2019 American Neuropsychiatric Association Annual Meeting Abstracts

Background: The presentation of corticosteroid-induced neuropsychiatric disturbances is pleomorphic with mood disturbance and overt psychosis being the most common manifestations. Additionally, pregnancy is a time of significant stress on a woman’s body. It is thus unsurprising that 15%−30% of women will develop a diagnosable mental illness at some point during their pregnancy. The following case represents the importance of keeping a broad differential for new psychiatric symptoms during pregnancy and rapidly initiating treatment. Case History: Patient is a 30-year-old woman with no past psychiatric history who is 12 weeks pregnant with her first child. She presents to the hospital reporting one month of no sleep, thought disorganization and intense feelings of fear. At the time of symptom onset, patient was being treated with corticosteroids for an ear infection. Patient underwent large neurologic evaluation for possible autoimmune encephalitis which was unrevealing. Psychiatry started patient on Olanzapine to help with psychotic symptoms which provided patient some relief. Primary service concerned patient having autoimmune response to pregnancy and suggested termination of the pregnancy. Patient discharged home on Olanzapine with plan to terminate pregnancy. Prior to termination appointment patient made suicide attempt. Patient again presented to hospital, admitted to psychiatric service and ECT initiated. Patient’s mental status rapidly improved and successfully kept pregnancy. Conclusions: This study illustrates the importance of keeping a broad differential when working with pregnant women with encephalopathic symptoms.

Background: Weather parameters are known to influence mood, behavior, and symptom severity in various disease states. Seasonal Affective Disorder is a well-established phenomenon. Additionally, admission rates for bipolar disorder and suicide frequency may positively correlate with ambient temperature. A single European investigator found an association between lowered barometric pressure and the incidence of psychotic depression. Objective: The purpose of this study is to evaluate further the effects of various changing weather parameters on the onset of psychotic depression. Methods: Weather events were examined in relation to the onset dates of 259 subjects with psychotic depression who participated in the National Institute of Mental Health STOP-PD (The Study of Pharmacotherapy of Psychotic Depression) between December 2002 and June 2007. Weather data were obtained from the National Oceanic and Atmospheric Administration. Longitudinal logistic regression models were used to determine the effect of a specific weather predictor event on the onset of psychotic depression. Results: Temperature, atmospheric pressure, wind speed, and precipitation deviations from average by 2–3 SDs within 60 days prior to onset were associated with a statistically significant increased odds (1.55 to 1.90) of developing psychotic depression. Deviations from the dewpoint average did not have any effect on disease onset. Conclusions: Extreme temperature, atmospheric pressure, wind speed, and precipitation events all increase the likelihood of developing psychotic depression. Given the known role of temperature in nerve conduction and the variety of neuropsychiatric symptoms seen at pressure extremes, these results support a physiological, neurological and neuroinflammatory basis for psychotic depression.

Background: Approximately 50% of individuals with Alzheimer’s disease (AD) develop hallucinations and/or delusions. While these symptoms likely arise from dissociable cognitive processes, they are typically modeled together as “psychotic” symptoms and associations with brain atrophy or genotype are explored separately. Objective: We aimed to test the hypothesis that distinct interactions between regional brain structure and genetic polymorphisms in cholinergic, dopaminergic or glutamatergic neurotransmitter systems give rise to the presence of delusions and hallucinations in patients with AD. Methods: Partial least squares correspondence analysis was used to analyze the relationship between structural neuroimaging measures and 15 single nucleotide polymorphisms (SNPs) in a cross-sectional cohort of 125 participants from the Alzheimer’s Disease Neuroimaging Initiative (AD+Hallucinations=19, AD+Delusions=22, AD+Hallucinations and Delusions=20, AD Controls=64). Results: Preliminary analysis identified one component (p=0.01) which showed an underlying association between brain structure and genetic data. Boot strap analysis showed that greater cortical thickness of the right superior parietal region and smaller volumes of bilateral nucleus accumbens were associated with rs1806201 in the GRIN2B gene and with both rs1076560 and rs1800497 within the DRD2 gene. In post hoc comparisons, this pattern of brain structure separated participants with hallucinations from those without, while the combination of SNPs separated participants with hallucinations and/or delusions from those without either symptom. Conclusion: Interactions between brain structure and genetic polymorphisms in dopaminergic and glutamatergic systems may mediate the development of hallucinations and delusions in AD.

Background: Studies suggest a complex relationship of manic behavior and bipolar disorder (BD) with behavioral variant frontotemporal dementia (bvFTD). Objective: To investigate all associations of manic-like behavior and bvFTD. Methods: Among a large well-characterized cohort of bvFTD patients seen over a 17-year period, we retrospectively evaluated their clinical presentations for manic-like behaviors and a personal or family history of BD. The findings were compared with a review of the literature. Results: Among 380 bvFTD patients, 21 (5.5%, versus 3% for U.S. population) had preceding BD of any type, and at least 20 had a positive family history. An additional 23 presented with loquaciousness with press of speech, tangentiality and derailment, flight of ideas, intrusiveness, and increased energy. Nineteen of these patients had a progressive, right temporal predominant bvFTD, and four did not progress and were deemed “FTD–phenocopies.” The literature suggested that manic symptoms can result from damage to right frontotemporal neural structures from neurological lesions and from longstanding BD itself. In addition, a few patients have a probable genetic predisposition (C9orf72 and GRN mutations) to both BD and bvFTD. Conclusions: Manic-like symptoms can result from damage to right frontotemporal neural structures involved in emotional behavior in both bvFTD and in some patients with a background of BD. Among these later patients, there are a number who present with a bvFTD illness that does not progress, and are a cause of the FTD phenocopy syndrome described in the literature. Finally, there are rare genetic predispositions for both.

Background: Patients with Dandy-Walker variant often get referred to neuropsychiatry for management of psychosis and behavioral disturbance. Optimal treatment strategies are unavailable. A case report of successful treatment with sodium divalproex is presented. The role of an hypoplastic cerebellum and mega cisterna magna, toward an understanding of its neuropsychiatric phenotype is briefly discussed. Case History: Dandy-Walker variant is considered a milder form of Dandy-Walker malformation, with variable cerebellar vermis hypoplasia, with or without an enlarged cisterna magna. Presentation is often with a schizophrenia-like psychosis but also affective disturbances, and in almost all cases, aggressive behavior, all in the background of cognitive deficits. Antipsychotics have been used with limited response. This is a 26-year-old male with deteriorating academic performance first noted at age 14, followed by prominent cognitive deficits, psychosis and behavioral disturbance, in the form of elopement, inappropriate sexual behavior, destruction of property, and violence toward others, including parents, with several instances of police involvement. He was diagnosed with schizophrenia at age 14 and been unsuccessfully treated with various psychotropics since. MRI was compatible with Dandy-Walker variant. He was tried on sodium divalproex, based on a review of his records and the available literature. Subsequent behavioral monitoring showed a dramatic and sustained response to monotherapy with sodium divalproex. Conclusion: Sodium divalproex may be considered first, for the treatment of psychosis and behavioral disturbances in Dandy-Walker variant, however controlled studies are needed. In addition to cognitive and affective disturbances, the cerebellum’s role in psychosis is explored via described corticocerebellar circuits.

Background: Our understanding of the laterality of certain brain functions is supported by commonly seen phenomena in right sided strokes. In addition to left sided hemiparesis, if temporal and parietal lobes are involved, patients often demonstrate left sided neglect, an inability to attend to left visual space. Patients can also have anosognosia, an unawareness of their physical deficit, anosodiaphoria, an inappropriate emotional response to their condition, or even somatoparaphrenia, regarding their paralyzed limbs as completely foreign to their body. Personification of limbs in hemiplegia has been described, however there were no case studies found, in which patients utilized personification as a tool to recover motor function. Case History: In 2013, a 24-year-old right handed female suffered a ruptured anterior communicating artery (ACA) aneurysm leading to subarachnoid hemorrhage which was treated with craniotomy and clipping. She subsequently developed vasospasm with bilateral ACA infarcts necessitating craniectomy and right sided lobectomy. She was initially akinetic and mute, but improved with acute inpatient rehab. 5 years later, sequelae include compulsive counting and impaired social cognition. Motorically, she has recovered full strength, but has named each of her limbs and verbally directs them in order to perform voluntary movements. Conclusions: This case highlights the complexity of neurologic connections and the brain’s ability to reconstruct, after severe insult. This patient has recovered her strength, but now must utilize language from her relatively intact left hemisphere, to complete motor tasks. Further research may yield new therapeutic strategies utilizing language in motor recovery, following right sided strokes.

Background: Malignant catatonia is a form of catatonia accompanied by autonomic dysfunction. The pathophysiology of catatonia is not fully understood. In depressed patients, it was shown that cortisol levels decreased following ECT. There is little research on the effects of catatonia and ECT on other endocrine systems. It is well known that there are hormone receptors (i.e. PTH) in the brain, making it possible that catatonia can lead to neuroendocrine dysfunction. In this case, a patient presented with catatonia and new-onset normocalcemic hyperparathyroidism, both which improved following ECT. Case History: Patient A is a 25-year-old female with autism admitted to an outside hospital for behavioral changes, including severe agitation and poor PO intake. Work-up was unremarkable aside from high PTH (233.5), prerenal AKI, low vitamin D (21.4), and pneumonia which was treated. Calcium was within normal limits. She became mute and her agitation worsened, leading to chemical sedation (and subsequent intubation). She was transferred to us for further workup. Soon after, she developed autonomic dysfunction and ECT was performed. After six treatments, she was hemodynamically stable, talking, eating, and significantly calmer. PTH was 28. Conclusions: To our knowledge, this is the first case of catatonia associated with normocalcemic hyperparathyroidism (with low vitamin D). The PTH normalizing once the catatonia was treated suggests catatonia- and/or ECT-induced neuroendocrine changes. PTH and vitamin D have been shown to affect dopamine signaling in the striatum and brain vasculature. Further research is needed to understand the effects catatonia can have on other organ systems.

Background: “Visual hallucinations” have been described in syndromes with vision loss including Anton-Babinski Syndrome and Charles Bonnet Syndrome. In Anton’s syndrome, visual anosognosia is associated with confabulations in the setting of blindness, resulting from bilateral occipital damage. Charles Bonnet Syndrome presents with visual hallucinations as a result of damage along the visual pathway, maintaining insight that the hallucinations are not real, absence of psychological conditions, while maintaining intact intellectual functioning. Literature review of Gabapentin and hallucinations found limited and contradicting case reports; attributing it to either the cause or treatment of visual hallucinations; recent studies in patients with chronic kidney disease have demonstrated psychosis as a result of Gabapentin toxicity. Case History: We present the case of a 70-year-old male, with no significant psychiatric history and a medical history of CKD on hemodialysis and CVAs, specifically old bilateral occipital and right frontal lobe infarcts. Two weeks after being started on Gabapentin, he complained of “blue eyes that burn my skin if I don’t look at them, but if I do look at them, they disappear,” which were not distressing, except for jerking behavior when he got “burned for not looking at them.” Discontinuation of Gabapentin resulted in resolution of the hallucinations. Conclusion: In hopes of expanding data in an area that requires further investigation, we present this case to illustrate the complexity of visual hallucinations and their etiologies. Further research would be beneficial as Gabapentin is a frequently prescribed medication and not one that is often considered as a cause for psychotic symptomatology.

Background: Mindfulness-based psychotherapies (MBT) are effective in many neuropsychiatric disorders. Mindfulness is a treatment modality worth exploring in psychogenic nonepileptic seizures (PNES). Objective: Determine efficacy of a manualized 12-session MBT for PNES. We hypothesized reductions in event frequency, intensity, and duration, and improvements in quality of life and psychiatric symptom severity at treatment completion. Methods: Between 08/2014 and 02/2018, 49 patients with documented PNES (with video-EEG) were recruited at Brigham and Women’s Hospital. Baseline demographic/clinical information and self-rating scales were obtained during the diagnostic admission (T0). Baseline event frequency, intensity, and duration were collected at the first follow-up postdischarge (T1). Frequency was obtained at each subsequent MBT session and analyzed over time with median regression analysis. Outcomes for other measures, including self-rating scales, were collected at the 12th MBT session (T3), and compared with baseline measures (T0 or T1) using linear mixed models. Results: Twenty-six patients completed the 12-session MBT program and were included in the analysis. Median event frequency decreased by 0.12 events/week on average with each successive MBT session (p=0.002). Seventy percent reported a 50% reduction in frequency from baseline and 50% reported remission at session 12. By treatment end, event intensity decreased (p=0.012), event duration trended toward reduction (p=0.100), quality of life improved (p=0.002), and psychiatric symptom severity had nonsignificant reductions. Conclusions: Completion of a manualized 12-session MBT for PNES provides improvement in event frequency, intensity, and quality of life. Randomized controlled trials and longer-term outcomes are needed to demonstrate the efficacy of MBT in PNES.

Background: Linguistic deficits in neurodegenerative disease have been well-described and most centrally include the primary progressive aphasias and dominant hemisphere atrophy. Affective aprosodia is a result of damage to a right-hemisphere analog of the left-dominant language network and has been less well examined in this population. Rare cases of primary degenerative aprosodia have been reported. We present a case (with audio) that demonstrates the importance of prosodic evaluation and highlights the anatomic basis of affective prosody and production of emotional facial expressions. Case History: A 58-year-old right-handed man presented with progressive motor speech impairment and flattening of his speech. An MRI showed right-predominant frontoinsular and peri-sylvian atrophy. His neurologic exam found mild parkinsonism and stereotypic mouth movements. He had mild deficits in processing speed, attention, fluency, and a mild retrieval deficit on visual memory. Language evaluation found moderate apraxia of speech, but relatively intact syntactic and single-word comprehension. He had marked impairment in the expression of affective prosody that was distinct from a patient with typical nonfluent variant PPA. Additionally, he had an impaired ability to produce intentional emotional faces, a deficit previously described in a case of progressive aprosodia and predicted by imaging literature. Conclusion: We present a case of a striking deficit in affective prosody and production of intentional emotional facial expressions. Affective prosody is tested far less frequently than linguistic components of language, which may make the preferential representation of degenerative aphasias at least in part a consequence of testing practices.

Background: The incidence of dementia is expected to increase in the coming decades. Alzheimer’s disease is the most common etiology of neurodegenerative dementias, and current understanding places onset of neuropathologic changes up to 30 years prior to the onset of clinical symptoms. Newly discovered mechanisms of brain waste removal (e.g., the glymphatic system), including proteins associated with neurodegenerative illnesses (e.g., amyloid, tau), provide an important framework through which to understand risk-reduction approaches. We highlight several factors, including sleep, physical activity, and diet and discuss how these are associated with dementia risk. Objective: The purpose of this exhibit is to synthesize and highlight the clinical and translational evidence behind commonly recommended “brain health” approaches to reducing risk for dementia. Methods: Review of the scientific literature and synthesis of information related to preventive approaches for risk reduction of neurodegenerative dementias. Results: Potentially modifiable risk factors for the development of dementia include low early life education, midlife hypertension, obesity, hearing loss, physical inactivity, smoking diabetes, depression, and social isolation. Each of these risk factors, to various degrees, interacts with others, making their relationship complex. Many of these factors affect generation of wastes within the brain and/or clearance mechanisms of waste removal. Conclusion: Emerging evidence for preventive strategies to reduce the incidence of dementia is promising. Early positive results of multimodal lifestyle interventions for the reduction of dementia incidence suggest that the application of a population health strategy may be able to shift the risk burden and ultimately help reduce dementia in the population.

Background: Catatonia is a psychomotor syndrome associated with a variety of psychiatric and general medical conditions. Cases of catatonia presenting with epilepsy and psychosis are relatively rare. Case History: A 62-year-old male with cerebral palsy, major depressive disorder, and a 5-year history of recurrent catatonia and psychotic episodes was admitted to the hospital with bizarre behavior, abnormal movements, and auditory hallucinations. He repeated the phrase “I am a sex addict” while simultaneously touching his nose with his right index finger for several minutes. He also reported hearing Satan laughing at him. Despite multiple similar admissions and extensive medical workups, the etiology of his neuropsychiatric symptoms remained unclear. Workups had included structural (CT, MRI) and functional (PET) neuroimaging of the brain, multiple EEGs, and CSF studies that included encephalitis panels. Four previous routine EEGs over a 4-year period were either normal or showed mild encephalopathy. However, on this admission, seizure-like activity preceding his behavioral changes was observed. Long-term video-EEG monitoring was ordered and revealed 6 focal seizures arising from the left frontocentral lobe and spreading to the right frontocentral lobe or arising from the right frontocentral lobe. Lacosamide 100 mg BID was started and no further seizures were noted. His catatonia was treated with lorazepam 2 mg TID. His psychosis and catatonia quickly resolved. At follow-up 2 months later, he had no symptoms of catatonia. Conclusion: Frontal lobe epilepsy and catatonia show significant syndromic overlap. Clinicians should be alerted to rare cases of frontal lobe epilepsy mimicking catatonia.

Background: Individual performance across different domains of cognition tends to be highly correlated, which is described as a domain-independent factor, g. The concept of g is pervasive (albeit controversial) in the cognitive neuroscience literature, but its neural correlates (if any) are not clear. Objective: This study aimed to provide a large-scale lesion-symptom mapping exploration of the neural correlates of g. Methods: 429 patients in the Iowa Neurological Patient Registry with focal brain damage received a battery of neuropsychological tests, including tests of language, memory, visuospatial ability, attention and processing speed. The g factor was modeled with confirmatory factor analysis based on the hierarchical Cattell-Horn-Carroll model. Multivariate lesion-symptom mapping of g was performed using the LESYMAP package in R. Results: The factor analytic model provided an adequate fit to the data (χ²=216.08, CFI=0.92, TLI=0.90, RMSEA=0.08, SRMR=0.07). The cross-validated correlation for the lesion-symptom map was statistically significant (r=0.32, p<0.001). The map identified damage to the left inferior fronto-occipital and longitudinal fasciculi, left frontal white matter, and the right posterior subinsula/claustrum as most strongly associated with deficits in g. Conclusion: Cognitive performance that spans multiple domains relies on large-scale brain networks and lesions that disrupt the white matter tracts connecting these networks are the most detrimental to general intelligence. In addition to enhancing our understanding of the neural basis of g this finding has prognostic implications for patients with acquired lesions to these sites.

Introduction: Hypoxic brain injury may cause impairments in consciousness, attention, speed of processing, and memory impairments, and executive dysfunction as well as somatosensory and motor deficits. Psychological impact of anoxic brain injury may correspond to physiologic location, degree of tissue loss, and mechanism of injury. Assessment of injury extent may be more challenging in patients with baseline cognitive deficits and preexisting psychiatric disorders. Case Presentation: 49-year-old male with a history of depression, chronic pain, severe alcohol use disorder, marijuana use, contractures and tremors of unknown etiology was admitted after attempting suicide by nitrogen gas inhalation. Laboratory and imaging studies were unremarkable. Patient continued to have impairments in recent and remote memory and myoclonic jerks. Divalproex sodium 500 mgs BID and Duloxetine 30 mgs were added for his myoclonic jerks and mood disorder. Neuropsychological testing during hospitalization yielded results inconsistent with patterns of known amnestic disorders; symptom exaggeration scale score was high despite no clear reason for secondary gain. Initial outpatient follow-up showed worsening of symptoms compared with baseline, but 8-month follow up findings were consistent with conversion disorder. Discussion: Deficits in memory and executive function are the most common deficits from hypoxic brain injury noted in literature. Inconsistency in memory impairment and likelihood of tremors being a conversion disorder both suggest that these cognitive deficits are driven by underlying depression. Assessment of the degree of cognitive impairment is challenging when there is comorbid depression.

Background: Several studies have reported promising results for the use of virtual reality (VR) and mirror visual feedback (MVF) in the treatment of phantom limb pain, as well as other unilateral motor-sensory disuse syndromes such as Complex Regional Pain Syndrome (CRPS). VR and MVF have also been reported to assist with physical therapy in children with Cerebral Palsy (CP). However, neither VR nor MVF has ever been reported for the treatment of adults with CP Case History: We report on a late-middle-aged female with a history of secondary right-sided dystonia, pain, and hemiplegia due to CP. Over a period of 18 months, she received weekly immersive VR-MVF experiences using a commercially available VR gaming device (HTC-VIVE) and customized software delivering an upper extremity limb-swapping illusion involving both gross and fine motor movement. Significant pain relief (ranging from 6.25%−38.5% improvement within the session), as well as improvement of dystonia, motor control, flexibility, and range of motion, was noted by the patient as a result of these interventions. Conclusions: This study provides the first case report that we know of involving the use of VR and MVF technology in an adult patient with CP. The results suggest that a low-cost, commercially available, immersive VR system can be a potentially valuable addition to treatment for adults with CP.

Background: Despite a growing number of migraine neuroimaging studies, inconsistent findings and high methodologic variability have limited attempts to unify this literature and to identify migraine-specific targets for neuromodulation. Objective: To determine if neuroanatomically heterogenous neuroimaging findings of migraine localize to a common brain network. Methods: Functional connectivity network maps of 11 meta-analysis coordinates of decreased gray matter volume in migraineurs were generated using a normative connectome (N=1000). Individual maps were then overlapped to identify common regions of connectivity across all maps. Specificity of our findings was evaluated using a region-of-interest (ROI) analysis and a whole-brain Bayesian Spatial Generalized Linear Mixed Model (BSGLMM) with comparison groups of chronic pain and a neurologic control (Alzheimer’s Disease). Results: Greater than 90% of migraine coordinates were positively connected with bilateral insula and negatively connected with the hypothalamus, bilateral posterior thalami and visual cortex (T=7, FWE-corrected p<10⁻⁶). Regarding the latter, a subregion localizing to left V3A was connected to 100% of coordinates. V3A connectivity was specific to migraine compared with chronic pain and our neurological control (ANOVA p=0.02; pairwise t tests p=0.03, p=0.003) and was the only brain region meeting a BSGLMM voxel-wise probability of ≥90%. Conclusions: We show that regions of decreased cortical volume in migraineurs localize to a common brain network defined by connectivity to visual cortex V3A. This area has been previously implicated as the potential origin of cortical spreading depression in migraine. Our findings provide new insight toward understanding migraine pathophysiology and offer a new migraine-specific target for neuromodulatory treatment.

Background: Pareidolia is a phenomenon of perception of familiar patterns, usually of faces, within vague or random stimuli. Folie à deux of pareidolia has not heretofore been described. Case History: Primary Member: A 37-year-old male presented with 13-years of delusions of embedded demon-like images. The images appear mainly on clothes, but may be embedded on any background. They are skeletons with sinister faces of only the eyes and mouth, without the nose. The images reappear 25 times a day, each remain for two minutes, then spontaneously disappear. During the same 13-year period, he also suffered from other types of delusions including control, nihilistic, guilt or sin, telepathy, reference, erotomania, grandiosity, and religious. Passive Member: A 50-year-old female presented with three years of delusions of embedded images, beginning soon after she met the primary member. When the primary member would see pareidolic images of a sinister countenance, the passive member would also envision an evil visage in the same object. During the interview, the primary member pointed to where he visualized a flagitious face. Upon hearing this, the passive member expressed that she, too, saw a wicked face in that location. She did not share any of the other delusions the primary member experienced. Conclusion: The fusiform gyrus is responsible for recognizing faces and is mainly responsible for pareidolia dysfunction of which may be the underlying pathology of this condition. Query as to the presence of pareidolia in those with folie à deux and other delusional disorder is warranted.

Background: Cerebellar lesions are known to lead to cognitive and affective symptoms, and more rarely, have been implicated in presentations of mania. Here we present a case of mania and cerebellar pontine angle (CPA) tumor, with postsurgical resolution of mood symptoms. Case History: A male in his 40s, with no past neuropsychiatric history, developed a first lifetime mania syndrome over several weeks including decreased need for sleep, severe emotional lability, and increased risky behavior. Initial exam demonstrated hyper verbal speech, tangential thought process and euphoric affect with confusion but no focal findings on physical neurological exam. MRI noted a 4 by 2.5 cm left CPA mass, with distortion of fourth ventricle. Sleep, thought process, concentration, and attention improved modestly with quetiapine prior to left retrosigmoid craniotomy and resection of the schwannoma. Postoperative course was complicated by delirium and MRI demonstrated left cerebellar edema. Delirium improved by two weeks postoperative on quetiapine 150 mg per day. Residual manic symptoms including grandiose delusions and disorganized thought process subsequently subsided completely over the next four weeks. Quetiapine was tapered off without symptom recurrence for three months. Conclusions: Many of this patient’s symptoms fit with the cerebellar cognitive affective syndrome (CCAS), including disinhibition, emotional lability, and irritability. However, his clustered manic symptoms, less commonly reported in CCAS, included decreased need for sleep, racing thoughts, pressured speech, and hyperthymia. Our case highlights the need for an evaluation of new onset mania which includes cognitive and neurologic examination and consideration of neuroimaging to evaluate for structural lesions.

Background: Several studies in the literature have suggested a possible link between early childhood infection, particularly Epstein Barr Virus (EBV) (and other members of the Herpesviridae family) and the development of Schizophrenia in adulthood. Further, data demonstrates a possible relationship between developing psychotic events later in life, following exposure to EBV. This further elucidates the possible relationship between infection and the development of psychosis. Case History: We present the case of a 48-year-old male with no significant psychiatric or medical history, who presented for a psychiatric evaluation, after his mother reported a two week history of him “not acting like himself, making nonsensical statements, not sleeping and talking to people who were not present in the room.” On interview, the patient was disheveled and gaunt, paranoid, and appeared to be responding to internal stimuli. Urine drug screen on admission was negative. The patient was a monozygotic twin and his twin brother had a history of Schizophrenia and multiple psychiatric hospitalizations. Elevated white blood count, TSH, and a sore throat raised suspicion for infection. The patient was found to be monospot-positive during his admission and was symptomatically treated. Simultaneously, he was treated with antipsychotic and responded well. Ultimately, his psychotic symptoms remitted and he was safely discharged home. Conclusion: Possible etiologies of the patient’s psychosis included: infection, other organic causes or substance abuse. A possible explanation for the patient’s presentation includes a genetic predisposition to Schizophrenia, as the patient was a monozygotic twin, in addition to his recent EBV infection.

Background: Autoimmune encephalitis (AE) is a rare disorder which is challenging to diagnose due to variable presenting symptoms, multiple subtypes, and scarcity of cases encountered by clinicians. Abrupt onset of neuropsychiatric symptoms is common. However, specific symptoms including psychosis, catatonia, mood lability, cognitive impairment, and seizures may vary. Despite increasing numbers of identifiable antineuronal antibodies associated with AE, a subset of patients remain seronegative, potentially leading to misdiagnosis or delay in treatment. Case History: A 14-year-old female without previous neuropsychiatric history developed prominent fatigue, persistent tachycardia, psychosis, catatonia, and short-term memory impairments over a 6-week period. Initially she was diagnosed with psychosis and started on risperidone, though experienced worsening delusions, auditory hallucinations, and suicidality with self-harming attempts. Extensive medical workup including MRI brain, CT head/abdomen/pelvis, CSF and serum paraneoplastic and autoimmune studies, and EEG yielded unremarkable or nonspecific results. Catatonia symptoms responded robustly to lorazepam, but psychotic symptoms persisted despite two antipsychotic trials. Mild improvement was observed after a course of empiric steroids and IVIG, and PET scan results showed occipital lobe hypometabolism, consistent with reported findings in autoimmune limbic encephalitis. Initiation of rituximab led to significant symptomatic improvement. Conclusion: This case illustrates the difficulty in accurately identifying and treating seronegative autoimmune encephalitis. There is a risk of delayed treatment initiation or misdiagnosis without the reassurance of detectable antineuronal antibodies. Given current evidence correlating early immunotherapy with improved patient outcomes, promptly recognizing and treating autoimmune encephalitis is critical.

Background: Attention-deficit/hyperactivity disorder (ADHD) is a prevalent heterogeneous neurodevelopmental syndrome associated with various environmental factors. Objective: This study examined the association between maternal preeclampsia and offspring ADHD at 7- and 10-years. Methods: The study cohort consisted of more than 7,200 children who participated in Avon Longitudinal Study of Parents and Children (ALSPAC) birth cohort study. We used data from the Avon Longitudinal Study of Parents and Children (ALSPAC). ADHD was diagnosed using parent reported Development and Wellbeing Assessment (DAWBA). Logistic regression and Generalized Estimating Equation (GEE) models were used to examine the association between maternal preeclampsia and ADHD in offspring. Results: The overall prevalence of ADHD was 2.04% and 1.62% at ages of 7 and 10 years, respectively. GEE analysis showed that pre-eclampsia was associated with increased risk of ADHD in offspring (adjusted odds ratio [OR] = 2.94, 95% confidence interval [CI]: 1.40–6.15). The results of multivariable logistic regression analysis at each time point also showed that preeclampsia almost threefold increase risk of ADHD. Conclusion: This study suggests that offspring of mothers with pre-eclampsia are at increased risk of ADHD adding to the growing evidence that uterine environment is a critical determinant of neurodevelopmental outcome. If our findings are replicated by others, early screening for ADHD and other developmental delays may be recommended in offspring of women with pre-eclampsia.

Background: Longitudinal studies suggest older adults with sensory deficits are at higher risk for developing cognitive impairment/dementia. It is unclear if the link between sensory and cognitive functioning reflects a common underlying cause or whether sensory deficits directly undermine cognition. We addressed this issue using a paradigm that manipulated sensory degradation and task demands. Objective: Compare ERP responses of young and old adults during a working memory paradigm that parametrically varied visual contrast levels and task demands. Methods: Young (18–32) and old (65–85) adults participated in a visual working memory task while ERPs were recorded. Before each block, participants studied 1–4 face pairs. One face of each pair was designated as a “target.” At test, individual faces were shown at evenly distributed, varying contrast levels (100%, 69%, 22%). Participants identified each face as target or nontarget. Results: In young adults, processing speed (P3 latency) decreased across levels of diminishing visual contrast or increasing demand. Compared with young, old adults had prolonged latencies in response to unfiltered stimuli or lower task demands but failed to generate differentiated responses across levels. Both groups generated smaller responses (P3 amplitude) to filtered stimuli. Young adults tended to generate larger P3 responses to higher task demands; old adults demonstrated the opposite. Conclusions: Processing speed was prolonged in old adults but did not vary across levels of contrast or demand. Filtering/degrading visual stimuli reduced the electrophysiological response magnitude equally in old and young adults. Old adults appear to deplete resources at lower levels of task demand.

Background: Witzelsucht, or “joke addiction,” is a rare behavioral sequela of damage to frontal-subcortical neural circuits first described by a German neurologist in 1888. This condition is characterized by compulsive joke telling, poor insight and impulse control, and can be associated with many different pathological processes affecting frontal executive function. We present a case of Witzelsucht secondary to behavioral variant of frontotemporal dementia (FTDbv) successfully treated with divalproex sodium. Case History: A 67-year-old male was referred to the Mood and Memory Clinic of Northern Light Acadia Hospital for personality change by his neurologist. He had been diagnosed with FTDbv by two neurologists, with symptoms onset four years prior to our seeing him. His family reported that he could not hold a conversation without inserting inappropriate jokes. On examination the patient had pressured speech and constant joke telling to the point where general cognition could not be tested. He had a normal sleep/wake cycle, normal level of psychomotor activity and no history of mood disorder. Previous trials of risperidone and trazodone were unsuccessful. An empiric trial of divalproex sodium 375 mg twice daily significantly reduced the compulsive joking and pressured speech. Conclusions: Witzelsucht is a socially debilitating frontal lobe syndrome that can be mistaken for willfully inappropriate behavior or bipolar disorder. Our patient had a positive response to divalproex sodium 375 mg twice daily allowing for short conversations without compulsive joking. Correct diagnosis and effective pharmacologic management significantly improved the quality of life for this patient and diminished caregiver distress.

Background: Individuals suffering from epilepsy are at an 8-times greater risk of having psychosis relative to the general population, with a prevalence of postictal psychosis in temporal lobe epilepsy of 7%. Psychosis in epilepsy can occur as postictal, interictal, antiepileptic drug-induced, as well as in de novo thought disorders. Each of these forms have characteristic presentations which aid in identification of the etiology of the psychosis. What confounds these characteristics is a clinical suspicious of psychogenic nonepileptiform seizures (PNES) for behavior and thought patterns that ultimately are more consistent with psychosis. Case History: A 45-year-old female with no past psychiatric history, and a past medical history of partial seizures with impaired consciousness underwent 3 days of continuous electroencephalogram (cEEG) without seizure activity noted. She was discharged to follow up on an outpatient basis, but one week after discharge she presented to an outside emergency department with paranoia and psychosis. She was transferred to our epileptiform monitoring unit for repeat cEEG monitoring. Initially, she had, what were presumed, psychogenic oral facial movements with 10 second periods of speech arrest, and a diagnosis of PNES was presumed. Subsequent repeat cEEG revealed her temporal-frontal seizure focus, and then she had a classic frontal lobe seizure. Conclusions: This case illustrates the importance of clinicians being familiar with the varying clinical presentations of types of psychosis in epilepsy, when the clinical course and timing of seizure activities is not readily available, and especially when “odd” behavior is more consistent with psychosis than PNES.

Background: Paraneoplastic encephalitis is increasingly recognized as a possible cause of neuropsychiatric symptoms in cancer patients, and a growing number of these conditions can now be identified via antibody testing. Here we report the unusual case of steroid-responsive psychosis with negative antibody testing in a patient with T-cell acute lymphoblastic leukemia (T-ALL). Case History: A 22-year-old woman with T-ALL in clinical remission abruptly developed confusion, echolalia, and paranoia during three chemotherapy cycles. No personal or family psychiatric history was identified, and neurological exam revealed no focal deficits. Extensive investigations were negative, including: CT, MRI, and EEG; toxic, metabolic, and infectious work-up; and serum and CSF antibody panels. LP revealed only a mild pleocytosis. All three episodes developed nine days following steroid taper (administered as part of her chemotherapy regimen) and resolved completely when steroids were resumed. In contrast, her symptoms responded minimally to antipsychotics. After discussion of the risks and benefits, she was maintained on continuous low-dose steroids. Her psychotic and cognitive symptoms have not recurred. We will discuss the approach to first episode psychosis in patients undergoing cancer treatment, with a particular emphasis on strategies to identify and treat toxicity related to chemotherapeutic agents. The clinical dilemma of steroid-responsive psychosis with negative antibody testing will also be explored. Conclusion: The case illustrates several challenges in the management of neuropsychiatric symptoms in cancer patients. In particular, organic etiologies of purely psychiatric presentations may be overlooked, and the neurotoxicity profiles of chemotherapy medications remain inadequately described.

Background: Electroconvulsive therapy is considered an extremely effective treatment in mentally ill patients. However it is also one of the most stigmatized and underutilized therapies in psychiatry. Objective: To systematically review available literature on attitudes of medical students toward electroconvulsive therapy (ECT). Methods: 27 electronic databases were searched medical literature including Pubmed, Psychinfo, etc. The keywords used were: medical students, attitudes, electroconvulsive therapy, ECT. Data extracted included aim, study design, sample size, response rate, the year of medical school which the students were in, year of publication, country where the study was conducted, interventions if any and main findings. Results: The initial search identified 190 papers. After removing duplicates and assessing abstracts and full articles against the inclusion criteria, 24 articles were included in the review. All the studies identified were qualitative studies and were cross sectional in design. 2 studies assessed attitudes to unmodified ECT. A majority of the studies were from India and USA (4 studies each) and conducted a pre and post analysis following interventions that included clerkships in psychiatry (5 studies). Other interventions included viewing a live ECT session, and attending a lecture on ECT. These interventions were efficacious in improving medical student attitudes toward ECT. Conclusion: Studies have used various methods to improve attitudes of medical students to ECT. Response bias should be considered while interpreting these results. However, the methods used can be adapted to medical curricula to improve the acceptability and utilization of ECT as a treatment method in psychiatry.

Background: Imbalances in maternal thyroid hormone level in early pregnancy may increase the risk of offspring psychosis. Objective: This study aimed to examine the association between maternal thyroid hormone dysfunction and the risk of offspring psychosis in early adolescence. Methods: Data were taken from the Avon Longitudinal Study of Parents and Children (ALSPAC). A total of 2277 mother-child pairs were included. Thyroid stimulating hormone (TSH) levels, free thyroxine (FT4) and Thyroid Peroxidase Antibodies (TPO-Ab) were assessed during the first trimester of pregnancy. Psychosis like symptoms (PLIKS) of children were assessed by the psychosis-like symptoms semistructured interview (PLIKSi) at age 12. The odds of offspring psychosis were estimated using logistic regression analysis. Results: None of the thyroid parameters [FT4 (OR: 95% CI; 0.93: 0.82−1.05), TSH (OR: 95% CI; 0.98: 0.85−1.13), and TPO–Ab (OR: 95% CI; 0.89: 0.70−1.13)] were associated with suspected or definite psychosis like symptoms (PLIKS) in the univariable analysis. We further examined for possible effects of confounder variables using multivariable analyses but results remained unchanged. Definite only psychosis like symptoms of children were also not associated with maternal thyroid parameters [FT4 (OR: 95%CI; 1.05: 0.86−1.28), TSH (OR: 95% CI; 1.02: 0.91−1.15), and TPO–Ab (OR: 95% CI; 0.69: 0.40−1.19)]. Conclusions: The results of this study show that maternal thyroid function during the first trimester of pregnancy was not associated with offspring nonclinical psychotic experiences in early adolescence.

Background: Social cognition is an emerging area of clinical neuroscience that encompasses emotional perception, Theory of Mind, and empathy. Clinicians often encounter impaired social cognition, but the neuroanatomic basis of this capacity is not fully understood. Objective: This project aimed to examine the role of white matter in normal social cognition, and in abnormal states that occur with structural brain disorders. Methods: A focused literature review was performed to consider the relationship between social cognition and white matter expansion over evolution, and to assess the effects of white matter pathology on social cognition. Results: The mammalian brain has enlarged over millions of years of evolution, resulting in the “social brain” of homo sapiens. White matter has expanded more than gray matter, particularly in the frontal and temporal lobes, regions most securely linked with social cognition. The rapid information transfer conferred by myelination likely enhanced cooperative behaviors necessary for survival and facilitated social cognition. Clinical evidence from the study of stroke, traumatic brain injury, Binswanger’s Disease, multiple sclerosis, glioma, and behavioral variant frontotemporal dementia supports a crucial role of white matter in the operations of social cognition, predominantly within a right cerebral network of cortical and subcortical structures. Conclusion: The expansion of frontal and temporal white matter has contributed to the cerebral representation of social cognition, primarily within a network of emotionally relevant structures in the right hemisphere. In clinical practice, an appreciation of white matter connectivity usefully informs the diagnosis and treatment of disorders that produce deficits in social cognition.

Background: Up to 1/3 of dementia cases are due to modifiable risk factors. There is growing consensus that adoption of certain healthy behaviors (e.g. exercise, Mediterranean diet, cognitively/socially stimulation) may prevent or slow cognitive decline and dementia. However, standard clinical practice does not systematically promote nor monitor these behaviors because providers often lack the time and resources to meaningfully impact patient behavior. Objective: To investigate the feasibility and efficacy of a novel, clinic-based, personalized health coaching intervention to augment brain-healthy behaviors in patients with MCI and mild dementia. Methods: We piloted a six-month, randomized, controlled investigation of 40 patients followed at the BWH Alzheimer Center with dementia, MCI, or subjective cognitive decline. In the intervention arm, patients and caregivers participated in weekly motivational interviewing phone calls and three additional visits with a “brain health champion” (BHC) health coach, who provided personalized support to set and update attainable goals. Changes in physical activity, diet, and cognitive/social engagement were measured using validated questionnaires. Secondary outcomes included quality of life (QOL), cognitive function, and neuropsychiatric status. Results: Compared with the standard-of-care control group, BHC participants had statistically significant and clinically meaningful increases in brain-healthy behavior scores and QOL. Cohen’s d effect sizes were in the large to very large range for physical activity (d=1.37, p<0.001), Mediterranean diet (d=0.87, p=0.016), cognitive and social activity (d=1.09, p=0.003), and QOL (d=1.54, p<0.001). Conclusions: Our pilot results demonstrate the potential efficacy of the BHC program, a low-cost, multimodal health coaching approach, in helping patients adopt brain health recommendations.

Background: Psychogenic nonepileptic seizures (PNES) are paroxysmal events, not caused by ictal epileptiform activity. Objective: We explored reported rates of military sexual trauma (MST), traumatic brain injury (TBI), childhood abuse, and intimate partner violence (IPV) in post 9/11 veterans as risk factors in PNES. Methods: This retrospective chart review included 414 veterans utilizing the VA healthcare system, diagnosed with PNES through video electroencephalograph from 2003–2016. Statistical analyses were conducted using SPSS version 24.0, Fisher’s exact results are reported. Results: Of the 414 veterans, 342 (83%) were men. TBI was reported by 158 (38%), MST in 49 (12%), and 32 (8%) reported both. IPV was reported in 21 (5%), with physical abuse in 14 (67%). Childhood abuse was reported in 112 (27%); of these, sexual abuse was reported in 64 (57%) and physical abuse in 62 (55%). Veterans with a history of childhood abuse were more likely to have suicidal intentions of any type (p=0.0001), with significant passive ideations (p=0.007), as well as attempts (p=0.0001). Veterans with either a history of IPV (p=0.75) or childhood abuse (p=0.85) were not more likely to seek out psychotherapy. Most (225, 54%) reported more than 30 seizures in the year preceding PNES diagnosis. Conclusion: Like the civilian population, a substantial proportion of Veterans with PNES report childhood physical and sexual trauma as well as IPV. Veterans have increased risk for PNES because of the potential exposure to MST. Future research will explore the role of psychotherapy in preventing PNES and interrupting the cycle of IPV.

Background: Neurodegenerative diseases such as behavioral variant frontotemporal dementia (bvFTD) are becoming increasingly prevalent. In addition, according to recent epidemiologic studies FTD is likely to be under diagnosed since they may present with atypical features, which can delay diagnosis and treatment (Young et al., 2018). Case History: A 58-year-old man without previous psychiatric history was admitted with acute-onset altered mental status and behavioral changes. Patient demonstrated spells of intermittent nonrhythmic jerking, eye fluttering, confusion, stereotypy, rigidity and combative behavior. MoCA was 23/30 with impaired attention, language and memory. Lorazepam challenge was positive and we diagnosed catatonia. Medical work-up revealed stage III malignant melanoma, but symptoms only transiently improved after melanoma excision. AMPA-receptor encephalitis associated with melanoma has been reported (Daneshmand et al., 2018), however, paraneoplastic panel was negative. PET scan demonstrated bilateral and symmetric hypometabolic activity within the temporal and parietal lobes. MRI brain showed mild frontotemporal greater than parietal volume loss volume loss. Symptoms improved with lorazepam and valproic acid treatment. Discharge and placement in a memory unit is pending further medical stabilization. Conclusion: bvFTD may present with neuropsychiatric symptoms that mimic catatonia, infection, inflammatory, neurologic, or paraneoplastic illness. Diagnosis of bvFTD is challenging, as it shares network dysfunction in the frontal-subcortical circuits, which may also be affected by catatonia (Tekin et al., 2002). Additionally, C9orf72 mutations are associated with both FTD and catatonia (Ducharme et al., 2017). In our case, the “red herring” of catatonia and melanoma delayed diagnosis and recognition of the patient’s neurodegenerative illness.

Background: West Nile is a virus most commonly transmitted to humans by mosquito bites. Clinical syndromes associated with West Nile virus (WNV) infection range from fever to neuroinvasive disease. Although age is a significant risk factor for neuroinvasive disease and death (increasing age associated with greater disease burden and mortality), the association of other cognitive and clinical factors is less definitive. There is also lack of data on pediatric population. A greater understanding of WNV disease burden is warranted for guiding clinical care and evidence informed policy making. Case History: The authors report neuropsychological findings from a 13-year-old, right-handed, Latina female with a medical history of West Nile Virus infection (WNV) with encephalitis. Medical history was further complicated by septic shock and meningitis. She was hospitalized for about 8 days and was discharged home in a stable condition. At the time of this evaluation (a month after discharge), parent report indicated no cognitive concerns and return to baseline functioning. Neuropsychological evaluation revealed intact IQ and several other cognitive strengths. A relative weakness was noted with aspects of attentional functioning. Conclusions: Consistent with research in this area, the young age of our patient might have contributed to a better outcome/prognosis despite having several other serious neural complications. Although her outcome appeared promising soon after hospital discharge, research has indicated that cognitive deficits may manifest later, regardless of the severity of WNV. Periodic neuropsychological assessments may provide an effective way to detect changes over time.

Background: Transient Global Amnesia (TGA) is characterized by abrupt onset of anterograde amnesia, disorientation to time and place, repetitive questioning, and lack of neurological deficits, that lasts anywhere between 4–8 hours. It commonly occurs in elderly patient’s although has been seen in the younger and middle age population. Etiology remains inconclusive although several hypotheses have been proposed including vascular causes (TIA), epilepsy, migraines or psychopathological in nature (anxiety, depression, certain personality traits, physical exertion, emotional stress.) Patients presenting with TGA can be challenging for many medical providers, as patients may present in other settings, not just ER departments. They can present in outpatient office settings, such as the case to be discussed here. Case History: A 71-year-old man with a medical history Wolff Parkinson White syndrome on flecainide, s/p R parietal hemorrhage with no noticeable residual effects and anxiety disorder, presented for weekly psychotherapy appointment working through anxiety surrounding termination with previous therapist. He suddenly became confused, disoriented, anxious, repetitive in questioning, diaphoretic and light-headed. He was sent to the ER for medical workup, which showed no overt explanation for amnesia. His mentation and confusion improved over four hours, allowing for discharge home with no medications. Conclusions: This condition remains a challenge for medical professionals, especially psychiatrists. This case illustrates the importance of awareness and ruling out more life-threatening causes of TGA, keeping in mind other likely causes including psychopathological ones. Further studies are necessary to better understand the pathophysiology of this syndrome to expedite the proper diagnosis and management.

Background: The internet allows sales of psychoactive agents, such as Tianeptine, Etizolam, and Phenibut, that are not regulated by the FDA. These medications have the potential for abuse potentially leading to altered mentation when intoxicated or withdrawing. This presents a challenge to clinicians who may not be aware of availability of such substances. Available cases have discussed the use of above substances individually, but how do you treat if there is use of more than one substance with different mechanism of actions? Case History: A 32-year-old male presented to the ED for altered mental status (AMS.) He was self-medicating with concurrent use of Tianeptine (atypical antidepressant with mu agonist properties,) Phenibut (Gaba mimetic) and Etizolam (a benzodiazepine like agent.) During his stay, he was agitated and delirious with reports of visual hallucinations. Neuroimaging and lab studies were within normal limits, EEG showed no seizure activity. He was started on Depakote for agitation, a Valium taper for suspected benzodiazepine withdrawal and prevention of seizures, Seroquel for delirium, and Baclofen for suspected GABAergic withdrawal symptoms. Patient’s AMS improved and discharged on hospital day 10. Conclusions: This case illustrates the difficulty managing polysubstance use/abuse and stresses the importance for physicians to screen for psychoactive agents purchased over the internet or over the counter to improve treatment outcomes. Continued discussions with patients regarding risks/benefits of use of such substances would be beneficial and help increase awareness.

Background: Many antiepileptic (AEDs) medications can cause adverse drug reactions. Behavioral side effects that can be associated with AEDs are often overlooked but are significant. Lacosamide (LCM) is an antiepileptic drug (AED) used as an adjunctive treatment for partial seizures. LCM associated psychosis has been reported but no reports on LCM and mania symptoms. This presentation presents similarly to symptoms observed in Bipolar Disorder. We present the first case of mania in a 71-year-old man after usage of LCM for epilepsy, with subsequent resolution following discontinuation of LCM. Case History: A 71-year-old man with a history of epilepsy, exhibited an increase in seizure activity, changes in personality, mood, and behavior (increased energy, paranoid delusions, grandiosity, aggression, impulsivity, memory impairment after initiation of LCM. Similar presentation last year when tried on Levetiracetam. Symptoms resolved after cessation of LCM, implicating LCM as the culprit and making Bipolar Disorder less likely. Conclusions: Case reports of many AED induced mania have been reported, however, to the best of our knowledge, this is the first case of LCM induced mania. This case illustrates the importance of recognizing the causal and temporal relationship of AED and manic symptoms as in such cases cessation of the medication and subsequent trial with the same medication is not recommended. Despite many published reports, the mechanism of AED induced mania remains unclear. Further studies are required to better understand the pathophysiology of this syndrome as it will affect the management of psychiatric disorders of epilepsy, prevent misdiagnosis and unnecessary treatment.

Background: Mild-Behavioral Impairment (MBI) is a neurobehavioral syndrome characterized by later-life onset of NPS as an at-risk state for dementia. While decreased white matter integrity in regions associated with NPS is identified in AD, evidence in predementia risk groups is sparse. Objective: To determine white matter neural correlates of neuropsychiatric symptoms (NPS) in an at-risk group for incident cognitive decline and dementia. Methods: ADNI subjects with diffusion tensor imaging (DTI) data and neuropsychiatric inventory questionnaire scores were included. DTI analysis examined the relation of NPS classified into MBI domains, and changes in large white matter tracts in those with normal cognition (NC; N=70), and Mild Cognitive Impairment (MCI; N=91). Multiple linear regression, adjusted for age, gender and education was conducted. Results: MBI domain specific analysis identified: 1) Impaired Drive/Motivation—reduced fractional anisotropy (FA) in posterior limb of the internal capsule(PLIC) in MCI; 2) Emotional Dysregulation—reduced FA in PLIC and cingulum in NC, and increased mean and radial diffusivity (MD; RD) in the uncinate fasciculus in MCI; 3) Impulse Dyscontrol—reduced FA in inferior fronto-occipital fasciculus, posterior thalamic radiation, cingulum, increased MD and RD in superior longitudinal fasciculus (SLF) in NC, and altered DTI parameters in SLF, and PLIC in MCI; 4) Social Inappropriateness—reduced FA within SLF in MCI; 5) Abnormal Thought/Perception—reduced axial diffusivity in corpus callosum, and cingulum in MCI. All aforementioned results were significant (p≤0.05). Conclusions: Distinct patterns of white matter changes associated with MBI domains were observed, thus improving our understanding of the role of NPS in neurodegenerative disease.

Background: Catatonia, a psychomotor dysregulation disorder of volitional behavior, occurs frequently in anti-N-methyl-d-aspartate receptor (NMDAR) encephalitis. Treatment relies heavily on benzodiazepines, but neurologically ill patients may not tolerate the doses necessary. The NMDAR antagonists amantadine and memantine are effective in catatonia with inadequate benzodiazepine response but their utility in anti-NMDAR encephalitis remains unknown. We present two patients with recent anti-NMDAR encephalitis admitted to inpatient neurorehabilitation with residual catatonic features who were treated with NMDAR antagonists. Case History: Case 1: A 20-year-old woman with anti-NMDAR encephalitis (serum antibody titer 1:640) treated with steroids, intravenous immunoglobulin (IVIG), rituximab, and ovarian teratoma resection. Catatonia responded to low-dose lorazepam, though titration was limited by sedation. Addition of memantine 10 mg twice daily resolved catatonia and reduced lorazepam requirement. Case 2: A 31-year-old woman with anti-NMDAR encephalitis (serum titer 1:640; CSF 1:512) treated with steroids, IVIG, plasmapheresis, rituximab, and cyclophosphamide. No teratoma was identified. Posttreatment serum titer was 1:640. Catatonia responded partially to lorazepam but titration was limited by sedation. Amantadine and memantine were administered sequentially but both produced agitation and were discontinued. Conclusions: NMDAR antibodies induce reversible internalization of the NMDAR, producing a state of NMDAR hypofunction possibly accompanied by extracellular glutamate excess. In Case 1, from whom a presumably antibody-generating teratoma was removed, memantine may have modulated glutamate excess at reemerging NMDARs. Case 2, whose circulating antibodies remained elevated, responded poorly to NMDAR blockade. We discuss proposed mechanisms of amantadine and memantine in catatonia and review the use of glutamate antagonists in anti-NMDAR encephalitis.

Background: According to Alzheimer’s Disease International, worldwide 50 million people are living with dementia in 2018 and this figure will triple to 150 million by 2050. The dementia diagnosis in young patients is a challenge and establishing an aetiological diagnosis is an important part of clinical care to choose the appropriate treatment. Case History: A 50-year-old Indian housewife presented with complaints of short-term memory problems. Her neuropsychological examination revealed impairment of all cognitive domains with functional impairment suggestive of a Dementia diagnosis. Her MRI Brain showed stable calcified meningioma in parafalcine area and no other abnormality or volume loss. She was investigated with Amyloid PET imaging using Flutemetamol F18 injection and the scans showed widespread amyloid deposition in bilateral temporal, parietal and posterior cingulate areas suggestive of Alzheimer’s pathology. Conclusion: The CSF biomarker and Amyloid PET in comparison, both were equally sensitive and specific to diagnose Alzheimer’s dementia at early stages. In summary this case illustrates that Amyloid PET will be the investigation of choice to diagnose Alzheimer’s dementia in young patients since it is more specific and noninvasive.

Background: The visual word-form area (VWFA) is a functionally specialized region of the inferior aspect of the dominant inferior temporal gyrus. This area is necessary for the integrated visual processing of whole words and, thus, is necessary for fluent comprehension of written language. This component of the ventral stream of visual processing straddles regions responsible for single-letter visual representations and higher-order lexical-concept integration. Isolated lesions to this area are associated with focal whole-word dyslexia, but, if surrounding circuits remain intact, other aspects of language, including letter-by-letter word comprehension, and semantic-phonological integration, may remain unaffected. Case History: A 75-year-old woman presented with gradual, new-onset, focal deficits in reading whole words. MRI revealed a glioblastoma involving the anterior aspect of the inferior left occipitotemporal cortex. To overcome her deficits, she would read individual letters out loud, sustain them in auditory working memory, and assemble the words phonologically letter-by-letter, which led to sudden verbal recognition and comprehension of the word. She could reconstruct even phonologically complex words. Her lesion spared posterior parts of the fusiform gyrus important for orthographic letter processing, thus preserving her ability to visually recognize individual letters and associate them with the appropriate sounds. We suspect this enabled an alternative pathway (not involving the VWFA) for ventral visual stream access to lexical-semantic concepts via the auditory/phonological system. This functional preservation allows her to read, albeit via a labored process. Conclusion: This case highlights the remarkable specificity of the dominant inferior temporal gyrus VWFA and emphasizes its specialization for visual lexical-concept integration.

Background: CADASIL is a well-described autosomal dominant syndrome. However, the reason for variability of severity, timing, and progression rate of the disease within families is unknown. A family of 3 sisters 2 of [which] diagnosed with CADASIL with varying degrees of progression, severity and functional impairment. Case History: 54-year old woman diagnosed with CADASIL, by cranial MRI combined with a positive NOTCH 3 gene mutation. Neuropsychological testing indicated severe functional impairment (MoCA: 18). CADASIL was initially diagnosed as depression. Subsequently, her 2 older sisters were evaluated, one diagnosed, and their father was the identified carrier. The sisters differed markedly in degree of functional impairment. The older sister continues functioning in the above range on the MoCA, is completely independent for ADL/IADL and is still working. Patients sisters describe significant childhood adverse events noting verbal/physical and possible sexual abuse of the patient which they were spared. DNA samples of the three siblings were sent for telomere length analysis. Conclusion: CADASIL symptoms and rate of progression may differ markedly inter/intra familialy. ACE scores correlate with mental and physical health in the general population. Higher ACE scores are correlated with shorter telomere length than the General population. Shorter telomeres have been shown in CADASIL patients compared with GP. CADASIL patients with greater functional impairment also appear to have shorter telomeres than their age matched diagnostic counterparts. Telomere shortening, related to severity of CADASIL, [may] be linked to elevated ACE score. Detailed inquiry about childhood abuse may become useful in establishing the prognosis of CADASIL.

Background: Neuroleptic-induced parkinsonism frequently decreases or resolves with medication changes. In this case we present a 50-year-old man with cognitive decline and parkinsonian features that persisted despite changes. These symptoms, as well as orthostasis, gait disturbance, and dysexecutive signs, continued to deteriorate over two years. The co-occurrence of parkinsonian signs and frontal dysexecutive signs may be caused by a mutation in the MAPT gene on chromosome 17. Case History: A 50-year-old Caucasian man with chronic schizophrenia occupying a long-term chronic psychiatric hospital, presented with 2 years of drug induced parkinsonism and cognitive decline. Paternal family history unknown, but a maternal uncle had significant cognitive decline in his early 70s after a lifelong course of severe mental illness. At initial evaluation, MoCA was 15/30 with poor attention, executive function and recall. Two years later his initial parkinsonian signs, including cogwheel rigidity, had improved off haloperidol. However, gait worsened with episodes of freezing, festinating gait, severe orthostasis, and significantly worse cognition (Repeat MoCA 5/30). Due to his age and presentation a genetic dementia syndrome such as MAPT mutation was considered. Conclusions: A precipitous cognitive decline in the setting of persistent motor symptoms, is an indication for genetic evaluation. The MAPT gene on chromosome 17 is related to neurodegenerative diseases including Parkinson disease, frontotemporal dementia, and Alzheimer’s disease and may have sporadic, autosomal dominant, or autosomal recessive inheritance. Psychotic disorders serious enough to result in chronic institutionalization may have components of neurodegenerative disorders, especially if associated with severe sensitivity to neuroleptic-induced parkinsonism.

Background: Neuropsychiatric symptoms (NPS) have been exclusion criteria for Alzheimer’s Disease therapeutic clinical trials. Mild Behavioral Impairment (MBI) is a neurobehavioral syndrome of emergent and sustained NPS as a risk state for dementia. The MBI Checklist (MBI-C) was developed to operationalize MBI, with applicability to predementia populations. Objective: To determine the predictive utility of the MBI-C and Neuropsychiatric Inventory Questionnaire (NPI-Q) in measuring NPS in relation to cognitive impairment, measured by the Montreal Cognitive Assessment (MoCA). Methods: The MBI-C (N=65) and NPI-Q (N=168) were administered to subjective cognitive decline (SCD; N=4 versus N=31), Mild Cognitive Impairment (MCI; N=10 versus N=42) and dementia (N=51 versus N=95) patients in a tertiary clinic over 6–25 months. We analyzed change in MBI-C and NPI-Q in relation to change in MoCA per month using response feature analysis. Results: As cognitive diagnosis progresses, NPS increases. Those with worse cognition tend to be older (p=0.676 versus 0.081), female (p=0.518 versus p=0.991) and have less education (p=0.922 versus p=0.943). For every point increase in MBI-C, there is a 0.002 point decrease in MoCA per month (p=0.511) while there is a 0.009 point decrease in MoCA per month for the NPI-Q (p=0.004). Apathy is the most predictive domain for both MBI-C (0.010; p=0.290) and NPI-Q (0.055; p=0.002). There is no modification but age confounds. Conclusion: The MBI-C may be used to detect NPS and has predictive utility. Earlier detection of dementia using NPS may serve as a treatment target.

Background: Poisons are classically divided into five categories: heavy metals, gases, organophosphates/solvents, complex metal ions, and drugs of abuse. CNS effects differ with each class. Exposures should be viewed in terms of length/amount of exposure, pre-exposure risk, and postexposure healthcare. Complex Metal Ion exposure can occur in occupational (included war-related), accidental, intentional overdose, or medical settings. Evaluations from previous ANPA presentations in this series (2015, 17, 18) were very positive, and indicated the need for more teaching products of this type. Incorporating feedback allows further refinement and adaption of materials for use in additional clinical conditions. Objective: Create new teaching materials in which color carries a significant portion of the information, allows large volumes of data on functional neuroanatomy and clinical presentation to be combined without overwhelming learners. Methods: New scientific and clinical research relevant to physiology of complex metal ions, particularly regarding comorbid war-related exposures, as well as medical and occupational exposures were reviewed, synthesized, and summarized into graphic rich original teaching materials (e.g. diagrams, charts, models). Results: Use of graphic-rich materials that connect functional neuroanatomy, physiology, and clinical practice deepens interest in the individual aspects of each patient, and enhances appreciation of co-occurring pathologies and prognosis. Conclusion: These newly revised tools support guiding learners’ through the intricacies of this complicated field. Use of guided experiences strongly promotes development of the active, integrated knowledge of functional anatomy required for practice of neuropsychiatry as it relates to assessment and treatment of complex metal ion exposures, particularly with comorbid war-related exposures.

Background: In 1998, the Vancouver Limbic Surgery Group was formed as a clinical program to offer surgical treatment for severe treatment resistant depression (TRMD) and treatment resistant obsessive-compulsive disorder (TROCD) for patients living in British Columbia, Canada. Bilateral anterior capsulotomy (BAC) was selected as the target for both conditions. Objective: This poster will present on the immediate, 2 month, and >1-year side effects of BAC. Methods: Since the program’s inception, 12 patients with MDD and 5 with OCD have been treated with BAC. Patients undergo a rigorous selection and vetting process. Results: One patient, aged 76 at the time of surgery, is excluded from the analysis. He developed postoperative akinetic mutism, confounded by the emergence of vascular dementia, and died within 2 years from renal failure. Of the remaining 16 closely monitored patients, followed for between 1 to 18 years, most obtained some or significant benefit. The long-term side effects of BAC, independent of the course of their underlying psychiatric condition or complicating psychosocial predicaments, are limited. Conclusion: The overall safety of BAC is reassuring and for most the benefits appear to be significant. This procedure should be available to patients who are severely disabled by depression and/or OCD who have failed all other available therapies. Long-term outcomes (>1 year) can be complicated by the course of an individual’s underlying psychiatric illness, pre- and postsurgical resilience, and confounding psychosocial circumstances. Identification of those few patients vulnerable to poor psychiatric outcome may not be possible.

Background: Traumatic Brain Injury (TBI) is common in the military population. The sequelae of mild traumatic brain injury (mTBI) have become a major focus of clinical research in the Department of Defense. Schizophrenia-like psychosis (SLP) has an incidence ranging between 0.7 to 9.8% in patients with a history of any severity TBI, often presenting over a year after the initial injury with an average time to symptom onset between 4–5 years. SLP differs from primary psychotic disorders as it presents with positive symptoms, but does not have negative symptoms or cognitive dysfunction. Case History: A 27-year-old male presented to the emergency department with recent onset of indistinct auditory hallucinations and mild paranoia, insight into his condition, and no cognitive dysfunction or disorganization. Careful review of the patient’s history revealed multiple mTBIs in high school and college from playing sports, followed by 4–5 additional mTBIs over the course of his military career. The most recent mTBI happened 1.5 years prior to symptom onset. The patient initially presented to mental health 6 months after the most recent mTBI with complaints of decreased concentration, depressed mood and anxiety. This case reviews the differences between SLP and schizophrenia and the evolving nature of this patient’s presentation. Conclusion: This case illustrates not only the delayed onset of psychiatric symptoms following mTBI, but the evolving course that can occur with those symptoms. Further research is needed to help determine how often these changes may occur and to more clearly establish incidence of these disorders.

Background: Veterans with posttraumatic stress disorder (PTSD) frequently report dream enactment behaviors (DEB). Whereas DEB are associated with PTSD, their clinical correlates and relationship with other sleep disorders, including rapid eye movement (REM) behavior disorder, warrant re-examination. Objective: To examine demographic and clinical characteristics of Veterans endorsing regularly occurring DEB versus infrequent or no DEB among Operation Enduring Freedom/Operation Iraqi Freedom, Operation New Dawn (OEF/OIF/OND) Veterans enrolled in an ongoing cohort study. Methods: 78 eligible participants were dichotomized as DEB+ (DEB at least once per week in the past month) versus DEB– (no DEB or less than once per week) according to responses on Item 1g of the Pittsburgh Sleep Quality Index Addendum for PTSD. Subjects completed semistructured assessments of mild traumatic brain injury (mTBI) exposures, PTSD symptoms, and other psychiatric disorders and self-report measures of sleep quality and antidepressant exposures. Sleep medicine histories were determined via systematic chart reviews. Results: As compared with DEB– (N=59), the DEB+ (N=19) group had poorer sleep quality, greater PTSD severity, a higher number of reported mTBI with loss of consciousness (LOC), and a higher likelihood of being diagnosed with sleep disorders. After adjusting for global sleep quality, a significant association persisted between DEB and number of mTBI with LOC, but not between DEB and PTSD. Conclusion: These results suggest that mTBI with LOC may disrupt neural circuits regulating REM sleep in OEF/OIF/OND Veterans, and this sample should be further characterized with standardized, polysomnographic assessment of muscle tone and behavioral events during REM sleep.

Background: Phase synchronization of slow waves (SW) and sleep spindles is proposed to facilitate sleep-dependent memory consolidation. The thalamocortical mechanism for initiation of SWs remains unclear, and some suggest that a 5–8 Hz “theta burst” precedes SWs, while others argue that the initiating event is a 9–12 Hz “slow spindle.” Objective: We developed a method to differentiate unique electroencephalographic (EEG) events that proceed SWs. Given that SWs occur in clusters, we sought to understand the relationship between order of SW and preceding EEG event-type through stages N2 and N3 sleep. Methods: We created a custom MATLAB function to detect SW events from an overnight EEG recording performed on a healthy control subject during N2 and N3 sleep. This program differentiated individual SWs into their sequence order and aligned each SW’s negative trough for subsequent time-frequency spectral analysis. Results: By segregating SW events in order, we observed that the first SW events during N2 are preceded by a 5–8 Hz theta burst event, whereas second and third SW events demonstrate a prominent 9–12 Hz slow spindle. During N3 sleep, 9–12 Hz slow spindles preceded all types of SWs. Both 5–8 Hz and 9–12 Hz events were more prominent over frontal (FZ) EEG position. Conclusion: Aging and neurodegeneration have been linked to breakdown of SW and sleep spindle coupling with associated deficits in sleep-dependent memory consolidation. Here we demonstrate a novel analysis of SW events and identify distinct subtypes of SW/spindle coupling that are dependent on sleep stage and SW order.

Background: Discerning the boundaries between longitudinal changes associated with idiopathic psychiatric boundaries and neurodegenerative disorders can be challenging absent specific diagnostic tests. Longitudinal follow-up focused on systematically characterizing the multidimensional trajectory of clinical signs and symptoms in conjunction with ancillary laboratory studies may eventually lead to a parsimonious, if not definitive, diagnostic formulation. Case History: A 64-year-old male was evaluated for possible behavioral variant frontotemporal degeneration. He carried a longstanding diagnosis of bipolar affective disorder managed by lithium, nefazadone, and venlafaxine. His wife reported a 2–3 year history of subtle personality changes including inappropriate and hostile behavior against a backdrop of lifelong “quirkiness.” Over a 2-month period he experienced two acute episodes of severe bifrontal headache, nausea and vomiting, which resolved over several days. Diagnostic work-up for each episode was similar: no routine laboratory abnormalities, normal MRI brain scan, and EEG findings of diffuse slowing, most prominent bifrontally. Neuropsychological testing revealed impairments in abstract reasoning, confrontational naming, fluency testing, and auditory and visuomotor learning, raising concern for “atypical” dementia. Initial diagnostic evaluation was inconclusive, but led to beneficial “un-treatment.” After a several year period of functional improvement, behavioral changes recurred in association with motor signs, and punctuated by three spells of headache and altered mental status similar to the previous episodes. Further medication adjustments and longitudinal follow-up culminated in clinical improvement and diagnostic disambiguation. Conclusion: Diagnosing and managing complex neuropsychiatric disorders demands careful consideration of multiple clinical, laboratory, and therapeutic variables over time, with particular attention to potential iatrogenicity.

Background: TBI is a costly public health concern. TBI patients suffer from neuropsychiatric sequelae requiring follow-up care after their injury. There have been challenges in providing outpatient TBI follow-up care in our region from lack of an organized system. Objective: We conducted a retrospective review of a resident-initiated and run outpatient system of care for mild TBI patients called BIONiC (Brain Injury Outpatient Neuropsychiatric Care). One year of data were reviewed to analyze efficacy in access to care. Methods: Organizational meetings with University of Massachusetts Medical School (UMMS) staff from Neurology, Psychiatry, Neuropsychiatry, Trauma, Neurosurgery, and Rehabilitative Medicine started in December 2016. Referrals for mild to moderate TBI from UMMS departments were made either directly to neuropsychiatry resident coordinators or via inpatient consultations completed by a nurse practitioner who would then refer to an academic-private partnership outpatient neuropsychiatry clinic (CNS) for follow-up. Initial intake was completed by neuropsychiatry residents from the UMMS Combined Neurology/Psychiatry Program on a biweekly basis with the assistance of CNS staff. Results: Over 12 months, 29 referrals were made, primarily by the UMMS Trauma Service. Of those, 16 (56%) established care with CNS. Four patients could not be reached or established care elsewhere, five patients were scheduled but not yet seen, and insurance issues limited follow-up care of four patients. Once care was established in the outpatient clinic, patients were more likely to continue follow-up (63%). Conclusions: Establishing a system of care for an underserved TBI population with extensive neuropsychiatric sequelae and disability requires interdepartmental collaboration.

Background: Successful voluntary tic suppression is a key factor of the behavioral interventions for tic disorder. Objective: This study aimed to examine tic suppression in children with recent-onset tics and whether it can predict their future tic symptom outcome. Methods: We tested 43 children with recent-onset tics whose tics began within the 6 months prior to the first study visit (baseline) and re-examined 39 of them at the 12-month anniversary of their first tic (follow-up). At each visit, children performed a tic suppression task in which they were asked either to feel free to tic or to suppress their tics in the absence or presence of reward. Results: At the baseline visit, these children, who had only had tics for a few months, could suppress their tics, especially when they received immediate and contingent reward for the successful tic suppression. At the 12-month follow-up visit, children still could suppress tics, but the difference in tic suppression between the reward-present and reward-absent conditions was not significant. Tic suppression ability measured at baseline visit was associated with age, such that older children could suppress tics more completely. Importantly, tic suppression ability measured in a reward condition at the baseline visit predicted YGTSS total tic score at 12-month follow-up: the children who could suppress tics better had greater improvement in tic severity at 12-month follow-up. Conclusion: These findings suggest that inhibitory control of tics is present within months of tic onset and may be an important marker predicting future tic symptoms outcome.

Background: Impulse control disorders (ICDs) and visual illusions/hallucinations (VHs) are known adverse effects of the dopaminergic medications used to treat Parkinson’s disease (PD). When medications lose efficacy or become intolerable, deep brain stimulation (DBS) is an effective intervention. Objective: We sought to test our hypothesis that susceptibility to treatment-emergent ICDs or VHs, potentially reflecting unique underlying network vulnerabilities, is associated with cognitive changes following DBS. Methods: Retrospective review identified 54 PD-DBS patients who completed pre- and postoperative neuropsychological testing. We noted any history of impulsivity or VH prior to DBS implantation. Linear regressions models were used to assess whether these independent variables predicted any changes in neuropsychological outcomes, controlling for surgical target and duration between evaluations. Results: History of ICDs was associated with improvements in visuospatial attention (regression coefficient b=6.684, p=0.055) and abstraction (b=8.083, p=0.024) that were not due to changes in visual perception. Visuospatial memory, however, weakened (b=−12.236, p=0.008). Any history of VH was associated with a decline in confrontation naming (b=−4.656, p=0.021) and visuospatial abstraction (b=−5.48, p=0.085). Neither history of ICDs nor VH predicted statistically significant cognitive changes in other domains. Conclusion: Treatment-emergent ICDs or VHs were associated with distinct cognitive changes following DBS, although cognition generally remained intact. History of ICDs was associated with improved visuospatial functioning, with the notable exception of worsened memory, while history of VH was associated with worsening of complex visuospatial functioning and naming. Neither history appears to be a contraindication to DBS, although patients with VH may warrant specific preoperative counseling.

Background: Posterior cortical atrophy (PCA) is a neurodegenerative dementia that presents with disruption of visual processing. It is the most common form of atypical Alzheimer’s Disease. Less frequently, PCA exhibits Dementia with Lewy Body pathology. Anxiety may be the initial presenting symptom. This is the first described case of PCA presenting with catatonia. Case History: A 72-year-old man with no psychiatric history prior to presenting at age 66 with panic attacks concerning abdominal pain. He was diagnosed with anxiety and prescribed citalopram. Within a week, he presented with altered mental status and rigidity, thought to be serotonin syndrome. He improved with lorazepam and cyproheptadine. For 6 years, he was stable on clonazepam, until he presented with severe catatonia (Busch Francis Catatonia Rating Scale 28 on lorazepam 1.5 mg QID). Laboratory studies were unrevealing. MRI brain showed bilateral parietal lobe atrophy with preserved hippocampi. He was transferred to a state psychiatric hospital and successfully treated with memantine, lorazepam and electroconvulsive therapy (BFCRS 8 after 3 ECT treatments). His neurocognitive exam revealed acalculia, poor supra-span recall, visuospatial impairments (incorrect registration and recall of asymmetric figures, clock and cube drawing), echopraxia and motor persistence. We plan to obtain lumbar puncture for protein analysis to better characterize his dementing process. Conclusion: This is the first case in which a patient with PCA presented with catatonia requiring ECT. Late onset anxiety and/or catatonia is an important diagnostic clue for a possible neurodegenerative condition. ECT may be an effective treatment modality for the associated psychiatric symptoms.

Background: Neurodegenerative disorders account for the bulk of early-onset dementia, with AD and FTLD being the most common degenerative pathologies. Initial clinical presentations vary, and may include cognitive deficits as well as neuropsychiatric symptoms. Auguste D, the first published case of AD in 1907, presented at the age of 51 with delusional jealousy, auditory hallucinations, and memory loss. Discerning the underlying etiopathology is paramount for prognosis, treatment, counseling, and life planning. How should clinicians approach cases in which the disease process remains elusive? Case History: A 53-year-old man was referred to the mental health clinic with new persecutory paranoia. Risperidone was briefly trialed and discontinued secondary to restlessness and mild parkinsonian signs with a positive DaT scan. He concurrently developed subtle speech hesitancy; neuropsychological testing evidenced executive dysfunction, impaired encoding, diminished semantic fluency, and slowed processing speed. He was admitted to the inpatient psychiatric unit with worsening paranoia, visual hallucinations, and further language decline. Workup demonstrated a structurally normal MRI, bilateral temporo-parietal hypometabolism, positive amyloid scan, and equivocal CSF AD biomarkers. APP, PSEN1, and PSEN2 genetic tests were negative. CSF was unrevealing for paraneoplastic or infectious processes. Parkinsonism worsened with olanzapine; clozapine and rivastigmine provided modest benefit. He was subsequently referred for neurometabolic DNA sequencing with negative findings. Conclusions: This case illustrates the complexity of phenomenology and challenges to definitive diagnosis in early-onset dementia. AD, FTD, DLB, PPA, or a combination remain on the differential, highlighting the need for reliable biomarkers to differentiate between etiologies.

Background: Metronidazole is a ubiquitous antibiotic found on the WHO’s List of Essential Medicines. We present a case of a 46-year-old man with alcoholic cirrhosis who presented with psychosis shortly after being prescribed metronidazole. Case History: A 46-year-old African American male with a history of alcoholic cirrhosis presented to the emergency department with sudden onset of paranoia, personality change, and visual hallucinations for two days. Psychiatrist history was notable for depression and PTSD. Psychiatry was consulted for concern of fugue state versus conversion disorder. Physical exam was notable for new onset ataxic gait. Further history revealed that the patient had recently been discharged from the hospital with metronidazole to treat c-difficile colitis. An MRI was obtained and was notable for symmetric T2/FLAIR hyperintense signal in the dentate nuclei bilaterally. Given the specificity of this radiologic finding in the context of his clinical story, a diagnosis metronidazole induced psychosis was made and the metronidazole was stopped. The patient’s symptoms promptly improved and he was discharged. Conclusions: Although the medical literature has typically described metronidazole induced psychosis as a rare occurrence after prolonged use of metronidazole, it should be on the differential in patients who present with acute neuropsychiatric symptoms after initiation of metronidazole regardless of duration. Bilateral increased T2/FLAIR signal of the dentate nuclei is a distinctive feature of metronidazole-induced neurotoxicity and should prompt clinical correlation in order to make a diagnosis of this reversible condition.

Background: Parkinson’s disease (PD) is a neurodegenerative disease with motor and nonmotor symptoms. Mounting evidence points that synaptic changes are paramount in PD pathogenesis and progression. Objective: This study assessed PD subjects using positron emission tomography (PET) imaging with ¹¹C-UCB-J, a recently developed PET radiotracer that binds to the synaptic vesicle glycoprotein 2A (SV2A) and can be used to measure synaptic density. Methods: Clinically established PD subjects (N=10) and matched healthy controls (HC) (N=10) were included in the study. Subjects were in good physical health and excluded for signs of dementia (MoCA score <21). Any PD medications were held during scan day to avoid potential confounds. Subjects received an MRI and then underwent a ¹¹C-UCB-J PET scan using a high-resolution research tomograph (HRRT). Primary regions included the striatum, substantia nigra (SN) and cortical regions. Secondary regions were also included for exploratory analysis. Regional binding potential (BP_ND) values were obtained using the centrum semiovale (a white matter rich area) as a reference region. Results: In PD subjects compared with HCs, there were large ¹¹C-UCB-J BP_ND reductions in the SN (46%, p value <0.001), red nucleus (32%, p value <0.01) and locus coeruleus (20%, p value=0.03). BP_ND values were not significantly different in cortical or striatal regions. Conclusion: ¹¹C-UCB-J PET revealed lower synaptic density for PD subjects in brain areas known to be involved in the pathogenesis of the disease. These data will be compared with ongoing studies of other neuropsychiatric disorders.

Background: PMR is an under-utilized Level A evidence-based treatment for migraine prevention. RELAXaHEAD is a smartphone application (app) that provides an electronic diary, has PMR audio recordings, and offers backend analytics to capture the amount of time spent playing the PMR audio recordings. Objective: To study the feasibility and acceptability of a smartphone application (app) based progressive muscle relaxation (PMR) intervention for the self-management of migraine in a neurology outpatient setting. Methods: In this exploratory single arm pilot study, adults with migraine (4+ headache attacks/month) were asked to use the app for 3 months by inputting daily diary information and performing PMR using the app (20 minutes/day). Backend analytics assessed adherence at 3 months, including the number and duration of PMR audio plays. Results: Fifty-one patients enrolled in the study. Ninety-four percent were female. Mean age was 39 years ±13. 32 (sd). The majority (63%) had severe migraine disability at baseline based on the migraine disability assessment scale (MIDAS). PMR was played a mean 26 days ±36 (sd), with a mean per session duration of 11 minutes ±7.1 (sd). Forty seven percent (311/663) of uses were 1+ time/week and 35% (230/663) of uses were 2+ times/week. There was attrition by week; most users of the app/PMR used it in the first 6 weeks of the 90-day period. Conclusion: About 1 out of every 2 migraine patients demonstrated uptake of the smartphone based PMR intervention based upon a brief, initial introduction to the app. Also, there appeared time limited acceptability of the intervention by 6 weeks.

Background: The role of cerebellum in language function is still controversial. The lesions in the cerebellum, most frequently on the right, are associated with the development of expressive aphasia. While the reason for this is not clear, the diaschisis between the cerebellar hemisphere and contralateral cerebral hemisphere was implicated as a mechanism for the deficit. Case History: A 72-year-old, right-handed man with sixteen years of education and no medical history presented to the emergency department after sudden onset of dizziness and vomiting, followed by brief loss of consciousness. Initial CT scan of the head demonstrated acute parenchymal hemorrhage in the right cerebellar hemisphere and vermis measuring 4.8×2.6 cm. Neurologic examination was notable for dysarthria and aphasia. He had difficulty expressing himself in full sentences and struggled to maintain a fluent conversation. He could name common objects but had difficulty with less common ones. Patient underwent comprehensive neuro-psychological testing, revealing a language deficient consistent with a variant of aphasia. Speech itself was dysarthric, effortful, and clumsy. Individual words were often broken up into separate syllables, separated by a noticeable pause, and with atypical emphasis. He periodically repeated phrases. Characteristic ataxic dysarthria / scanning speech was observed during reading and naming tasks. Conclusion: Based on the clinical presentation, neuropsychological testing results, and neuroimaging findings, we concluded that a hemorrhage in the right cerebellar hemisphere caused aphasia. The other findings, such as dysarthria and coordination deficits seen in this patient are classical symptoms of cerebellar function impairment.

Background: There are no evidence-based guidelines or gold standard criteria for the diagnosis of functional movement disorders. Sudden onset, spontaneous remissions, and variability over time are considered useful “red flags” suggestive of a functional movement disorder. However, clinical symptom variability and spontaneous remissions can occur in nonfunctional disorders including paroxysmal dyskinesias and focal seizures. Case History: A 40-year-old woman with bipolar disorder was referred to the emergency room for mania in the setting of medication noncompliance. Her exam was notable for intermittent right sided facial spasm with posturing of her right arm and moaning vocalization with fluctuating arousal. Brain MRI along with CSF autoimmune studies were unremarkable. 24-hour EEG was a normal study, though the abnormal movements were not captured. She subsequently developed depressive symptoms which were treated with lamotrigine. Three months later she developed similar episodes of abnormal movement. The movements were in a right sided craniofacial distribution, occurred exclusively in the late afternoon/evening, and were precipitated by stress, sleep deprivation, and alcohol. CBT for conversion disorder was started but the movements continued. Lithium was initiated for residual depressive symptoms and the movements ceased for 3–4 weeks. When lamotrigine was decreased from 200 mg to 100 mg, the movements briefly re-emerged before resolving. Conclusion: Differentiating a “functional” from “organic” movement disorder can be diagnostically challenging based on clinical phenomenology. Pharmacologic interventions to address underlying psychiatric disease often affect circuity shared by both disorders. Abnormal corticostriatal connections may be involved in the pathophysiology of bipolar disorder and abnormal movement.

Background: Though originally described in women with ovarian teratomas, anti-NMDAR encephalitis is now recognized as an autoimmune disorder that may occur without an associated tumor. Isolated psychiatric episodes are reported as rare (∼4%). The comorbidity of other autoimmune diseases with NMDA receptor encephalitis has not been well defined, though patients without associated tumor are more likely to have overlapping demyelinating syndromes. Case History: A 29-year-old woman with a 9-year history of bipolar disorder presented with decreased need for sleep, heightened creativity, increased productivity, and grandiose delusions. Three weeks into her hospitalization she became disoriented, tachycardic, and intermittently catatonic. Work-up revealed CSF anti-NMDA antibodies. MRI pelvis was negative for teratoma. Her symptoms resolved with IVIG. 19 months after discharge she developed left sided numbness and was found to have transverse myelitis. Upon review of outside records she was found to have anti-ds DNA antibodies 5 months prior to her manic episode. Conclusion: Isolated psychiatric presentations of anti-NMDAR encephalitis reported as rare, but the evidence is biased toward patients who obtain ancillary testing for concerning symptoms. We present a patient with a nine-year history of isolated mood episodes without movement abnormalities, dysautonomia, or seizures prior to her diagnosis. Patients without an associated tumor may be more prone to autoimmune disease. Studies that include a longitudinal history of psychiatric symptoms preceding a diagnosis of anti-NMDAR encephalitis are needed. Other disease-specific antibodies should be screened for. The clustering of diseases may shed light on a common autoimmune mechanism.

Background: Neurodegenerative diseases cause progressive irreversible loss of specific neuronal populations. The disrupted neural circuitry often involves system disturbances, which extend beyond the diseased territory in the brain. Objective: This review aims to synthesize the available data regarding the interactions between the neuroendocrine system (including the hypothalamic-neurohypophyseal system and hypothalamic-pituitary-adrenal / thyroid / gonadal axes) and various neurodegenerative disorders (Alzheimer’s, Parkinson’s, ALS and Huntington’s). Method: A PubMed literature review was done to identify relevant articles published within the past twenty years. Results: Our original search criteria produced 1993 articles, of which 123 were applicable. They yielded evidence of many interactions which will be discussed in this review. Several common findings include HPA axis hyperactivation, impaired CNS insulin signaling and disrupted circadian rhythms. As examples, HPA axis hyperactivation impacting neuronal loss and homeostasis has been demonstrated in Alzheimer’s, Parkinson’s, ALS, and Huntington’s. Type II diabetes mellitus is an overall risk factor for dementia, however evidence suggests that disrupted central insulin signaling may influence amyloid-beta deposition and tau hyperphosphorylation in Alzheimer’s and dopaminergic transmission in Parkinson’s. Melatonin not only regulates sleep cycles but may have a neuroprotective benefit that when lost, contributes to neurodegeneration. Conclusions: Neuroendocrine disturbances are common components of neurodegenerative disorders and often unaddressed. Some may be markers of progression of disease, some may aggravate the underlying neuropathology, and others may have a direct role in the primary pathogenesis. Thinking “neuroendocrine” has therapeutic potential in prevention and management of both the primary neurodegenerative disease and associated general medical conditions.

Background: In the epilepsy monitoring unit (EMU), patients are routinely taken off of their anticonvulsants to provoke seizures. Subsequent agitation or violence from postictal confusion or postictal psychosis are safety concerns. Yet, neurology residents, nurses, and police are not routinely taught specifically about this subject. Objective: This quality improvement project aimed to use an educational lecture and supplementary materials to increase comfort and knowledge about postictal safety concerns. Methods: We presented a 1-hour lecture for neurology residents and collected 16 pre- and posttests assessing comfort level (5 likert questions) and knowledge base (5 multiple choice questions). We presented a 15-minute lecture for EMU nurses, and collected 17 pre- and posttests for knowledge (3 multiple choice questions). A 30-minute lecture for campus police will be conducted in the future. A paired-T test determined statistical change. Distributed resources included the slide show and video of the presentation, and a laminated pocket card with a list of risk factors, management guidelines, and medication options. Results: For the neurology residents, there was a significant improvement in all 5 comfort level questions: 1* (p=0.004), 2* (p<0.001), 3* (p<0.001), 4* (p=0.002), 5* (p=0.0145). For knowledge, there was improvement in the first 3 questions: 1* (p=0.0011), 2* (p=0.0074), 3* (p=0.0364), 4 (p=0.1439), 5 (p=0.2162). For the EMU nurses, there was improvement in the first 2 knowledge questions: 1* (p=0.0078), 2* (p=0.0486), 3 (p=0.4495). Conclusion: Formal lectures and resources can be helpful for residents and nurses to learn about recognition and management of postictal agitation and postictal psychosis.

Background: Schizophrenia typically begins from age 16–30 and can result in eventual cognitive decline. Frontotemporal Dementia (FTD) typically begins from age 45–65 with unrelenting progressive cognitive decline. The most common genetic cause of familial FTD is a noncoding hexanucleotide repeat in the C9orf72 gene. The clinical presentation of C9orf72 carriers often includes psychiatric symptoms, yet psychotic symptoms are not included in the criteria for FTD. Diagnosis is complicated by the fact that the psychotic symptoms in C9orf72 are not known to constitute a distinct syndrome. We present a patient who appears to have had psychosis related to C9orf72 with onset in young adulthood. Case History: A 51-year-old right-handed Vietnamese woman with a history of schizophrenia presented with a one-year history of progressive cognitive decline associated with disinhibition, loss of empathy, repetitive rituals, hyperorality, incontinence, and aphasia. Her brain MRI revealed moderate diffuse atrophy, and CSF studies were inconsistent with Alzheimer’s disease. She had been diagnosed with schizophrenia at age 24 when she presented with auditory hallucinations and delusions, but her symptoms remained stable and untreated for 26 years. Her current symptoms met criteria for bvFTD, which was confirmed with genetic testing showing >44 repeats in the C9orf72 gene. Conclusion: C9orf72 repeat expansion can manifest with a syndrome that meets DSM-5 criteria for schizophrenia with stable symptoms for decades before exhibiting deterioration consistent with FTD. Progressive cognitive decline in patients with schizophrenia should not simply be attributed to schizophrenic deterioration but should prompt a search for other causes of dementia.

Background: We present the novel case of a 66-year-old woman who was diagnosed with Amyotrophic Lateral Sclerosis (ALS) after the onset of an episode of MDD with psychotic features. MDD is an uncommon prodromal symptom of ALS. This case highlights the multidisciplinary approach to management of patients’ with MDD with comorbid ALS. Case History: Ms. S is a 66-year-old woman who was seen on the psychiatry consultation-liaison service on an account of 3-month history of depressed mood and weight loss. She had previously been relatively well except for a recent diagnosis of ALS prior to which she had an onset of depressive episode. She complained of hearing demeaning voices, poor sleep, anhedonia and a 40 pounds weight loss. She exhibited poor oral intake and paranoid delusional thinking. She was noted to have bradykinesia, chelitis, and impaired speech. Her chief compliant was she should be “left alone to die.” Conclusion: This case adds to the literature that points to an association between MDD and ALS. The management of MDD with comorbid ALS requires a multifaceted approach. The patient was started on olanzapine dissolving tablet 7.5 mg nightly and sertraline 100 mg daily. Given the severity of her symptoms, ECT was initially considered. However, careful deliberation with neurology, pulmonology and anesthesiology teams deemed she was a poor candidate for ECT. Over the course of the hospitalization, olanzapine and sertraline were titrated to 20 mg QHS, and 175 mg daily, respectively. Depression and psychosis resolved and she was subsequently discharged in stable condition.

Background: In the biopsychosocial formulation of Functional Neurological Disorders (FND), little is known about relationships between social behavior and other concurrent neuropsychiatric factors. Objective: The study investigated how patient-reported social network size related to predisposing vulnerabilities, symptom severity, and structural brain profiles in motor FND patients. We hypothesized that reduced social network size would correlate with trauma burden, depression/anxiety, personality traits, symptom severity, and structural brain alterations within salience/reward processing areas. Methods: In 38 motor FND patients (25 woman, 13 men), we explored how Social Network Index (SNI) network size related to demographics, risk factors, and symptom severity. Data from 23 patients with MRIs were used to perform FreeSurfer analyses adjusting for age, gender, and total intracranial volume. Cortical thickness analyses were corrected at the cluster-wise level and subcortical analyses were Bonferroni corrected. Results: In univariate psychometric analyses, social network size positively correlated with physical and mental health, graduating college and working full-time; social network size inversely related to lifetime trauma burden, PTSD severity, and neuroticism. Across motor FND subtypes, patients with psychogenic nonepileptic seizures showed a tendency toward increased social network size compared with other motor FND subtypes. In structural neuroimaging analyses, a larger social network correlated with left nucleus accumbens (p_corrected=0.045) and hippocampal (p_corrected=0.009) volumes; both results remained significant when adjusting for depression scores. Conclusion: This cohort study preliminarily suggests that risk factors for the development of FND negatively impact social behaviors and supports a role for the nucleus accumbens in social behaviors across clinical and nonclinical populations.

Background: The number of Behavioral Neurology & Neuropsychiatry (BNNP) fellowship training programs accredited by the United Council of Neurologic Subspecialties (UCNS) and the number of UCNS Diplomates in BNNP have grown since the inception of the subspecialty in 2004 and the first BNNP subspecialty certification examination in 2006. However, challenges to the further growth and development of this subspecialty merit the collective consideration of practitioners and thought leaders in this and related clinical disciplines. Objective: The present project evaluates the state of UCNS-accredited BNNP training programs and explores barriers to the further growth and development of the field with respect to recruitment of qualified trainees, posttraining career opportunities, and the sustainability of BNNP fellowship training programs. Methods: Publicly available information on BNNP fellowships and Diplomates was obtained and integrated with information on these matters maintained by the UCNS as part of fellowship accreditation and practitioner certification processes. These data were compiled and analyzed with respect to several metrics on information available to trainees, fellowship programs, and certification. Results: There are 33 UCNS-accredited BNNP fellowship training programs in North America. More than 400 practitioners have been certified as BNNP subspecialists by the UCNS, among whom 382 are current Diplomates in this subspecialty. Conclusion: BNNP has grown rapidly over the last 15 years, and is now the third largest UCNS-accredited subspecialty. Actionable barriers to growth are reviewed, and recommendations for the continued growth and development of this subspecialty based on the assessments undertaken in this project are discussed.

Background: Creutzfeldt-Jakob disease (CJD) is a rapidly progressive dementia associated with prion protein accumulation and neurodegeneration. Average disease duration is 6 months. Diffusion-weighted imaging (DWI) is highly sensitive and specific for CJD, especially in conjunction with cerebrospinal fluid studies. We present an atypical case of sporadic CJD with slow progression of symptoms over six years and late development of typical MRI findings. Case History: A 59-year-old Caucasian female with no prior medical or family history presented with a six-year history of gradually worsening balance, coordination, and memory. Thorough neurological evaluation three years earlier was inconclusive, with MRI brain demonstrating mild generalized atrophy and neuropsychological testing indicating nonspecific mild cognitive impairment. She remained functionally independent, but her balance and cognition continued to decline. Our neurological examination revealed a MoCA score of 21/30, cerebellar signs, lower extremity spasticity, and diffuse hyperreflexia. Repeat MRI brain showed worsened cortical and cerebellar atrophy, but no DWI abnormalities. An extensive ataxia workup was unremarkable. Three months later, she experienced rapid cognitive decline. Repeat MRI brain demonstrated new asymmetric DWI hyperintensities in bilateral cingulate and insular cortices. CSF 14-3-3 protein was negative, RT-QuIC was positive. The patient entered hospice, expiring after two months of precipitous decline. Conclusion: Sporadic CJD is typically associated with rapid progression and DWI is usually a sensitive marker for disease presence. An atypical presentation with slow symptomatic progression and absence of typical imaging findings may present a diagnostic challenge and a high index of suspicion must be maintained for timely diagnosis.

Background: Limb apraxia is a cognitive deficit in motor programming that leads to an inability to correctly execute skilled purposeful movements, and results in errors either of the spatiotemporal processing of the movements or in the content of the actions. Limb apraxia is distinguished from other causes of impaired movement including elementary motor deficits, primary sensory deficits, neglect, agnosia, and other movement and cognitive disorders. Several studies in the last few years have generated advancements in our understanding of limb apraxia. Objective: This study summarizes the advances that have been made in limb apraxia research in recent years. Methods: A PubMed search for “limb apraxia” from 2013–2018 produced 155 articles. The articles were evaluated for significant new developments and 62 pertinent articles were further reviewed. Relevant information was subsequently extracted from half of the reviewed articles. Results: A patient’s quality of life can be detrimentally impacted by limb apraxia. Progress has been made in the localization of limb apraxia, characterization of limb apraxia in different types of dementia and other neurological diseases, rehabilitation of the apraxic limb including the use of novel technologies in rehabilitation, and the development of better screening tools for limb apraxia. Conclusion: Knowledge of recent advancements in clinical and biomedical research of limb apraxia can potentially aid in the diagnosis of various neurological diseases, enhance precision in localization of deficits, and bring about more efficacious methods of rehabilitation.

Background: False reports, not due to deliberate lying, can result from neurological disorders. Their nature and characteristics differ depending on whether they are delusions or a number of other related conditions. Objective: To report a patient with “fantastic thinking” after a lesion involving the right claustrum and to review the causes of nondeliberate false reports from neuropsychiatric disorders. Methods: We present an 81-year-old man with stroke involving the right claustrum and the emergence of an “inner world” where he was a successful CEO and general who could overcame bad people, had superpowers, and was able to perform other feats. The patient could come and go from this alternate world and endorsed that it was internal, but, nevertheless, held on to it tenaciously. We review the different causes of false reports and how they differ. Results: This patient, and a review of the literature, suggests that neuropsychiatric disorders can result not only in delusions of different types, but also in false memories, magical thinking, provoked confabulations, fantastic confabulations, and fantastic thinking. A comparison of the criteria and characteristics for these conditions suggests that the patient’s lesion in the claustrum, which has a role in integrated conscious experience, may blur the distinction between inner and outer experience resulting in “fantastic thinking.” Conclusions: False reports not due to deliberate falsehoods, may range from delirium to fantastic thinking. We discuss the differential diagnosis between them, and specifically discuss the potential relationship of fantastic thinking to acquired brain lesions.

Background: Central Pontine Myelinolysis (CPM) is a neurological disorder associated with demyelinating lesions in the central pons. It may coexist with extrapontine myelinolysis (EPM). It often presents with dysphagia, dysarthria, quadriplegia, pseudobulbar palsy, encephalopathy, or coma. Neuropsychiatric manifestation includes personality changes, inappropriate affect, emotional lability, disinhibition, catatonia, psychosis and delirium. None of the previous reports have suggested occurrence of prominent manic symptoms followed by catatonia in patients with CPEM. Case History: A 72-year-old man was admitted to the cardiothoracic surgery for aortic valve repair and coronary artery bypass graft. His serum sodium level was corrected rapidly before surgery. After two days of surgery, he developed manic symptoms in the form of persistently elated mood, decreased need for sleep, and perceived increase in physical energy. His speech became loud and excessive. On the mental status exam, he had elated mood, grandiose and persecutory ideas, impaired judgement, and absent insight. Subsequently, MRI brain was done and axial T2W images showed central hyperintensities in the pons, bilateral caudate and lentiform nuclei, as well in the thalami. Based on overall history, examination and neuroimaging findings, a diagnosis of CPEM secondary to rapid correction of hyponatremia was made. Conclusion: Neuropsychiatric symptoms such as psychotic symptoms, mood symptoms, catatonic symptoms, etc. developing in the background of rapid correction of serum sodium should be investigated thoroughly and should not be assumed to be a part of a primary psychiatric disorder. Such rare psychiatric presentations of CPEM could provide us mechanistic details of the psychiatric symptoms and perhaps, mental disorders.

Background: Speech and language are often impaired early in the disease course of several NCDs such as Alzheimer's disease and may offer a useful automated screening tool for early detection. Automated speech analysis in atypical dementias such as behavioral variant frontotemporal dementia (bvFTD) and primary progressive aphasias (PPA) has not been well studied. Objective: To test automated classification algorithms to determine a) whether or not someone had a dementia; b) whether the patient had PPA, FTD or AD and c) what kinds of features were most useful in predicting diagnosis based off recorded conversational speech. Methods: 124 individuals with FTD, PPA, AD or healthy controls engaged in a 10 minute conversation. Acoustic features were extracted from the audio recording using open-source tools including the openSMILE package and the Google speech recognition API. Noisy features were removed by a selection process. Results from multiple classification algorithms were then compared. Results: a) We achieved 92% accuracy in NCD from HC. Precision and recall were each over 90%. b) We achieved accuracy scores of 70% at distinguishing between NCD subtypes. c) Cepstral coefficients, linear spectral frequencies, fundamental frequency, voicing probability, and intensity were the most important acoustic features in distinguishing dementia patients from healthy controls. Conclusion: Conversational speech would likely serve as a useful screening tool for dementia, though further work is needed to distinguish between dementia types. These results should be replicated in an independent sample to guard against over-fitting.

Background: Akathisia is a neuropsychiatric syndrome characterized by psychomotor restlessness, an intense sensation of unease and almost compulsory need to move to feel relieved. Although its pathophysiology is not fully clear, it is more often observed with use of dopamine type-2 receptor blockers, including typical and atypical antipsychotics. Akathisia is classified into acute, subacute, chronic, tardive, withdrawal-related, and “pseudo” subtypes. It is often underdiagnosed or misdiagnosed with other psychiatric conditions including psychosis, anxiety and agitated depression. This can delay or prevent the initiation of appropriate treatments and increase the occurrence of adverse outcomes such as poor adherence to medications, worsening of the underlying psychiatric condition, and even aggression, violence, and suicide. Treatments include reducing the dose of the responsible antipsychotic or switching to another one. Alternatively, beta-blockers, benzodiazepines, anticholinergics and mirtazapine can be used. Case History: We report a case of a 50-year-old woman with a history of cocaine, marijuana and alcohol use disorder, and psychotic disorder, emergently hospitalized twice after discontinuing risperidone. Both times she was provided a diagnosis of anxiety and sent home after restarting risperidone. Here we review aspects of her presentation that help differentiating the diagnosis of anxiety from akathisia and treatment strategies. Conclusion: This case exemplifies the clinical challenges of akathisia particularly when the underlying primary psychiatric condition could similarly manifest. Careful investigation of the nature of the clinical manifestations and their chronological onset and progression remains a cornerstone for the correct diagnosis and choice of treatment.

Background: Untreated psychosis has been associated with worse neurological and psychiatric outcomes. Further, duration of untreated psychosis has been shown to have an effect on long-term clinical outcome and prognosis. Several barriers, such as psychosocial factors, stigma, and social support predict adherence. Literature review demonstrates a relationship between certain genetic markers in some cancers and Schizophrenia. Patients with untreated psychosis who develop cancer may develop complicated sequelae, not only due to untreated psychosis, but also due to untreated cancer. Case History: We present the case of 74-year-old Caucasian female with a 30-year history of “behavioral disturbances,” which included paranoid delusions regarding surveillance and “people getting in through gaps in the window pane” resulting in showering while in her bathrobe. Prior to presentation, she was found by police on the side of the road after she had run out of gas, with a 20-cm, necrotic, fungating mass covering much of the right side of her face. She described the mass as a “Band-Aid” and was admitted for medical and psychiatric evaluation and treatment. She was psychiatrically stabilized with antipsychotic and once stable, was able to consent to have the mass, determined to be squamous cell carcinoma, removed via resection. Conclusion: This case illustrates the complexities of untreated psychosis and demonstrates the need for further exploration into the relationship between genetic factors in psychosis and cancer. Her outcome demonstrates the benefit of antipsychotic treatment in improving insight and psychotic symptom amelioration.

Background: Syntax is a uniquely human aspect of language that allows for infinite generativity with the use of finite linguistic means. This important aspect of language is impaired to varying degrees in the nonfluent variant of primary progressive aphasia (PPA), a neurodegenerative disease that predominantly affects language. To date, most measures of agrammaticality in PPA have been relying on the subjective ratings of clinicians. Objective: The aim of this study is to use computational linguistics to measure agrammaticality in the language of patients with the nonfluent variant of PPA (nf-PPA). Methods: The study includes language samples from 34 PPA patients, 13 patients were diagnosed with nf-PPA and 21 with other variants of PPA. We measured syntactic complexity using Stanford Dependency Parser which then allowed the measurement of other linguistic features such as the number of content words, embedded clauses, etc. We trained a prediction model using the logistic regression (nf-PPA=1, other variants of PPA=0) on 20 patients. The model was then tested on a hold-out set of 14 patients. Results: In the training set, the combination of syntactic complexity, verb to content words ratio, and noun to content words ratio resulted in 100% accuracy of prediction (Wald's χ²(3)=25.90, p<0.001). The accuracy of prediction continued to be at 100% for the hold-out set (Wald's χ²(3)=19.12, p<0.001). Conclusion: Quantitative analysis of grammar using computational linguistics can offer an accurate and cost-effective technique in the diagnostic assessment of language in PPA patients.

Background: Prolonged electroencephalographic (EEG) monitoring is performed frequently in the neurological intensive care unit (ICU), but the utility of prolonged EEG monitoring in the acute inpatient neurorehabilitation setting has yet to be established. Objective: To describe a series of patients who were found to have epileptiform abnormalities with prolonged EEG monitoring in the inpatient rehabilitation setting. Methods: Charts were retrospectively reviewed to identify patients who had at least one prolonged EEG performed at the TIRR Memorial Hermann inpatient neurorehabilitation unit during their acute inpatient rehabilitation episode between January 2012 to January 2016. EEGs of at least 3-hour duration were performed under standard guidelines. Patients with a known history of epilepsy or of a prior EEG demonstrating epileptiform abnormalities were excluded. Results: We identified 17 patients who underwent prolonged epilepsy monitoring, and of these, five (29.4%) had at least one prolonged EEG detecting epileptiform activity. Their ages and time-post injury ranged from 18 to 64 years old and 110 to 202 days, respectively. All of the patients had severe functional deficits on admission. In 2 patients, electrographic seizures were captured during the recordings. Conclusion: This case series suggests that prolonged EEG may be useful for the detection of epileptiform activity in patients without a known history of epilepsy when conducted during the acute neurorehabilitation period. Prospective studies are needed to determine the optimal duration of EEG monitoring in this clinical setting.

Background: Mood disorders and anxiety are overrepresented among persons with epilepsy. Anxiety is particularly common in pediatric epilepsy and associated with a variety of seizure types. Broad spectrum anticonvulsants are highly effective treatments both for mood and anxiety disorders and for epilepsy. Clobazam may be an anticonvulsant with a similar “dual role,” and has been found effective for epilepsy and for anxiety in Europe and Asia. Objective: To assess the impact of clobazam on seizure control as well as in reducing symptoms of anxiety. Methods: This is an open-label, adjunctive, proof of concept, clinical trial. At baseline, DSM-V diagnoses are established with a semistructured interview (K-SADS), and symptom measures are obtained with standardized parent and child questionnaires. The trial is for 10 weeks and involves a flexible dose paradigm, starting at 5–10 mg BID and increasing to 10–20 mg BID. Outcome measures include clinical global improvement (CGI-I) as well as scores on specific measures. Results: Ten participants have been enrolled, two dropped out, and five have completed the trial. Anxiety symptoms and seizure control improved in all of the completed subjects as evidenced by CGI-I scores of 1 or 2 and clinical significance threshold changes in anxiety scales. Three subjects had tiredness at maximal dosages, but improved and remained in the clinical trial when the dosages were reduced. Conclusion: Preliminary results suggest that clobazam is effective in the treatment of both anxiety and epilepsy in pediatrics. The flexible dosing paradigm utilized in the trial may have important implications clinically.

Background: The Delirium Motor Subtype Scale DMSS and its short form, the DMSS-4 were derived from 30 characteristics reflecting delirium motor phenomenology and demonstrated correlation with objective measures of hyperactive, hypoactive and mixed subtypes. Objective: To develop the DMSS-Spanish (DMSS-S; 7 hyperactive items, 8 hypoactive) and the DMSS-4-S (2 hyperactive, 2 hypoactive items), from the original English instruments, following the ISPOR principles for good translation/cultural adaptation. Methods: The process included: Three independent forward translations of both instruments by native Spanish psychiatrist. Reconciliation of forward translations, and then, back-translation to English by independent native English translators from an on-line company. Review of the back translated tools by their original author. Harmonization by four psychiatrists from Colombia and Spain, according to the recommendations from the original author. Finally, “cognitive debriefing”: 20 experts were asked to complete an anonymous electronic survey about comprehensibility of language and content of hyperactive and hypoactive items of each scale (four questions for scale). According to the compressively, each question could be rated from 1 (not at all) to 6 (absolutely). Results: Thirteen psychiatrists sent ratings, 7 (53.8%) from Colombia, 6 (46.1%) from Spain. Median scores regarding language and content comprehensibility of the DMSS-S ranged between 5.0 and 6.0. Median scores for the DMSS-4-S were all =6.0. None of the ratings was <3. The new instruments can be downloaded here: https://goo.gl/zc3jZU. Conclusion: The DMSS-S and the DMSS-4-S are culturally adapted to be used by native Spanish language clinicians. Validation studies in Spain and Hispano-America are needed.

Background: Temporal lobe epilepsy (TLE) is associated with a wide range of psychiatric sequelae and has been reported as a cause of catatonia—a neuropsychiatric state with a diverse variety of psychiatric and medical etiologies. Case History: A male in his 20s presented with recurrent admissions for catatonia—without a clear underlying psychiatric, neurologic, or medical diagnosis—requiring electroconvulsive therapy (ECT) and benzodiazepines for several years. In 2015, he experienced an episode of fixed gaze and rhythmic eye blinking, and electroencephalography (EEG) demonstrated new bilateral anterotemporal sharps suggestive of epileptiform activity without electrographic seizures. Differential considerations included nonconvulsive seizures driving his behavior versus electrographic sharps as an after-effect of hundreds of lifetime ECTs. Valproate trial lead to modest stabilization but was eventually discontinued due to pancytopenia and hyperammonemia with subsequent decompensation. In 2018, he developed worsening of catatonia exhibited by perseverative speech, agitation, and disinhibition, partially improved on ECT and lorazepam. An electrographic seizure was captured on EEG. Initial antiepileptic drug (AED) trials proved unsuccessful at suppressing frequent spikes on scalp EEG. Due to the unclear correlation of epileptiform potentials and behavior, intracranial foramen ovale electrodes were placed. Intracranial EEG demonstrated frequent (2–10 per hour) right temporal electrographic seizures with left temporal spread. Aggressive treatment with multiple AEDs resulted in reduced seizure frequency and correlated with clinical improvement, providing a diagnosis of TLE-induced catatonia. Conclusions: TLE is a potential cause of catatonic behavior. As scalp EEG has known limitations in detecting TLE, intracranial monitoring can be considered in refractory cases.

Background: Hyperactive delirium is a form of delirium mainly characterized by agitation, restlessness, orbitofrontal dysfunction. These features can also be seen in delirious mania that was first described by Luther Bell in 1849. Delirious mania remains a rare or possibly underdiagnosed condition and little is known about its underlying neurophysiology as compared with hyperactive delirium. It is crucial to differentiate between these two conditions because the treatment for one condition is contraindicated for other. Case History: The author describes a case of 38-year-old male with past history of paraplegia post motor vehicle accident, Bipolar disorder type 1, left thalamic stroke and similar presentation of acute altered sensorium. Patient had undergone extensive neurological testing including EEG, CSF examination, MRI imaging. The patient was diagnosed with delirium mania. He responded well to intravenous lorazepam and was discharged home on valproate. Conclusions: Delirium mania is a fatal condition. The clinical picture can resemble hyperactive delirium which is due to overlapping neurophysiology. Early suspicion and close monitoring of the patient is required for accurate diagnosis and treatment.

Background: Somatization is hypothesized to contribute to persistent symptoms after mild traumatic brain injury (mTBI). We sought to characterize the type and extent of somatic symptoms in individuals with post-concussion syndrome. Methods: We administered a self-report inventory of somatic symptoms (Patient Health Questionnaire-15) and post-concussive symptoms (the Rivermead Post-Concussion Symptom Questionnaire) to 36 individuals with mTBI more than 30 days prior, and 15 healthy controls. We split the mTBI patients into those with post-concussion syndrome (PCS) and those without (recovered). To assess somatic symptoms not directly due to mTBI, we excluded PHQ-15 items common in mTBI, including headache, dizziness, fatigue, and insomnia. This produced an “atypical somatic symptom score” comprised of somatic complaints including: stomach, chest, and back pain; pain in arms, legs or joints; menstrual cramps; fainting spells; palpitations; shortness of breath; sexual dysfunction; constipation or diarrhea; nausea and dyspepsia. Results: Rivermead scores were expectedly significantly different between groups (F_(2,48) = 51.548, p<0.0001, η² = 0.682), with post hoc comparisons showing that the PCS group endorsed significantly higher RPQ scores than the control and the recovered group (p<0.0001). The MANOVA also showed a significant difference in atypical somatic symptoms (F_(2,48) = 15.231, p<0.0001, η² = 0.388), with post hoc comparisons showing that the PCS group endorsed significantly higher atypical somatic symptoms than the control or recovered groups (p<0.0001). Conclusion: Atypical somatic symptoms frequently accompany persistent post-concussion syndrome, and somatization may represent an important, modifiable factor in mTBI recovery.

Background: Right Hemisphere Syndrome (RHS) is a constellation of cognitive and behavioral deficits occurring after injury to the right cerebral hemisphere. It includes mood lability, spatial neglect, abnormal prosody, impairment of pragmatics and anosognosia. Research on treatment of RHS has often, with sound methodological justification, recruited patients with well-demarcated parenchymal damage in the absence of other injuries. The clinical presentation of RHS arising from traumatic brain injury (TBI), however, may be complicated by additional injuries, subsequent falls and seizures, impoverished histories of pre-event functioning and lack of access to treatment resources. Case Histories: A 41-year-old was first seen in this clinic two years after right temporal hemorrhagic contusion and left occipital suture fracture sustained by falling from standing while intoxicated. Over the following 8 years she experienced significant improvement interspersed with multiple episodes of decompensation and significant medication side effects. A devoutly religious man with an identical twin was admitted 15 years after an automobile accident which caused three-lobe right hemisphere injury. Over 17 years of treatment, his anosognosia, pragmatic deficits and spatial neglect caused significant social difficulty in his religious community. A 55-year-old admitted with extensive right hemisphere damage from a motor vehicle accident 30 years earlier worsened significantly over the ensuing decade due to repeated injury from falls and accumulating seizure damage. Conclusions: The real-world clinical management of RHS from TBI is neuropsychiatrically complex. Patient, precise medication titration, individualized socialization management, reduction in falls and seizures, and multidisciplinary cognitive and physical therapy may be beneficial.

Background: Autistic children have deficits in social functioning and communication skills. Studies have shown a 30%−50% prevalence of self-injurious behaviors in this patient population. Similarly, aggressive, noncompliant and disruptive behaviors can be relatively common in autistic children. Although medication and behavioral treatments have been widely used to address these behaviors, they are not always successful in controlling those behaviors that are especially violent. The Graduated Electronic Decelerator (GED) is a device that applies a brief 2-second electric shock to the skin remotely by a practitioner when the participants show eminent signs of engaging in violent behavior or at the beginning of a dangerous act. Case History: At the Judge Rotenberg Educational Center (JRC), GED has been applied for a subgroup of clients with the diagnoses of autism spectrum disorder (ASD) and/or moderate to severe intellectual disability who demonstrate extremely dangerous behaviors. Self-injurious behaviors include severe self-mutilation, and assaultive behaviors result in hospitalization of staff and other patients, and PTSD among these victims is common. While the dangerous behaviors displayed by a subset of these participants do not respond to conventional pharmacologic and behavioral interventions, there is consistently seen a rapid and dramatic decline with the initiation of GED. As control of these behaviors is achieved, GED can often be faded and discontinued. Conclusions: GED has been shown to be a significantly effective and reliable therapeutic option when other treatment options fail for individuals with ASD and ID.

Background: Reversible lesions within the splenium of the corpus collosum have been attributed to seizure disorder, antiepileptic usage, alcohol use, encephalitis, among other causes. Few case reports demonstrate reversible splenium lesions in neuroleptic malignant syndrome (NMS) and the clinical significance remains unresolved. Case History: We studied a 40-year-old male with schizophrenia, admitted for severe agitation and psychosis. He was initially trialed on olanzapine and lorazepam and developed respiratory failure attributed to pneumonia and severe OSA. Due to sedation, he was switched from olanzapine to valproic acid and haloperidol. He soon developed autonomic instability with leukocytosis and elevated creatinine kinase. His developed clinical features of rigidity, myoclonus, and negativism, which combined with fever of 105.1F prompted concern for NMS. Neuroleptics were held and he was started on dantrolene, bromocriptine, and lorazepam. Emergent ECT was performed. After 3 sessions of ECT, MRI demonstrated restricted diffusion in the splenium with mild flair hyperintensity. Fifteen days later after a total of 9 sessions of ECT, repeat MRI demonstrated resolution of the area of restricted diffusion in the splenium. At this time NMS symptoms had mostly resolved though fever and psychotic symptoms continued. While the cessation of NMS symptoms coincided with the resolution of the splenium lesion, we cannot fully exclude other causes including valproate usage, ECT, or yet undiscovered causes of restricted splenium diffusion. Conclusions: This case adds to the limited literature demonstrating reversible splenium lesions in NMS and underscores the evidence that splenium lesions may be expected to resolve following NMS treatment.

Background: Fyodor Dostoevsky was a 19th century author of Russian literature whose works are considered to be widely influential and often noted for their philosophical, spiritual, and psychological content. Notably, Dostoevsky suffered from epilepsy, which is presumed to be of temporal lobe origin and is a common topic in his writings. Objective: While previous authors have focused on the semiology of his epilepsy and his biopsychosocial development as influences on his writing, few authors have explored the effect that underlying cognitive changes related to his epilepsy may have had on his writing. Methods: We used standard natural language processing techniques to analyze 140 English language translations of Dostoevsky and his contemporaries downloaded from Project Gutenberg with a particular focus on cognitive changes seen in temporal lobe epilepsy (TLE) described in the current literature. Results: Cognitive changes associated with TLE include reduced verbal fluency, reduced naming ability, and deficits in theory of mind tasks. When compared with his peers, we found subtle changes in Dostoevsky’s use of language suggestive of these changes including reduced vocabulary, reduced use of nouns, increased use of pronouns, and increased use of first-person perspective. Conclusion: Here we present the results of a novel analysis that suggests cognitive changes associated with Dostoevsky’s epilepsy may have contributed to his unique writing style. Future directions include attempting to lateralize Dostoevsky’s epilepsy using cognitive evidence, investigating interictal behavior in his writing, and validating results in original Russian transcripts.

Background: Tourette Syndrome (TS) is highly heritable, though Mendelian analyses have failed to identify “the Tourette gene.” A prior genome-wide association study (GWAS) suggested that TS is highly polygenic, indicating that aggregated polygenic risk score (PRS) analyses might be fruitful in understanding the significant phenotypic heterogeneity of the disorder. Objective: To conduct a second-stage TS GWAS of 4,819 cases and 9,488 ancestry-matched controls and to use ancestry-adjusted PRS analyses to test whether polygenic risk may underlie relationships between TS, non-TS tic disorders, and tic severity. Methods: A multicenter, European ancestry-matched case-control GWAS and ancestry-stratified meta-analysis was performed. TS cases all met DSM-5 criteria; a subset were assessed for worst-ever tic severity using the Yale Global Tic Severity Scale (YGTSS). Analyses of TS aPRS as a predictor of tic spectrum disorder status and worst-ever tic severity were performed using logistic and linear regression. Results: Genome-wide analyses confirmed a high polygenic contribution to TS heritability. TS PRS demonstrated enrichment of TS genetic risk in variants regulating gene expression in human BA9/DLPFC (p=1.2×10⁻⁴). TS PRS predicted TS (p=5.3×10⁻⁹) and non-TS tic spectrum disorder (p=4.2×10⁻⁴) status in an independent population-based sample. TS PRS in familial cases also correlated with lifetime worst-ever YGTSS (p=0.026). Conclusions: TS and other tic disorders appear to represent a continuous spectrum of polygenic risk. These genetic results support previous efforts to reclassify tic disorders as a single nosological entity (tic spectrum disorder).