2021 American Neuropsychiatric Association Annual Meeting Abstracts

Background: COVID-19 has been linked to neuropsychiatric symptoms, including delirium, depression/anxiety, PTSD, and rarely, severe neuropsychiatric impairment. However, much remains unknown. We present a case of anti-NMDA receptor encephalitis in a patient with concurrent COVID-19 infection. Case History: A 27-year-old male who carried diagnoses of unspecified mood versus psychotic disorder was admitted with atypical psychosis and suicidal ideation. Patient initially presented to primary care with racing thoughts, delusions, depression (PHQ-9=17), anxiety (GAD-7=10), and new onset cognitive symptoms along with olfactory hallucinations. He endorsed daily suicidal ideations and reported using two cellphones to block suicidal waves and enhance his memory. He was admitted to inpatient psychiatry where he exhibited disorganized behavior and paranoid delusions, and reported visual hallucinations. Initial workup of EEG, brain MRI, and TSH were unremarkable. Two months after admission, he developed sore throat and fever and tested positive for COVID-19. Patient developed streaky opacites on chest X-ray, was transferred to the ICU, and intubated due to agitation. Once extubated, he experienced repeated epileptic seizures despite multiple antiepileptics, and lumbar puncture ultimately revealed anti-NMDA receptor antibodies. Symptoms slowly improved with plasmapheresis, steroids, and Rituximab. Conclusions: Case reports suggest that some patients may present with neuropsychiatric symptoms or experience neuropsychiatric sequelae following COVID-19 infection. Infection itself can precipitate an autoimmune encephalitis and may also cause neurological damage which can unmask other neuropsychiatric conditions. This case highlights that research is needed to understand the intersection between COVID-19 infection and mechanisms implicated in other neuropsychiatric disorders, including the spectrum of autoimmune encephalitides.

Background: Medical students have been shown to have increased rates of anxiety compared with the general population. Specifically, in medical students, anxiety and depression may be inversely associated with academic performance. Objective: The aim of the study is to evaluate whether resilience, engaged living, spirituality and loneliness are significantly correlated to the development of anxiety in medical students. Methods: Eighty first year medical students were recruited into the study via electronic and physical bulletins. Subjects were asked to complete a series of demographic screening questionnaires. Students also completed a series of scales: CD-RISC 10 (resilience), DeJong Gierveld scale (loneliness), DUREL (spirituality), ELS (engaged living), PHQ-9 (depressive symptoms), GAD-7 (anxiety symptoms), and PSY (wellbeing and happiness). Results: The sample had a mean GAD7 score of 4.34±3.82 and mean ELSL, DUREL, ELS, CD-RISC 10, and PSY scores of 2.20±1.57, 18.00±7.44, 50.26±7.25, 31.15±4.42, 151.70±14.56, respectively. GAD7 scores positively correlated with ELSL (r=0.34, p=0.002) and PHQ (r=0.57, p=0.000). GAD7 scores negatively correlated with ELS (r=−0.36, p=0.001), CD-RISC 10 (r=−0.27, p=0.02), and PSY (r=−0.32, p=0.004). Conclusion: Depression and loneliness were positively correlated with anxiety. Standard of living and resilience were negatively correlated with anxiety. Age, standardized exams, and religiosity were not found to have a significant correlation to anxiety. These results may be used to understand and manage anxiety in medical students.

Background: Bilateral repetitive transcranial magnetic stimulation (rTMS) protocols have been used in an effort to improve response rates to TMS treatment, especially in patients with comorbid anxiety. Objective: To determine if adding low-frequency (LF) right-sided rTMS treatment to the standard high-frequency (HF) left-sided treatment confers any additional benefit for depressive or anxiety outcomes. Design/Methods: A retrospective chart review of patients treated with rTMS was conducted, from 2015 through 2018, yielding 361 patients. All were treated with a figure-of-8 coil for a major depressive episode. The protocol was either HF left-sided treatment or bilateral treatment. The Generalized Anxiety Disorder 7-item scale (GAD-7) was the anxiety outcome measure, and the Patient Health Questionnaire (PHQ-9) was the depression outcome measure. Results: There was no significant difference in GAD-7 change scores between unilateral (GAD change=4.2) versus bilateral rTMS (GAD change=4.5). Unilateral showed greater improvement in PHQ-9 than bilateral (7.2 versus 5.0; p=0.011). Switching from unilateral to bilateral midcourse correlated with overall poorer outcomes. Conclusions: This large, naturalistic study provides no support for a bilateral protocol to treat patients with combined depression and anxiety. The overall results do not show an advantage to bilateral treatment in any group or condition examined, and for depression outcomes, there appears to be a deficit with bilateral versus unilateral treatment. Unilateral treatment is better for depression (PHQ-9) outcomes and is no worse for anxiety (GAD-7). The results of this study have immediate clinical applicability and are a cautionary note regarding the use of combination protocols in rTMS treatment.

Background: Psychogenic nonepileptic seizures (PNES) disorder can be challenging to properly diagnose, which can lead to delays in treatment regimes. Physical symptoms, currently thought to be derived from underlying psychological conditions, are often associated with comorbidities, influencing misdiagnosis. Effective treatment therefore varies across individual cases. Currently, the standard treatment is cognitive behavioral therapy and psychoeducation; however, due to differing semiologies and comorbidities, there is a lack of understanding in treatment efficiency. In many cases, treating the comorbidity can improve the condition of patients with PNES. More research is needed to address the acceptance of the condition following diagnosis, the challenges of specialized treatment, and what factors influence the long-term prognosis. Case History: We present the pathway to diagnosis for a 44-year-old woman initially rushed to the emergency room due to an attack of primarily left-sided paralysis and an inability to speak. This attack was described as an unusual moment of altered consciousness with no immediate resolution. In the coming months, following multiple daily attacks and visits to five different medical providers, a series of tests led to the conclusion that the individual was experiencing PNES disorder. While the patient pursued a number of different treatments thereafter, she ultimately ceased pursuing treatment. Conclusions: We use the case study as a means of exploring the complexities of treating individuals with PNES. Ultimately, we suggest a path forward for explicit research into the patient’s perspective on their experience with treatment that can be used to improve the prognosis for other PNES patients.

Background: Underserved TBI patients suffer a heavy burden of disease requiring extensive care continuity. Barriers to care include early detection, inpatient treatment, and establishment of outpatient care. Objective: This study aimed to test the hypothesis that a proactive, collaborative, resident-led Neuropsychiatry Consultation Service (NCS) in inpatient medical care settings will improve identification of hospitalized TBI patients and allocation of outpatient services using the BIONiC model. Methods: 38 TBI patients admitted to the Neurology Intensive Care Unit (NICU) and 39 TBI patients admitted to the inpatient medical floors (IMF) at UMass Memorial Medical Center from July to December 2020 were referred to NCS. NICU consultations were discussed during primary team rounds. IMF primary teams directly consulted NCS. Each consultation consisted of chart review, neuropsychiatric examination, collateral gathering, and family education. Results: 77 consultations were completed, of which 38 were NICU patients, 20 of which were followed upon transfer to the inpatient medical floors, 6 were discharged home, 32 were discharged to rehabilitation, and 2 died. Of the 38 NICU patients, 33 (87%) established outpatient care at UMass, 3 established outpatient care outside of UMass. Of the 39 IMF patients, 35 (90%) established outpatient care at UMass, 4 established care outside of UMass. 100% of all patients who established outpatient care at UMass attended their first appointment. Conclusion: Establishing NCS in the NICU and IMF for TBI patients was feasible with early interdepartmental collaboration. It provided a novel BIONiC-focused method for early identification of neuropsychiatric sequelae, treatment, monitoring, and outpatient resource allocation.

Background: Since the onset of the COVID-19 pandemic, healthcare facilities throughout the U.S. have received guidance to minimize the spread of the virus. One of the major outcomes of this has been a rapid transition to telemedicine for many subspecialties of neurologic care. While the use of telemedicine in fields such as acute stroke care had been extensively studied prior to the pandemic, fewer studies have addressed the role of telemedicine in other subspecialties of neurology, such as memory and cognition. Objective: The goal of this pilot study was to assess the ways in which the transition to telemedicine had affected providers’ experiences with neurologic care as of July 2020. Methods: An online survey was emailed to neurology providers who are members of various professional organizations. The survey assessed the amount of telemedicine use in daily practice, which telemedicine platforms were utilized, and how provider satisfaction with telemedicine has changed since the onset of COVID-19. Additionally, memory and cognition providers were asked about cognitive tests they have been able to utilize during telemedicine visits. Results: Preliminary analysis of 16 responses showed a significantly increased use of telemedicine in average daily caseload; however, insufficient data prevented conclusions about provider satisfaction and memory and cognition testing use. Conclusion: Telemedicine has become a fixture in various subspecialties of neurology. We hope the results of this pilot study will contribute to our understanding of the use of telemedicine in neurology and expect that future studies will reveal more about provider experiences with telemedicine.

Background: We previously reported on the efficacy of a manualized 12-session mindfulness-based therapy (MBT) for psychogenic nonepileptic seizures (PNES). Completion of MBT provided improvements in PNES frequency, intensity and quality of life. Objective: Determine sustainability of improvement at 3- to 6-month follow-up after treatment completion in previously reported measures, plus newly reported measures on illness perception/ attribution, worry, and mechanisms. Methods: Patients with documented PNES were recruited from 2014 to 2018. Baseline measures were collected at time of diagnosis (T0) and/or at first follow-up postdiagnosis (T1). Outcomes are reported at treatment completion (T3) and follow-up (T4). The Wilcoxon signed-rank test was used for pairwise comparisons of PNES frequency; linear mixed models were used for other variables. Results: Fourteen of the 26 MBT completers attended follow-up (median 147.5 days between T3 and T4). PNES frequency, intensity and number of days/week with PNES remained reduced at T4 (p<0.01 for all; median frequency reduction 1.3/week from T1). Illness perception and feeling understood remained improved at T4 (p<0.001 for both) as did worry about PNES (p<0.05). Identifying PNES as “mental” versus “physical” disease changed from T0 to T3 (p<0.01), not to T4. Quality of life did not maintain improvement at T4. Hypothesized psychological mechanism did not change over time. Conclusion: Previously reported improvements in PNES frequency and intensity with MBT at treatment conclusion were maintained at 3- to 6-month follow-up. This study also demonstrates sustained improvement in illness conceptualization and symptom worry. Long-term benefits of MBT need to be established with randomized controlled trials.

Background: Focal brain lesions can cause spontaneous confabulation, a type of memory error in which false information is conveyed by the patient as true. This symptom shares features with amnesia and delusions but is thought to be distinct with a distinct neuroanatomical substrate. Lesions in several nonoverlapping locations can result in spontaneous confabulation, leaving the neuroanatomic localization unclear. Objective: To determine if lesion locations associated with spontaneous confabulation localize to a unique network of brain regions. Methods: 24 cases of spontaneous confabulation due to focal brain lesions were identified in the medical literature. Lesion locations were mapped to a common brain atlas and lesion network mapping was used to identify brain regions functionally connected to each lesion location. Specificity was assessed through comparison to lesion networks for amnesia (N=53) and delusional misidentification (N=15). Results: Lesions associated with spontaneous confabulation mapped to a common brain network: over 90% of lesions were positively connected to the mammillary bodies, anterior limb of the corpus callosum, and bilateral parahippocampal gyri (t>7, p<10⁻⁶). Lesions causing confabulation were significantly more connected to the orbitofrontal cortex than lesions causing amnesia and significantly more connected to memory regions (e.g. bilateral parahippocampal gyri, bilateral mamillary bodies) compared with lesions causing delusions (FWE, p<0.05). Conclusion: Our results identify a causal substrate for spontaneous confabulation that is dissociable from networks causing amnesia and delusional misidentification.

Background: Several studies of normobaric hyperoxia in some neurological conditions have demonstrated clinical benefits. Oxygen enriched air may increase oxygen pressure in brain tissue and have biochemical effects such as on brain erythropoietin gene expression, even in patients without lung disease. Objectives: This pilot, randomized, double-blind study examined the efficacy of normobaric hyperoxia as a treatment for depression. Methods: Fifty-five consenting patients aged 18–65 years with mild to moderate depression were included in the study. Participants underwent a psychiatric inclusion assessment and a clinical evaluation by a psychiatric nurse at baseline, 2 and 4 weeks after commencement of study intervention. Participants were randomly assigned to normobaric hyperoxia of 35% fraction of inspired oxygen or 21% fraction of inspired oxygen (room air), through a nasal tube, for 4 weeks, during the night. Patients were rated blindly using the Hamilton Rating Scale for Depression (HRSD); Clinical Global Impression (CGI) questionnaire; Sheehan Disability Scale (SDS). Results: The present study showed a significant improvement in HRSD (p<0.0001), CGI (p<0.01) and in SDS (p<0.05) among patients with depression who were treated with oxygen-enriched air, as compared with patients who were treated with room air. In CGI, 69% of the patients who were treated with oxygen-enriched air improved compared with 23% patients who were treated with room air. Conclusions: This small pilot study showed a beneficial effect of normobaric hyperoxia on some symptoms of depression.

Background: A diagnosis of functional neurological disorder (FND) may be relevant to litigation involving personal injury, psychiatric disability, or medical malpractice. However, no empirical studies on the courtroom use of FND have been conducted. Objective: To review case law involving FND in U.S. federal and state courts. Methods: The legal database Nexis Uni (formerly LexisNexis Academic) was searched for U.S. case summaries or overviews containing the search terms “functional neurological disorder” or “conversion disorder.” Cases were current through December 2020. Results: The Nexis Uni search yielded 38 cases: 20 were from U.S. federal courts and 18 from various state courts. Federal court cases primarily involved Social Security disability claims for FND (N=7; 35%), veterans’ benefit claims for service-connected FND (N=6; 30%), and claims brought under the National Vaccine Injury Compensation Program for injuries (including FND) allegedly caused by vaccination (N=3; 15%). Most state cases (N=17; 94%) involved claims of FND arising from workplace injuries; one additional case involved a malpractice claim due to FND misdiagnosis. Although some plaintiffs successfully received compensation for work-related FND, others failed to demonstrate a causal connection between their FND and a workplace injury (N=3) or a permanent disability (N=1). Conclusion: FND may be implicated in multiple legal contexts. Forensic experts evaluating claimants with FND should be prepared to testify regarding the potential cause(s) of claimants’ symptoms.

Background: There are many potential neuropsychiatric complications of coronavirus disease (COVID-19). While catatonic presentations were common during past pandemics (e.g. encephalitis lethargica), few case reports have identified this syndrome in patients with COVID-19. Here, we present a case of acute catatonia associated with COVID-19. Case History: The patient was a man in his 60s with a history of hypertension and a distant psychotic episode (20 years ago) who presented to the ED with three days of altered mental status. Symptoms included agitation, verbigeration, insomnia, and refusal of food and water. He was observed at home pacing with his arms outstretched in odd postures. On arrival to the ED, he was diaphoretic, tachycardic, and hypertensive. He was initially mute on interview. Physical examination was notable for staring, perseveration, ambitendency, rigidity, and gegenhalten. Fifteen minutes following a lorazepam challenge, his Bush-Francis Catatonia Rating Scale score decreased from 27 to 9. He quickly became calm, conversant, and better oriented. His laboratory results were notable only for a serum creatine kinase level of 1,187 U/L (530 U/L after fluid administration) and a positive PCR test result for COVID-19. Brain MRI showed mild probable microvascular ischemic disease. EEG and additional serologies were normal. Lumbar puncture was not obtained. Τhe patient was discharged on a lorazepam taper on hospital day 4 with a recommendation for outpatient psychiatric follow-up. Conclusion: Catatonia is a potential complication of COVID-19. Our case is consistent with the literature demonstrating catatonia responds at high rates to benzodiazepine treatment, regardless of its etiology.

Background: In Lewy body dementia, there is a well-documented phenomenon of neuroleptic hypersensitivity. This phenomenon may also present in other dementias, though there is currently little research on this topic. It is important for clinicians to recognize that neuroleptic hypersensitivity may occur not only in Lewy Body dementia, but in other types of dementia as well. Case History: A 60-year-old African American female with a past diagnosis of schizophrenia, later determined to be frontotemporal dementia, presented to inpatient psychiatry with disorientation, incoherent speech, socially inappropriate behavior and hyperorality after unremarkable medical work up. While inpatient, she was sent to the ED for stroke evaluation on three occasions after experiencing acute onset of difficulty swallowing, drooling, and dysarthria. Each incident was preceded with a relatively slight increase in antipsychotic medication dosage, with a delay of up to five days between dose increase and symptom onset. Additional workup for acute dysphagia and dysarthria in the ED was negative. A head CT scan did not show signs of stroke or other acute findings. Two of these reactions were successfully reversed with intramuscular benztropine. This is suggestive of an acute dystonic reaction, occurring in response to doses of antipsychotic medications that were relatively low when compared with doses previously tolerated in the treatment of presumed schizophrenia. Conclusions: This case suggests that as the patient’s dementia progressed, she became increasingly sensitive to antipsychotic medications. In this poster, we detail this presentation of neuroleptic hypersensitivity in frontotemporal dementia.

Background: Familial frontotemporal dementia (FTD) is a neurodegenerative disorder caused by three main autosomal dominant mutations. Objective: To provide an examination of the impact of these mutations on the cerebellum as a cause of neuropsychiatric symptoms. Methods: 413 participants from the GENFI dataset were included in this study (40% noncarriers). We used the MAGeT Brain algorithm to estimate the cerebellar lobule volumes from standard T1-weighted images. Partial least square analysis was used to identify a set of latent variables (LVs), that explain patterns of covariance between “brain” and “demographic/neuropsychiatric” data with the constraint that LVs explain as much of the covariance between the two matrices as possible. Here, our “brain” data included each cerebellar lobule volume and total brain volume. Our “demographic/neuropsychiatric” data contained age, sex, years of education, estimated years of onset, genetic status, and 11 behavioral scores from the Cambridge Behavioral Inventory (CBI). Permutation testing and bootstrap resampling were performed to statistically test each LV and to assess the contribution of each “demographic/neuropsychiatric” data on these LVs, respectively. Results: Two LVs were significant in each hemisphere. LV1 demonstrated lower overall cerebellar volumes to be associated with high CBI scores, being a mutation carrier, older, closer to expected disease onset, female sex and low education. LV2 exhibited higher lobule X volumes to be related to higher CBI scores in behavior, memory and everyday skills. Conclusion: Within genetic FTD individuals, subjects with larger lobule X volume seem to be at a higher risk for neuropsychiatric symptoms.

Background: The ongoing NewTics study examines children who have had tics for less than 9 months (NT group)—a population on which little research exists. Objective: Here, we further investigate relationships involving subcortical surface deformation and tic symptom severity. Methods: 138 children were assessed at baseline and a 12-month follow-up—79 with NT, 27 tic-free healthy controls (HC), and 32 with chronic tic disorder (CTD) or Tourette syndrome (TS) (the TS group)—using T1-weighted MRI and total tic scores (TTS) from the Yale Global Tic Severity Scale to evaluate symptom change. Subcortical surface maps were generated using FreeSurfer-initialized large deformation diffeomorphic metric mapping, utilizing automated brain segmentations based on multiple template images. Linear regression models were constructed to correlate structural shapes with TTS while accounting for covariates, with relationships mapped onto structure surfaces. Results: Baseline volumetric analyses using one-way ANOVA and post hoc tests showed NT subjects having smaller average pallidal, thalamic, and caudate volumes than HCs. TS subjects also had smaller average thalamic and caudate volumes. Surface maps illustrate inward shape deformity (localized volume loss) compared with controls in the nucleus accumbens, thalamus, and pallidum of both NT and TS children, with NT also exhibiting deformity in the putamen and caudate. The accumbens and caudate also show inward deformation relating to TTS increase from baseline to 12-months (worsening of symptoms). Conclusion: These results demonstrate distinct patterns of subcortical deformation in NT, and in some cases TS, which may further provide insight into prognostic biomarkers in TS-CTD.

Introduction: Estimates are that lifestyle interventions and adequate control of blood pressure could substantially reduce the incidence of brain disease, cerebrovascular or neurodegenerative, as well as mood disorders. Patients and clinicians are increasingly interested in the steps to take to prevent common forms of brain disease and promote brain function. Methods: The McCance Center for Brain Health developed and piloted a 12-point Ideal Brain Care Score (IBCS). IBCS was derived from evidence-supported interventions associated with reduced risk of brain diseases, building upon and expanding AHA Life’s Simple Seven and recommendations from the Alzheimer Association. Practitioners administered IBCS in an outpatient practice with individuals at high risk for brain disease but without active disease. After completing IBCS, personalized strategies were developed for improving scores at 6 months. Results: We report data from the first 45 patients completing IBCS, 24 male/21 female, Average age 63 years old (age range 30–86). Average score 7.5(±1,4). Points were commonly lost (in descending order) for Meditation, Body Mass Index, physical activity, blood pressure, sleep and diet. Patients were receptive and appreciative of the heightened awareness around needed lifestyle modifications to better their scores. Conclusion: IBCS can be administered in routine clinical care with direct feedback identifying evidence-based steps that patients can take to reduce the risk of brain disease and protect brain health. Next steps are to report data from an expanded cohort, follow-up data at 6 months. Ultimately, IBCS validity requires a large diverse population to assess performance and improvement as patients return for follow-up.

Background: While prior TBI may be associated with the onset of psychiatric disorders, psychosis is relatively rare, occurring in only 0.9%−8.5% of patients. Post-TBI mood and anxiety disorders are well-described in the literature; thorough characterization of post-TBI psychosis and treatment options is lacking. Case History: A 32-year-old male presents for inpatient psychiatric admission following multiple heroin overdoses with suicidal intent. Neuropsychiatric history significant for in utero exposure to several substances and alcohol, early-life neglect, depression, opioid use disorder, frequent cannabis use, and a prior severe TBI following a 2010 vehicular accident. Immediately following this TBI, he perceived daily command auditory and infrequent visual hallucinations, leading to numerous suicide attempts, escalating substance use, worsening depressive symptoms, and chronic nightmares. Psychotic and mood symptoms were unremitting despite several antidepressant, mood stabilizing, and antipsychotic trials. MOCA on admission of 13/30. A workup including CT, inflammatory markers, anti-NMDA assay, and cosyntropin stimulation were unrevealing. Clozapine titration complicated by new stuttering, which can be ictal in nature. Routine EEG without epileptiform activity. ECT allowed modest objective improvement in affect, though this was complicated by marked worsening of amnestic impairment and lack of a subjective relief from his profound melancholia. Conclusion: A thorough history and temporal correlation is imperative to making a diagnosis of post-TBI psychosis. This is a case of schizophrenia-like psychosis following TBI, and underscores the complex interactions of TBI with premorbid psychopathology, development, addiction, as well as nuanced considerations in treatment selection, e.g. adverse cognitive effects and seizure threshold.

Background: Behavioral variant frontotemporal dementia (bvFTD) and catatonia can present with many similar overlapping symptoms and thus provides a complicated diagnostic picture. Further clouding this issue is that catatonia is noted to be a presenting symptom of bvFTD. Unfortunately, little guidance is provided in the literature to help the differentiation of bvFTD and catatonia. Case History: Our patient was a 56-year-old male with a history of depression who presented to the hospital with altered mental status along with new onset paucity of speech, impulsivity, immobility, refusal to eat or drink, and overall lack of engagement with providers. Initial presentation resembled catatonia and given a positive screen on a Busch Francis Catatonia Scale; a lorazepam challenge was administered. Symptoms were noted to modestly improve following lorazepam; however, continued treatment did not show any continued response. Furthermore, cessation of lorazepam showed no worsening functional decline. Extensive altered mental status work-up was largely noncontributory asides from an MRI Brain that noted mild brain atrophy throughout and including the frontal region along with modest brain atrophy in the temporal region. The authors review the clinal presentations and distinguishing features of both bvFTD and catatonia. Conclusion: This case highlights the diagnostic difficulties that arise from the phenotypic overlap that exists between bvFTD and catatonia. The authors, in an effort to help supplement diagnostic clarity, provide guidelines for both approach and management of this neuropsychiatric challenge.

Background: Like those with Multiple Sclerosis (MS), patients with Radiologically isolated syndrome (RIS), characterized by incidental lesions suggestive of MS on MRI without typical symptoms of MS, have high rates of mood disorders and less so psychotic symptoms. Neuropsychiatric signs and symptoms occur frequently in individuals with MS, either as the initial presenting complaint prior to a definitive neurological diagnosis or more commonly with disease progression but not much is known about RIS in this context. To date, the literature is sparse on RIS and associated psychiatric symptoms. Case History: An 18-year-old man got admitted to the first-break psychosis unit for new-onset psychosis characterized by intense command auditory hallucinations and a paranoid delusional system of four months duration. Work-up for organic causes of psychosis yielded multifocal areas of T2 hyperintensity in white matter and corpus callosum on MRI Brain. The lesions were nonenhancing. Additionally, he had elevated IgG index and oligoclonal bands in CSF. Otherwise, medical work-up for autoimmune, infectious, toxic, and metabolic causes was unrevealing. In the absence of any clinical neurological event, the patient was deemed to have RIS. He was treated with Olanzapine with improvement in auditory hallucinations. Conclusions: This case illustrates that it is important to not ignore even the so-called “coincidental” findings and contextualize them clinically, especially when patients present with atypical/rare symptoms. Future studies should explore the relationship between RIS and psychiatric syndromes as it may yield a better characterization of neuroanatomical basis of psychiatric symptoms.

Background: The potential dawn of a biological therapeutic for Alzheimer’s disease highlights the need for a very rapid screen for disease severity. While short questionnaires such as the Functional Activity Questionnaire (FAQ) or Dementia Severity Rating Scale (DSRS) exist, even these may be too long to be adopted by most primary care providers (PCPs). Dr. Daniel Kaufer designed a brief screen intended for PCPs, with a 4-question section on functional independence, which also emphasizes higher-risk activities such as financial management and driving. Objective: We here establish how Dr. Kaufer’s very brief screen compares with better established measures of disease severity. Methods: Care partners of patients seen at the University of Colorado Memory Clinic filled electronic versions of the Kaufer questionnaire, as well as the FAQ (n=21) and DSRS (n=16). In addition, neurobehavioral status examinations on 13 patients were evaluated using the Montreal Cognitive Assessment (MoCA). Results: With ordered logistic regression, the Kaufer questionnaire correlated well with scores on the FAQ ($\widehat{\beta }$=0.67, p<0.001, CI=[0.31; 1.02], pseudo-R²=0.41) and DSRS ($\widehat{\beta }$=0.30, p=0.001, CI[0.11;0.48], pseudo-R²=0.21). No correlation was found with the MoCA (p=0.15). A suggested cutoff score of 4 or>1 to any question on the Kaufer questionnaire may best support a diagnosis of dementia based on thresholds of the better-established scales of functional independence. Conclusion: The Kaufer questionnaire’s 4-question section on functional independence has potential as a very brief initial screen for neurocognitive disease severity. Further work is needed to better understand the properties of this short questionnaire.

Background: Synesthesia is a cross-sensory experience that occurs when stimulation of one sense results in an internally generated experience in another sense. Synesthesia can be broken down into an inducer-concurrent pair and into three forms: genuine, acquired, and drug-induced. We present a case of a patient who was referred for evaluation of psychosis due to worsened visual hallucinations after starting fluoxetine who described both genuine auditory-visual synesthesia and components of drug-induced synesthesia. With this case we review synesthesia and discuss the literature regarding SSRI-related synesthesia. Case History: 33 y/o male who reported a past history of only depression/anxiety developed new onset psychosis after two weeks of starting fluoxetine. On interview, he showed no signs of a primary thought disorder. He described both new and old visual phenomena. Patient reported a life-long history of seeing color when listening to music. Since starting fluoxetine, the phenomena began to develop patterns, occurring move vividly and with additional colors. The patient was cross titrated to bupropion with return to baseline visual experiences. Conclusions: Consult providers need to be prepared to assess and recognize synesthesia as it can be part of a differential for psychosis. While not considered a usual substance that precipitates synesthesia, our case suggests that some patients may be more sensitive to this occurrence. Being prepared to screen for and discuss this potential side effect will help consult providers avoid unneeded interventions.

Background: Alzheimer’s disease (AD) is the most prevalent dementia and its progression rises with age. Caregivers are liable for giving physical, social, economic, and emotional aid to the patient and caregivers often are the spouses or children of the patient. Care burden is a multidimensional reply to physical, psychological, social and financial stressors associated with caregiving. This research was to identify the agents significantly predicting caregiving burden of spousal and adult-children caregivers of patients with AD. These predictive factors were depression, positive and negative mood affects, and caregiver grief. Method: Inventories and demographic information forms were used with descriptive and correlational research design. Participants were recruited from the Alzheimer's Association, Alzheimer's Foundation, Akdeniz University Neurology Clinic and two Facebook groups for Alzheimer’s carers. Of the 103 caregivers, 84 of whom were women and 19 of whom were men. Caregiving burden was measured with ZBI. Result: In this study, statistical (stepwise) regression was chosen to create a multiple linear regression model. The regression model showed significance F(3,99)=4.33, p=0.04, R2=0.38. Conclusively, 38% of the variance in the caregiving burden can be described by depression, personal sacrifice burden, negative affect. Conclusion: Caregivers who provide care to their spouse reports higher caregiving burden, as well as caregivers who needed psychological help, caregivers who participated in social support activities, caregivers who wanted to participate in support activities or groups, and caregivers who took daily medications for personal chronic health problems.

Background: In the adult population, both cerebral small vessel disease (SVD) and psychiatric illness have been individually associated with a higher risk of developing cognitive impairment (CI). There is little information regarding the characteristics of the subjects who have SVD and psychiatric illness together. Objective: Our hypothesis suggested that CI is higher in frequency in the psychiatric population with SVD than the general population with SVD (9.1%). Thus, the principal aim of this study was to estimate the frequency of CI in a psychiatric population with SVD. Method: A cross-sectional study was implemented in a psychiatric adult population of the National Institute of Psychiatry Ramón de la Fuente Muñiz in Mexico. We determined the severity of SVD with Fazekas and mRankin scales, and the presence of CI with MoCA. Associations between CI and known vascular risk factors, including those specific in the psychiatric population, were determined. Results: From a total of 47 patients studied, with a mean age of 63 years, a 68% of CI was found. There were no differences between patients with or without CI except for the use of mood stabilizers, p=0.020. Correlations were made to exclude confounders such as age, level of education, Fazekas and mRankin scales. Conclusion: Psychiatric patients with SVD using mood stabilizers have a higher frequency of CI than the general population with SVD. Results hold regardless of the age, education, sex and comorbidities commonly associated with CI and SVD.

Background: Over 80% of the global population consider themselves religious with even more identifying as spiritual, but the neural substrates of spirituality and religiosity remain unresolved. Objective: We apply lesion network mapping to test whether lesion locations associated with spiritual and religious belief map to a specific human brain circuit. Methods: Focal brain lesions were converted to lesion networks using a normative connectome (N_connectome=1,000). Permutation analysis of linear models (PALM) was used to identify peak association between connectivity to neurosurgical resection sites (N1=88) and changes in spiritual acceptance following neurosurgery. In a second, independent dataset of focal brain lesions (N2=105), we tested whether lesion connectivity to the peak region derived in dataset 1 was significantly associated with religiosity. For cross-validation, we used dataset 2 to localize peak association with religiosity, and dataset 1 to test whether lesion connectivity to this region correlated with changes in spiritual acceptance following neurosurgery. Results: Changes in spiritual acceptance and religiosity both localized to periaqueductal gray (PAG) (dataset 1, p<0.001; dataset 2, p<0.002). Connectivity between lesion locations in dataset 2 and the PAG peak from dataset 1 predicted religiosity (p<0.02), and connectivity between lesion locations in dataset 1 and the PAG peak from dataset 2 predicted changes in spirituality (p<0.02). Conclusions: We conclude that spirituality and religiosity map to a common brain circuit centered on the periaqueductal gray, a brainstem region previously implicated in fear conditioning, pain modulation, and altruistic behavior.

Background: The combination of posttraumatic stress disorder (PTSD) with traumatic brain injury (TBI) produces a syndrome more severe than PTSD or TBI alone based on prior clinical reports. Both PTSD and TBI produce a long-lasting neuroinflammation, which potentially contributes to their chronic affective and cognitive deficits. Objective: To study the interaction of TBI and PTSD using animal models. Methods: Using C57BL/6 mice, five groups of mice received either: 1) Sham-treatment 2) closed head injury (CHI), a model for TBI 3) chronic variable stress (CVS), a model for PTSD, or two models of combined TBI & PTSD that differed in the order of the insults, 4) CHI → CVS, 5) CVS → CHI. Results: The CVS → CHI group had significantly larger cognitive deficits based on performance on a spatial task, Barnes Maze, and acquiring the area of shock zone in the Active Place Avoidance (APA) task. The cognitive and affective deficits of CVS → CHI group were accompanied by increased hippocampal inflammation as measured by Iba−1 and Arginase-1 levels. Conclusion: These results support a central role of neuroinflammation in inducing neurobehavioral deficits. The combined CVS → CHI model had persistent memory and cognitive deficits. The neurobehavioral deficits were accompanied by alteration of Iba−1, and tau phosphorylation level.

Background: Post stroke depression (PSD) is the most common psychiatric complication of stroke with an estimated prevalence of 33%, classically triggered by frontal lesions. Persistent postural-perceptual dizziness (PPPD) is a chronic functional vestibular disorder manifesting nonspinning vertigo, unsteadiness, and hypersensitivity to motion stimuli, often triggered by structural vestibular disorders. Pathophysiologic mechanisms responsible for persistent symptoms in these two illnesses are incompletely understood. Herein, we present the case of a woman who developed new onset depression and PPPD following a right insular stroke with possible insights gained from the location of this infarct. Case History: A 40-year-old female with a history of generalized anxiety disorder, chronic migraine with aura, and obesity sustained a localized stroke to the right insula. Shortly after hospital discharge, she developed new onset dizziness and her first episode of depression that together gradually worsened and disrupted her daily life. A collaborative workup including Neurology, Otorhinolaryngology, Psychiatry and Optometry concluded that the insular stroke was the trigger for both her PSD and PPPD and that disruption of neural networks through the insula was the biological correlate of ongoing symptoms. Conclusion: Structural neuroimaging studies of voxel-based morphometry have shown significant insular gray matter reduction in patients who have major depressive disorder. For PPPD, functional neuroimaging studies previously identified decreased activity and connectivity in vestibular networks centered about the insula. This unique case calls attention to the insula as a key node in networks that underlie two critical human functions, affective regulation and mobility.

Background: Cotard’s syndrome is characterized by the bizarre delusion that one is dead, decaying, or nonexistent. Underlying neurological disease including neurodegenerative conditions, as well as acute medical precipitants are often implicated in its pathogenesis, even in individuals with pre-existing psychiatric disorders. While coronavirus disease 2019 (COVID-19) has been reported as an acute medical precipitant of psychosis, an associated case of Cotard’s syndrome has yet to be reported. Given its often multifactorial nature, the occurrence of Cotard’s syndrome in COVID-19 offers an opportunity to examine a spectrum of neuropsychiatric morbidity associated with the infection and its treatments. Case History: A 57-year-old woman with bipolar I disorder stable for the preceding two years was hospitalized for severe respiratory COVID infection, treated with dexamethasone, remdesivir, and oxygen, recovered, and then subsequently developed Cotard’s syndrome associated with depressed mood and catatonic features. Her course was complicated by the development of seizure activity and encephalopathy with diffuse EEG slowing. Her paranoid and nihilistic delusions were florid and protracted, lasting over a month. MRI Brain showed dense T2 hyperintensities in the bilateral subcortical and deep white matter, likely vascular in etiology. She recovered after antidepressant, antipsychotic, and anticonvulsant mood stabilizer treatment. Conclusion: This case describes the development of Cotard’s syndrome in a post-COVID patient. The patient experienced a range of neuropsychiatric disturbances suggesting evolving underlying CNS dysfunction in the post-COVID state. Consistent with prior analyses of Cotard’s syndrome, pre-existing neuropsychiatric and neurodegenerative morbidity and acute medical precipitants ultimately interacted in generating the patient’s presentation.

Background: Transcranial Magnetic Stimulation (TMS) is not FDA approved for use in bipolar depression and most insurance plans do not cover TMS for bipolar disorder. Objective: To determine if patients with bipolar depression (BPD) patients respond as well to rTMS as those with unipolar (UPD). Design/Methods: A retrospective chart review of patients treated with rTMS was conducted, from 1/2015–12/2018, yielding 291 UPD and 36 BPD patients. All were treated with a figure-of-8 coil for a major depressive episode, with either high-frequency (HF) left-sided treatment or bilateral treatment with both HF left-sided and low frequency (LF) right-sided treatment. The outcome measures were the Generalized Anxiety Disorder 7-item scale (GAD-7) and the Patient Health Questionnaire (PHQ-9). Results: BPD patients had more rapid response in PHQ (8.4 versus 11.2 by session 30, p=0.012) and greater change by end of treatment (PHQ change=8.1 versus 5.8, p=0.036). There were no significant differences in the GAD changes. The PHQ-9 difference between bipolar and unipolar patients occurred largely in patient receiving unilateral treatments (BPD versus UPD PHQ change: 10.2 versus 6.7, p=0.011). Regression analyses predicting PHQ-9 change prepost treatment showed the only significant predictors were number of unilateral treatments (p=0.007) and BPD diagnosis (p=0.011). Conclusions: In our sample, rTMS was a potentially more effective treatment in BPD than in UPD. The greatest PHQ-9 change was seen in BPD patients treated with unilateral rTMS. This large naturalistic study supports the use of HF left-sided rTMS in the treatment of BPD.

Introduction: Approximately one third of adults report insomnia symptoms, which are associated with adverse psychological and functional outcomes. Unfortunately, few over-the-counter sleep aids have demonstrated efficacy in controlled trials, and those that improve sleep usually also cause sedation and impaired daytime function. Objective: This study investigated whether an over-the-counter polyphenol botanical blend (PBB) could improve sleep without compromising neurocognition. Methods: We conducted a 30-day randomized, double-blind, placebo-controlled trial in 88 adults. Sleep was measured by diaries, actigraphy, and questionnaires, while neurocognitive functioning was assessed using a Motor Praxis Task (motor speed), Visual Object Learning Task (visual learning), N-back (working memory), Abstract Matching (abstraction), Line Orientation Task (spatial orientation), Digital Symbol Substitution Task (visual tracking), Balloon Analog Risk Task (risk decision making), and the Psychomotor Vigilance Task (vigilant attention). Analyses tested group, time, and group-by-time effects using linear mixed effects models. Results: PBB improved sleep quality (p<0.05) and insomnia symptoms (p<0.05) while reducing attentional lapses (p<0.05) and response times (p<0.01). PBB did not deteriorate neurocognition and improved N-back sensitivity (p<0.05) and accuracy (p<0.05), reduced Line Orientation Task errors (p<0.05) and increase mean pumps on the BART (p<0.01), versus placebo. Conclusion: The PBB improved sleep quality, reduced insomnia symptoms, and improved sustained attention without neurocognitive compromise. This is in contrast to most sleep aids that cause sedation at the expense of cognition. This suggests an opportunity for botanicals to improve sleep in those with sleep complaints but not sleep disorders.

Background: Stress is implicated in psychosis etiology and exacerbation, but pathogenesis toward brain network alterations in schizophrenia remain unclear. White matter connects limbic and prefrontal regions responsible for stress response regulation, and white matter tissues are also vulnerable to glucocorticoid aberrancies. Objective: Using a novel psychological stressor task, we studied cortisol stress responses over time and white matter microstructural deficits in schizophrenia spectrum disorder (SSD). Methods: Cortisol was measured at baseline, 0-, 20-, and 40-minutes after distress induction by a psychological stressor task in 121 SSD patients and 117 healthy controls (HC). White matter microstructural integrity was measured by 64-direction diffusion tensor imaging. Fractional anisotropy (FA) in white matter tracts were related to cortisol responses and then compared with general patterns of white matter tract deficits in SSD identified by mega-analysis. Results: Differences between 40-minutes poststress and baseline, but not acute reactivity poststress, was significantly elevated in SSD versus HC, time x diagnosis interaction F_2.3,499.9=4.1, p=0.013. All SSD white matter tracts were negatively associated with prolonged cortisol reactivity but all tracts were positively associated with prolonged cortisol reactivity in HC. Individual tracts most strongly associated with prolonged cortisol reactivity were also most impacted in schizophrenia in general as established by the largest schizophrenia white matter study (r=−0.55, p=0.006). Conclusion: Challenged with psychological stress, SSD and HC mount similar cortisol responses, and impairments arise in the resolution timeframe. Prolonged cortisol elevations are associated with the white matter deficits in SSD, in a pattern previously associated with schizophrenia in general.

Background: Down syndrome (DS) is the most common chromosomal cause of intellectual disability. Individuals with DS may exhibit acute neuropsychiatric symptoms as young adults. These symptoms include psychomotor retardation, mutism, apathy, emotional instability, anorexia, insomnia, myoclonus, obsessive-compulsive behaviors, memory impairment, delusions, and hallucinations. Since life expectancy has increased in the last few decades for patients with DS, rising comorbidities have also been reported. There have been very few reported cases of hallucinations and late-onset myoclonus in such patients, with no established criteria of diagnosis. More research is compelled to understand the neuropsychiatric symptoms of patients with DS which impact on their quality of life, and efforts are needed toward providing excellent patient-centered care. Case History: Ms. R is a 34-year-old, single Hispanic female with DS and no reported past psychiatric history. She presented for psychiatric evaluation for sudden mood changes, anxiety, and noncommanding type auditory and visual hallucinations after a dental surgical procedure in 2017. Prior to this presentation, the patient was reported to be happy and highly functional. A detailed review of this patient's condition revealed late-onset myoclonus and choroid plexus mass. Conclusions: This case serves to illustrate the complex psychiatric presentation and treatment in patients with DS and evidence of late-onset myoclonus coupled with choroid plexus mass shown on brain MRI imaging. More research is needed to fully understand and treat neuropsychiatric symptoms in patients with DS.

Background: Parkinson’s disease (PD) is one of the most common neurodegenerative movement disorders seen in a neuropsychiatric clinic. It can present with a number of neuropsychiatric syndromes, most common being depression and anxiety. Rarely, some patients with PD may demonstrate functional neurological symptoms, confounding the clinical picture, demanding extensive investigations, and complicating treatment. Case History: We assessed a 74-year-old right-handed white man with previous history of macular degeneration, subclinical hypothyroidism, and hypertension, who presented for an evaluation of depressive symptoms after a recent inpatient admission investigating gradual weight loss over one year. He was experiencing progressive subjective discomfort with swallowing solid foods for several months. He lost 30 lbs consequently. Extensive work-up for dysphagia and weight loss was negative. His clinical symptomatology was concordant with major depression and parkinsonism. We recommended sertraline for depression which led to improvement in dysphagia as well as depressive symptoms and helped him regain lost weight. His parkinsonian symptoms had started at the same time as depressive symptoms. His DaT scan findings were consistent with a diagnosis of neurodegenerative parkinsonism. Conclusions: Our case yields some relevant clinical insights. Depression may herald the onset of PD or both motor symptoms and depression may present simultaneously. Functional neurological symptoms (dysphagia in our patient) may complicate diagnosis when accompanying PD and it is important to distinguish them from neurodegenerative motor symptoms.

Background: Osmotic Demyelination Syndrome (ODS) is a rare, but well-known entity characterized by a range of neurological and neuropsychiatric symptoms, including alteration of consciousness, quadriplegia, dysphagia, dysarthria, extrapyramidal symptoms, catatonia, psychosis, manic symptoms, etc. It is classically associated with rapid correction of hyponatremia, heavy alcohol use, hyperglycemic hyperosmolar coma, diabetic ketoacidosis, malnutrition, and hepatic transplantation. It is rarely described in patients with hypernatremia. Case History: A search on PubMed for “Osmotic Demyelination Syndrome” resulted in 384 hits. We found only 7 papers that described ODS occurring in the context of hypernatremia. We evaluated a 22-year-old right-handed Emirati man who presented for the management of depression and cognitive symptoms. Prior to presentation, he was admitted to a medical ICU for hypernatremia-related complications secondary to ingestion of an unknown quantity of salt tablets followed by prolonged inpatient rehabilitation stay. His brain MRI showed pontine and extrapontine T2 FLAIR hyperintensities. The patient manifested aprosodic speech, bradykinesia, and mask-like facies, poor concentration, reduced processing speed, and the full complement of depressive symptoms. He became fully functional with supportive treatment. Conclusions: This case illustrates that seemingly benign salt tablets can be highly dangerous in overdose. Resulting hypernatremia may lead to ODS, especially in those with risk factors. It also highlights that the prognosis of ODS is not grim universally. There is a need to spread awareness regarding the dangers of salt tablets to prevent overdoses, and regarding other causes of ODS, to speed diagnosis and aid management of this life-threatening complication.

Background: Neuropsychiatric symptoms such as depression, anxiety, fatigue, and apathy are common sequelae of stroke. While the incidence of psychotic symptoms after stroke ranges from 1% to 5.3%, they tend to be underdiagnosed and undertreated despite their association with poor functional outcomes. Case History: A 53-year-old woman without psychiatric history presented with six-week history of progressive visual hallucinations and delusions. Seven months prior, she suffered a large ischemic right MCA territory stroke complicated by hemorrhagic conversion. She had one principal delusion of her husband’s infidelity with a neighbor. Physical exam was notable for mildly impaired attention/memory, intact visual fields, left-sided facial droop and hemiparesis with upper motor neuron signs, and ataxia. Laboratory work up was unremarkable, and brain MRI redemonstrated chronic ischemic changes in the right MCA territory. We initiated treatment with risperidone 0.75 mg nightly, and her delusions and hallucinations remitted several days later. Conclusion: Poststroke psychosis is more common than originally thought and associated with a high mortality rate. Damage to the right hemisphere has been strongly implicated. Neuroanatomic and neurophysiologic explanations for poststroke delusional syndrome are being investigated. In our patient, stroke-related misperception of her physical surroundings, that is, a perceived absence of continuity in the walls of her apartment, may have given rise to a theory of her husband’s infidelity. Delusional jealousy has also been described as a rare isolated sequalae of right cerebral infarctions. Cross-specialty collaboration between neurologists, psychiatrists and physiatrists may be the best approach to develop appropriate identification and management guidelines for poststroke psychosis.

Background: Powassan encephalitis (PE) is a CNS inflammatory condition associated with the tick-born flavivirus, Powassan virus. Symptoms can include a wide range of constitutional symptoms as well as focal neurological deficits and, rarely, severe symptoms including coma and death. A subset of patients, appear also to have an as yet poorly described neurobehavioral profile of persistent prolonged, postinfection symptoms. We present two cases of neuropsychiatric PE in the hopes of adding to the literature describing this condition. Case Histories: 1) An 8-year-old boy with premorbid, suspected ADHD contracted Powassan virus at age 5 with initial course complicated by seizures. Following acute treatment, he developed severe behavioral sequelae including persistent hyperphagia, OCD-like symptoms, anxiety, and new-onset aggression and dysregulation. Symptoms continue 3 years postinfection with mild benefit from symptomatic treatments including stimulants and alpha agonist. 2) A 6-year-old girl presented at age 5 with initial course complicated by suspected vasculitis. Prolonged symptoms have included choreiform movement disorder, indiscriminate kissing, hyperorality/pica, vocal tics, anxiety, emotional lability and new-onset ADHD-like symptoms. Symptoms continue to wax and wane after a year with some benefit from a stimulant and alpha agonist as well as tetrabenazine. Conclusion: There is a striking preponderance in both cases of compulsive, repetitive behaviors. Both patients have extensive subcortical white matter and basal ganglia involvement on MRI suggestive of disruption of cortico-striato-thalamacortical (CSTC) loops. Notably, disruption of CSTC pathways is hypothesized to play a role in cases of secondary obsessive-compulsive disorder. PE may be characterized by a specific endophenotype with these features.

Background: Down syndrome disintegrative disorder (DSDD) is a general term for the syndrome of regression in adolescents or young adults with Down syndrome characterized by loss of previously acquired cognitive, adaptive and other skills. Hypotheses for potential causes vary, but substantial overlap with catatonia syndrome is well-characterized in the literature and a range of medical, neurobehavioral and autoimmune factors are posited to potentially contribute to this regression. Case History: A 16-year-old woman with trisomy 21, Hashimoto’s thyroiditis and acute lymphoblastic leukemia in full sustained remission presented with subacute onset of catatonia, psychosis and dramatic functional regression. Her Bush Francis Catatonia Scale was 32. Extensive work-up included normal brain MRI and EEG. Serum lab abnormalities included elevated anti-TPO antibody at 402 IU/mL (normal: <16 IU/mL) and glutamic acid decarboxylase (GAD) 65 antibody at 1.1 nmol/L (normal: <0.02 nmol/L). CSF revealed matched oligoclonal bands and was otherwise bland. CSF autoimmune encephalopathy panel was negative (Medical Mayo Laboratories). No psychiatric etiologies were suspected. After her first intravenous methylprednisolone dose, she evidenced dramatic improvement with transient return to 80% baseline. She ultimately achieved catatonia resolution and sustained return to 95% functional baseline with Rituximab. Conclusion: This is a case of dramatic functional regression and catatonia with near full restoration of baseline function. Such cases have been reported, but we have rarely witnessed such dramatic functional restoration. This case adds evidence for the need for careful medical work-up and consideration of autoimmune etiologies of DSDD for which specific immunotherapies may be profoundly beneficial.

Background: Although obesity in midlife may predict later cognitive decline, obesity in older age may paradoxically protect against cognitive decline. Limitations in the measurement of obesity and cognition may confound this relationship. Objective: This study aims to explore associations between body composition and cognition in an obese sample of community-dwelling older adults, while controlling for physical frailty, sex, and diabetes. Methods: This is a cross sectional analysis of 81 older adults with obesity. Cognition was assessed using age-adjusted total composite score from the National Institutes of Health Toolbox Cognition Battery (NIHTCB). Obesity was measured both by body mass index (BMI) and truncal fat mass from dual energy X-ray absorptiometry. Physical frailty was assessed using the Physical Performance Test (PPT). Multiple linear regression investigated whether addition of either measure of obesity improved on a model limited to physical frailty, sex, and hemoglobin A1c. Results: Multiple linear regression analyses revealed that in separate models, BMI (β=−0.68; 95% CI=−1.23, −0.14) and truncal fat mass (β=−0.47; 95% CI=−0.89, −0.06) were both significant predictors of cognition. The BMI model explained 38.8% of the variation in cognition (p=0.014), which represents an additional 5.0% when compared with the limited model. The truncal fat mass model explained 38.0% of the variation in cognition (p=0.025), which represents an additional 4.3%, when compared with the limited model. Across all models, PPT (i.e. degree of frailty) consistently demonstrated strongly significant, positive correlation with NIHTCB. Conclusion: Extent of obesity is associated with cognition, though physical frailty appears to have great importance.

Background: Dominant stroke imaging methods focus on relating symptoms to stroke location. Objective: We apply a wiring diagram of the brain (i.e. the connectome) to test whether lesion connectivity may add predictive value to lesion location in assessing behavioral outcomes following stroke. Methods: MR images of stroke locations in two independent datasets (N1_total=125; N2_total=439) were converted to lesion networks using a normative connectome (N_connectome=1,000). Acute behavioral measures of NIH Stroke Scale scores (NIHSS) were obtained for all patients. Dataset 1 was used to calculate both a voxel lesion symptom-based map (VLSM) and a lesion network map (LNM) of NIHSS severity. In dataset 2 (N2_total=439), lesion intersection with VLSM and LNM topographies from dataset 1 were quantified and correlated with NIHSS severity. Results: Both lesion location and lesion connectivity were significantly associated with NIHSS measures (VLSM r=0.53, p<0.001; LNM r=0.55, p<0.001). When both variables were combined in a single linear model, VLSM and LNM each represented independent variance in NIHSS measures (r_combined=0.56; VLSM p=0.04; LNM p_<0.001). Conclusions: Stroke lesion location and lesion connectivity each represent independent variance in behavioral measures of stroke severity. Future work will examine these relationships longitudinally relative to stroke onset and explore ways to optimize clinical utility of these tools.

Background: Rabbit Syndrome acutely manifesting after cerebellar hemorrhage has not been described. Cerebellar dysfunction is posited as causality of disease. Case History: A 67-year-old right-handed male suffered a fall without loss of consciousness. Initial work-up revealed a left cerebellar hemispheric hemorrhage, requiring a decompressive craniotomy. Subsequently, the patient had gait instability, left hand clumsiness, dysarthria, change in cadence of speech, and difficulty with fine motor movements of his left hand, which gradually resolved. He also developed persistent chin tremor with vertical movement of the chin without tongue involvement. Voluntary movements of the chin and the mouth inhibit these movements. There were no somatosensory complaints and no chin tremors pre-existed the trauma. Neurological examination: Cranial Nerve (CN) examination CN I: Alcohol Sniff Test: 5 (anosmia). CN III, IV, VI: Saccadic horizontal eye movements. Motor examination: spontaneous vertical tremor of the chin and lower lip not involving the tongue. 1+cogwheel rigidity right upper extremity. Gait: unstable, wide based, with dystonic posture of the left upper extremity. Cerebellar examination: Bilateral finger to nose dysmetria, left>right. Dysdiadochokinesia of the left upper extremity. Holmes rebound: positive ipsilaterally. Conclusion: This could be understood given that there is a direct reciprocal connection between cerebellum and basal ganglia, from dentate nucleus of the cerebellum to the striatum via the thalamus and from the cerebellar cortex to the subthalamic nucleus via the pontine nucleus. This suggests that cerebellar dysfunction may be a primary or alternative abnormality as an origin for Rabbit Syndrome, warranting further research.

Background: Frontotemporal Lobar Degeneration (FTLD) is a family of neuropathologic diseases that tend to affect frontal and anterior temporal brain systems and lead to one of a variety of Frontotemporal Dementia (FTD) syndromes. The two major types of FTLD are FTLD-tau and FTLD-TDP43. One extremely rare (∼60 cases in the literature) type of FTLD-tau is Globular Glial Tauopathy (GGT), characterized by 4-repeat tau globular inclusions in astrocytes and oligodendrocytes. Patients with GGT usually present with an FTD syndrome but sometimes with an ALS/PLS motor syndrome and occasionally with a progressive amnestic dementia. Here, we present a case and discuss clinical and imaging features that may raise the possibility of GGT. Case History: MS presented at age 73 with 3 years of personality and behavioral symptoms consistent with bvFTD, along with features of Geschwind Syndrome. Imaging revealed atrophy in the right temporal pole, right amygdala, and right hippocampus. White matter hyperintensities were observed subjacent to regional atrophy. She died at age 84. An autopsy showed many globular glial tau inclusions in frontal and temporal white matter and brainstem white matter (GGT type III); substantial Alzheimer’s Disease Neuropathologic Changes were also present (A3B3C2). The burden of both neuropathologic processes was heaviest in the frontal and temporal lobes. Conclusions: In patients presenting with an FTLD clinical syndrome, especially when accompanied by white matter hyperintensities subjacent to regional atrophy, GGT should be considered a rare member of the differential diagnosis of possible neuropathologic etiologies.

Background: Neurological disorders may present with antecedent psychiatric symptoms, though such cases are often misdiagnosed as primary psychiatric illness. For example, obsessive-compulsive symptoms occur in a wide range of neurological disorders and a particular association with epilepsy has been noted. Typically seizures precede the onset of obsessive compulsive symptoms; an estimated 10%−20% of patients with seizures in the frontal or temporal lobes or ACC later develop OCD. However in rare cases OCD may be the presenting symptom of epilepsy. Suggested mechanisms range from development of personality characteristics to a kindling effect whereby localized seizures generalize to the limbic region overlapping with the neurocircuitry of OCD (the cortico-striatal-thalamic-cortical loop). Case History: A 13-year-old boy with no neuropsychiatric history developed one year of progressive obsessions and compulsions with impaired functioning related to contamination fears. No other neurological symptoms were noted. Initial workup including MRI, EEG, CTAngio, and neuroimmunology yielded mildly abnormal, nondiagnostic results. The patient was diagnosed with obsessive-compulsive disorder and did not respond to multiple treatment modalities. Over the following 6-months he developed syncope and GTCs. Repeat EEG was notable for an epileptogenic process in the absence of clinical seizure activity during exam. A diagnosis of epilepsy was given and treatment with an AED coupled with behavioral therapy led to remission of OCD symptoms. Conclusion: This case highlights the integrated nature of neurologic and psychiatric symptomatology and considers psychiatric symptoms as the presenting signs of underlying CNS disease. This case further elucidates our understanding of the neurocircuitry of OCD.

Background: Isolated myoclonus and opsoclonus myoclonus ataxia syndrome (OMAS) as an initial manifestation of the coronavirus disease 2019 (COVID-19) has not yet been described. Case History: A 55-year-old right-handed Hispanic woman, with no history of neurological dysfunction, was asymptomatic without fever, headaches, respiratory symptoms, myalgia or chemosensory dysfunction until four days prior to presentation when she gradually lost muscle control with uncontrollable arrhythmic nonrepetitive jerking and shaking throughout, involving her abdomen, arms, face and hands both with intention and at rest. Later that same day, she observed oscillopsia, whereby her visual field flickered vertically. On the fourth day after onset of symptoms, the patient’s COVID-19 RT-PCR on nasopharyngeal swab test was positive. Physical examination on day five: Afebrile. Cranial Nerve (CN) examination: CN III, IV, VI: Opsoclonus, spontaneous conjugate multidirectional eye movements without nystagmus and intersaccadic interval not restricted to a horizontal or vertical gaze. CN VII: Intermittent rapid closing and fluttering of eyelids. Gait: Unable to stand. Cerebellar examination: Finger-to-nose testing: Severe intention myoclonus. Myoclonic jerks were present on drift testing with inability to raise the arms due to upwards and negative myoclonic movements. Negative myoclonus on wrist extension. Lumbar puncture on day five: WBC count: 2 cells/µL, RBC count: 0 cells/µL, protein 26 mg/dl, gram stain negative, viral serology negative. Discussion: Those who present with myoclonus, oscillopsia, ataxia or opsoclonus without preexisting respiratory or chemosensory symptoms warrant evaluation for presence of COVID-19 infection.

Background: The COVID-19 pandemic has increased mental health issues worldwide. Patients with cognitive disorders may be at particular risk of neuropsychiatric decompensation. Telehealth may be an effective means of delivering care to these patients. Objective: To characterize neuropsychiatric symptom exacerbations reported by patients of a neuropsychiatry outpatient practice during the COVID-19 pandemic and evaluate the perceived efficacy of telehealth in addressing these symptoms. Methods: Patients who completed at least one telehealth visit at our practice after March 1, 2020 were invited to enroll in this prospective, single site study. Telephone surveys were conducted assessing neuropsychiatric symptoms and satisfaction with telehealth. Descriptive statistics summarize our findings. We used Fisher’s exact test to compare responses across demographic and diagnostic categories. Results: Thirty-eight patients completed the survey; 31 (82%) were white, 18 (47%) were female, and median age was 61. Diagnoses included acquired brain injury (traumatic, N=12, 32%; nontraumatic, N=9, 24%); mild cognitive impairment (N=9, 24%); dementia (N=5, 13%); and other (N=3, 5%). Exacerbations of anxiety (63%), irritability (61%), depression (58%), and memory impairment (58%) were most common. Symptom reports did not differ across age, race, or diagnosis, but women were more likely to report worsened memory (83% versus 35%, p=0.004), disorientation (76% versus 20%, p=0.001), and impulsivity (39% versus 5%, p=0.016). Thirty-seven patients (97%) reported overall satisfaction with telehealth. Conclusion: Multidomain neuropsychiatric symptoms increased during the pandemic in a population with access to telehealth. Women may be at greater risk. Telehealth can be an effective way to deliver care to these patients.

Background: The tau positron emission tomography (PET) ligand [18F]flortaucipir (FTP) has strong in vivo and postmortem evidence supporting its sensitivity and specificity for the measurement of tau pathology in Alzheimer’s disease. Its utility in Frontotemporal Lobar Degeneration (FTLD) appears limited, but few cases have been reported with imaging and postmortem examination. Objective: To examine the utility of our genetic FTLD model for the evaluation of tau PET ligands, investigating in vivo FTP PET and postmortem examination of two patients with genetic mutations predicting FTLD-TDP43 pathology. Methods: Our genetic FTLD tau PET model predicts that patients with GRN or C9orf72 mutations should not have elevated tau PET signal, while those with MAPT mutations should. One patient had a GRN mutation (65-year-old, behavioral variant frontotemporal dementia (bvFTD)) and the other had a C9orf72 expansion (52-year-old, bvFTD). They each underwent detailed clinical evaluation, MRI scan, PiB (amyloid) PET scan, and FTP scan, and were followed to autopsy. Results: We were surprised when each of these two cases showed elevated FTP PET signal localized in atrophic regions on MRI; the magnitude of signal increase was lower than that typically seen in AD. Neither case showed any evidence of tau neuropathologic changes, but rather the expected subtype of FTLD-TDP43 neuropathology typically associated with each genetic abnormality. Conclusion: These results further demonstrate the nonspecificity of the [18F]flortaucipir ligand as a biomarker for tau pathology in FTLD. This study supports the use of a genetic FTLD model for the evaluation of next-generation putative tau PET ligands.

Background: Syndrome of the Trephined (SoT) is a rare complication of decompressive craniectomy causing alterations in the blood-brain barrier, intracranial pressure, and cerebrospinal fluid volume; leading to headache, seizures, focal weakness, midbrain syndromes, cognitive deficits (worsened during paradoxical herniation). This warrants timely evaluation and management of emerging neuropsychiatric symptoms. How should a neuropsychiatrist approach evaluation of pertinent differential diagnoses? Case History: 58-year-old woman with bipolar I disorder suffered a right-MCA ischemic stroke with residual left-sided hemiparesis and seizures. Months after undergoing decompressive hemicraniectomy, she develops sinking skin flap syndrome with a 7mm right-to-left midline shift with paradoxical herniation. With altered mental status, right-sided hemiparesis, aphasia and dysphagia, she is diagnosed with SoT. Psychiatry was consulted for psychotropic reconciliation to optimize alertness prior to cranioplasty. On evaluation, she meets criteria for stuporous catatonia and hypoactive delirium, without evidence of worsening premorbid mood or seizure disorders. Neuroimaging showed chronic severe encephalomalacia of right frontal, temporal, and parietal lobes. We recommended discontinuing Olanzapine and Aripiprazole. Despite suspicion of catatonia, benzodiazepines were withheld given concurrent delirium, postictal encephalopathy, and frontal lobe injury. Conclusion: This is the first case-report of SoT presenting with catatonia, postictal encephalopathy, hypoactive delirium and deficits from postischemic encephalomalacia. Medically ill patients with neurotrauma are susceptible to similar symptomatology of altered sensorium and cognitive deficits, raising the hypothesis of frontal-subcortical circuit disturbance similar to Normal Pressure Hydrocephalus or Intracranial Hypotension presenting with catatonia or akinetic mutism. This warrants comprehensive neuropsychiatric evaluation to inform management for emerging sequalae, before and after cranioplasty.

Background: Neuropsychiatric symptoms cause considerable distress for patients and caregivers. Objective: To investigate the prevalence and level of distress that caregiver-reported mood and behavioral symptoms cause for patients and caregivers. Methods: A year-long descriptive and analytical study was conducted using the 10-item Neuropsychiatric Inventory (NPI) in a group of 79 patients with idiopathic Parkinson disease, in our specialized out-patient consultation. A corollary questionnaire was administered to characterize dopamine dysregulation syndrome. Results: 95% of caregivers reported at least 1 symptom in patients, with an average of 4 symptoms per patient. The most frequent symptoms were depression (77%), irritability (67%), and anxiety (57%). The least frequent were apathy (16%), delusions (14%), and hallucinations (14%). Dopamine dysregulation syndrome was present in 17.2% of our patients. Sleep problems were the most distressful to patients, while sleep disorders, aggressiveness and euphoria were particularly distressful for caregivers. Conclusion: Mood and behavioral symptoms are frequent in Parkinson disease from caregivers’ perspective. These symptoms cause considerable distress in patients and caregivers alike and, therefore, warrant a systematic and thorough assessment as well as specific treatment.

Background: Functional neurologic disorders, sometimes with la belle indifference, are often considered conversion reactions, rather than malingering or factitious disorders. However, repeated presentations with identical semiology to multiple hospitals over years suggests a factitious disorder imposed on the self. Clearly, the boundaries between conscious and subconscious behavior in medically unexplained neurological syndromes can be difficult to detect. It is even more challenging when both the underlying conflicts and motivations are vague and the falsification of symptoms is not directly associated with an identified deception. An organized interprofessional approach to such cases is needed to protect the patient, the healthcare system, and families from adverse effects. Case History: A 40-year-old male presented to the emergency department for acute flaccid paraplegia with complete anesthetic hypoesthesia below the T-10 to L-1 level. He had notable hyperreflexia with nonsustained clonus in the context of a negative workup, la belle indifference, and pseudologia phantastica. There were multiple, almost identical admissions to other hospitals for exactly the same scenario over a number of years. We review the distinguishing features between conversion disorder, Munchausen syndrome, and malingering in a patient with no apparent underlying stressors or incentives. Conclusions: This case highlights the importance of distinguishing between factitious disorder, conversion, and malingering when symptoms and underlying motives are discordant and, thus, potentially misleading. Treatment options are considered.

Background: Neuropsychiatric symptoms (NPS) and neuroimaging biomarkers are independent risk factors for cognitive decline in old age. Objective: To examine NPS with PiB-PET versus NPS with FDG-PET abnormalities in predicting cognitive trajectories. Methods: We conducted a longitudinal study in the setting of the population-based Mayo Clinic Study of Aging in Olmsted County, MN, including 1886 cognitively unimpaired persons aged≥50 years (median age 72 years, 1013 males, 530 APOE ɛ4 carriers). NPS at baseline were assessed using Neuropsychiatric Inventory Questionnaire (NPI-Q), and Beck Depression (BDI-II) and Anxiety Inventories (BAI). Glucose hypometabolism was measured by FDG-PET and defined as an SUVR≤1.47 in regions typically affected in Alzheimer’s disease; cortical amyloid deposition was measured using PiB-PET and an abnormal load was defined as an SUVR≥1.48. Neuropsychological testing was done approximately every 15 months, and we calculated global and domain-specific cognitive z-scores (memory, language, attention, visuospatial skills). Results: Linear mixed-effect models adjusted for age, sex, education and previous cognitive testing revealed statistically significant three-way interactions between PiB-PET and BDI-total score with global cognitive, attention, language and visuospatial z-scores, indicating that persons with higher amyloid deposition and higher BDI-II-assessed depression had more pronounced cognitive decline over time. In addition, we observed several additional significant three-way interactions, for example between PiB-PET and NPI-Q-assessed appetite change, depression, disinhibitions, hallucinations, and irritability with faster decline in attention z-score. Conclusion: NPS and increased brain amyloid deposition but not glucose hypometabolism interact in accelerating global and domain-specific cognitive decline in community-dwelling older adults.

Background: Despite the first identification of the classic purple dermatological plaques by Hutchinson in 1869 and the revolutionary advancements in our understanding of complex multisystem disorders, neurosarcoidosis remains a clinical entity with a myriad of presentations. Involvement of the nervous system is seen in 5%−15% of cases (with meningeal invasion being more common than parenchymal infiltration) and requires prompt intervention with glucocorticoids, glucocorticoid sparing immunosuppressants, or TNF-α inhibitors. Reported neuropsychiatric presentations include psychosis, mood disturbances, cognitive impairment, delirium, and personality changes. Here we present a case of a patient with a history of sarcoidosis but no known psychiatric history who presented with multiple neurobehavioral symptoms including personality changes, hypnopompic hallucinations, somnambulism, and familial concerns for psychosis. Case History: Our patient was a 42-year-old woman brought in by her mother due to concern for worsening delusional and hallucinatory behavior over the last week. We were consulted to assess for underlying psychosis. However, after multiple interviews, she consistently failed to demonstrate evidence of a primary thought disorder as it became evident that her aberrant behavior (such as brandishing a butter knife at night) was misinterpreted by her family. MRI imaging of her brain and spine revealed diffuse meningeal and spinal enhancing lesions. Thus, we recommended holding all anticholinergic medications, not starting scheduled antipsychotics, and aggressively treating her neurosarcoid flare resulting in a phenomenal response of her neurobehavioral symptoms. Conclusion: Consultants should include neurosarcoidosis in a broad differential when assessing neuropsychiatric behavioral disturbances of dubious origins in the general hospital setting.

Background: Loneliness and wisdom are personality traits with contrasting relationships with health and well-being. Loneliness is consistently associated with worse health outcomes. Wisdom is a complex trait consisting of empathy/compassion, emotional regulation, decisiveness, acceptance of diverse perspectives, and self-reflection. It is usually associated with better mental health. Recent reports indicate that wisdom is inversely correlated with loneliness; however, the neurobiological correlates of the two traits have not been systematically examined. Objective: To identify neurobiological correlates of loneliness and wisdom. Methods: We conducted systematic review of publications containing measures of loneliness or wisdom and of neurobiology. Results: Many publications highlighted involvement of several similar brain regions in both loneliness and wisdom: medial and lateral prefrontal cortex (PFC), insula, amygdala, and temporo-parietal junction. These seem to be somewhat differentially activated in individuals exhibiting high loneliness versus high wisdom. Medial PFC plays a prominent role in in self-referential processing involved in loneliness and in several components of wisdom (empathy/compassion, emotional regulation, and self- reflection). Wisdom is associated with lower amygdala reactivity, while loneliness is believed to lead to hypervigilance in response to negative or stressful stimuli. The overlap in neurobiology of loneliness and wisdom is partial; however, they seem to be, in part, associated with opposite neurobiological correlates. Conclusion: Loneliness and wisdom are multidimensional traits with far-reaching implications for mental well-being. This review provides preliminary evidence of an inverse neurobiological association between loneliness and wisdom. Increasing the level of wisdom could reduce loneliness, though this hypothesis warrants empirical testing.

Background: Few case reports of catatonia following hyponatremia are found in the literature. Tethered to schizophrenia for decades as a result of early conceptualizations by Kraepelin and Bleuler, catatonia is better characterized as its own condition found in not only idiopathic psychiatric disorders, but also medical and neurological maladies. Cotard’s syndrome, also known as walking corpse syndrome, is a rare delusional disorder. Case History: A 62-year-old man with a longstanding bipolar diathesis was admitted in the setting of self-neglect and repeated decompensations. Over the course of several months and unsuccessful brief attempts at reentering the community, he began endorsing a debilitating sense of anxiety different in both quality and intensity from prior affective states. Upon being found unresponsive, a workup in the intensive care unit revealed urinary retention and a drop in sodium to less than 110. What followed was a new neurobehavioral profile composed of perseveration, withdrawal, immobility, and nihilistic delusions of being dead or having lost his blood and limbs. The patient shed more than 60 lbs in two months’ time. MRI T2 FLAIR and DWI sequences were not consistent with osmotic demyelination syndrome. Lorazepam trial evidenced negligible benefit, yet subsequent bilateral ECT with memantine augmentation demonstrated modest but clinically significant effects. Conclusions: This case highlights the complex neuropsychiatric sequelae resulting from acute hyponatremia not attributable to osmotic demyelination. Consequent phenomenology resembling a catatonic-like state and Cotard’s syndrome may respond to ECT and memantine after failure of a benzodiazepine trial.

Background: The microtubule-associated protein tau (MAPT) gene is the site of one of the three most common mutations in genetic frontotemporal dementia (FTD). Clinically, the MAPT mutation is often associated with certain distinguishing features, including earlier age at symptom onset and death than other forms of genetic FTD, more prominent behavioral symptoms, Parkinsonian features, and atrophy especially concentrated in the anteromedial temporal lobes, orbitofrontal lobes, and insula. This report features the first case of a patient with a MAPT mutation presenting with progressive cerebellar ataxia as the chief symptom. Case History: Heterogeneous clinical manifestations of the MAPT mutation are well-documented in the literature; however, cerebellar ataxia represents a novel presentation. This report describes a 48-year-old man with a family history of behavioral variant frontotemporal dementia presenting with isolated progressive cerebellar ataxia. Magnetic resonance imaging revealed disproportionate cerebellar atrophy. After a four-year delay featuring visits with many different specialists, a causative MAPT mutation was identified. Worsening cerebellar ataxia remained his only notable symptom, although he also manifested tinnitus early in the disease course, and later began displaying very slight behavioral changes and mildly reduced fluency compatible with a nonfluent primary progressive aphasia phenotype secondary to a MAPT mutation. Conclusion: This case highlights to clinicians that a MAPT mutation should be suspected in patients with cerebellar ataxia—particularly with a family history of neurodegenerative disease suggestive of FTD—and further serves as a reminder of the heterogeneous clinical profiles manifested by MAPT mutations.

Background: Since the 1990s, virtual reality (VR) has been employed as a technological alternative for 3D imaging needs in the medical field. In addition to VR, augmented reality (AR) and mixed reality (MR) are emerging imaging technologies progressively being applied as valuable adjunct tools in medicine (i.e. neurosurgery, neuropsychiatry) and medical education (i.e. anatomy). Objectives: To disseminate peer-reviewed information regarding the advantages of VR technologies in clinical medicine and medical education; and to increase the knowledge and applicability of VR technologies into neuroanatomy and clinical neuroscience pedagogies. These technologies have the potential to facilitate increased learning by extrapolating medical imaging data (e.g. neuroanatomical structures, pathologies). It also fosters the application of clinical knowledge translatable to the “bedside.” Methods: New clinical and research findings regarding VR technologies, particularly relevant to neuropsychiatry and medical education, were reviewed, synthesized and summarized. The most relevant information and functional descriptions including advantages and disadvantages of VR technologies were integrated into graphic depictions and instructional representations. Results: The literature postulates interesting differences and functional nuances between VR technologies. The potential for superior integration of basic neuroscience and clinical neuropsychiatry into improved clinical outcomes is a major advantage. The high cost, logistics and cumbersome design of most VR hardware, along with the scarcity of VR neuroanatomy software remains a challenge for the use of these emerging technologies. Conclusion: VR technologies warrant more attention from both medical education and neuropsychiatry. Innovations in AR and MR subsets appear to have higher potential in neuroscience and medicine.

Background: Abuse of substances such as opiates, cocaine, and inhalants is known to cause destruction of brain myelin leading to toxic leukoencephalopathy, but little is known about recovery or prognosis in this disorder. In light of the ongoing opiate epidemic in the United States, it is important to understand the natural history of patients who have neurological complications from illicit drug exposure. Objective: To conduct a scoping review of the literature regarding prognosis in described cases and case series of substance abuse related toxic leukoencephalopathy. Methods: A systematic review of the literature was conducted using the terms “toxic,” “leukoencephalopathy,” “prognosis,” “opiate,” and “substance abuse” in PubMed, Ovid, and Google Scholar databases. Cases and case series were eligible for inclusion if they described acute leukoencephalopathy with a clear temporal association with opiate, cocaine, or inhalant abuse. Results: Of 51 articles identified, 18 were eligible for inclusion in the review, yielding a total of 73 cases of substance abuse related toxic leukoencephalopathy. Of these patients, 19 died at an average time from onset to death of 23.6 days. Of those who survived with descriptions of long-term follow-up, 12.3% (N=9) had partial recovery, and 6.8% (N=5) had full recovery at an average follow-up time of 20.2 months. Conclusion: Toxic leukoencephalopathy related to substance abuse is associated with a wide range of clinical outcomes. Death is common, but among patients who survive, there is potential for partial recovery and, in some cases, full recovery after a protracted course.

Background: Parkinson’s disease (PD) is a neurodegenerative disorder often associated with high rates of neuropsychiatric symptoms. The development of nonmotor symptoms in PD is thought to be related to the neurologic changes rather than reactive to the disease-state or disability. Objective: The aim of the study was to investigate the relationship between degradation of frontal white matter (WM) tracts and the presence of depression, anxiety, and apathy in patients with Parkinson’s disease. Methods: PD participants were subgrouped into with neuropsychiatric symptoms (Neuropsych+) and without (Neuropsych–). Controls were age and sex matched. FLAIR-DTI sequences were captured on 3T scanner. Depression, anxiety, and apathy were measured with the Geriatric Depression Scale, GAD-7, and Apathy Inventory. We analyzed the fornix, bilateral uncinate fasciculus. DTI tractography was performed by hand and checked for intra- and interrater reliability. Volume measurements of the nucleus accumbens, amygdala, caudate, hippocampus, and putamen for secondary analysis were performed with FreeSurfer. Results: No significant differences in WM tract degradation were found between the PD groups and control groups, nor between Neuropsych+and Neuropsych–. No DTI measurements of degradation were associated with severity of neuropsychiatric symptoms. Secondary analysis revealed a significant relationship between presence of neuropsychiatric symptoms and decreased volume of the left and right hippocampus, and right nucleus accumbens. Conclusion: PD patients with neuropsychiatric symptoms had preserved structural integrity of relevant frontal WM tracts. The presence of neuropsychiatric symptoms does not hinge on subatrophy scale neurodegeneration. This refutes that neuropsychiatric symptoms may be fixed or difficult to treat because of degenerative changes in these areas.

Background: Individuals with Mild Cognitive Impairment (MCI) have a higher dementia progression rate than the healthy elderly. However, they are also known to revert to normal cognition, so early intervention during the MCI stage is required. MCI is reported to be associated with a reduction in frontal lobe volume, blood flow, and metabolism; dysfunction of the frontal lobes has also been reported to increase the risk of progressing to dementia. Objective: This study verifies the effects of cognitive rehabilitation targeting executive dysfunction of the frontal lobes in MCI. Methods: 10 who were suspected of having MCI based on MoCA-J were used as the subjects of this study. The subjects took part in a one-hour cognitive remediation therapy once or twice a week for a total of 22 sessions. The cognitive remediation therapy used a Frontal/Executive Program (FEP) that was formulated by focusing on the frontal lobe/executive function. Results: The intervention showed effects on verbal memory, working memory, verbal fluency, executive function, conversion of sets, and persistent wrong answers. These effects on verbal memory, verbal fluency, and conversion of sets were maintained for a period of three months. In addition, 60.0% of the subject reverted to and maintained normal cognition for three months. Conclusion: Improvements were seen in the executive function of the frontal lobes, which are subject to the risk of progression from MCI to dementia, due to cognitive rehabilitation targeting frontal lobe executive function. A high rate of reversion was also seen from MCI to normal cognition.

Background: Neuroscience Education Therapy (NET) has been successfully used for numerous overlapping pain conditions, but few studies have investigated NET for migraine. Objective: We sought to (1) review the literature on (NET) used for the treatment of various pain conditions to assess how NET has been studied thus far and (2) recommend considerations for future research of NET for the treatment of migraine. Methods: Scoping Review. Results: Overall, a NET curriculum consists of the following topics: pain does not equate to injury, pain is generated in the brain, perception, genetics, reward systems, fear, brain plasticity, and placebo/nocebo effects. Delivered through individual or group sessions, NET treatments often incorporate exercise programs and/or components of other evidence-based treatments e.g. cognitive-behavioral therapy, biofeedback, and relaxation. NET has significantly reduced catastrophizing, kinesiophobia, pain intensity, and disability in overlapping pain conditions. In migraine specific studies, when implemented together with traditional pharmacological treatments, NET has emerged as a promising therapy by reducing migraine days, pain intensity and duration, and acute medication intake. Conclusion: NET is an established treatment for pain conditions, and future research should focus on refining NET for migraine, examining delivery modality, dosage, components of other behavioral therapies to integrate, and migraine-specific NET curricula.

Background: An overarching explanation for schizophrenia eludes us. No single theory accounts for the various phenotypes associated with the disease. However, rare cases in which psychosis arises from focal neurological lesions offer us clues to potential underlying mechanisms. 3 key principles have been proposed for establishing a cause-effect relationship between psychosis and another condition: an atypical presentation of psychosis, temporality, and explicability (i.e. the psychosis is not better explained by a primary psychotic disorder). Such a case of secondary psychosis can support or challenge existing theories for aspects of schizophrenia, for example the generation of positive symptoms by dysfunction of the mesolimbic pathway. Case History: After 2 months of hearing voices, a 46-year-old woman with no relevant psychiatric history came to the emergency room. CT detected a brain abnormality, and she was hospitalized. MRI and angiogram revealed a de novo (a brain MRI taken 12 years earlier had been normal) arteriovenous malformation (AVM) deep in the right hemisphere, which distorted the medial temporal lobe and entire mesolimbic pathway. A continuous EEG was unremarkable, and the hallucinations did not respond to antiepileptic or antipsychotic medications. Conclusion: To our knowledge, this case is the first reported example of psychosis as an initial manifestation of a de novo brain AVM. In satisfying proposed conditions for secondary psychosis, it supports dysfunction of the mesolimbic pathway as a model for the generation of positive symptoms. This case is an example of how secondary psychoses can help to elucidate the pathophysiology of primary ones like schizophrenia.

Background: Primary progressive aphasia (PPA) is a debilitating syndrome marked by progressive loss of language skills from neurodegenerative disease. No current effective PPA treatments exist. Noninvasive brain stimulation, such as transcranial direct current stimulation (tDCS), when paired with language therapy, has demonstrated the ability to enhance language outcomes in PPA. However, variability in tDCS response is not well understood. Objective and Methods: In a blinded, within-group crossover pilot study, PPA patients (N=12) received two-weeks intervention of high-definition-tDCS (HD-tDCS) with constraint-induced language therapy (CILT). Multilevel linear regression using backward-fitted models were performed to assess whether baseline cortical thickness or volume of regions involved in language function predict tDCS-induced naming improvements (WAB-naming subtest), at 0-weeks (immediate) and 6-weeks postintervention. Results: Greater pars opercularis thickness predicted naming gains at 0-weeks. At 6-weeks, greater middle temporal gyrus and lower posterior-superior temporal gyrus thickness predicted naming gains. Thickness did not predict naming gains in sham. Volume did not predict 0-week performance in active. At 0-weeks, greater pars orbitalis and MTG volume, but less posterior-STG volume predicted naming gains in sham. At 6-weeks, greater volume of pars triangularis and MTG, but lower posterior/anterior-STG significantly predicted naming gains in active; volume did not predict gains in sham. Conclusion: Frontal cortical thickness predicted 0-week tDCS-induced gains and temporal areas at 6-weeks (active, not sham), suggesting a broader network may maintain treatment gains. Volume predicting 0-week sham gains may indicate the immediate behavioral therapy response. Collectively, cortical measures predicted gains in active, not sham, suggesting that pairing HD-tDCS+CILT may be important for maintaining treatment effects.

Background: Functional neurological disorder (FND) is a core neuropsychiatric condition. To date, promising yet inconsistently identified neural circuit profiles were observed in patients with FND, suggesting important gaps remain in our systems-level neurobiological understanding. As such, other important physiological variables including autonomic, endocrine and inflammation findings need to be contextualized for a complete mechanistic picture. Objective: Here, we performed a systematic review and meta-analysis of available case-control and cohort studies in FND. Methods: PubMed, PsycINFO and Embase databases were searched from January 1, 1900 to September 1, 2020 for studies that investigated autonomic, endocrine and/or inflammation markers in patients with FND. Results: Sixty-six of 2,056 screened records were included in the review representing 1,699 patients, with data from 23 articles used in meta-analyses. Findings show that children/adolescents with FND versus healthy controls (HCs) have increased resting heart rate; there is also a tendency toward reduced resting heart rate variability in patients with FND across the lifespan versus HCs. In adults, peri-ictal heart rate differentiated those with functional seizures from individuals with epileptic seizures. Other autonomic and endocrine profiles in patients with FND were heterogeneous, with several studies highlighting the importance of individual differences. Inflammation research in FND remains in its early stages. Conclusion: Moving forward, there is a need to use larger sample sizes to consider the complex interplay between functional neurological symptoms and behavioral, psychological, autonomic, endocrine, inflammation, neuroimaging and epigenetic/genetic data. More research is needed to determine whether FND is mechanistically (and etiologically) similar or distinct across phenotypes.

Background: An improved understanding of long-term psychiatric complications can inform counseling and diagnostic screening of survivors of autoimmune encephalitis. Objective: We aimed to characterize long-term psychiatric symptoms and disorders in patients with autoimmune encephalitis. Method: We retrospectively identified patients ages 18–100 treated at NYULMC from 2007–2017 with a diagnosis of 1) antibody receptor positive and clinically possible autoimmune encephalitis, 2) definite autoimmune limbic encephalitis, and 3) probable seronegative autoimmune encephalitis, using Graus diagnostic criteria. Patients were then evaluated prospectively using Mini Neuropsychiatric Inventory (MINI) 7.0.2 and Profile of Mood States-2 (POMS-2). Results: 14 subjects (4 males) with a mean age of 41.2 years were included. Median time to follow-up was 5.8 years. Subtypes included anti-NMDAR (29%), anti-GAD65 (21%), anti-LGI1 (14%) and antibody negative (36%) autoimmune encephalitis. 35% of subjects had been previously diagnosed with a psychiatric disorder. 64% had a new diagnosis of a psychiatric disorder on follow-up (as per MINI) and 21% reported mood disturbance (as per POMS-2). New psychiatric diagnoses included Major Depression (35.71%), Bipolar Disorder 1 & 2 (7.1% each), Panic Disorder, current (14.2%) & lifetime (35.71%), Agoraphobia and Social Anxiety Disorder (14.2% each), and Current Mild Alcohol Use Disorder (7.1%). 28% of subjects reported worsening of prior psychiatric disorders. Only 22% of those with a new psychiatric diagnosis were receiving treatment. Conclusion: There is a high prevalence of psychiatric comorbidity in patients with autoimmune encephalitis and a significant proportion of these patient remain undertreated. Patients with autoimmune encephalitis may need continued follow-up with mental health providers.

Background: Behavioral variant frontotemporal dementia (bvFTD) is easily misdiagnosed as a primary psychiatric disorder (PPD) such as bipolar, autism spectrum, or attention deficit disorder. While dedicated scales are being developed to confirm a bvFTD diagnosis, primary care doctors and psychiatrists may be more likely to initially screen for more common disorders. Objective: We investigate the probability of PPD screens being positive in bvFTD. Methods: The care partners of 21 patients with bvFTD who presented to a University Memory Clinic filled electronic packets including questionnaires targeting PPD. These included the Mood Disorders Questionnaire (MDQ), Adult ADHD Self Report Scale (ASRS 1.1), and the Ritvo Autism and Asperger Diagnostic Scale (RAADS-14). We describe the proportion of patients with bvFTD who are positive on each screening questionnaire and suggest refined methods of interpretation when considering possible bvFTD. Results: Of the three psychiatric scales, the MDQ had the best performance in bvFTD with only 14% of patients screening positive for possible bipolar disorder. Diagnostic certainty may be further augmented by a low reported prevalence of sleep loss in bvFTD (< 5%). 62% of bvFTD patients screened positive for ADHD, and 81% screened positive for autism spectrum disorder (ASD). Over 75% of reported symptoms on the RAADS-14 occurred exclusively in adulthood, however—a pattern that might alert a clinician to possible bvFTD. Conclusion: With the exception of the MDQ, the psychiatric screens we examined may mislead unwary clinicians regarding bvFTD, but further attention to details within the scales may point toward an accurate bvFTD diagnosis.

Background: There is a subset of Covid-19 patients who, despite relatively benign initial disease course, develop symptoms persistent beyond that which is typically expected. Patients with functional neurological disorder (FND) are a vulnerable population that often are seen by many subspecialists leading to a delay in diagnosis. The framework of FND may help to explain some patients with persistent symptoms, labeled “long-haulers.” Case History: A 49-year-old woman developed symptoms consistent with Covid-19 infection with positive PCR test, fever for 3–4 days, without need for hospitalization. She presented to clinic 9 months later due to persistent symptoms of brain fog, emotional lability, speech problems, memory difficulties, dizziness, insomnia, and feeling overwhelmed by sensory stimuli, all of which were variable throughout her nine-month course. Notably, prior to the Covid-19 infection, the patient suffered from fibromyalgia, multiple concussions with prolonged recovery time, and chronic Lyme disease, all of which shared symptoms similar to her current complaints. Other pertinent history included childhood trauma and posttraumatic stress disorder, with multiple psychotropic medication trials that were not well tolerated. She was diagnosed with FND and is planned to begin psychotherapy and cognitive rehabilitation. Conclusions: The case illustrates the importance of considering FND in patients presenting with chronic symptoms attributed to Covid-19 infection, as a more precise diagnosis can more effectively inform treatments and explain course. Little is known regarding the extent of neuropsychiatric sequelae of Covid-19; one can consider FND coexisting with or a perpetuating factor for chronic symptoms postinfection.

Background: Approximately 10% of human spongiform encephalopathies are genetically transmitted. Both single point mutations and octapeptide repeat insertions of varying lengths have been discovered within the open reading frame of the human prion protein (PRNP). Some mutations have been correlated with distinct clinical course and neuropathology. Case History: A 35-year-old female with a strong family history of early onset dementia (mother and grandmother) presented to our cognitive disorders’ clinic with several years of depressive symptoms and apathy, later, developing cognitive decline and dementia. The initial workup including MRI (parietal atrophy) and neuropsychological testing (verbal and nonverbal memory impairment) resembled that of early onset Alzheimer’s disease but genetic testing revealed genetic mutation in PRNP gene yielding a diagnosis of familial human spongiform encephalopathy/prion disease. The patient has experienced a slowly progressive course with cognitive, functional, and behavioral decline. Neurobehavioral symptoms have responded to psychotropic medications. Conclusions: This case illustrates considering family history as well as prion disease in the differential of young onset dementia. The progression and clinical course in this case resembled individuals with early onset AD dementia.

Background: Parkinson’s disease (PD) is known to have multiple motor and nonmotor manifestations ranging from depression to dementia. However, catatonia is a rare presentation of Parkinson’s disease in fact being described in only 4 cases so far. Case History: This case describes a 68-year-old female who presented for a new patient visit. She reported a previous diagnosis of Parkinson’s disease characterized by slowing of gait with short shuffling steps, loss of facial expression, and tremor in her right arm and a one-year history of episodes where she would “lock down,” have difficulty swallowing and choking. During these episodes the patient would not get up or move and would be noted to have minimal interaction with her surrounding environment. She was also noted to have repetitive movements without any purpose during these episodes such as swaying of her arms and rocking back and forth. Duration of these episodes would last from 30 minutes to 8 hours. ENT specialist was unable to find a structural cause of her dysphagia. Her neurologist prescribed increasing doses of carbidopa-levodopa as well as a dopamine infusion pump with minimal improvement. The patient also had trials with clonazepam and ropinirole which caused fatigue and dizziness. Patient’s primary care physician prescribed a course of lorazepam which was effective in aborting the catatonic episodes in about 10 minutes. Patient underwent a full panel of diagnostic investigations including blood work and radiological investigations which were noncontributory. Conclusion: Catatonia in patients with PD is a very uncommon presentation.

Background: Risperidone is a second-generation antipsychotic that has been associated with hyperprolactinemia. While MAO and D2 receptor polymorphisms and variations in CYP2D6 metabolic factors have been implicated, one primary contributing factor is hypothesized to be an imbalance between 5HT2A antagonism (which inhibits prolactin release) and D2 antagonism (which promotes prolactin release). While there are multiple reports of reducing dosages or switching agents in response to risperidone-induced hyperprolactinemia, another potential approach would be to further antagonize the 5HT2A receptors. Case History: A 22-year-old female with childhood-onset PTSD with prominent dissociation, disorganized thinking and nightmares was started on risperidone 0.5 mg nightly with significant symptomatic relief. She then reported an onset of amenorrhea with an onset approximately one month later. Prolactin level six months into treatment was found to be 103.08 ng/mL (ref. range 3.34–26.72). The patient then tried switching agents successively to aripiprazole, ziprasidone and iloperidone with worsening of symptoms, but normalization of menstrual cycles. She elected to resume risperidone 0.5 mg nightly with a repeat prolactin level in six weeks which was found to be elevated at 70.4 vg/mL. Due to significant symptom relief, the addition of a 5HT2A antagonist was offered. Hydroxyzine 25 mg nightly was added to her regimen with the prolactin level falling to 66.5 ng/mL with normalization of menstrual cycle at week 18 and 22.5 ng/mL at week 54 on the combined regimen. Conclusion: Risperidone-induced hyperprolactinemia can be reversed with adjunctive 5HT2A antagonists.

Background: Hashimoto’s Encephalopathy (HE); was first described in 1966, and roughly 200 cases have been reported since. The prevalence of thyroid disorders in children between ages 11–18 is 1% and Hashimoto’s thyroiditis is the most common cause. Patients with HE can present with altered mental status, hallucinations, tremors, mood changes, and anti-TPO elevation. Untreated HE has been reported to cause schizophrenic-like presentations in elderly patients, and to our knowledge, this would be one of the few reported cases of a young child with a schizophrenic-like presentation. The aim of this case is to illustrate how to differentiate between primary psychiatric conditions and HE. Case History: We present a 12-year-old female, seen in the emergency department, with depressed mood and suicidal ideation. She also complained of schizophrenic-like symptoms such as auditory and visual hallucinations and is noted to have flat affect, and psychomotor retardation. Her mother reported declining school performance and severe fatigue. She was also found to have chaotic saccadic eye movements and a jaw tremor. Basic labs showed TSH of 21.2 μIU/dL and TPO antibodies of 430 IU/mL. Neuroimaging and EEG were normal. When the clinical presentation was correlated with labs, the diagnosis of HE was suspected. The patient improved with Escitalopram, Aripiprazole, and Levothyroxine. Conclusions: This case highlights the need to broaden our differential diagnoses when children present with depression, psychosis or any abnormal behaviors. This case educates providers in delineating psychiatric symptoms due to Hashimoto's Encephalopathy from primary psychiatric problems and further discusses the treatment modalities.

Background: Friedrich Ataxia (FRDA) is the most common cerebellar ataxia with multisystemic consequences. Mean age of death is 36.5 years. The cerebellum is associated with emotional regulation. Higher scores of the Beck Depression Inventory-II are reported with correlation to ataxia severity. Although suicide is a cause of death in FRDA, few studies discuss psychiatric management. We describe a case and discuss the importance of interventions for depression and suicidality. Case History: A 27-year-old Caucasian man with no previous psychiatric diagnosis, developing ataxia at 14 years old, diagnosed with FRDA at 22 years old, was admitted after a hanging attempt under the influence of alcohol. He had discontinued a prophylactic antidepressant trial prescribed at time of FRDA diagnosis due to lack of perceived effect. Upon hospitalization, he was diagnosed with Major Depressive Disorder. He exhibited severe bilateral cerebellar ataxia. EKG was positive for ischemic disease. A family meeting revealed several years of ongoing neurovegetative symptoms, emotional lability, with recent financial issues and an ongoing divorce. He was initiated on sertraline 50mg daily. Physical, occupational, and speech therapy was consulted. He was discharged on day 4 following improvement in suicidality. Conclusions: Regardless of the origin of depression in FRDA, the disease’s burden poses significant impact on the quality of life. Depression is likely undertreated in the presence of striking physical symptoms. We urge routine psychiatric assessments and intervention in FRDA. A multidisciplinary treatment plan should be pursued, including pharmacotherapy and psychotherapy, along with the usual interventions for the patient’s well-being.

Background: Stiff person syndrome (SPS) is a rare neurologic disorder with characteristic muscle spasms and painful rigidity. While psychiatric comorbidities are suspected, a decisive link has yet to be established. Objective: This retrospective cohort study aimed to identify features in patients’ past medical histories that predict SPS. Methods: 322 past medical history items from 23 patients carrying SPS diagnoses and 25 controls, all anti-GAD positive, were vectorized as binary features. Using only features present in 4 or more patients (27 features), we generated a support vector machine (SVM) model using a Gaussian radial basis function kernel with inputs randomly split into training and test groups following a repeated stratified cross-validation scheme over 40 iterations, and feature importance assessed on the aggregate results. Features with the highest permutation importance scores were isolated as inputs for an optimized SVM model following the aforementioned iterative algorithm. Feature importance analysis was performed on the aggregate results. Results: The initial model (following the first feature reduction step) yielded an accuracy of 61% (CI₉₅[42%−80%]) and identified 8 features with high predictive power (depression, dysphagia, joint pain, headache, anxiety, hypothyroidism, gastroesophageal reflux disease, dyslipidemia; highest to lowest importance). The subsequent model trained on these features yielded an improved accuracy of 82% (CI₉₅[67%−97%]). Conclusion: The final model predicted SPS with an 82% accuracy based only on patients’ past medical histories and ranked depression and anxiety as important predictors. This highlights SPS’ association with psychiatric conditions and warrants an in-depth exploration for possible pathophysiological connections.

Background: Intermittent theta-burst stimulation (iTBS) was recently demonstrated to be noninferior to 10Hz rTMS (repetitive transcranial magnetic stimulation) in treating major depressive disorder (MDD). Few studies exist directly comparing early clinical improvement between modalities. Objective: Our study sought to test the hypothesis that early clinical improvement could predict treatment response in both iTBS and 10Hz rTMS groups. Methods: Retrospective analyses of 105 participants with MDD that received open-label 10Hz rTMS (N=68) and iTBS (N=37) investigated clinical response to treatment using PHQ-9 (Patient Health Questionnaire 9) scores. Percent changes from treatment 10 and end of treatment compared with baseline were used to assess clinical response (defined as percent change>50%), as well as data-driven kernel density estimates to find distinct ‘responder’ subgroups. Results: We predicted nonresponse to 10Hz rTMS with 73.7% and 83.9% certainty if patients failed to achieve at least 20% improvement by treatment 10 using 50% and 40% as final response criteria. Likewise, nonresponse was predicted in iTBS groups with 65% certainty using both 50% and 45% final response criteria. As we decreased improvement criteria by treatment 10 from 20% to 10% and 0%, predictive values decreased for both 10Hz rTMS and iTBS. Conclusion: Patients who fail to achieve at least 20% improvement by session 10 in both 10Hz rTMS and iTBS groups have ∼70% chance of nonresponse to full courses of treatment. By predicting nonresponse in patients who do not rapidly respond to treatment, this information may assist psychiatrists in switching or adapting treatment strategies to optimize outcomes.

Background: The occurrence of psychosis in patients with multiple sclerosis (MS) has been described, both as emergence of new psychotic symptoms in a patient with MS, as well as secondary to MS itself. Current treatments for MS may also result in secondary psychosis. The relationship between MS and development of psychotic symptoms remains ill-defined. Case History: We present a case of a 34-year-old woman with MS presenting with affective symptoms after initiating treatment with Tecfidera (dimethyl fumarate). This adverse reaction has not been described in the literature to the best of our knowledge. The patient had no prior psychiatric history. She presented with abrupt onset of insomnia, aggression, hyper-religiosity and auditory hallucinations. She was admitted to hospital for observation. No antipsychotic medications were initiated. MRI was performed three months prior to presentation, and it remained stable when repeated. Her psychotic symptoms resolved upon discontinuation of Tecfidera. It was suggested her acute manic symptoms were precipitated by Tecfidera. This medication was not reinitiated. She represented to hospital after two months, exhibiting manic symptoms despite stable neurological illness. Her presentation was consistent with a new bipolar illness, but the authors cannot conclude whether this emerged secondary to MS rather than a comorbid diagnosis. Conclusion: The emergence of psychotic symptoms secondary to MS is described in the literature, however our clinical case demonstrates the complex interplay that might exist between a patient’s predisposition to psychiatric illness, neurological disease and medications and the challenges this can present when trying to establish a definitive diagnosis.

Background: Catatonia and delirium are mutually exclusive diagnoses in DSM-5. Both may have primary infectious etiology. Treatment of catatonia includes benzodiazepines and ECT, which may worsen delirium in typical elderly and frail patients. It’s important to treat primary cause. Case History: We present a case of recurrent catatonia as presenting signs of recurrent urinary tract infection in an elderly African American female with no previous psychiatric diagnosis. She initially presented frequently with confusion. Gradually presentations become more consistent with catatonia, given prominent rigidity, posturing, mutism as well as negativism. Initial benefit from Ativan was later negated by worsening confusion. Use of ECT improved her catatonia. However, recurrent UTI would worsen her status even during acute ECT course to the point she can’t consent for ECT voluntarily. This leads to repeated cycles of hospitalization, acute voluntary and involuntary ECT then infection and catatonia again with significant hospital utilization. Eventually placement of chronic catheter by Urology modified her disease course, improved her quality of life. Despite intermittent positive urine cultures, she is able to transition to outpatient maintenance ECT and regular urology clinic visit. Family noted more confusion with longer interval during tapering of ECT. She currently has maintenance ECT at 5–6 weeks and did not have any decompensation to severe catatonia or delirium. Conclusion: This is the case where ECT maintenance is used to treat and to prevent decompensation from catatonia secondary to underlying difficult-to-resolve chronic recurrent UTI.

Background: Attempting to localize depression with lesion-symptom mapping studies has led to inconsistent and conflicting findings. Multivariate lesion-symptom mapping is a new brain-behavior correlation method which may have advantages over mass univariate approaches when disease implicates multiple nodes of a network. Objective: To identify brain regions that may result in higher or lower depression symptom burden when lesioned, leveraging the largest lesion-symptom mapping dataset to date. Methods: 526 subjects with focal brain lesions were recruited across 2 sites. Subjects had brain imaging and a Beck Depression Inventory completed>3 months after lesion onset. Lesion-symptom mapping used sparse canonical correlation analysis to identify brain regions correlating with higher or lower depression symptom burden (“risk” or “resilience” regions, respectively). The regions were used as seeds in a functional connectivity analysis to identify “risk” and “resilience” brain networks. Results: Peak “risk” regions were bilateral insula and left prefrontal cortex (PFC). Peak “resilience” regions were right ventromedial prefrontal cortex (vmPFC), right orbitofrontal cortex (OFC), and right inferolateral temporal cortex. Cross-validated correlation was 0.12 (p=0.0064). Seed-based network analysis demonstrated peak “risk” region overlap with the ventral attention/salience network (correlation coefficient 0.69) and the peak “resilience” region overlap with the default mode network (0.60). Conclusions: Anterior insula and left PFC lesions pose the greatest risk of high depressive symptom burden and right OFC, vmPFC, and inferolateral temporal lobe lesions associate with lower depressive symptom burden. “Risk” lesions correspond with nodes of the ventral attention/salience network and “resilience” lesions correspond with nodes of the default mode network.

Background: The Symbol Digit Coding (SDC) test assesses attention and processing speed and is a putative cognitive marker for major depression. Transcranial Magnetic Stimulation (TMS) targets the left dorsolateral prefrontal cortex (DLPFC) in treating depression, an area of the brain important for these cognitive functions. Objective: To assess the hypothesis that targeting the left DLPFC with TMS will improve SDC scores in patients who have significant clinical response (at least a 50% improvement on the PHQ9). Methods: Subjects included 10 treatment-resistant major depression patients who had significant clinical response to left DLPFC TMS. They did the SDC and PHQ9 at baseline and at the end of the standard TMS treatment course (30 sessions). Results: There was a mean improvement on 2.2 on the SDC standard score and a mean improvement of 16.7 on the PHQ9 score after TMS. There was no significant correlation between change in SDC and PHQ9 scores using linear regression: F(1,8)=0.5524, p=0.4786. With logistic regression, there was no significant correlation between change in SDC score and probability of remission on the PHQ9: Chi-Square=3.2256, p=0.0725. Conclusion: Contrary to the expectation that TMS targeting the left DLPFC will improve cognition in patients getting TMS for major depression, we did not find a significant correlation between improvement in depression and improvement in SDC scores. This could be due to the SDC not being a very sensitive marker of cognitive improvement in depression, or alternatively, that the cognitive effects of left DLPFC TMS are not captured by the SDC.

Background: Logopenic variant Primary Progressive Aphasia (vlPPA) is a neurodegenerative process with a progressive course, without, yet, definitive treatment. Anticholinesterases, recommended by the regulatory authorities for the treatment of this entity have limited efficacy. Transcranial magnetic stimulation (TMS) has been used for the treatment of several neuropsychiatry conditions and a new form of it – theta burst stimulation (TBS) has recently demonstrated efficacy similar to the regular TMS with some advantages (possibility of giving more pulses in a shorter time). Some case reports used TMS for the treatment of PPA but not the use of TBS. Case History: Two patients (72 and 62 years) with symptoms of language impairment began to present a progressive decline of verbal communication characterized by difficulty notably in naming objects, impairment in finding words, and dysnomia that caused pauses in speaking. MRI and 18F-FDG PET compatible with vlPPA. They were submitted to 15 sessions of TBS. Both patients showed improvement in cognition, especially in language skills, one showed clinically relevant improvement in different domains of cognition, especially in lexical semantic processing, directly impacting the improvement of oral language production. Conclusions: These two cases illustrate the importance of new treatments for the treatment of PPA. Although both patients had reduction of their symptoms, one had a maintained improvement through several months. Current and former military service members who are evaluated for posttraumatic stress disorder would benefit from being screened for hypomania. Research with randomized, controlled clinical trial is needed to evaluate the efficacy of this technique.

Background: Peduncular hallucinosis (PH) is a rare phenomenon involving lesions in the cerebral peduncle that are often associated with complex visual hallucinations. While the pathophysiology of these hallucinations is unknown, current hypotheses suggest disturbance of thalamic inhibition, possibly mediated by dysfunction in the cholinergic and serotonergic pathways. The varied etiologies of these lesions, as described in case reports, include ischemia, hemorrhage, neoplasm, central pontine myelinolysis, and multiple sclerosis. Case History: A 31-year-old female with a history of spinal muscular atrophy and multiple sclerosis presented with a 12-year history of distressing, multimodal hallucinations. She had no other symptoms of primary psychosis and retained partial insight. Due to her complex past psychiatric history, her hallucinations were largely presumed to be part of her psychopathology until an MRI of her brain was completed. Imaging showed lesions in her pons, cerebral peduncles, and thalami, which were determined to be the etiology of her hallucinations. She was treated effectively with a low dose of quetiapine. Various symptom patterns including retained insight, the absence of other psychotic symptoms and a nonfluctuating time course helped to differentiate PH from other causes. Conclusions: One can differentiate PH from more common presentations of visual hallucinations by its identifiable lesion on imaging. The nature of the hallucinations themselves also differs in their extensive detail and vivid imagery, their nonpersecutory nature, and their absurdity causing many PH patients retain some insight. This case demonstrates the importance of a broad differential to avoid misdiagnosing an organic illness presenting with psychiatric symptomatology.