novel mutation in SLC6A1, a gene that regulates the reuptake of GABA from the synapse. This mutation was found to likely be autosomal dominant; the patient passed it along to her daughter, who also had problems with developmental delay and autism. The mutation was found after the daughter was tested, given her family history and clinical course. Conclusion: This gene has been associated with seizure disorder and autism. However, in this patient’s case, she has severe problems with psychosis. This has recently been proposed as a gene responsible for psychosis in molecular psychiatry literature. This family provides real life replication of these findings and demonstrates the heritability of these symptoms.

Background: Catatonia is a motor dysregulation syndrome associated with dysfunction in fronto-cortico-striato-thalamic circuits and has been seen in pathology affecting the basal ganglia. Metabolic derangements, including hyperammonemia, have been associated with bilateral signal intensities of the basal ganglia. Here we present a case of a patient with catatonia associated with bilateral globi pallidi hyperintensities on MRI. Case History: A 27-year-old male with classical Hodgkin lymphoma, complicated by hemophagocytic lymphohistiocytosis, and no prior psychiatric history presented initially with hallucinations, confusion, and neck pain. Extensive infectious, toxic, and metabolic workup was remarkable for hyperammonemia of uncertain etiology with new bilateral globi pallidi FLAIR hyperintensities on MRI. The patient became progressively emotionally labile, impulsive, and disorganized, with an examination demonstrating stereotypies, echolalia, verbigeration, and automatic obedience consistent with catatonia. He subsequently responded positively to a lorazepam challenge and ultimately had significant improvement in mental status with scheduled benzodiazepines despite persistent hyperammonemia. Conclusions: This report describes a possible case of catatonia precipitated by hyperammonemia, with corresponding bilateral basal ganglia hyperintensities on MRI, in a patient with no psychiatric history. Further research exploring the relationship between such clinical presentations and imaging findings may help clarify the pathophysiology of catatonia.

Background: Seizure-like events are common manifestations of functional neurologic disorder (FND-seizures). Although traditionally associated with psychological precipitants, neurological disorders may trigger FND-seizures. Babinski described four cases of FND symptoms linked to migraine in 1890. More than a century later, the neurobiological basis of this relationship is poorly elucidated. Objective: 1) Complete a systematic review of potential associations between migraine and FND-seizures. 2) Conduct a retrospective study of patients with migraine and FND-seizures, including response to migraine prophylaxis. Methods: 1) Using PRISMA methods, we completed a systematic review of EMBASE and Scopus databases from inception to March 31, 2021, for literature on migraine and FND-seizures. 2) Our multi-disciplinary team, including subspecialists in psychosomatic medicine, epilepsy, and headache disorders, reviewed consecutive patients diagnosed with migraine and FND-seizures to assess potential causal associations and response to migraine prophylactic medications. Results: 1) We retained six studies from 125 screened manuscripts (N=1,170 patients with FND-seizures; mean age 38.7 years; 72.6% female). All found associations between migraine and FND-seizures compared with epileptic seizures, but provided limited information on treatment response. 2) Our subspecialists reached unanimous consensus that migraine triggered FND-seizures in 29/43 (73%) patients in our series (mean age, 38.8 years; 74% female); 19/26 (73%) patients with adequate follow-up data showed concomitant reductions (>50%) in headache and FND-seizure frequency on treatment with migraine prophylactic medications alone. Conclusion: Data from published reports and our case series suggest an association between migraine and FND-seizures, which may respond to migraine prophylaxis. Fully-powered prospective investigations are needed to validate these observations.

Background: The Neurobehavioral Symptom Inventory (NSI) assesses persisting symptoms among persons with mild traumatic brain injury (TBI), including Veterans. Validity of the NSI and its factor structure depends upon the population to which it is applied. Objective: This study examined the Vanderploeg et al. (2015) NSI four-factor structure in a predominantly Veteran cohort in an intensive outpatient program (IOP) for persisting symptoms after mild TBI and co-occurring psychological health conditions at the Marcus Institute for Brain Health (MIBH). Methods: Consecutively evaluated patients at MIBH between 2017 and 2022 with chronic mild TBI (>6 months post-injury) as identified with the Ohio State University TBI Identification Method were included in the present analyses. Demographic and clinical data were extracted from the program evaluation record. NSI total and factor scores (Cognitive, Emotional, Sensory/Somatic, Vestibular) were calculated at IOP admission and discharge for the entire study group and validation subgroups. Results: The cohort included 149 patients (134 men, 15 women; 143 Veterans) age 42.0±8.9 years with a modal education of 12–16 years (modal N=112). Mean total NSI score=45.1±14.1. The four-factor structure robustly modeled NSI scores at IOP admission and discharge in the entire study group and the validation subgroups. Patients whose NSI was obtained at IOP admission and had Validity-10 scores ≤22 were identified as the index cohort for future assessment of IOP efficacy and durability. Conclusion: Persisting symptoms after mild TBI and IOP-related changes in patients receiving care at MIBH are modelled well by the Vanderploeg et al. (2015) NSI four-factor structure.

Background: McLeod syndrome is a rare X-linked neuroacanthocytosis disorder specifically affecting the XK gene and results in the development of movement disorders, neuropathy, psychiatric symptoms, neurocognitive deficits, and seizures. These symptoms typically present in adulthood and progress into more severe neuropsychiatric symptoms such as epilepsy and dementia. A paucity of research exists with only several hundred case reports of patients diagnosed with this syndrome. No case reports exist that report post-surgical complications secondary to choreiform movement or impulsive behavior in patients with McLeod Syndrome. How can physicians successfully treat these symptoms in this rare disease? Case History: A 66-year-old Caucasian man with a history of McLeod syndrome, epilepsy, hypertension, hypothyroidism, mild spinal stenosis, and multiple hip and knee replacements underwent above-the-knee amputation following a left femoral fracture following a fall at home. Impulsive removal of surgical dressings and involuntary choreiform movements complicated recovery and placed the patient at greater risk of postoperative infection and falling. We review his neuropsychiatric history, imaging studies, and previous medications trials. We discuss treatment with first- and second-generation antipsychotics as well as a benzodiazepine. Conclusions: This case illustrates many of the key features of McLeod syndrome and previously unreported post-surgical complications secondary to impulsivity and choreiform movements. Furthermore, haloperidol did not appear to reduce symptoms. Atypical antipsychotics may be more useful to reduce impulsivity and choreiform movements due to antidopaminergic and serotonergic properties.

Introduction: Chronic Traumatic Encephalopathy (CTE) is a debilitating neurodegenerative disease, which is often the sequelae of repetitive head trauma. Although the definitive diagnosis of CTE is made postmortem, there are proposed clinical algorithms aimed at identifying characteristic features of CTE, based on a combination of clinical history, serum, cerebrospinal fluid (CSF) and neuroimaging biomarkers. There are promising new advances in PET neuroimaging, including tau specific ligands, which will potentially provide a robust assessment as well as an exploratory tool of the disease semiology and progression. Case Report: Here is a unique case of an ex-football player, who suffered multiple prior traumatic brain injuries (TBIs) throughout his career, and presented to our clinic with significant episodic memory, visuospatial and executive functioning deficits, as well as comorbid mood and behavioral changes in the absence of prior psychiatric history or substance use. His clinical presentation and biomarkers were consistent with a suspected diagnosis of CTE comorbid with AD, which comprises a significant portion of overall CTE cases. Conclusion: This case report presents a patient with a subtle case of dementia, which could be easily mistaken for behavioral variant frontotemporal dementia (bvFTD) or primary progressive aphasia (PPA). This in turn highlights the importance of detailed longitudinal history taking, as well as rigorous biomarker studies.

Background: White matter in the human brain occupies roughly the same volume as the gray matter, but has received far less attention in behavioral neurology and related disciplines. In particular, the cerebral cortex has dominated thinking about the organization of brain-behavior relationships, and subcortical structures, most notably the white matter, have been accorded limited neuroscientific study. Objective: To examine the background and development of corticocentrism, particularly as it impacts the study of white matter. Methods: A focused literature review was conducted to consider the origin and present status of the corticocentric bias, and how emerging investigation impacts this issue. Results: The influence of corticocentrism can be explained by several factors, including historical precedent in neurology strongly emphasizing the importance of the cortex, a preponderance of available investigative methods that selectively target this structure, and a misunderstanding of comparative neuroanatomic data gathered from normal brains that overstates cortical volume compared to that of the white matter. Neuroscientific developments have recently begun to redress this bias, and considerable progress is evident in the study of white matter. Conclusion: Corticocentrism has exerted a powerful impact in thinking about brain-behavior-relationships. Recent years have witnessed heightened focus on white matter, however, promising to expand knowledge of the normal brain and improve understanding of many neurologic and psychiatric disorders. A complete appreciation of brain-behavior relationships requires an understanding not only of the outermost layer of the cerebral hemispheres, but also white matter connectivity that links gray matter regions into distributed neural networks subserving cognition and emotion.

Background: The cellular and molecular pathogenesis of obsessive-compulsive disorder (OCD) is largely unknown, but brain imaging studies have suggested that hyperactivity in decision-making regions of the brain, specifically the orbitofrontal cortex (OFC), is associated with OCD symptoms. Recent work has shown significant differences in the expression of excitatory genes in human patients with OCD compared to unaffected comparison subjects. Based on these studies, we predicted these transcriptional alterations may have an impact on dendritic spine architecture. Objective: Therefore, our objective is to measure the dendritic spine density in OFC of individuals with OCD and compare to matched unaffected comparison subjects (N=11). Methods: Dendritic spines were measured by staining with a combination of spinophillin and phalloidin in tissue sections of OFC using confocal microscopy. Furthermore, the gray matter was divided into layers I–VI, and dendritic spine density was measured within each layer. Additionally, given the importance of spine morphology in its function, we calculated the differences in spine density among varying spine sizes between OCD individuals and healthy controls. Results: Together, we were able to measure layer and size-specific dendritic spine density changes in post-mortem samples of individuals with OCD. We found a decrease in overall dendritic spine density in individuals with OCD. Interestingly, there did not appear to be any specificity for this effect in different cortical layers, or among different spine sizes. Conclusion: From these experiments, we were able to determine the nature of changes to dendric spine density in post-mortem human brain tissue among individuals with OCD.

Background: Neuroscience-based patient education has become an evidence-based strategy for chronic pain conditions (1). Advances in the neuroscience of functional neurological disorder (FND) may allow for similar approaches to be developed and disseminated to clinicians, given the public health need for greater provider awareness and expertise around the condition (2). Objective: We developed an online multimedia module for clinicians on delivering neuroscience-based psychoeducation for FND. This quality improvement project tested whether this online intervention would be associated with changes in clinician perception of FND patients and knowledge about the condition. Methods: The online intervention was developed based on multidisciplinary feedback and includes an eight-minute scripted video modeling neuroscience-informed diagnosis delivery. Pre- and post-intervention survey data was collected from participants including self-assessment of FND-related perceptions and knowledge, as well as multiple-choice assessment of neuroscience content retention. Paired t tests and McNemar’s tests were used for statistical analysis (p<0.05). Results: Forty participants provided complete pre- and post-intervention data out of 103 submitted surveys. Self-assessment items showed significantly greater comfort with diagnosis delivery and treatment options (p<0.01), as well as decreased stigma towards FND patients following the intervention (p<0.01). Percentage of correct responses significantly increased on a multiple-choice assessment of the functional neuroanatomy of FND (p<0.01). Conclusion: An online neuroscience-based educational intervention was effective for increasing clinician knowledge about FND as well as comfort with diagnosis delivery and treatment options. Web-based formats may be a viable and cost-effective approach to disseminating neuroscience-based patient education strategies to clinicians.

Background: Though hippocampal volume reduction is a pathological hallmark of schizophrenia, the molecular pathway(s) responsible for this degeneration remains unknown. Recent reports have suggested the potential role of impaired blood-brain barrier (BBB) function in schizophrenia pathogenesis. However, direct evidence demonstrating an impaired BBB function is missing. Objective: To measure BBB leakage of the hippocampus and surrounding temporal cortex in schizophrenia patients and compare with controls. Method: Postmortem human hippocampus sections (N=27 controls, N=25 SSD) were obtained from the NIH NeuroBioBank and Maryland Brain Collection, that were age, gender, race, and postmortem interval frequency-matched. Leakage phenomena was observed using a secondary IgG-only (Vector Laboratories, 1:250) staining technique, to demonstrate endogenous IgG extravasation, a marker of BBB compromise. IgG leak was quantified using unbiased stereology (MBF Bioscience, VT). Analyses was corrected for multiple comparisons using false discovery rate with q<0.05 where applicable. Results: A significantly higher incidence of IgG leak in schizophrenia patients compared to controls (t₅₀=2.8, p<0.008). Further, BBB permeability was significantly higher in old schizophrenia patients compared to controls (t₃₉=2.5, p<0.01). Male schizophrenia patients also demonstrated a significant increase in IgG permeability compared to control males (t₅₁=2.7, p<0.009). The extravasated IgGs also demonstrated selective immunoreactivity for neurons in distinct hippocampal compartments and neuronal subpopulations of cell types. Conclusion: A significantly higher incidence of sIgG leak was shown in schizophrenia patients compared to controls. Extravasated sIgGs also demonstrated selective immunoreactivity for neurons. We suggest that BBB dysfunction and sIgG autoantibodies could be two key missing pathoetiological links underwriting schizophrenia hippocampal damage.

Background: Catatonia is an understudied complex neuropsychiatric syndrome which can occur as a standalone syndrome, but is more commonly associated with general medical/neurological diseases and psychiatric illnesses. Certain medications, substances of abuse, and withdrawal states may also lead to catatonia. Benzodiazepines (BZD) and electroconvulsive therapy are the mainstay of treatment. Akin to delirium, treating the underlying cause is crucial. Infrequently, catatonic illness may acquire BZD-dependence, analogous to steroid-dependent nephrotic syndrome, that is distinct from catatonia occurring initially in the context of substance-use withdrawal. A PubMed search (since its inception) for the term “Catatonia” returned 3,626 hits, while “Recurrent Catatonia” had only 133 hits. Here, we describe two cases of BZD-dependent recurrent catatonia and review the existing literature on this rare entity. Case History: Two elderly gentlemen presented to our neuropsychiatry clinic for the management of recurrent catatonia, characterized by mutism, negativism, and refusal to eat, with episodes triggered by BZD taper attempts following sustained symptom remission. Both the patients had comorbid mood symptoms, but lacked any history of psychotic symptoms, substance use, or family history of psychiatric illness. Comprehensive medical work-up was negative. Risk of falls and cognitive side effects was high in both. Conclusions: This case series highlights the dilemma faced in managing frail, elderly patients with BZD-dependent Recurrent Catatonia. It also emphasizes that this entity should not be confused with Periodic Catatonia or Catatonia secondary to substance use withdrawal. Systematic studies are required to characterize and understand this enigmatic phenomenon.

Background: Peduncular hallucinosis (PH) is a rare cause of visual hallucinations following injury to brainstem structures, thalamic nuclei, and the basal ganglia. First described by Lhermitte in 1922, PH is characterized by vivid, well-formed hallucinations that are usually ego-dystonic. PH is well-documented in adults, much less in children. As often occurs in pediatric neuropsychiatry, the child’s psychiatric presentation and course are influenced by features of their developmental level and stage of life. We present a case of PH in an adolescent with stroke whose developmental stage and psychological features markedly impacted his hallucination presentation, leading to diagnostic confusion yet developmentally-focused treatment opportunities. Case History: A 15-year-old male with left MCA stroke from focal cerebral arteriopathy at age 13 years presented with worsening visual hallucinations. Hallucinations initially developed several months post-stroke, at which time he described seeing shapes, animals, and figures he could identify as unreal. He then began seeing ghosts. With interests in superheroes and horror consistent with his age, he began to view his ability to see ghosts as “a super-power.” Over time, however, these experiences progressively became agitating and upsetting. Treatment included extensive psychoeducation, moratoria on certain media content, and fluoxetine. While hallucinations persisted, they ceased being distressing except following viewing certain YouTube videos. Conclusion: While PH is usually considered ego-dystonic and many patients have intact reality testing, important features of normal childhood development, such as media content intake, can impact interpretation of presumed neurological phenomena, complicating diagnosis and treatment of classic neuropsychiatric syndromes in children.

Background: Sleep disturbances are common in neuropsychiatric disease. Sleep derangement is a known symptom of autoimmune encephalitis, particularly anti-NMDAR and anti-IgLON5 encephalitis. Anxiety and insomnia are frequently reported as early symptoms before the eventual development of psychosis, autonomic instability, and catatonia in anti-NMDAR encephalitis. Hypersomnia and confusional arousals are typically noted later in the course of disease. Suicidality is less frequently described as a presenting symptom in autoimmune encephalitis. We report a case of a confusional arousal associated suicide attempt as the presenting symptom of anti-NMDAR encephalitis. Case History: A 57-year-old woman presented to the emergency department after a suicide attempt by overdose. On assessment, she described feeling compelled to kill herself after experiencing a sleep-wake junction misperception in which her husband had died. Additional history was notable for a 6-week subacute neuropsychiatric course marked by insomnia, confusion, and auditory hallucinations. Examination revealed deficits in memory, attention, and executive function, speech changes, paraphasic errors, gait disturbance, and hyperreflexia. Toxic-metabolic-infectious evaluation was unremarkable. EEG demonstrated diffuse slowing. CSF was notable for elevated oligoclonal bands and 14-3-3 protein - autoimmune panel was sent. Her course was complicated by catatonia. History, examination, and course drove empiric initiation of steroids. CSF autoimmune panel returned positive for anti-NMDAR antibodies. Additional immune therapies were initiated. Conclusion: Sleep disturbances are increasing recognized as a feature of autoimmune encephalitis. Suicidality is a less common presenting symptom of autoimmune encephalitis. This case of sleep disorder related suicidality supports improved screening for sleep derangement and suicidality in auto-immune encephalitis.

Background: Deletions and duplications of the 15q11-13 chromosomal region are known to cause neurodevelopmental syndromes including Prader-Willi and Angelman syndromes. In addition, maternal 15q11-13 duplication syndrome (maternal dup15q) is a genetic disorder thought to be caused by overexpression of maternally inherited genes in the 15q11-13 region and is characterized by intellectual disability, autism spectrum disorder (ASD), and epilepsy. While psychiatric comorbidities such as mood disorder have been reported with maternal dup15q, there have been no reports of catatonia. We offer a case report of a patient with maternal dup15q treated with electroconvulsive therapy (ECT) for catatonia with severe features. Case History: Patient with known maternal dup15q presented with sudden onset withdrawal, rigidity, and mutism consistent with catatonia in the months following carbamazepine discontinuation. The patient was previously ambulatory and interactive on a regimen of lamotrigine and valproate for epilepsy and carbamazepine for bipolar disorder. Catatonic features showed minimal improvement on high dose benzodiazepine treatment, with progressive clinical deterioration until initiation of ECT. The patient is currently returning to verbal and motor baseline with continued ECT, with sustained remission of mood symptoms after reinitiation of carbamazepine. Conclusion: To our knowledge, this case is the first report of catatonia in a patient with maternal dup15q. Notably, the catatonia symptoms were life threatening and refractory to standard pharmacologic treatment but responsive to ECT. This case expands our clinical knowledge of maternal dup15q and sheds light on areas of interest in severe catatonia.

Background: Rapidly progressive dementia (RPD) can include treatable conditions, and the recognition of patients with such an etiology is critically important. Non-convulsive status epilepticus (NCSE) is one such potential etiology that requires a high index of suspicion for accurate diagnosis. We present a complex case of RPD that highlights the relevance of thorough and systematic approach to the evaluation of RPD and of recognizing neuropsychiatric abnormalities along the ictal to postictal spectrum. Case History: A 60-year-old right-handed woman with a medical history of temporal lobe epilepsy, not on anti-seizure medications presented with rapidly progressive cognitive decline. Initial symptoms were described as compulsive behaviors, leading to a referral to psychiatry, which progressed over 6 months to persistent inability to complete ADLs prompting an evaluation for an RPD. MRI found known left hippocampal sclerosis, and CSF analysis was normal. An initial routine EEG was unrevealing, requiring ambulatory monitoring, which found abrupt onset rhythmical slowing associated with behavioral change concerning for non-convulsive status epilepticus, requiring admission to an Epilepsy Monitoring Unit (EMU). Symptoms improved with treatment of seizures, but total improvement was only seen with initiation of lorazepam for post-ictal catatonia. Conclusion: We present a case of RPD due to NCSE and associated postictal psychosis and catatonia. In patients with a known history of epilepsy, particularly those with recent medication changes, a high index of suspicion is necessary to capture subclinical seizures. Neuropsychiatric manifestations may be the primary expression of postictal symptoms and can present as a reversible RPD.

Background: Despite the important role of written language in everyday life, abnormalities in functional written communication have been sparsely investigated in Primary Progressive Aphasia (PPA). Objective: We analyzed written functional communication between PPA variants: nonfluent (nfvPPA), semantic (svPPA), and logopenic (lvPPA); as well as a comparison between written and spoken communication. Methods: We developed a Python program to quantify content units (CU) and total utterances in language samples. We analyzed written descriptions of the WAB Picnic scene, based on a pre-defined CU corpus, from a cohort with 95 participants (20 controls, 28 nfvPPA, 30 lvPPA, 17 svPPA). Results: One-way ANOVAs revealed patients with lvPPA and svPPA wrote fewer CU than controls (mean±SD 11.97±7.87 and 10±4.5, vs. 18.5±9.32) (F(3, 91)=[4.897], p=0.003). There was a trend towards a decrease in CU in nfvPPA (13.89±6.33) (p=0.144). Patients with all PPA subtypes (nfvPPA 34.64±18.89; lvPPA 38±24.54; svPPA 28.88±20.36) wrote fewer total utterances than controls (61.7±27.86) (F(3, 91)=[7.778], p<0.001). The CU/utterance ratio was higher in nfvPPA and svPPA than controls and lvPPA (0.42±0.14 and 0.43±0.22 vs. 0.3±0.05 and 0.32±0.12 respectively) (F(3, 91)=[5.592], p=0.001). The CU/utterance ratio was higher in written than spoken language for all groups (Two-way ANOVA F(3, 86)=[9.46], p<0.001). Patients with nfvPPA and lvPPA followed consistent patterns in written and spoken language, which was not the case for patients with svPPA. Conclusion: We found differences in written language between the PPA variants, with varying production of CU and utterances. Deficits and coping mechanisms may differ in written from spoken language in svPPA.

Background: There are numerous secondary causes of neuropsychiatric symptoms, including infections and stroke. Some infections can also cause stroke. We present a case of new-onset psychosis in a patient found to have Bartonella endocarditis and a thalamic stroke. We review the literature related to these two rare causes of neuropsychiatric symptoms. Case History: A 49-year-old right-handed female with a history of poorly-controlled hypertension presented with a delusion of pregnancy. Mental status evaluation was notable for impaired concentration, delusions, and auditory and visual hallucinations. She scored 15/30 on a Mini-Mental Status Examination. MRI revealed an acute left medial thalamic stroke. A transthoracic echocardiogram showed an aortic valve vegetation. Blood cultures were negative, but serological findings for Bartonella quintana were indicative of active infection. She was treated with antipsychotics with minimal improvement. Cognition and thought content started to improve after initiation of antibiotics. Left thalamic strokes can infrequently cause psychosis. This is thought to be caused by damage to the thalamic reticular nucleus causing hallucinations. Psychosis may also be seen after strokes in the right hemisphere involving regions connected to the limbic cortex. Bartonella bacteremia can rarely cause endocarditis and stroke. It has also been linked more directly to neuropsychiatric symptoms—memory loss, language dysfunction, and delusions—even in the absence of overt stroke or abscess. Conclusion: This case highlights a patient with neuropsychiatric symptoms potentially due to two rare overlapping etiologies: post-stroke psychosis and Bartonella bacteremia. Clinicians must have a broad differential when assessing new onset psychosis.

Background: Fahr’s disease is a rare neurodegenerative disorder characterized by idiopathic basal ganglia calcifications which manifests in various neurologic and psychiatric symptoms such as seizures, movement disorders, cognitive symptoms, and psychosis. Management of the psychiatric symptoms, particularly psychosis, is not well described and there is a dearth of research on this subject. A PubMed search for “Fahr’s Disease” and “psychosis” yields only 26 results, with the majority being case reports. There is little consensus on treatment, thus medication classes and dosages have varied greatly, generally favoring low-dose neuroleptics. We present a case of Fahr’s psychosis that required greater neuroleptic dosage and potency than previously described in the literature to achieve remission of psychotic symptoms. Case History: A 43-year-old Caucasian male with history of psychosis, intellectual disability, and seizures presented with worsening auditory and visual hallucinations, disorganization, hypersexuality, intrusiveness, and speech perseveration. Careful review of this patient’s history, including MRI and EEG, supported a diagnosis of Fahr’s disease. He was treated on the inpatient psychiatric unit with high-dose olanzapine. We review the clinical features and diagnostic criterion of Fahr’s disease. Conclusions: This case illustrates the importance of awareness of Fahr’s disease as a rare etiology of psychosis. Uniquely, this case illustrates the tolerability and occasional need for higher-dose antipsychotics in the management of Fahr’s psychosis. Research is needed to further guide ideal pharmacological management of patients with Fahr’s disease.

Introduction: We aim to describe a novel case about a patient with schizoaffective disorder who presented for behavioral changes. After ruling out secondary causes, he was found to have a restricted lesion in the splenium of the corpus callosum (SCC) that resolved after 1 month, coinciding with his return to baseline. Case History: We report a case of a 47-year-old man with schizoaffective disorder who presented for delirium with episodes of inappropriate behavior. He was maintained on Haloperidol, diazepam, promethazine, and lithium; the last two replaced by valproid acid and olanzapine upon admission. We were able to rule out neuroleptic malignant syndrome by a negative dantrolene trial. All secondary causes were ruled out with an extensive infectious/inflammatory and rheumatologic screen, including a lumbar puncture done twice. MRI and MRA of the brain done showed restricted diffusion and faint FLAIR signal in the SCC with severely diseased vessels raising the possibility of CNS vasculitis. Digital subtraction angiography however was negative for vasculitis. Repeat MRI of the brain 1 month later showed complete resolution of the callosal lesion with improvement of patients’ symptoms back to baseline. Conclusion: This is the first case report of reversible splenial lesion syndrome (RESLS) in a patient with schizoaffective disease presenting with altered mental status and found to have a transient splenial lesion with symptoms resolution after 1 month. Therefore, RESLS should be included in the differential diagnosis of patients with known psychiatric disease on treatment presenting with delirium especially in the setting of poly-pharmacotherapy.

Background: We present the hardship of neurology residents at AUBMC during the raging COVID 19 pandemic, Lebanon GDP downfall and the crumbling health care system topped by the worst explosion in recent world history of Beirut Port in August 2020. Content: Educational Experience: Until 2020, the neurology residency training at AUBMC was the only accredited ACGME-I program worldwide enrolling nine residents. The outpatient experience covered 10 clinics soon dropped to five clinics with specialists’ brain drain. The inpatient service world-renowned for its stroke, multiple sclerosis, epilepsy, and neuromuscular teams suffered the most with patients unable to afford costs or avoiding the hospital fearing COVID. Neurology residents’ duties shifted to COVID floors with hectic work hours. Ordering COVID PCR in CSF became the norm; previously healthy adults presented with embolic strokes. Research projects halted. Senior residents filled the mentoring gap, established case discussions and core curriculum reviews weekly and biweekly reading assignments. Then came the blast! Neurology residents were called to evaluate trauma, suture wounds, and stabilize fractures or discharge floor patients to increase capacity for trauma victims. For weeks treating traumatic brain injury and prognosticating for brain death were priority. Moral injury was huge and long-lasting. With the responsibility to serve and bring hope came exhaustion and anger. Emotional numbing sat in with survival rooted in robotic daily activities. Conclusion: The world quickly forgets suffering. No, it is not business as usual! For this period, we need to evaluate what truly happened to educational journeys in training programs everywhere.

Background: Sural nerve conduction studies are crucial in diagnosing disorders of the peripheral nervous system. Multiple factors, such as age and gender, may affect its responses. A consensus in the Middle East region seems lacking when it comes to its normative data, specifically in elderly population. Objective: We aim to explore the effect of age, gender and diabetes mellitus on sural nerve conduction study parameters in a sample of Lebanese subjects. Methods: This is a retrospective chart review study of older subjects (>50 years), done at the American university of Beirut Medical Center, Beirut, Lebanon. Sural nerve conduction study parameters were gathered and compared between different age groups, genders and diabetic subjects. Results: 480 patients were included (276 healthy, 204 diabetics). We found that sural sensory nerve action potential amplitude decreases with age (17.4 µv in 50–59 years vs. 8.94 µv in ≥80 years), peak latency increases (3.19 ms in 50–59 years vs. 3.47 in ≥80 years) and conduction velocity gets slower (54 m/s in 50–59 years, vs. 48.85 m/s in ≥80 years). Diabetic subjects compared to healthy ones had a lower sensory nerve action potential amplitude (14.19 µV vs. 9.16 µV), longer peak latencies (3.27 ms vs. 3.50 ms), and slower conduction velocities (52.24 m/s vs. 50.51 m/s). Conclusion: Sural nerve conduction study parameters differ in reflection to age, gender and both the chronicity and burden of diabetes.

Background: People with functional seizures have complex etiologies and benefit from specialized mental health (MH) care. Access to and utilization of psychotherapy is not characterized in the Veterans Administration (VA), a national health care system with robust MH focus. Objective: In this retrospective cohort study, we examined psychotherapy access and utilization after a diagnosis of functional seizure. Methods: Veterans diagnosed with functional seizures between 2002 and 2018 were identified from the national VA electronic health record. We reviewed psychotherapy engagement, treatment setting, drop out and treatment modalities used. Results: Of the 1,032 veterans diagnosed with functional seizures and known treatment status, the median time from first documented seizure to diagnosis was 39.3 months (range 0–394). After diagnosis, 67% engaged in psychotherapy within a median of 1.5 months (range 0–89.2). Approximately, 95% were treated by MH staff, 88% in an individual setting and 48% dropped out of treatment. In 65% of cases, two or more indications were cited for psychotherapy, with functional seizure as the primary indication in 13% of cases. Only 37% had documented cognitively informed therapy (cognitive behavioral therapy or cognitive processing therapy), all others had supportive therapy. Conclusion: In a national cohort of Veterans diagnosed with functional seizures, a majority started psychotherapy after diagnosis, however, most were treated for other indications. A minority received treatment based on cognitively informed or specialized therapy. We identified gaps in the delivery of evidence-based treatment for functional seizures in the VA. Future analysis will assess seizure outcomes and health care utilization associated with treatment.

Background: Reports of patients presenting with an amnestic syndrome after opioid overdose reversal have been steadily emerging. Yet, there is a paucity of data examining whether patients managed for opioid overdose and withdrawal receive a neuropsychiatric assessment or workup. A PubMed search did not find any articles evaluating the utility of neuropsychiatric assessment after overdose reversal. Given the main goal of management is to medically stabilize these patients for discharge, the phenomenon of opioid-associated brain injury may be missed by clinicians. This case study poses the question: could there be benefit to neuropsychiatric screening of patients after opioid reversal therapy? Case History: A 64-year-old man was found unconscious with heroin beside him. After opioid-reversal, the patient was admitted for management of opioid withdrawal and Acute Kidney Injury secondary to rhabdomyolysis. Neuropsychiatric assessment was notable for retrograde and anterograde amnesia, including most autobiographical information. Additional findings included abulia, anosognosia, docility, diminished affect, and poverty of speech. Neuroimaging showed bilateral diffusion restriction at the hippocampus and bilateral T2-FLAIR hyperintensities at the globus pallidus. The patient’s amnesia did not resolve and he was discharged to a nursing home. Conclusions: This case illustrates the importance of neuropsychiatric screening for patients with opioid intoxication. We propose clinicians conduct a brief neuropsychiatric assessment as part of their management. This recommendation has the potential to better understand opioid-related neuropsychiatric syndromes and manage the disabling deficits patients with opioid use disorders can develop over time.

Background: Neuroleptic Malignant Syndrome (NMS), Malignant Catatonia (MC) and Serotonin Syndrome (SS) are neuropsychiatric syndromes with overlapping symptomatology that manifest in encephalopathy, autonomic instability and motor findings. While exact neurobiological correlates are unknown, hypothesized pathophysiologies include aberrant neurotransmission (dopamine, GABA, glutamate, and serotonin in MC and NMS; serotonin, norepinephrine, GABA, glutamate in SS) and neurocircuitry (cortico-striatal-thalamo-cortical in MC and NMS; various cortical and subcortical structures and the spine in SS). In a patient with damage to brain regions implicated in MC, NMS and SS pathophysiology, how can each neuropsychiatric syndrome be distinguished from one another, and/or from the underlying brain injury? Case History: A 14-year-old boy with pineal gland teratoma status post debulking, left parietal-occipital junction and thalamus encephalomalacia, and residual pontine and cerebellar tumor presented after attempting suicide. His mood and dysexecutive symptoms from posterior fossa syndrome improved with fluoxetine and aripiprazole. After receiving haloperidol for agitation, he developed dysautonomia, stupor, tremor, clonus, hyperreflexia, rigidity, and opisthotonos consistent with NMS, MC and SS. After concurrent onset, NMS and MC resolved within three weeks, non-malignant catatonia persisted for 2 months, and SS resolved within 2 weeks but recurred in the third week attributed to fentanyl. Frequent exams, neuroimaging and multidisciplinary discussions were necessary in distinguishing one neuropsychiatric syndrome from another, and/or from the manifestation of tumor growth causing mass effect on the brainstem. Conclusions: This case illustrates difficulties and strategies in assessing and treating acute-on-chronic neuropsychiatric syndromes in a pediatric patient with critical illness.

Background: Anorexia nervosa (AN) is a devastating eating disorder with one of the highest mortality rates among all psychiatric illnesses. Current pharmacological treatment options demonstrate limited efficacy in treating AN. Recently, newer non-invasive neuromodulation approaches have been refined to aid in the treatment of this condition. Objective: This study summarizes the recent therapeutic approach of neural circuit manipulation with repetitive transcranial magnetic stimulation (rTMS) in the treatment of AN. Methods: A PubMed query was conducted using the search terms of (anorexia nervosa) AND (transcranial magnetic stimulation). The results were systematically evaluated by three independent researchers to determine eligibility for inclusion Results: Out of 33 results from the search terms applied, 17 primary studies were identified. Most of these studies (12 total) investigated the application of rTMS to the dorsolateral prefrontal cortex (DLPFC). rTMS to the insula and the dorsomedial prefrontal cortex (DMPFC) were examined in one and four studies, respectively. Conclusion: While rTMS has been a breakthrough therapy for some AN patients, studies have also revealed a pattern of patients for whom it is not effective. Moreover, small studies on rTMS to the DMPFC of patients with AN have shown that baseline differences in structural connectivity may influence response to rTMS. Overall, the existing literature indicates that rTMS is safe and well-tolerated, and may be an effective treatment for patients suffering from AN. However, large randomized controlled trials comparing real versus sham rTMS on various brain regions are needed to develop evidence-based recommendations to optimize outcomes for these patients.

Background: The cerebellar cognitive affective syndrome comprises symptoms of executive dysfunction, disinhibition, poor working memory and emotional regulation deficits. The hypothesis was based on the clinical findings of Chiari Malformation type 1 lesions in the posterior cerebellum and vermis. Adult ADHD displays deficits in executive functioning, poor working memory, impulsivity and impaired emotional self-regulation. ADHD symptoms are not better explained by another psychiatric or medical condition. There are case reports on Chiari Malformation and ADHD regarding overlapping symptoms. How should a clinician differentiate between these two disorders? Case History: Twelve years after Chiari Malformation type 1 decompression, a 28-year-old university student on Atomoxetine for ADHD which was diagnosed before 2009 surgery presented with worsening of neurocognitive symptoms, inability to initiate and plan for long, difficulty in recalling recent events or names, feeling of memory loss, headache, dizziness and problem with balance. MRI Brain showed some crowding at the foramen magnum with reduced CSF flow posteriorly. Atomoxetine was stopped to commence on low dose Lisdexamfetamine. Referral to the National Disability Insurance Services for community neurorehabilitation completed. Conclusion: This case illustrates the overlapping neurocognitive symptoms in the borderland of neurology and neuropsychiatry. The ADHD symptoms may be better explained by Chiari Malformation type 1 due to the presence of neurosurgical and autonomic symptoms. However, the case also demonstrates the need for ongoing stimulant medication under the State Legislation for Adult ADHD. Research is needed to operationalize the distinction of these two conditions.

Background: Plasma-derived biomarkers of Alzheimer’s disease (AD) and neuropsychiatric symptoms (NPS) are both independent risk factors for cognitive decline in old age but studies examining their association are limited. Objective: To examine the associations between plasma-derived AD and neurodegeneration biomarkers and NPS in community-dwelling older adults. Methods: We conducted a cross-sectional study in the setting of the population-based Mayo Clinic Study of Aging, including 1,005 persons aged ≥50 years (mean age 74 years, 564 males, 276 APOE ɛ4 carriers, 118 cognitively impaired). Plasma-derived biomarkers included neurofilament light, amyloid beta 40 (Aβ40) and 42 (Aβ42), phosphorylated tau181 (pTau181) and 217 (pTau217), and total tau. NPS were assessed using Neuropsychiatric Inventory Questionnaire, and Beck Depression and Anxiety Inventories. We conducted logistic regression analyses with z-scored plasma-derived biomarkers as predictors and NPS as outcomes, adjusted for age, sex, education, APOEɛ4 status and medical comorbidities. Results: We observed statistically significant associations between Aβ42 (odds ratio [95% confidence interval], 1.39 [1.01, 1.91], p=0.045), pTau181 (2.06 [1.41, 3.00], p<0.001) and pTau217 (1.7 [1.10, 2.61], p=0.016) with appetite change. Higher levels of pTau181 and pTau217 were statistically significantly associated with increased symptoms of agitation (1.93 [1.20, 3.11], p=0.007; and 2.03 [1.21, 3.42], p=0.007), delusion (2.43 [1.06, 5.54], p=0.035; and 2.49 [1.06, 5.88], p=0.037) and disinhibition (2.39 [1.45, 3.93], p=0.001; and 2.3 [1.33, 3.98], p=0.003). Conclusion: Higher plasma levels of pTau181 and pTau217 are associated with increased symptoms of appetite change, agitation, delusion and disinhibition in community-dwelling older adults. Prospective studies are needed to validate study findings.

Background: COVID-19 has been recognized to have multiple neuropsychiatric manifestations, including delirium, epilepsy, mood disorders, catatonia, and acute psychotic disturbances. NMS is characterized by hyperthermia, muscle rigidity, autonomic instability, and altered mental status. It is considered a medical emergency with high lethality due to an adverse reaction to D2 blocking medications. Although there have been some cases reporting the association between COVID-19 and NMS, all involved either starting or titrating a D2 blocker. We are reporting the first case of NMS in a patient on a previously stable dose of antipsychotics, without recent changes in medication or a previous history of psychotic spectrum disorder, precipitated by COVID-19. Case History: A 32-year-old male with history of attention deficit disorder, intellectual disability, autism spectrum disorder, and significant developmental delay presented to the emergency department with mild COVID-19 symptoms. He had been prescribed risperidone 1 mg twice daily for multiple years to prevent episodes of agitation associated with autism. After 5 days of isolation, he represented with altered mental status along with hyperpyrexia (temperature 106.4°F), cogwheeling rigidity in upper extremities, and severely elevated CK of 59,573. We review the distinguishing clinical features of NMS, possible pathophysiological mechanisms relating to COVID-19, and treatment based on current clinical guidelines. Conclusion: Given the potential lethality, it is of paramount importance to recognize NMS early, even in patients who may be using stable and low dose antipsychotics. This case adds NMS to the growing literature of acute neuropsychiatric complications of COVID-19.

Background: Primary lateral sclerosis (PLS) is a neurodegenerative upper motor neuron (UMN) disease. PLS is comparatively rare to amyotrophic lateral sclerosis (ALS) which involves upper and lower motor neurons. Prion-like aggregations of TDP-43 proteins has been described in neurodegenerative disorders including ALS, PLS, and chronic traumatic encephalopathy (CTE). The relationship between CTE and sporadic ALS is under ongoing investigation and is often referred to as CTE-ALS. Given the similarities between ALS and PLS, is there any correlation between CTE and PLS? Case History: A 46-year-old male with clinically presumed CTE and chronic muscle weakness was admitted to a state psychiatric hospital for worsening aggression. During his prolonged hospitalization, he continued to have sub-acute progression of chronic weakness. Careful review of his history and detailed neurological examination revealed “probable” PLS. We review the PLS diagnostic criteria and distinctions from similar neurodegenerative disorders. To our knowledge, this is the first reported description of presumed CTE with PLS. Conclusion: This case highlights the diagnostic criteria for PLS and distinguishing features from other UMN diseases. The role of TDP-43 aggregations has been described in neurodegenerative disorders including ALS, PLS, and a subset of CTE. Given this overlapping pathological underpinning and the current investigations into CTE-ALS, PLS may also be a novel presentation of a subset of CTE cases. A clinical case of “CTE-PLS” has yet to be described in the literature and further research is required to assess this relationship. Lastly, psychiatrists should remain vigilant for primary neurologic conditions presenting with behavioral sequelae.

Background: Patients and care partners readily use the internet for health information and advice, which may not be accurate or evidence based. Providing education in clinical settings can be time-consuming, and not all the patient’s carers may be able to attend clinical appointments. While web-based care partner interventions have been shown to be effective, few resources conform to best practices in e-learning instructional design. Objective: Our objectives were to design, build, disseminate, and evaluate an internet-based educational platform for dementia care partners. Methods: Developed by experts in geriatrics, psychiatry, and e-learning from McMaster University in collaboration with lived-experience dementia care partners, iGeriCare is a free, open-access internet-based program that allows for care partners to access essential content about dementia from their own homes, at their own pace and to easily share the experience with family members and other care partners. iGeriCare features 12 multimedia lessons, resources, e-mail-based subscription learning, and live, online events where viewers can interact directly with experts. Results: Since July 2018, over 165,000 unique visitors have come to iGeriCare with extensive use of the lessons and videos of the live events. Web analytics, user surveys and key informant interviews were used for multimodal evaluation. Feedback has been consistently positive for all components, with visitors identifying various ways that the education is relevant, useful, and beneficial. Conclusion: The award-winning iGeriCare site provides an evidence-informed resource that can be prescribed for care partners to complement comprehensive dementia care. A blended patient and family education strategy can assist in providing high-quality, family-centered care.

Background: Post-stroke mania is an uncommon but well-documented post-stroke neuropsychiatric disorder. We present the case of a 62-year-old male with no psychiatric history who developed instantaneous hypersexuality after a right hemispheric stroke. Case History: A 62-year-old man fell at home with left sided paralysis after undergoing chiropractic cervical manipulation earlier that day. While still fallen, the patient began to caress his wife’s buttocks with his non-paralyzed right hand while she called emergency medical services. Hospital staff were amazed by his “excellent mood” during hospitalization. His hypersexuality continued after discharge. Ignoring orders to avoid strenuous activity, the patient repeatedly attempted to initiate sex while still wearing a neck brace. He also developed pressured speech and impulsive behavior, attempting to ride dirt bikes. He developed delusional jealousy, inspecting his wife’s body with a flashlight to look for any signs of infidelity. After a year, his primary care physician prescribed 5 mg of olanzapine and his mania subsided within days. The patient then developed severe depression. After various medication trials, he responded well to the combination of olanzapine, fluoxetine, and bupropion. Conclusion: What this case adds to the existing literature is the immediate onset of manic symptoms which went undetected and untreated by medical professionals for almost a year while his wife suffered. This case reinforces the importance of probing thoroughly for neuropsychiatric disorders after stroke as underrecognition will lead to undertreatment and preventable distress for the patient as well as their caregivers. It may also shed light on the neurologic pathways for mania.

Background: Ketamine has long been used to treat various chronic pain syndromes, especially those with a neuropathic component. More recently, ketamine has emerged as a promising treatment for treatment-resistant depression with transient dissociative side-effects. There have been 10 case reports of individuals developing mania after receiving ketamine IV infusions. We add to this a unique case report of a patient developing mania after oral application of topical ketamine. Case History: A 68-year-old man with a diagnosis of trigeminal neuralgia sought treatment with numerous headache specialists. Neither surgical intervention nor medical treatment with carbamazepine, oxcarbazepine, topiramate, or gabapentin proved effective. Due to intractable headaches, the patient sought care with a pain specialist who prescribed topical ketamine. This also proved ineffective. In parallel, the patient developed oral lichen planus and independently decided to use his ketamine ointment on his tongue. He soon developed classic symptoms of mania with pressured speech, auditory and visual hallucinations, impulsivity and excessive spending, and spoke with an Australian accent. During the resultant psychiatric hospitalization, his use of topical ketamine was discovered and discontinued. His mania resolved. Conclusions: Given the increasing off-label use of topical ketamine, especially in the treatment of pain, it is important for physicians to be aware of the risk of manic switch. This case also highlights the importance of performing a careful review of patients’ medication during psychiatric hospitalization.

Background: The historical records emerging from well-known anatomists, led to the canonical classification of the 12 pairs of cranial nerves as recognized today in most medical textbooks and the anatomical nomenclature. However, very little is known regarding cranial nerve zero (CN 0). This nerve has been given many names, such as nervus terminalis (NT), nerve of Pinkus, tractus olfacto-commissuralis, the new nerve, terminal nerve, nerve nulla (i.e., nothing, zero), and cranial nerve 13. Objectives: To disseminate new peer-reviewed information regarding the clinical relevance of CN 0; and to increase the level of awareness about its neuroanatomical nuance, functions, and implications in clinical neurosciences and medicine. Methods: Previously known scientific information was reviewed, summarized, and integrated with new clinical evidence regarding CN 0. There was a particular focus on areas relevant to clinical neurosciences and neuropsychiatry. The most pertinent concepts, including its neuroanatomical characteristics, neurophysiological aspects and clinical extrapolations were contextualized into graphic-rich instructional resources and neuroanatomical depictions. Results: CN 0 poses a neuromodulatory role in human reproductive behavior, via the gonadotropin releasing hormone (GnRH) and the hypothalamic “kisspeptin neural circuit.” Kisspeptin is linked to the modulation of mood, anxiety, and reward, potentially influencing various structures of the limbic and paralimbic networks. Conclusion: CN 0 is a highly functional neuroanatomical structure with important roles in the development of the GnRH system. Its connection with the hypothalamic kisspeptin neurocircuitry suggests an intricate regulatory involvement, potentially modulating the behavioral mechanisms of mood, anxiety, and reward via varied neurophysiological pathways (i.e., mesocorticolimbic).

Background: Visual hallucinations (VH) are a heterogenous and transdiagnostic phenomenon with multifaceted pathophysiology. Typically associated with neurodegenerative conditions (Parkinson’s, Charles Bonnet Syndrome, Peduncular Hallucinosis) and psychotomimetics, primary psychotic disorders (Ex: schizophrenia) can also be connected; an area believed to be under reported/diagnosed. We use this case to highlight the need for systematic approaches both diagnostically and phenomenologically to drive multidisciplinary care appropriate for a presenting symptom of VH. Case History: A 77-year-old female with a history of prior stroke, atrial fibrillation, and diabetes mellitus presented to the ED delirious, combative, and dysarthric. Neurological examination showed no focal deficits, NIHSS of 7 and use of Xarelto contraindicated thrombectomy, TPA. Neurological workup included a head CT, neurological examination, and SS which were unremarkable. She reported visual hallucinations within 24 hours, seeing a figure “steal her money” The report of perceptual disturbance and disorganized thinking and behavior was initially interpreted as a primary psychiatric symptom signaling a psych consult; however subsequent MRI revealed acute infarctions in the left temporal and lower occipital lobes—a topographical map implicating the dorsal and ventral attention networks associated with VH. The patient was discharged post-symptom remission after 12 days of conservative management. Conclusion: Visual hallucinations are a transdiagnostic symptom indicating challenging exploration and interpretation, particularly when presenting as an isolated symptom superimposed on subtle mental status changes. Careful evaluation is required to rule out multiple neurological and psychiatric etiologies.

Background: Functional neurologic disorder (FND) has a prevalence of 15% in outpatient neurologic settings and is often comorbid with primary neurologic illness. Distinguishing between functional and primary neurologic processes can be challenging. Case History: A 60-year-old woman with post-traumatic stress disorder and bipolar II presented for evaluation. After falling asleep at the wheel and crashing her car, she had experienced stuttering, depression, panic, forgetfulness, trouble operating devices, and intermittent right leg weakness. Noncontrast MRI brain was unrevealing. On examination, she was tearful, with stuttering that improved with distraction. She was able to give detailed descriptions of recent events and demonstrated normal lower extremity strength. Due to inconsistencies between her complaints and examination, a diagnosis of FND was made. Four months later, she became catatonic and was found to have a left frontal glioblastoma. Subsequent exams have not demonstrated leg weakness. Conclusions: This patient’s glioblastoma may have precipitated her car accident and cognitive symptoms. Her FND symptoms appear to have emerged in response to the car accident, or possibly due to disruptions in frontal networks caused by the incipient glioblastoma. Although this patient has several FND risk factors (female sex, trauma, a recent stressor, psychiatric comorbidities), the presence of these risk factors is not required to diagnose FND. This case highlights the importance of clinicians remaining open to primary neurologic processes in patients diagnosed with FND.

Background: Investigators report greater parietal tau deposition and alternate frontoparietal network involvement in early onset Alzheimer’s Disease (EOAD) with onset <65 years as compared with typical late onset AD (LOAD). Objective: To determine whether clinical brain MRI volumes reflect these differences in EOAD compared with LOAD. Methods: This study investigated the clinical MRI of 45 persons with Clinically Probable AD with onset <65 years and compared them to 32 with Clinically Probable AD with onset ≥65 years. Brain volumes on their T1 MRI scans were quantified with a program, called Neuroreader, that calculates percentage differences from normative scans, and regional volumes as fraction of total intracranial volume (TIV) were compared between both groups. Receiver operating characteristic (ROC) analyses were performed. Results: Persons with EOAD had significantly smaller parietal lobes (volumetric percentiles) than LOAD. They also had decreased total white matter and right pallidum, whereas, LOAD had a smaller left putamen and hippocampus among other regions. ROC analysis showed an area under the curve (AUC) of 96.5% with brain region delineation of EOAD compared to LOAD. Conclusion: When adjusted for age-related differences, MRI scans of the EOAD patients were significantly different than those for LOAD patients. EOAD patients had distinctly smaller parietal lobes, out of proportion to any other differences and consistent with increased distribution of neuropathology, particularly cortical neurofibrillary tangles, in EOAD compared to LOAD. This study indicates the presence of parietal atrophy at less than 30% of normal on clinical MRI scans is suggestive of the diagnosis of EOAD.

Background: Understanding the temporal sequence of change in cognitive and behavioral domains is important for the early detection of individuals at higher risk of developing Alzheimer’s disease (AD). Objective: To identify the temporal sequence of changes among five cognitive domains plus apathy and whether these sequences differ between men and women with a family history of AD. Methods: We examined 145 women (age=64.26±4.74) and 49 men (age=65.03±4.69) over 55 years old with a first-degree relative with AD who were followed in the longitudinal PREVENT-AD cohort at McGill University. They were examined at baseline, 24 and 48 months using the RBANS subindexes (attention, language, delayed memory, visuospatial, and immediate memory) and the apathy evaluation scale. The temporal sequence of changes in the RBANS and apathy were examined through a Lead-Lag analysis. Results: Leading variables included increased attention (lead-lag coefficient: 2.415) in women and increased attention (0.580), and decline in language (0.289) in men. Among lagging variables, increased apathy (women: –2.170, men: –1.942) preceded visuospatial decline (women: –3.550, men: –1.942) in both sexes, while an immediate memory increase lagged all variables in men (–10.724) but not in women (–2.053) where it preceded increased apathy and the visuospatial decline. Conclusion: The temporal changes in cognition are led by a clear pattern of decrease in attention, followed by changes in language and delayed memory recall in both sexes. The lagging patterns differed between men and women, with women first experiencing a decline in immediate memory recall, while men experience this element last.

Background: Caregiving for a person with developmental disorders (DD)/intellectual disability (ID) can often be a positive experience. However, negative consequences have also been described, including stress, reduced psychological well-being, poorer physical and mental health, and lower quality of life in caregivers. Objective: 1) To understand which barriers limit this community’s access to support. 2) To assess the impact of a short-term virtual support group on caregivers’ feelings of support, confidence, knowledge about the relevant DD, and prioritization of their own self-care. Methods: Caregivers of adults with DD/ID were recruited to participate in a virtual support group over the course of 4 weeks. Each group session had a specific focus and consisted of introduction of educational material, significant time for discussion, and a brief therapeutic intervention that fostered self-care. Participants (N=12) completed a pre- and post-participation survey regarding barriers to support as well as confidence, support, knowledge, and prioritization of own self-care rated on a five-point Likert scale of agreeableness. Results were converted to integers for statistical analysis. Results: Time (58%), opportunity (58%), financial restraints (50%), and transportation (42%) were the most significant barriers reported. After completion of the group, participants reported significantly increased feelings of support (p=0.001), though no change in confidence (p=0.08), knowledgeability (p=0.32), or prioritization of self-care/needs (p=1) as it relates to being a caregiver. Conclusion: Community outreach groups for caregivers of adult persons with DD/ID in a virtual format may help increase feelings of support in a way that addresses the significant barriers faced by this demographic.

Background: Catatonia is a clinical condition characterized by immobility, and withdrawal, and its prevalence is 0.6%–17% in inpatient youth. Schizophrenia is a disorder associated with delusions, hallucinations, and disorganized speech, with a lifetime prevalence of 1%, and its onset usually happens between the ages of 15 and 24 years old or later. Both schizophrenia and catatonia typically manifest in patients of adult age, much rarely in children. We highlight the case of a 12-year-old boy with both catatonia and schizophrenia in the setting of a genetic mutation. Case History: A 12-year-old boy with previously normal social and neurotypical development presented progressive cognitive decline, social withdrawal, bizarre behavior, and personality changes over 2 years. Genetic testing revealed mutations on chromosomes 2 and 3, the latter of which disrupts a single copy of the CNTN4 gene and is of uncertain clinical significance. Due to the exacerbation of his cognitive symptoms, he was diagnosed with catatonia. Treatment included benzodiazepines followed by ECT upon worsening catatonia. After starting ECT sessions, catatonia symptoms improved, and benzodiazepines were weaned, but psychotic symptoms such as paranoia, anxiety, and mood disorders manifested. He was diagnosed with an early-onset schizo-affective disorder treated with atypical antipsychotics. Conclusion: This case highlights that progressive cognitive decline in children with previous normal social and neurological development could be a prodrome of a psychotic disorder. The presence of the CNTN4 gene mutation raises the question about its implication in an uncommon presentation of catatonia and psychosis in a 12-year-old boy.

Background: Bilingualism is increasingly recognized as protective in persons at risk for Alzheimer’s disease (AD). Objective: Compare MRI measured brain volumes in matched bilinguals versus monolinguals with AD. Methods: This study analyzed T1 volumetric brain MRIs of patients with criteria-supported Probable AD. We identified 17 sequential bilinguals (any native language) with Probable AD, matched to 28 (62%) monolinguals on age and MMSE. Brain volumes were quantified with Neuroreader. Regional volumes as fraction of total intracranial volume (TIV) were compared between both groups, and Cohen’s D effect sizes were calculated for statistically significant structures. Partial correlations between bilingualism and brain volumes adjusted for age, gender, and TIV. Results: Bilinguals had higher brain volumes in 37 structures. Statistical significance (p<0.05) was observed in brainstem (t=2.33, p=0.02, Cohen’s D=0.71) and ventral diencephalon (t=3.01, p=0.004, Cohen’s D=0.91). Partial correlations showed statistical significance between bilingualism and larger volumes in brainstem (rp=0.37, p=0.01), thalamus (rp=0.31, p=0.04), ventral diencephalon (rp=0.50, p=0.001), and pallidum (rp=0.38, p=0.01). Bilingualism positively correlated with hippocampal volume, though not statistically significant (rp=0.17, p=0.26). No brain volumes were larger in monolinguals. Conclusions: Bilinguals demonstrated larger thalamic, ventral diencephalon and brainstem volumes compared to matched monolinguals with AD. This may represent a neural substrate for increased cognitive reserve in bilingualism. Future studies should extrapolate this finding into cognitively normal persons at risk for AD.

Background: Electroconvulsive therapy (ECT) is the most effective treatment for Major Depressive Disorder (MDD). Despite its clinical effectiveness, the mechanism of action of ECT remains unclear. Objective: We used diffusion tensor imaging (DTI) to evaluate the effects of ECT in the medial forebrain bundle (MFB), a prominent fiber pathway of the mesocorticolimbic system. We hypothesize that ECT would lead to variations in DTI measures in the MFB, which would correlate with a decrease in depression severity (syndromal efficacy) and anhedonia (dimensional). Methods: DTI data were acquired in 11 patients with MDD who underwent treatment with right unilateral (RUL) ECT. Depression severity was assessed with the Quick Inventory of Depressive Symptoms (QUIDS) and anhedonia with the Snaith Hamilton Pleasure Scale (SHAPS). The MFB was extracted using multi-tensor tractography. We compared fractional anisotropy (FA), radial diffusivity (RD), axial diffusivity (AD), and trace diffusivity indices before and after RUL-ECT. We also evaluated the associations between changes in DTI measures and clinical response. Results: Analysis revealed that RUL-ECT lead to a significant decrease in AD in the right MFB (t=2.81, p=0.018). We observed a significant association between greater AD decrease and improvement in depression severity (r=0.66, p=0.02), and anhedonia levels (r=0.69, p=0.018). Conclusion: RUL-ECT is associated with right-lateralized white matter neuroplastic changes in the MFB that explain the syndromal (categorical) response, as well as dimensional improvement in anhedonia. Our results suggest that therapeutic response after ECT is achieved through the modulation of pathological networks involved in mood regulation, particularly positive affect and reward pathways.

Background: The sense of self-agency (action-authorship) results from a matching of the predicted sensorimotor consequences of our actions and incoming afferent sensory information. The right temporoparietal junction (rTPJ) is involved in perceiving discrepancies between motor intentions and consequences and has been implicated in the pathophysiology of functional neurological disorder (FND). Here, we present a case of functional weakness in a patient with a chronic rTPJ stroke. Case History: A 44-year-old right-handed woman with a past medical history notable for fibromuscular dysplasia presented to a tertiary-care emergency room complaining of acute left lower extremity weakness. She was cleaning a window at work, when she suddenly felt light-headed and her left leg “went dead.” She reported anxiety regarding her financial situation and feelings of loneliness. Her neurological examination on admission was notable for a positive Hoover’s sign, inconsistent motor strength and preserved reflexes. Brain and spine MRIs were negative for an acute stroke or other pathologies, and a computed tomography angiography of the left lower extremity showed an intact vasculature. Her brain MRI did show multiple areas of chronic encephalomalacia including involvement of the right temporoparietal junction, suggestive of previous strokes. During an FND clinic visit, here symptoms had resolved with a non-focal neurological examination. A line bisection test was slightly right-lateralized, but there was otherwise no evidence of a visuospatial or sensorimotor neglect syndrome. Conclusion: Within the context of the biopsychosocial model, we formulate that the patient’s old rTPJ infarct represented a possible predisposing vulnerability for the development of FND.

Background: Traumatic brain injury (TBI) is a common disorder with complex neuropathology, and diagnosis of neurobehavioral deficits can be complicated by comorbid psychological disorders. Military veterans who have been exposed to combat are at risk for both TBI and a range of psychological disorders, and determining the contributions of these problems to the clinical picture can be challenging. Tree drawing analysis (TDA) may offer insight into these diagnostic issues and has not been systematically studied in TBI. Objective: Our goal was to examine tree drawings as a diagnostic instrument in well-characterized veterans with TBI and associated psychological disorders at the Marcus Institute for Brain Health (MIBH). Methods: A total of 102 drawings were rated from veterans (91 M; 11 F) seen consecutively at the MIBH. Ratings were conducted blindly by three independent practitioners. Both normal and abnormal tree drawing features were derived from the Diagnostic Drawing Series and the Koch Baum Tree-Drawing Test. Areas of the tree that were examined included the crown (branches and foliage), the trunk, and the roots. After discussion of each feature, a consensus rating was reached. Results: Among the 102 drawings, impairment in one or more tree areas was observed in 89%. A particularly striking finding was an abnormal tree crown in 82%. Conclusion: Impairment of tree drawing is highly prevalent among veterans with TBI and comorbid psychological disorders. Whereas further research is warranted, these preliminary observations suggest that TDA may be useful in the assessment of individuals with TBI who may also have psychological dysfunction.

Background: Women victims of interpersonal violence have increased risk of developing PTSD with greater severity, comorbidities and functional impairment which may be related to cognitive deficits. Although there is evidence of cognitive disturbances in general population with PTSD currently there are few studies in women victims of interpersonal violence. Objectives: To determine if there are cognitive deficits in women victims of interpersonal violence with PTSD and if there are differences according to severity, illness duration, comorbidities, and treatments. Methods: We included 30 patients from the National Institute of Psychiatry Mexico City and used the Neuropsi test for cognitive assessment and “symptoms severity scale for PTSD.” We excluded patients with neurologic comorbidities, psychotic, and bipolar disorders. Results: Cognitive deficits were found in 43% of patients. Alterations were found in executive function, attention, and evocative memory. There were significant differences in severity of symptoms and in patients receiving antiepileptic drugs. There were no significant differences in PTSD duration, history of traumatic brain injury, dissociative symptoms, and psychiatric comorbidities. All patients had depressive disorders. Conclusion: We found cognitive deficits in executive function, attention, and evocative memory. We found that patients receiving antiepileptic drugs and those with higher severity had increased frequency of cognitive deficits. Although all our patients had treated depressive disorders not all of them had cognitive deficits implying that depression may not be an associated factor. These findings suggest that changing severity of illness, comorbidities and pharmacological treatment could have an impact on the cognitive aspects in patients with PTSD.

Background: The Montreal Cognitive Assessment (MoCA) is a commonly used screening tool for the diagnosis of neurocognitive disorders, including mild cognitive impairment (MCI) and Alzheimer’s Disease (AD). The current threshold for detection of MCI and AD on the MoCA increases risk for false positives, particularly in ethnic minorities. It is therefore important to establish a standardized cognitive screening test independent of language and cultural norms, and to clarify cut-offs for AD plasma biomarkers in minorities. The Visual-based Cognitive Assessment Test (VCAT) is a new language-neutral cognitive screening test that is comparable to the MoCA. Objective: Our study will correlate VCAT scores to MRI brain findings and established AD plasma biomarkers in African Americans (AA) and Caucasians. Methods: Fifty AA and Caucasians with MCI, AD, and normal cognition were recruited. Plasma, CSF, and MRI brain imaging data were obtained, and the VCAT and MoCA were completed. Phosphorylated-tau 181 (p-tau 181) was measured in the samples using a Quanterix HDX device. Results: Preliminary results reveal that p-tau 181 is elevated (from a cut-off value of 1.81 pg/ml) in all patients, and highest in those with both CSF findings consistent with AD and a history of cardiovascular diseases (MI, CKD, and/or stroke). Conclusion: Established cut-off values for p-tau 181 in the literature likely underestimate these results in AA patients. In addition to elucidating the normative values for plasma AD biomarkers in a diverse cohort, our goal is to validate the VCAT, a language-neutral screening assessment. This will allow for application to multilingual populations.

Background: A subset of patients with Bipolar Disorder (BD) develop a dementia that can overlap with the features of behavioral variant Frontotemporal Dementia (bvFTD). The clinical features of this population have not yet been determined. Objective: To characterize the clinical features and course in patients with typical or early-onset BD (EOBD) and late-onset BD (LOBD) who develop dementia with frontal features. Methods: A systematic review identifying all reports of patients with BD who developed a dementia with frontal features was conducted. The sample was divided in two groups: EOBD and LOBD. Clinical features and course were analyzed using chi-square analysis. Results: Seventeen articles met the inclusion criteria from which 53 unique patients were identified; 31 patients had a history of EOBD and 20 had LOBD. Three different phenotypes of dementia were observed based on evaluation of available descriptions of the symptoms, cognitive, imaging, pathologic features, and disease course. Forty-one percent of patients developed features that met criteria for bvFTD, 6.9% had a course consistent with bvFTD phenocopy, while 51% developed a BD-frontal dementia that current lacks diagnostic criteria. Most patients with LOBD met criteria for bvFTD (60%) or bvFTD phenocopy syndrome (30%). The BD-frontal type dementia was characterized by very slow progression and frontal cognitive and behavioral dysfunction not meeting criteria for possible bvFTD. Conclusion: Three different dementia phenotypes were detected in patients with a history of BD. Specific diagnostic criteria for the BD frontal-type dementia are proposed to facilitate identification and development of future research of this phenotype.

Background: Anton Babinski Syndrome (ABS) is an uncommon condition with a limited number of case reports in the literature. It consists of cortical blindness combined with visual anosognosia and confabulation. It is essentially a neuropsychiatric disturbance usually resulting from bilateral lesions to the occipital cortex in the presence of an intact pregeniculate visual pathway, most commonly due to ischemic stroke. Case History: We present a patient with ABS and quadriplegia in the setting of delayed post- hypoxic leukoencephalopathy (DPHL). This is the case of a 26-year-old male who became comatose after an overdose with opioids, which resulted in cardiorespiratory arrest. Upon regaining consciousness, he developed cortical blindness, visual anosognosia and confabulation, in addition to quadriplegia. A few days later he developed an acute neuropsychiatric presentation with agitation, mood dysregulation, paranoia and auditory hallucinations. T2/Flair weighted images from an MRI without IV contrast showed extensive leukoencephalopathy involving both cerebral hemispheres, extending to the posterior corpus callosum. Conclusions: DPHL typically occurs after a period of prolonged cerebral anoxia. Our patient endured cerebral anoxia due to respiratory failure (anoxic anoxia) and critical hypotension (ischemic anoxia). Possible mechanisms include delayed post-hypoxic demyelination, potentially caused by a variety of mechanisms including alterations in myelin turnover and oligodendrocytes apoptosis. The presence of a disconnection syndrome may be involved in the pathogenesis of visual anosognosia and confabulation. Recovery of visual function typically will depend on the underlying etiology and response to rehabilitation. Further research is needed in the field of neuropsychiatric manifestations secondary to substance abuse.

Background: It is important to understand relationships between cognitive dysfunction and impairments in instrumental activities of daily living. Objective: We completed an exploratory investigation looking at relationships between cognitive dysfunction and impairment in daily living activities in older patients with neurocognitive disorders. Methods: Sixty-eight patients (average age=72.3 years) completed neuropsychological testing assessing for cognitive dysfunction. Patient family members completed the Functional Activities Questionnaire (FAQ) to document observed problems that the patients have in carrying out instrumental activities of daily living. Spearman correlations were calculated to examine the relationships between cognitive dysfunction and impairment in daily living activities. Results: The FAQ total score significantly correlated with only one cognitive domain: executive functioning. However, individual items from the FAQ correlated with a variety of cognitive domains. Traveling correlated with executive functioning and visuospatial skills. Financial management and delayed memory correlated. Shopping correlated with attention, executive functioning, and immediate memory. Operating basic kitchen appliances was correlated with attention, executive functioning, and visuospatial skills. Tracking of current events and immediate memory correlated. Attending to, understanding, and discussing media correlated with immediate memory, delayed memory, and executive functioning. Remembering activities and events was correlated with executive functioning and attention. Conclusion: Executive functioning is the primary cognitive domain relating to global functional ability. When looking across individual daily living activities, all were strongly correlated with all cognitive domains except the language domain. Findings suggest that neuropsychological testing might be useful for determining which functional activities are likely to be impaired in patients with neurocognitive disorders.

Background: Research has indicated that individuals with dementia can experience improved mood, reduced agitation, and increased social engagement from listening to personally enjoyable music. Objective: Our community’s Alzheimer’s Association chapter distributed MP3 players to individuals diagnosed with or suspected to have dementia living in residential care facilities. Each MP3 was loaded with music previously identified as enjoyable to that individual. The aim of this study was to examine for observed effectiveness of utilizing the MP3 music-based intervention for addressing certain neuropsychiatric symptoms. Methods: Surveys were sent to the care providers of those individuals using the MP3s. The surveys included six questions asking about the individual’s utilization of and reaction to the music-based intervention; 79 surveys were returned. Results: Nearly all (98%) care providers were satisfied or very satisfied with the intervention. Ninety-four percent reported that the individual enjoyed listening to the music; 61% of providers reported that the music was listened to at the same or increased frequency across time. Regarding mood of the individuals during the music intervention, 78% showed improved mood, 4% showed worsened mood, and 18% showed no mood change. For those with improved mood, the most frequently reported benefits were an improvement in general happiness (71%), a reduction in anxiety (68%), and an improvement in positive emotional expression (55%). Conclusion: The personalized music-based intervention was typically viewed as being beneficial by care providers and resulted in mood improvements in the majority of individuals diagnosed with or suspected of having dementia.

Background: Functional neurological disorder (FND) presents with neurological symptoms such as weakness, speech impairment, paralysis, pseudoseizures or movement problems, which don’t fit any specific neurological disorder. There have been some cases of FND post COVID-19 vaccine but there is an overall lack of published research and cases regarding this. Here we present three cases of FND post COVID-19 vaccine. Case History: Ms. A, a 38-year-old woman without significant medical history, developed acute onset thirst, headache, neck pain, palpitations, low energy, and left-sided hearing loss after COVID-19 vaccination. Symptoms abated over some months but the exercise intolerance, phonophobia, left neck and chest discomfort and “internal tremors” remained. Neurological examination, audiology testing and brain MRI were unremarkable. Her symptoms improved with education and meditation. Ms. B, a 47-year-old woman with a history of PTSD and bipolar I disorder, developed acute left sided weakness and sensory loss following her second COVID-19 vaccine. Brain MRI revealed nonspecific white matter lesions consistent with small vessel ischemia. Over the following months these symptoms abated but she reported tinnitus, facial paresthesia and dysgeusia. Ms. G, a 30-year-old woman with a history of migraines, non-epileptic seizures, possible SLE, reported acute dizziness and headache following her first COVID-19 vaccine. She also began having episodes of facial twitching, stuttering, dystonic turning of her left foot. Unremarkable brain MRI and EEG confirmed these were non-epileptic. Conclusions: These cases illustrate possible presentations of FND post COVID-19 vaccination. Vaccine’s role in the etiology of FND requires further research.

Background: Functional neurological disorder (FND) is a disorder which exhibits neurological symptoms such as weakness, speech impairment, paralysis, pseudoseizures or movement problems, but the symptoms don’t fit into any specific neurological disorder. Recently, there have been a few reports of cases of FND appearing post COVID-19 vaccination. Objective: This study aimed to review the published literature of FND post COVID-19 vaccination. Methods: A PubMed search for “covid,” “sars-cov-2,” “vaccine,” “functional neurological disorder” was done on February 11, 2022. This yielded 182 results, from which a total of seven cases from three articles were found which matched FND symptoms. Results: Six out of the seven cases presented with symptoms after the first dose. Initial symptom presentation time varied from a few minutes to 13 h post vaccine. In two cases, the symptoms appeared a few minutes after, receded and then a different set of symptoms re-emerged at a later date (ranging from next day, to a couple of weeks later). Finally, most cases had no prior pertinent medical history. Conclusion: FND is important to consider as a differential diagnosis by clinicians. As seen in the review, the symptoms typically arise from the first dose, but may spontaneously recede and reappear days or weeks later. The patients also were mostly healthy individuals. Overall, early detection will allow prompt treatment of the patients, improving outcomes. Additionally, early diagnosis and patient education will limit the misinformation spread by those experiencing symptoms (1).

Background: Catatonia has been reported as an infrequent manifestation of neuropsychiatric systemic lupus erythematosus (NPSLE) but is not formally recognized in SLE classification criteria. First-line treatment for non-malignant catatonia is benzodiazepines; ECT is recommended if catatonia persists. Limited guidance has been published for ECT treatment of catatonia in patients with preexisting epilepsy on newer antiepileptic drugs (AEDs) and/or with cerebral palsy. What must clinicians consider when catatonia develops in a patient with these neuropsychiatric comorbidities? Case History: An 18-year-old Latino man with epilepsy and cerebral palsy presented with clinical findings, lab abnormalities and imaging consistent with NPSLE. He developed catatonia 33 days into a hospitalization with BFCS scores (Bush Francis Catatonia Scale) ranging from 13 to 26 not responding to lorazepam and multiple immunomodulatory therapies. Only after 20 ECT treatments did catatonia resolve, 201 days after onset. Careful modifications to the AED regimen (perampanel, lacosamide, and midazolam PRN) were made for ECT. Conclusions: ECT for catatonia with NPSLE in a young male with comorbid epilepsy and cerebral palsy has not been described previously in the literature. Potential multifactorial causes of catatonia were considered. A recent review included 39 catatonia cases associated with NPSLE: five patients improved with immunomodulatory monotherapy; another review described 81% of cases received benzodiazepines and 38% received ECT, with session counts from 6 to 20. ECT should be prioritized in patients unresponsive to immunomodulation and benzodiazepines. It can be safely and effectively used in patients with cerebral palsy and epilepsy on AEDs, but factors such as medication half-life must be considered.

Background: Delusions and aggression can be seen in hepatic encephalopathy and mania with psychosis. While delirium is typically thought to be “organic” and mania “purely psychiatric,” both are disorders of the brain, may require treatment with medication, and may impair insight. However, the legal implications of these diagnoses differ in states where standards for involuntary treatment apply only to “purely psychiatric” conditions. Case History: A 56-year-old man with a history of alcohol-associated cirrhosis, depression and PTSD was referred for involuntary admission due to acute onset delusions and aggression causing him to pose a danger to himself and others. An outside hospital treated hepatic encephalopathy and medically cleared the patient, attributing continued symptoms to psychiatric illness. At our hospital, the patient had fluctuating levels of arousal, poor attention and visual hallucinations. Delirium due to hepatic encephalopathy was diagnosed and proceedings for involuntary treatment were deferred. Symptoms persisted after weeks of treatment for decompensated cirrhosis despite normalized ammonia levels and unremarkable EEG. Lithium was initiated and symptoms improved; tapering lithium led to worsening symptoms. A history of grandiosity, excessive spending and impulsivity was thought to possibly represent unrecognized prior hypomanic episodes. The patient was expected to require continued psychiatric medication and so a court order for treatment was pursued. Conclusions: This case illustrates the difficulty in diagnosing bipolar disorder in the setting of recent decompensated cirrhosis. This is especially true given the time and diagnostic constraints imposed by court proceedings in an involuntary setting and by limitations of objective testing.

Background: Smoking is the leading cause of preventable morbidity worldwide and therefore developing effective smoking cessation strategies is a public health priority. Currently, most studies focus on short-term effects of smoking abstinence. However, it is completely unknown what brain networks support maintenance of smoking cessation in the long-term. Objective: To identify individual differences in the brain structure and function underlying successful and sustained smoking cessation. Methods: We analyzed baseline resting-state functional magnetic resonance imaging (fMRI) data in a longitudinal cohort (PREVENT-AD) of 23 smokers (M_age=61.52±3.71; cognitively normal). Self-reported smoking status and amount were recorded at baseline and repeated after 4 years. We investigated the effect of smoking behavior change on functional brain connectivity using a seed-to-voxel approach. We examined a-priori regions of interest including the reward network (ventromedial prefrontal cortex [vMPFC] and ventral striatum [VS]) and the right insula. We hypothesized that reward valuation and self-regulation brain networks (vmPFC, VS and insula) are associated with smoking cessation behavior. Self-regulation is promising target mechanism given prior behavioral research linking it to smoking cessation. Results: Our results revealed that successful behavior change (reduced smoking) was associated with reduced connectivity between VS and middle frontal gyrus and enhanced connectivity between right insula and middle temporal gyrus (voxel p<0.001, cluster p<0.05 FDR corrected). However, change in smoking did not reveal any significant effects in the vMPFC. Conclusions: Our findings suggest that successful smoking behavior change is associated with altered reward network and insular functional connectivity in the long term.

Background: Three years into the pandemic, studies have established the presence of diverse post-acute covid infection sequelae, referred to as post-COVID 19-syndrome, or long COVID. These conditions may be multisystemic and range from mild symptoms to debilitating complaints. Psychiatric symptoms were apparent, requiring an in-depth search into this ailment. Objectives: We aim to investigate the psychiatric symptoms of post-covid-19 syndrome described in the literature. Methods: PubMed database was used. The terms included were: psychiatric illness, mental health disorders, long COVID, and persistent COVID. Studies including the child and geriatric population were disregarded to limit the search to the adult population. 306 studies were found. Results: Around 30% of patients had persistent psychiatric symptoms following acute COVID-19 infection, with anxiety being the most common diagnosis. Studies showed a high prevalence of depression and PTSD in adults with long COVID symptoms. In addition, OCD and psychotic disorders were less likely, but possible sequelae of COVID infections. Last, but not least, insomnia, cognitive disorders, loss of concentration, and fatigue were also frequent concerns. Conclusion: Psychiatric sequelae of COVID-19 infection are prevalent. Diagnosis and treatment of these symptoms are imperative to achieve full recovery. Further research is necessary for adequate treatment options.

Background: Depression is a heterogeneous illness comprised of a constellation of symptoms including cognitive and somatic clusters. Depression can present variably across individuals, and attempts to associate specific brain lesions with depressive symptoms have been inconclusive. Objective: Here we present results of the largest lesion-symptom mapping of depressive symptoms to date, focusing on unique sub-categories of depressive symptoms as opposed to depression as a single construct. Methods: 526 individuals with focal, stable brain lesions received neuroimaging and a Beck Depression Inventory-II in the chronic phase (>3 months) post-injury. Sparse canonical correlation analysis was used to identify brain lesion locations that correlated with higher or lower depressive symptom burden for individual depression items, as well as for cognitive and affective symptom sub-scales as determined by PCA and prior literature. Results: Symptoms with statistically significant correlations included sadness (r=0.113, p=0.0097), pessimism (r=0.143, p=0.000995), guilt (r=0.089, p=0.0406), self-dislike (r=0.131, p=0.00258), indecisiveness (r=0.094, p=0.0306), and concentration difficulty (r=0.098, p=0.0248), in addition to cognitive and somatic symptom subscales. Regions associated with higher depression symptom burden included the prefrontal cortices, the left dorsal cingulum, and the bilateral insula. Regions associated with lower depression symptom burden included the ventral prefrontal regions, the right anterolateral inferior temporal gyrus, the right inferior parietal lobule, and the right posterior insula. Conclusion: Some symptoms of depression have stronger associations with site-specific brain lesions than others, based on a multivariate lesion-symptom mapping approach in a large sample of subjects. Associations were stronger for cognitive as opposed to somatic symptom categories.

Background: New psychiatric symptoms in older adults should raise suspicion for underlying medical etiologies. Neurological insults like brain infarcts can cause psychiatric symptoms extremely similar to those seen in primary psychiatric illnesses. Even small infarcts in key areas of the brain can produce dramatic symptoms. For instance, case reports of infarcts in the thalamus have suggested these can lead to mania-like presentations and hallucinations in multiple modalities. Case History: A 79-year-old female with mild cognitive impairment but no other psychiatric history was hospitalized after developing new decreased need for sleep, increased goal-directed activity, agitation, and hypersexuality. She also endorsed seeing a male friend on the unit, whom she frequently attempted to engage sexually. Neurological work-up included MRI of the brain, which showed a right thalamic infarct. Interestingly, the patient’s manic symptoms resolved with treatment, but her visual hallucinations and romantic preoccupations persisted (although less hypersexual). Implications for our understanding of the thalamus and neuropsychiatric symptoms are discussed, as is our rationale for diagnosis and treatment in such circumstances. Conclusion: This interesting case strengthens the association between thalamic infarcts and mania and hallucinations (namely, peduncular hallucinosis), and adds the novel finding that, in such patients, hallucinations and some delusional preoccupations may persist even after the manic symptoms have resolved. Additionally, this report aims to help clinicians improve their diagnostic reasoning skills, including determining when to attribute symptoms to findings on imaging and when to seek other explanations. It also demonstrates the importance of being vigilant for medical causes of psychiatric symptoms.

Background: The Perception of Emotions Test (POET) can potentially be used as a biomarker for depression response, with patients with major depression particularly fast at recognizing negative faces. Transcranial Magnetic Stimulation (TMS) targets the left dorsolateral prefrontal cortex (DLPFC) in treating depression, an area of the brain important in modulating affective networks, and so may modify response time to negative faces. Objective: To assess the hypothesis that targeting the left DLPFC with TMS will show changes in response times to negative faces along with improvement in Hamilton Depression (HAMD17) scores. Methods: We assessed 12 treatment-resistant major depression patients who had left DLPFC TMS and who did the HAMD17 and POET at baseline and at the end of a standard TMS treatment course. Results: There was a trend towards significance between change in POET and HAMD17 scores using linear regression: F(1,10)=4.371, p=0.0631. With logistic regression, there was a trend towards significance between change in POET score and probability of response (at least 50% improvement) on the HAMD17: Chi-Square (1)=3.1971, p=0.0738. Three patients had at least 1 SD change in POET score, and all three were responders on the HAMD. Conclusion: There was a trend towards significance between improvement in depression and change in POET scores with left dorsolateral prefrontal TMS, but statistical significance was not reached, potentially because of the small sample size. Given the above and that all patients with at least 1 SD change in POET scores were responders, studies with a larger size may be warranted.

Background: Over 70 million Americans endure a chronic sleep disorder. Mobile app benefits have been postulated to expand patient access to scientifically-based interventions in aiding their sleep disorders. It is critical that information regarding these mobile apps are sufficiently analyzed. Objective: Analyze characteristics of commercially available sleep-exclusive apps using the Mobile Health Index and Navigation (MIND) apps database published by the Division of Digital Psychiatry at BIDMC for app review. Methods: Using pre-specified criteria, we identified 106 sleep related mobile apps in the iOS and Google Playstores, and rated them using a 105 question review as part of the MIND database based on: Accessibility, Privacy & Security, Clinical Foundation, Engagement Style, and Interoperability. Features of these 106 apps were compared to a control group of non-sleep apps to evaluate the features and limitations sleep apps bear relative to the remainder of the marketplace. Results: The most common features of sleep apps were mindfulness (68.9%), deep breathing (54.7%), and psychoeducation (30.2%). 39.6% of apps have accessibility features and 49.1% can be used offline. Sleep apps lack sleep trackers (22.6%), exportability features (21.7%), and opportunities to collaborate with one’s provider (7.6%). Only 10.4% of sleep apps have an efficacy study. Conclusion: In their current state, sleep apps can only assist the user as a self-help tool. The lack of sleep tracking, support, exportability, the inability to collaborate with one’s provider and efficacy studies limit the potential of implementing sleep apps for clinical use.

Background: The neuropathology of autism spectrum disorder (ASD) is poorly understood at the molecular level. Evidence from animal models, genetics, post-mortem studies, and single-gene disorders suggests possible involvement of mGluR5. Here, we use positron emission tomography (PET) to quantify mGluR5 receptor density in autistic adults. Objective: This project aims to quantify metabotropic glutamate receptor 5 (mGluR5) receptor density in ASD and assess the association with validated clinical measures. Methods: Ten individuals with ASD (mean age [SD] 27 [5]; seven males), and 10 demographically matched typically developed controls (HC; 29 [4]; seven males) participated in an [¹⁸F] FPEB PET scan. Volume of distribution (V_T: ratio of activity in tissue relative to blood) was the primary outcome measure and computed with equilibrium analysis using a venous input function. Partial volume corrections were applied to control for possible volumetric differences with Freesurfer. t tests were calculated for between group differences, and p values were uncorrected for multiple comparisons given the exploratory nature. Results: We observed significantly lower mGluR5 availability in ASD compared to HC in the left frontopolar cortex (–18%, p=0.03), left accumbens (–17%, p=0.04) with nonsignificant differences in multiple regions including the isthmus of the cingulate cortex (–16%), parahippocampal cortex (–16%), cerebellar cortex (–16%) and thalamus (–16%). Conclusion: This in vivo investigation with mGluR5 PET in ASD is the largest sample to date (to our knowledge) and found preliminary evidence of lower mGluR5 availability. Additional data collection and the correlations with validated clinical measures are being explored in the expanded sample.

Background: Recruiting participants for neuropsychiatric clinical trials is a time consuming and intensive process. Natural language processing (NLP) and network algorithms are effective solutions to facilitate patient identification and prioritization, however, require domain expertise. Moreover, these solutions do not address the manual chart review process, which remains a key bottleneck in the recruitment process. Objective: Create a web-based application to facilitate patient screening and recruitment to neuropsychiatric clinical trials. Methods: We obtained a test corpus of 1,274,023 free-text notes for 10,896 patients with a psychotic disorder or related diagnosis from our hospital’s medical record. We used standard NLP techniques to prioritize patients with keywords related to the inclusion and exclusion criteria from a recently completed clinical trial. We created a network of patients using the cosine similarity between each patient’s notes and implemented a Personalized PageRank (PPR) algorithm to further refine patient prioritization. Finally, we developed a web application called ChartReviewR. Results: When ranking 36 gold standard cases against 10,860 controls we obtained an Area Under the Receiver Operating Characteristics curve (AUC) of 0.826. The PPR algorithm increased AUC to 0.857. ChartReviewR includes the ability to input a set of keywords, automatically highlight passages of relevant text, and store screening results. Conclusion: ChartReviewR is a web-based application that 1) is effective in prioritizing patients, 2) allows clinicians access to NLP and PPR, and 3) streamlines the chart review process. Additional work is required to optimize integration and scalability with a hospital-wide electronic medical record.

Background: Mood disorders after traumatic brain injuries (TBI) are not uncommon in the general population. The diagnosis and management of mania secondary to TBI is not well defined, especially in populations with repeated head trauma. We present a case of a military veteran with multiple past TBIs who developed new-onset mania. Case History: A 36-year-old military veteran with a psychiatric history only notable for combat-related PTSD and a medical history of chronic hip pain presented to the emergency department (ED) with new-onset headache after a recent fall at home. During his initial ED workup, the patient appeared anxious and with pressured speech. However, the patient discharged from the ED against medical advice before any significant workup or imaging could be completed. The following day, the patient presented to the ED in the custody of police for “threatening to kill his wife.” He endorsed a four-day history of decreased need for sleep, increased caffeine intake, and auditory and visual hallucinations. He exhibited pressured speech, increased distractibility, and bizarre behavior. The patient endorsed approximately 20 previous concussions sustained during combat. Urine drug screen was positive for opioids, which he was regularly prescribed. The patient’s symptoms and presentation were consistent with mania. Subsequently, mirtazapine and olanzapine were added and he was stabilized and discharged. Conclusion: This case explores the possible neuropsychiatric manifestations of traumatic brain injuries. It also highlights the importance of continued discussion and research on TBIs.