2017 American Neuropsychiatric Association Annual Meeting Abstracts

Background: The concept of catatonia has evolved from its DSM-1 description as a schizophrenia subtype. In the DSM-5, catatonia is described as either due to another mental condition, a medical condition, or as unspecified (Tandon et al. 2013). While this description allows for catatonia to be associated with any psychiatric illness and acknowledges subclinical presentations, most clinicians view catatonia as a categorical diagnosis associated with psychotic disorders, mood disorders or secondary to a general medical condition. We present a case series that raises the possibility of a dimensional approach to catatonic behavior allowing focus on individual catatonic symptoms in a range of neuropsychiatric conditions. Cases: Our cases include 7 men, ages 20 to 61-years-old, and 2 women, ages 44 to 92-years-old. These 9 patients had individual components of the catatonic syndrome and could be considered as having unspecified catatonia. Their symptoms occurred in a variety of neuropsychiatric conditions including Cerebellar Cognitive Affective Syndrome, dissociative states, nonepileptic seizures, severe anxiety, panic disorder, PTSD, obsessive compulsive disorders, ADHD, dementia and delirium. Core symptoms included stupor, mutism, stereotyped speech and agitation, but not other major catatonic symptoms such as posturing, negativism, catalepsy, and mannerisms. Conclusions: A dimensional rather than categorical approach to catatonia may help elucidate mechanisms in common to many disorders, including dysfunction within thalamocortical (Carroll et al. 2007; Daniels 2009) and corticocerebellar circuits. A dimensional approach may also allow clinicians to consider individual catatonia components as treatment targets in diverse conditions.

Carroll BT, Goforth HW, Thomas C, et al: Review of adjunctive glutamate antagonist therapy in the treatment of catatonic syndromes. J Neuropsychiatry 2007; 19:406–412

Daniels J: Catatonia: clinical aspects and neurobiological correlates. J Neuropsychiatry 2009; 21:371–380

Tandon R, Heckers S, Bustillo J, et al: Catatonia in DSM-5. Schizophr Res 2013; 150:26–30 [Web]

Background: Capgras syndrome describes a condition in which an individual incorrectly identifies or reduplicates persons, places or events. Current supports bifrontal or diffuse cortical disturbance to produce this finding. We report a patient admitted with familial schizophrenia and traumatic head injury who manifested a misidentification syndrome of self. Theories of two anatomically independent pathways for facial recognition, a ventral route (explicit recognition) and a dorsal route (emotional significance) of faces support a possible disruption of our patient’s dorsal route, diminishing the emotional significance but preserving the semantic knowledge of himself, family and familiar places. Case: The patient is a 51-year-old male with Schizophrenia admitted involuntarily to the inpatient psychiatry due to threatening and bizarre behavior to neighbors. His delusions included beliefs that the individual who bore his legal name had been replaced by another one named “head of household” following an accident that occurred one year prior during which he was reported to have been unconscious for 5 hours. He referred to family members in a manner void of any emotional attachments e.g. “WWII Veteran,” stating it was “awkward” to use words like mother, brother or father in describing them. His family noted this pattern of speech was not observed during prior decompensations. He improved with antipsychotics. Conclusions: Our patient demonstrated a perturbation with no apparent replacement resulting in what may be termed an “incomplete capgras phenomenon.” We highlight the neuropsychiatric aspects of this case while searching for possible neuroanatomical correlates of this unique symptom constellation.

Background: Nitrous oxide is an inhaled anesthetic that has recently been proposed for use in treatment-resistant depression (Nagele 2015). A case of seasonal pattern depression associated with chronic N2O inhalation reveals the possible detrimental effects of its chronic use. Case History: A 55-year-old male dentist presented with a twenty-year history of seasonal pattern depression. He suffered sadness, crying spells, anhedonia, impaired concentration, fatigue, insomnia, apathy, decreased libido, anorexia, and progressive extremity paresthesias. History revealed the patient inhaled nitrous oxide weekly for twenty years, inducing transient euphoria, epistaxis, vomiting, and syncope. Physical exam revealed bilateral absence of vibration and areflexia in the lower extremities. Lab values revealed a decreased Vitamin B12 (190 pg/ml), an elevated intrinsic factor antibody (15 [N:0.0–1.1]), an increased hematocrit (54.1%) and MCV (102.1 FL). Treatment consisted of ceasing nitrous oxide use, vortioxetine (5 mg/d), and B12. There was a rapid and significant improvement in the patient’s depressive symptoms and he remained asymptomatic on follow up. Conclusion: Inhalation of nitrous oxide has been shown to induces psychosis (Hartman 1995), polyneuropathy and CNS dysfunction by producing a functional B12 deficiency (Waclawik 2003) and neuronal apoptosis in the posterior cingulate cortex of adult rat brains (Jevtovic-Todorovic 2003), the area that is associated with depression in humans (Leech 2013). This case study sheds light on a link between depression and chronic nitrous oxide exposure raising questions about the long-term repercussions of using N2O as a treatment for depression.

Background: Carotid atherosclerosis is a risk factor for cerebral ischemia and has been associated with altered brain structure and cognitive dysfunction. In this study, we examined the relationship between carotid atherosclerosis and cerebral cortex thickness, and investigated whether alterations in cortical thickness mediate the relationship between carotid atherosclerosis and cognitive decline. Methods: We assessed 554 community-dwelling subjects from the Lothian Birth Cohort of 1936 (LBC1936) study who underwent brain MRI and carotid Doppler ultrasound studies. Linear generalized models were applied to investigate the relationship between carotid atherosclerosis markers and cerebral cortex thickness (mean age=73 years), controlling for extensive vascular risk factors (VRFs) and IQ at age 11. In 347 individuals, separate linear models were employed to examine the association between the degree of carotid atherosclerosis at baseline and progression of cortical thinning over three-year follow-up period. A structural model was utilized to examine if the relationship between carotid atherosclerosis and cognition is mediated by alterations in local cortical thickness. Results: Independent of VRFs and the side of carotid narrowing, a widespread negative association was identified between percent of carotid artery narrowing and cerebral cortical thickness bilaterally. However, over the follow-up period, no statistically significant relationship was evident between the degree of carotid artery narrowing and progression of cortical thinning. A relationship between fluid intelligence and carotid artery narrowing was demonstrated, which appeared to be partly mediated by the identified alterations in cortical thickness. Conclusion: Asymptomatic carotid artery narrowing is associated with a widespread cerebral cortex thinning independent of VRFs and IQ at age 11. This association may mediate the observed relationship between carotid artery narrowing and cognitive decline in older individuals, although other VRFs that were not accounted for in this analysis could be responsible for this relationship.

Background: Postmortem and in vivo studies suggest that abnormalities in the structure and/or function of the anterior cingulate cortex (ACC) may contribute to suicide risk in major depressive disorder (MDD) and bipolar disorder (BD). These types of abnormalities are amenable to assessment using resting-state functional connectivity (rsFC). Objective: This study compared rsFC of the ACC subdivisions between individuals with MDD or BD during a depressive episode with and without lifetime history of suicide-related behaviors (SB). Methods: 42 individuals with MDD or BD and a history of SB were compared with 26 individuals with MDD or BD and no SB (non-SB) and to 40 healthy comparators (HC). Functional 3T magnetic resonance imaging was performed and rsFC of the subgenual, perigenual, rostral, dorsal, and caudal subdivisions of the FCC were calculated using a seed-to-voxel approach. Statistical significance was set at p<0.05 FWE-corrected. Results: After controlling for age, gender, psychosis, and severity of depression, ANCOVA demonstrated increased connectivity between the left rostral ACC and the visual cortex bilaterally in SB compared with both non-SB and HC participants (right BA-19, p<0.001; left BA-18, p=0.003). In the SB, the altered connectivity with right BA-19 negatively correlated with the Big Five Inventory openness dimension (r=−343, p=0.026). Conclusion: A history of suicide-related behaviors in MDD or BD was associated with altered rsFC of the rostral ACC, a region involved in conflict detection and error monitoring. Replication of these findings and further study of their clinical implications are needed.

Background: Non-epileptic seizures (NES), while gaining recognition, are frequently diagnosed without adequate evaluation. Making a diagnosis of NES without appropriate workup can lead to mismanagement of other serious and potentially reversible conditions. Case History: We describe an 18-year-old female admitted to a freestanding psychiatric hospital inpatient unit for roughly 1 month of failure to thrive, anxiety, catatonia, and attacks of shaking initially concerning for NES in the wake of numerous psychosocial stressors. The patient was repeatedly transferred to a medical emergency department for seizure evaluation, however workup was limited based on reported suspicion of NES. On the third such occasion a brain MRI demonstrated sequelae of epileptic seizure and she was transferred to a tertiary care center Neuro ICU for status epilepticus confirmed by EEG. Her seizures were adequately treated and anti-NMDA receptor encephalitis was confirmed with positive CSF antibodies. Treatment included IVIG, methylprednisolone, and a full course of rituximab. After a 2-month medical hospitalization, she had nearly returned to baseline and was discharged home. Conclusions: Patients with NES are most frequently diagnosed with conversion or somatoform disorder and only one case report of association with anti-NMDA receptor encephalitis appears in the literature. Anti-NMDA receptor encephalitis is rare and presents with an array of neuropsychiatric symptoms making early diagnosis difficult thus delaying treatment and prolonging recovery. Early diagnosis of NES without appropriate workup may influence subsequent providers’ care and cause delay in accurate diagnoses of such conditions and thus affect prognosis and recovery.

Background: Cognitive deficits in stroke are associated with greater disability and mortality rates. Detecting cognitive deficits in acute stroke is critical for appropriate care, but appropriate cognitive assessment can be difficult for inpatient services. A 5-minute MoCA protocol has been validated in outpatients with stroke and TIA (1), but further study is needed to determine performance of this screen for acute stroke inpatients. Objective: To determine if the 5-minute MoCA predicts disability in acute stroke and compare its predictive value with more detailed screening. Methods: Subjects included 154 acute stroke inpatients. Patients were administered a newly developed 20-minute cognitive assessment designed for acute stroke use (LASS–I, Lexington Acute Stroke Scale–Inpatient) and rated by the Barthel Index (BI). 5-minute MoCA scores were extracted from this testing. Results: 5-minute MoCA was predictive of BI score (R²=0.16, F(1, 153)=28.63, p<0.01); adding total LASS-I added significant predictive value (R²=0.22, F(2, 152)=21.37, p<0.01). 5-minute MoCA score was no longer significant in that model (β=–0.10, t=–0.12, p=0.90). Conclusion: Results support that cognition significantly predicts disability in acute stroke. In the present data, both brief screening and more comprehensive assessment have utility in evaluating cognitive deficits in acute stroke. However, analyses suggest that more thorough screening indeed has more robust predictive value. Further analysis will be required to identify which acute stroke patients are most appropriately assessed with more in-depth screening versus those for whom brief screening has best utility.

1. Wong A, et al. The MoCA 5-min protocol is a brief, valid, reliable and feasible cognitive screen for telephone administration. Stroke 2015; 46:1059–1064

Background: Conversion Disorder (CD) is a neuropsychiatric condition with functional neurological symptoms. Psychological stressors play a role but little is known about objective markers of stress. Objective: This study aims to explore 1) objective (biomarkers) and subjective (self-reported) responses to a social stressor and 2) links between stress biomarkers, psychological factors (life adversities) and somatic awareness in CD patients. Methods: 16 CD patients and 15 matched healthy controls performed the Trier Social Stress test(TSST). Saliva samples and subjective evaluation of stress scores were collected before and after TSST. Cortisol (HPA axis) and α-amylase (adrenergic axis) were compared between groups and correlated with life events scores (Amiel-Lebigre) and awareness of bodily perception(BPQ). Results: Cortisol and α-amylase concentrations were overall significantly higher in patients. Objective stress response did not differ, but subjective stress was reported significantly higher in patients following TSST. Stress-induced α-amylase positively correlated with the self-reported stress in controls only. Cortisol values positively correlated with life adversities only in patients, although number and impact of these events did not differ between groups. Finally, cortisol levels negatively correlated with awareness of bodily perception in the CD group only. Conclusion: These findings reveal a tonic but not phasic hyperactivity of stress systems in CD patients when confronted to a social stressor, though self-reported stress did not align with somatic markers as in controls. Cortisol level correlated positively with life adversities and negatively with body awareness in patients suggesting, altogether, a disconnection between emotion awareness and somatic states in CD mediated by a dysregulation of HPA axis.

Background: Rapid eye movement (REM) sleep behavior disorder (RSBD) is characterized by dream enactment behaviors (DEB) and REM sleep without atonia. However, disruptive nocturnal behaviors (DNB), including DEB, are commonly reported in posttraumatic stress disorder (PTSD). Studies utilizing polysomnogram (PSG) and neuroimaging have demonstrated the presence of several overlapping features. We present a case highlighting the potential limitations of clinical history and polysomnography in differentiating RSBD from DNB associated with PTSD. Case History: The patient is a right-handed male veteran in his early fifties with a diagnosis of early onset Parkinson’s disease (PD), Hoehn and Yahr Stage 2.0, status post deep brain stimulation with electrode leads placed bilaterally in the globus pallidus interna. The veteran was referred for neuropsychiatric evaluation of PTSD and sleep disturbances. He reported a longstanding history of nightmares, DEB, and nocturnal vocalizations. He met criteria for chronic PTSD per the Diagnostic and Statistical Manual of Mental Disorders (DSM-5). He carried the diagnosis of RSBD without PSG confirmation. However, the PSG that was obtained following our assessment was inconclusive, as the patient never achieved REM sleep. Conclusions: The confounding effects of pharmacological treatment for PD, RSBD and PTSD and the similarities in the reported DNB can create a diagnostic dilemma. The etiologies of RSBD will be discussed and compared with PSG abnormalities and brain stem alterations described in PTSD. Given their different prognostic implications and treatments, more work is needed to delineate the potential neuroanatomical and pathophysiological associations between these disorders.

Background: Encephalitis can present with headache, fever, and confusion or as severe as seizures, hallucinations, and coma. Infectious etiologies are commonly viral, with herpes simples being the most common nonepidemic encephalitis in the United States¹. N-Methyl D-aspartate receptor (NMDA) antibody positive encephalitis is another common entity². Damage to the brain from these etiologies can lead to deficits that may be transient or permanent. Case History: We present a case of a 23-year-old female with fever, confusion, seizure activity, auditory and visual hallucinations. Care was managed by Medicine, Infectious Disease, Neurology and Psychiatry. Elevated WBC at 20,000. Head CT showed left temporal swelling, hemorrhage, and uncal edema. MRI showed bilateral areas of mixed cortical and subcortical edema with diffusion restriction on bilateral temporal lobes, mesial frontal lobes, right basal ganglia and insula, highly suggestive of herpes encephalitis. With a Glasgow Coma Scale of 7, she was managed in the intensive care unit. CSF evaluation confirmed HSV encephalitis, thus Acyclovir was initiated. She was hyperoral, hyperphagic, inappropriate and hypersexual with an eighty pound weight gain. Temporal lobes involvement with this presentation, led us to diagnose Kluver Bucy Syndrome. Conclusions: Early diagnosis and treatment is imperative for an appropriate outcome. This patient was started on antivirals late, resulting in severe brain damage and poor outcome.

1. Meningitis and Encephalitis Fact Sheet. NINDS. April 2004

2. Dalmau J, Lancaster E, Martinez-Hernandez E, et al: Clinical experience and laboratory investigations in patients with anti-NMDAR encephalitis. Lancet Neurol 2011; 10:63–74. Available at doi:10.1016/S1474-4422(10)70253-2

Background: Catatonia is a complex psychomotor phenomenon that may coexist with a variety of neurological and psychiatric conditions. While recognition of catatonia does not directly inform the underlying diagnosis, catatonic symptomatology may contribute significantly to treatable clinical morbidity. Case History: We report a patient who was diagnosed with Lewy body dementia following an acute postoperative encephalopathy that was punctuated by a medical illness in his son. A series of follow-up consultations led to diagnoses of psychogenic movement disorder, restless leg syndrome, and REM sleep behavior disorder. His complex presentation included severe headaches, debilitating anxiety, and relatively preserved cognitive function. His symptoms were refractory to standard treatments, and his wife reported that he was remarkably normal upon awakening for about an hour, after which his symptom complex returned. After being hospitalized for work-up of acute headache exacerbation, he was transferred to the in-patient Geropsychiatry unit. Follow-up Neurology consultation raised suspicion for the diagnosis of catatonia, which was supported by a positive response to intravenous lorazepam challenge. Subsequent ECT combined with lorazepam treatment resulted in virtually complete symptom resolution. Conclusions: Catatonia has protean clinical manifestations that can mimic acute or chronic neuropsychiatric conditions. Accurate recognition of catatonia depends on clinical suspicion associated with factors such as acute onset in conjunction with a significant psychosocial stressor, atypical parkinsonian-like psychomotor signs, refractoriness to standard therapies, and idiosyncratic clinical features. The clinical morbidity and cost associated with unrecognized catatonia and the nascent understanding of its underlying neurobiological basis demand more systematic clinical and investigative attention.

Background: Video-EEG is known as a diagnostic tool for psychogenic nonepileptic seizures (PNES). Objective: Finding specific electrophysiology markers for successful treatment of psychogenic seizures. Methods: We combined continuous video-EEG recordings as a therapeutic tool in a cognitive-behavioral therapy (CBT) protocol of a treatment-resistance PNES patient. We therefore had a unique opportunity to record psychogenic seizures, failed attempts to suppress seizures and successful suppression of seizures in a PNES patient that was undergoing continuous video-EEG. For comparison we analyzed psychogenic seizure recordings of another six PNES patients. Results: We describe the clinical case, the modified CBT protocol and the topographical analysis of the bandpass filtered EEG epochs. We found an increased theta range (4–8Hz) activity at the left temporoparietal cortex during psychogenic seizures in the PNES patient and the control patients. Similar increased theta range activity at the left temporoparietal cortex was found during failed attempts to suppress seizures. However, during successful suppressed seizures an increased theta range activity was located at the right frontal cortex. Conclusions: These findings suggest that successful treatment of psychogenic seizures does not simply reverse the changes of the activity at the temporoparietal cortex but also involves specific right frontal processes.

Background: While there are no FDA approved medications to treat chronic TBI-related neuropsychiatric symptoms, previous work suggests that targeting cortical dopaminergic signaling could improve outcomes in patients with TBI. Tolcapone—a CNS penentrant COMT inhibitor—has been shown to modulate prefrontal cortical dopamine tone and improve working memory performance in normal controls. Objective: To evaluate the use of tolcapone for the treatment of chronic neuropsychiatric symptoms due to TBI. Methods: This study is an open-label 2-week trial of tolcapone (200 mg TID) for patients with a history of mild to severe TBI and neuropsychiatric complaints. Outcome measures include patient-reported outcomes (TBI-QOL, FrSBe, GDS), informant-reported symptom questionnaires (FrSBe, NPI, MOAS) and neurocognitive testing (NIH Toolbox Cognition, HVLT, BVMT). Results: 25 patients have consented and thirteen patients have completed the study to date. At this point, group-level statistics (Fisher’s t test) show significant improvement in various patient- and informant-reported outcome measures, including the FrSBe domains of apathy (p=0.011), disinhibition (p=0.001) and executive dysfunction (p=0.07; all FRSBE domains p=0.040). Similar results were obtained with an independent patient reported outcome measurement (TBI-QoL). Cognitive testing also improved while patients were taking the study medication. Modest but significant improvements were shown in the NIH toolbox fluid composite (p=0.005) while other cognitive measures showed trends toward improved functioning. Conclusion: In this preliminary analysis of an ongoing study, we find modest improvements of neuropsychiatric symptom ratings and cognitive testing in patients with TBI following tolcapone treatment.

Background: Recent calls have suggested that the NIH Toolbox Cognitive Battery (NIHTB-CB) is ready for clinical use. Cross-validation studies comparing NIHTB-CB with well-established tests have produced mixed findings, and have focused on combined scores rather than individual tests. No studies have looked at Veteran samples. Objective: This study evaluated relations among individual NIHTB-CB tests and measures common in clinical use. We hypothesized that tests would be associated according to the domains they purported to measure as per related manuals. Methods: Combat veterans (N=51) enrolled in an ongoing study completed a standard neurocognitive test battery. Scores were chosen from the battery a priori based on likely cognitive constructs measured. Correlations were calculated to assess relationships between tests. Results: The NIHTB-CB List Sorting Working Memory Test (LSMW) was correlated (p<0.01) with WAIS-IV working memory scores except for Digits Backward. The NIHTB-CB Pattern Comparison Processing Speed Test (PCPS), Dimensional Change Card Sort (DCCS), and Flanker Inhibitory Control and Attention Test (Flanker) were correlated (p<0.01) with hypothesized scores, respectively (Trail Making A, WAIS-IV Symbol Search, Coding, Cancellation, Processing Speed Index; Trail Making B; Trail Making B, WAIS-IV Cancellation). The Flanker and DCCS were also associated with the Controlled Oral Word Association Test (COWA; p<0.05). Conclusions: Results indicated concurrent validity between NIHTB-CB tests and common domain congruent tasks in a Veteran population. Digits Backward was an exception, and appeared to measure a construct unique from simple attention span/working memory tasks. Future work should address discriminate validity.

Background: PBA results from neurologic injury and is characterized by sudden, involuntary outbursts of laughing and/or crying. DM/Q 20/10 mg twice daily remains the only treatment FDA-approved for PBA. Objective: To evaluate persistence of effect for DM/Q in PBA treatment. Methods: 12-week, OLE for patients with PBA secondary to amyotrophic lateral sclerosis or multiple sclerosis completing a 12-week, double-blind (DB), phase 3 trial (NCT00573443). Patients entered the OLE ≤14 days of last DB dose. DB treatment arms included placebo, DM/Q 20/10 mg, or DM/Q 30/10 mg twice daily; during OLE, patients received DM/Q 30/10 mg twice daily. Center for Neurologic Study-Lability Scale (CNS-LS) scores were measured at all clinic visits and allowed ad hoc evaluation of persistence of efficacy. Results: Of 253 enrolled OLE patients, 92.9% completed and 4% discontinued for adverse events. Regardless of DB treatment assignment, PBA symptoms significantly improved from DB baseline (CNS-LS mean score [SD] of 20.4 [4.8]) throughout the OLE. Mean CNS-LS changes from DB baseline to each OLE visit (OLE Days 15 [N=245], 42 [N=241], and 84 [N=237]) were –9.4 [5.5], –9.3 [5.5], and –9.2 [5.6], respectively (all p<0.001). Patients with a >48-hour gap in DM/Q treatment between DB and OLE had a significant return of PBA symptoms while off treatment (mean [SD] CNS-LS increase=4.5 [5.2]; p<0.001; N=52). Conclusions: DM/Q showed persistent efficacy in treating PBA throughout 24 weeks of DB and OLE treatment. Patients with a greater than 2-day gap in DM/Q therapy between DB and open-label experienced a return of symptoms. Results here support prolonged effectiveness of DM/Q as PBA treatment.

Background: Altered sense of limb ownership (ASLO)—encompassing asomatognosia, somatoparaphrenia, feelings of transformation or strangeness, and personification—usually results from right hemisphere lesions, particularly those involving the parietal lobe and/or insula, and typically involves left-sided limbs. We report a case of right-sided ASLO following a left parietal meningioma. Case History: A 61-year-old right-handed man underwent inpatient rehabilitation following resection of a left parietal meningioma. He reported that his right arm and leg felt like they did not belong to him, although he retained insight that this perception was incorrect. He said his right limbs felt separate from him, and absent at times; and did things of their own accord. He called his right arm and leg by the name “Jimmy”. He had mild anomia and mild right-sided weakness. He did not show extrapersonal neglect on bedside testing. Preoperative brain MRI revealed a large left parietal meningioma impinging on frontal and temporal lobes, with surrounding edema; on postoperative MRI, the edema extended further into adjacent areas as well. During his 28-day rehabilitation stay, the ASLO symptoms diminished. At discharge, he once again felt that his right-sided limbs fully belonged to him and acted only under his command; he no longer called them “Jimmy.” Conclusions: Only a few prior reports describe ASLO following left hemisphere lesions. Our patient's lesion involved the parietal lobe, a region frequently implicated in right hemisphere forms of this disorder. His other cognitive functions showed typical laterality, suggesting that laterality of body ownership can be reversed in isolation.

Background: Serotonin Syndrome is a potentially life-threatening condition. Little is known about mild cases which are seldom recognized. Less is known about prevention. Recognition bias is partly due to the early criteria which included many nonspecific symptoms and favored severe autonomic instability. More recent Hunter criteria demonstrate improved sensitivity and specificity with clonus/hyperreflexia as the primary criterion. Objective: Identify the prevalence of mild Serotonin Syndrome (SS) in an outpatient psychiatric cohort. Show usefulness of ankle clonus as a proxy test for SS. Test the hypothesis that failure to recognize SS results in polypharmacy. Clinical description and management are illustrated. Methods: Subjects included 146 consecutive outpatients to a Friday clinic over a 1 year period. Serotonin Syndrome was clinically diagnosed using Hunter criteria. All patients were tested for ankle clonus. Serotonergic antidepressants (SRI) were present in 74 patients. Extracted records were reviewed for diagnosis, descriptors and course. Results: Mild Serotonin Syndrome was identified in 10 of the 74 patients on SRIs (13.5% prevalence). One non-SRI case was diagnosed SS. Clonus was present in all SS cases. As a marker for SS, ankle clonus showed a Sensitivity of 100% and Specificity of 98%. Curiously, long-term patients with polypharmacy (3 or more agents) showed less risk of clonus (Fisher’s p=0.010). Conclusion: Mild Serotonin Syndrome is common in outpatients. Ankle clonus is the best marker for SS. We recommend routine use of brief focused neurological testing for clonus and tremor. Failure to recognize SS may lead to polypharmacy or increased Serotonin Syndrome severity.

Background: The practice of clinical neuropsychiatry relies, often implicitly, on fundamental assumptions about how brain function affects mental states and behavior. This modern formulation of the mind-body problem has been the focus of sophisticated theoretical work and has far-reaching implications for the understanding and management of neuropsychiatric conditions. Objective: This review aimed to identify and analyze the most influential theories on the mind-body problem from both neuroscientific and philosophical perspectives. Methods: A systematic literature review was conducted across the Medline, EMBASE and PsycINFO databases, as well as the Stanford Encyclopedia of Philosophy and David Chalmers’ MindPapers online bibliography, focusing on theoretical articles on the relationship between mind and brain and the mind-body problem. Results: Although most neuroscientific models have been developed in recent years based on our understanding of brain function (e.g. “global workspace theory” and “integrated information theory”), traditional philosophical constructs formulated centuries ago persist in modern-day neuropsychiatric narratives (e.g. Cartesian dualism). Overall, neuroscience-based theories converge on materialism or physicalism, whereby mental events are reduced to their underlying neural substrates, whereas philosophical theories allow multiple ontological or explanatory levels. Notable exceptions exist within both fields (e.g. Nobel Prize-winner neuroscientist John Eccles, who developed a form of dualism-interactionism, and philosophers of mind Paul Churchland and Daniel Dennett, who developed models of eliminative reductionism). Conclusion: This review revealed a wide range of theoretical positions, with considerable overlap between the traditional framework of the mind-body problem and the “hard problem” of consciousness, both in neuroscience (“neural correlates of consciousness”) and philosophy (“qualia”).

Background: Withdrawal effects from benzodiazepines are myriad. Reduction of benzodiazepines in the older population may reduce the risk of falls, clarify diagnoses, reduce confusion, and identify alternative treatments with lower risk. Even relatively low dose discontinuation can precipitate withdrawal including seizures, catatonia, hallucinosis, and panic attacks. The constellation of the withdrawal symptoms has been less well studied in its import for specifying underlying neuropathology. This presentation of a case of apparent benzodiazepine withdrawal is followed by a discussion of the withdrawal literature on the question of determinants of withdrawal severity and type. Case: The patient is a 75-year-old female presenting to the emergency department with aggression and agitation at her nursing home. Neuroimaging prior to admission showed small old right temporal white matter infarct and findings suggestive of small vessel ischemic changes and arterial calcification. Her regimen of lorazepam 1.5 mg thrice daily was tapered over 72 hours period while antidepressants were optimized. Quetiapine was added for agitation and sleep. In the last day of lorazepam, the patient developed bilateral intermittent myoclonic jerks of her upper extremities and jaw accompanied by momentary perplexity and word finding difficulties. She did not lose consciousness and her vitals were stable. The jerking movements disappeared and subsequent EEG was normal. Conclusions: We present an unusual case of benzodiazepine withdrawal with myoclonic fits in a woman with established cerebral pathology and review the literature on withdrawal symptoms in relation to underlying disease.

Background: While neutralization of dysgeusic taste via food combinations has been demonstrated, food combination dependent ageusia has not heretofore been described. Case History: A 60-year-old, right-handed female, was nasute until one year prior to presentation, when she fell on ice, suffering occipital head trauma and loss of consciousness. A few days later she noted trouble tasting, wherein individual foods would have some flavor, but when combined would be tasteless. For instance, alone peanut butter is 30% of normal taste, blackberry jelly is 10% for flavor and 70% for sweetness, while bread alone is totally tasteless. When these ingredients were combined into a sandwich, they had no taste. Similarly, chicken salad alone had a taste of 30%−40% of normal, whereas when placed into a sandwich it had no taste. Chemosensory Testing: Normosmia on: Brief Smell Identification (11). Pocket Smell (3). Olfactometer Identification: left (16), right (20). Alcohol Sniff (19). Retronasal Smell Index: 2 (abnormal). Gustation: Propylthiouracil Disc Taste: 9 (normogeusia). Taste Quadrant: hypoguesia to citric acid on posterior tongue and palate. Conclusion: For both smell and taste, the overall intensity of the combination of different foods may be less than each individual ingredient. This suppressive effect can be asymmetric, wherein one ingredient may be more suppressed than another (Stevenson, 2012). In this subject, the bread may have suppressed the taste of the other ingredients in the sandwich. Query as to the combination of flavors and their effects on taste in those with chemosensory complaints is warranted.

Laing DG: Characteristics of the Human Sense of Smell when Processing Odor Mixtures, in The Human Sense of Smell (254). Edited by Laing DG, Doty RL, Breipohl W. Berlin, Germany, Springer-Verlag, 1991

Lima DP, Simão FC, Abib SC, et al: Quality of life and neuropsychological changes in mild head trauma. Late analysis and correlation with S100B protein and cranial CT scan performed at hospital admission. Injury 2008; 39:604–611. Available at doi: 10.1016/j.injury.2007.11.008

Mese H, Matsuo R: Salivary secretion, taste and hyposalivation. J Oral Rehabil 2007; 34:711–723. Available at doi: 10.1111/j.1365-2842.2007.01794.x

Schubert MM, Izutsu KT: Iatrogenic causes of salivary gland dysfunction. Dentistry. Oral Surgery & Medicine 2007; 66:680–688. Available at doi: 10.1177/00220345870660S213

Stack KM, Papas AS: Xerostomia: Etiology and Clinical Management. Nutr Clin Care 2001; 4:15–21 Retrieved from http://web.b.ebscohost.com.ezp.waldenulibrary.org/ehost/detail/detail?vid=4&sid=afeb2e9a-fee3-4600-9264-4a532000caa5%40sessionmgr105&hid=124&bdata=JnNpdGU9ZWhvc3QtbGl2ZSZzY29wZT1zaXRl#AN=5521752&db=a9h

Stevenson RJ: The Psychology of Flavour. Oxford, UK, Oxford University Press, 2009

Stevenson RJ: Multisensory Interactions in Flavor Perception, in The New Handbook of Multisensory Processing (290). Edited by Stein BE. Cambridge, MA, Massachusetts Institute of Technology, 2012

Background: Anti-NMDA receptor encephalitis is an acute, severe form of autoimmune encephalitis. Because patients with this condition often present with prominent psychiatric and cognitive symptoms, neuropsychiatry may be among the first to evaluate these individuals. Improved awareness of the condition in neuropsychiatry is essential for timely care. Case History: A 36-year-old African-American female with no significant medical history was brought to her local Emergency Department following two-weeks of progressively bizarre behavior, anxiety, nonsensical speech, confusion, and visual hallucinations. She required restraints for agitation and antipsychotic medication for nonsensical yelling, spitting, and hypersexual language. Basic labs were normal. She was admitted to inpatient psychiatry for ‘acute psychosis.’ Despite treatment, psychiatric symptoms worsened and she developed motor dysfunction, seizures, and autonomic instability. She was transferred to intensive care for unresponsiveness and acute respiratory failure. Lumbar puncture revealed elevated white blood cell count; syphilis, herpes, cryptococcal, West Nile virus, and enterovirus tests were negative. Following transfer to an urban medical center, CSF demonstrated positive anti-NMDA antibodies and an ovarian teratoma was discovered and removed. Treatment included high dose steroids, PLEX, and IVIG. As alertness improved, agitation, impulsivity, paranoia, hypersexual language, perseveration, and delirium reemerged. Immediate psychiatric management included use of restraints, Haldol, Seroquel, clonidine, and clonezapam. Ten-months after initial admission, psychological symptoms had fully resolved. Conclusions: Anti-NMDA receptor encephalitis can be life-threatening in the absence of early detection and treatment. Presentation of acute onset psychosis, altered mental status, and cognitive dysfunction in otherwise healthy adults should prompt early and thorough involvement of neuropsychiatry.

Background: The syndrome of catatonia may be a manifestation of psychiatric, medical, or neurological conditions, including hypoxic-ischemic brain injury (HIBI). Treatments of catatonia following HIBI are underdeveloped, and the available literature suggests variable response to first-line treatments. The present report adds to this literature by suggesting that partial response of HIBI-associated catatonia to lorazepam, a first-line treatment of catatonia, may be usefully augmented with memantine. Case History: A 36-year-old, previously healthy woman sustained a HIBI due to cardiac arrest. Computed tomography of the head performed two-months postinjury demonstrated bilateral caudate and putaminal hypodensities, at which time she was admitted to inpatient rehabilitation in a “minimally conscious state.” Examination revealed catatonic features, including stereotypies, negativism, waxy flexibility, and mutism. Intravenous lorazepam 1 mg markedly but transiently improved level of consciousness, social interaction, and behavior. Oral lorazepam 2.5 mg every six hours produced sustained benefits: she conversed, danced, and participated in self-care activities. Improvement in catatonia was accompanied by severe cognitive impairment, intermittent crying, fearfulness, hallucinations, and paranoid ideation. The addition of memantine, but not amantadine, to lorazepam improved the emotional and behavior accompaniments of her HIBI-induced neurocognitive disorder. Conclusions: Catatonia following HIBI is an uncommon but identifiable and potentially treatable condition. First-line treatments of catatonia, including lorazepam, may effectively treat this condition. Other neuropsychiatric sequelae of HIBI become more apparent as the severity of catatonia wanes. Selection of medications that improve these symptoms without worsening catatonia is paramount; memantine may be one such agent. Prospective study of this possibility is recommended.

Objective: To determine the neural correlates of criminal behavior in patients with focal brain lesions. Background: Brain lesions can cause a previously normal person to engage in criminal behavior, a condition known as acquired sociopathy. Why lesions in certain brain locations but not others cause this syndrome, and how this relates to brain regions normally involved in moral decision-making, remains unknown. Here, we utilize a new technique called lesion network mapping to investigate the hypothesis that (1) symptoms emerge from sites functionally connected to a lesion location, not just the lesion location itself, and (2) these identified regions will be involved in regulating moral behavior. Methods: First, 16 cases of acquired criminal behavior were identified. Second, lesion network mapping was used to identify brain regions functionally connected to the lesion locations. Third, regions involved in moral cognition, and in specific components of moral cognition, were identified using meta-analyses of prior fMRI studies, and compared with control lesions. Results: Lesions causing sociopathy occurred in different brain locations, but were all functionally connected to regions involved in moral cognition (p<0.0001). Lesions causing sociopathy were specifically connected to regions involved in value-based decision-making (p<0.0001) and theory of mind (p<0.0001), but not empathy or cognitive control. This connectivity was specific to lesions causing sociopathy vs. control lesions (p<0.0001), and perfectly separated lesions causing sociopathy from control lesions using logistic regression. Finally, connectivity of lesions predicted more utilitarian decisions. Conclusions: Our results suggest that brain connectivity can lend insight into the development of criminal behavior.

Background: Tinnitus is the sensation of hearing a sound with no external auditory stimulus present. It is a public health issue correlated with noise exposure, military service, traumatic brain injury, small vessel disease, smoking, stress, and socioeconomic status. Clinical experience and a recent literature review point at tinnitus as a neuropsychiatric condition involving both auditory and nonauditory cortical areas of the brain and affecting brain-auditory circuitry. Objective: The aim of this study is to evaluate the correlation between tinnitus and comorbidities measured using common survey instruments that quantify tinnitus, cognitive functioning, depression, and anxiety. Methods: A retrospective chart review for 400 adults seen in the Comprehensive Tinnitus Clinic from 2011–2016 was completed. Demographics, questionnaire regarding symptoms of tinnitus, medical history, neurological exam, and Tinnitus Handicap Inventory (THI) scores were analyzed. In most charts Montreal Cognitive Assessment, Beck Depression Inventory (BDI) and Beck Anxiety Inventory (BAI) were also available. Results: Moderate to severe scores on THI correlate directly with BDI and BAI scores. Catastrophic cases accounted for ∼2% of cases and were highly correlated with addiction. Cognitive impairment correlated in some cases with higher scores on THI. Comorbidities associated with all levels of THI were attention difficulties, frontal lobe executive dysfunction, anxiety, depression, hearing loss and obstructive sleep apnea. Cerebrovascular burden of moderate small vessel disease was correlated with moderate to severe THI. Conclusion: Tinnitus remains a challenging condition to evaluate and treat. A neuropsychiatric circuitry approach would best lead the way in advancing the understanding of the disease and proposing therapeutic breakthroughs for symptom relief.

Background: Focal reversible lesions of the splenium of the corpus callosum have been described in several of pathological entities including acute withdrawal of antiepileptic drugs. The pathophysiology remains unclear. Clinical presentation has been described as psychiatric and/or neurologic symptoms. We describe three cases with a transient lesion of the splenium in psychiatric patients. Cases history: Case 1, a 21-year-old woman with Bipolar Disorder (BD) with a severe depressive episode. Case 2, a 32-year-old woman with unspecified affective disorder presenting a catatonia with psychosis episode. Case 3, a 42-year-old woman with BD with a mania and psychosis episode. All the cases had history of acute withdrawal of antiepileptic drug. An MRI was performed at admission, the three MRIs from each patient showed a single ovoid lesion in the splenium of corpus callosum, been hyperintense on T2W and FLAIR, restriction in DWI sequence and no enhacement with gadolinium administration. Other functional and structural studies were performed to rule out other possible causes. Patients were treated with quetiapine and had a complete remission of the symptoms. Later MRIs were performed showing absence of the splenial lesion. Conclusions: Splenial lesions in the MRI have been well described and associated to several conditions. Little is known until now about the clinical manifestations of the splenium involvement. We discuss the role of the corpus callosum, specially the splenium in the neurobiology of psychiatric symptoms in these patients.

Background: The cerebellar cognitive affective syndrome (CCAS) has been well described since 1998. Besides coordination and motor functions, different cerebellar lesions are responsible for cognitive and affective symptoms. Specifically the posterior cerebellar lobe and associated nuclei has been implicated in the modulation of supramodal, higher order functions. Case History: A 54-year-old woman, who worked until 3 years ago as an elementary school teacher. She has a severe tobacco use disorder for 40 years and a 5-year history of Hypertension. Three years ago, her family noticed slurred speech and personality changes that led to impaired work and social functioning. A depressive episode with psychotic symptoms was then diagnosed and was treated with several antidepressives with partial improvement. The neurological examination revealed: impaired attention, executive dysfunction, blunted affect, inappropriate behavior, decreased verbal fluency, impaired visuospatial construction as well as other apraxias. She has dysarthria, scanning speech, generalized hypotonia, wide based gait and dysdiadochokinesia. Brain MRI showed bilateral hyperintensities in the superior, middle and inferior cerebellar peduncles and scarce small frontoparietal hyperintensities due to small vessel disease in T2 and FLAIR. No cerebellar hemispheric lesions were demonstrated. Brain SPECT showed left cerebellar hypoperfusion and bilateral orbitofrontal and temporal cortex hypoperfusion. A DTI MRI was performed to assess neural circuits disconnection between cerebral cortex and the cerebellum. Conclusions: We discuss a particular case of CCAS due to lesions in the cerebellar peduncles and describe the anatomical circuits that link the cerebral cortex and the cerebellum affected in this case and its clinical correlation.

Background: Capgras Delusion (CD) is characterized by delusional belief that some relatives have been replaced by impostors. It is probably due to visuoanatomical disconnection, secondary to damage in the neural circuit responsible for emotional response to familiar faces observation, with neural tract of face recognition unaltered. The Neuroanatomical tracts involved are the inferior fronto-occipital fasciculus (IFOF) for emotional processing and the inferior longitudinal fasciculus (ILF) for face recognition. Objective: Determine the Fractional Anisotropy with Diffusion Tensor Imaging MRI to evaluate the structural integrity of bilateral IFOF and ILF in 3 patients with CD and 3 paired controls. Methods: Case 1, 58-year-old woman with interictal psychosis and long evolution focal epilepsy; CD was presented without reduplication phenomenon, associated Frégoli, Delusion, hyperfamiliarity, paranoid and erotomaniac ideas, somatic nihilistic thoughts and complex auditory hallucinations. Case 2, 64-year-old woman with bipolar depression; CD was presented with reduplication phenomenon, delusions of harm and erotomaniac ideas. Case 3, 34-year-old woman with schizophrenia; CD involved her family and cat, harm and magical-religious delusions and auditory hallucinations. DTI MRI was performed in the 3 patients and paired controls and FA was determined for each tract. Results: IFOF and ILF integrity alterations were founded in each case, been the main finding significant reduced FA in unilateral IFOF and contralateral ILF. Conclusions: The expected reduced IFOF connectivity was found, but the associated contralateral reduced ILF connectivity differs from previous reports. We discuss how these findings suggest a more complex visuoanatomical disconnection theory in CD.

Background: Neuropsychiatric symptoms are common in Parkinson´s disease (PD), they occur in a higher prevalence than control groups of the same age and have a significant impact in the quality of life. Among the neuropsychiatric manifestations founded in PD are cognitive impairment and dementia (84 and 48% respectively), depression 58%, apathy 54%, anxiety 49% and hallucinations 44%. Apathy is one of the most dysfunctional symptoms for the patient and the caregiver. Objective: To determine the frequency of apathy, depression and cognitive impairment in patients with PD in Mexico City. Methods: A cross-sectional study was conducted in patients with PD. All participants were evaluated through a set of scales for specific neuropsychiatric symptoms including: MDS-Unified Parkinson's Disease Rating Scale, Montreal Cognitive Assessment, Beck Depression Inventory and the Lille apathy rating scale (LARS). Results: A total of 98 patients with Parkinson were included. The age media was 67.7±12.1 years. The PD evolution in years was 4.58±3.31. The frequency of apathy was 25.5%, apathy associated to depression and cognitive impairment 13.26% and 18.36% respectively, only 3 patients with apathy had no depression nor cognitive impairment. Conclusion: There are no epidemiologic data about Neuropsychiatric disorders in PD in Mexico. Given the impact of these symptoms on quality of life, identification and proper treatment is essential.

Background: Psychomotor slowing is often a feature of depression, especially in the elderly. Secondary parkinsonism is frequently caused by neuroleptic medications and cerebrovascular disease. We describe refractory depression presenting as a mimic for Parkinson’s disease (PD). Case History: A 75-year-old Caucasian man presented with six months of worsening balance and abnormal gait. He had hypophonia, hypomimia, bradykinesia, asymmetric cogwheeling in upper extremities, rigidity in lower extremities and an anteflexed posture with UPDRS-III 37. Gait was wide based, without arm swing and with en-bloc turning. There was no constipation, orthostasis, or resting tremor. MoCa score was 26/30, with deficits in visuospatial and working memory tasks. He had depressed mood with congruent affect, poor sleep, anhedonia, apathy, negative thought patterns, low energy, and psychomotor slowing. He had no prior exposure to antipsychotic medications. He had an inadequate trial on carbidopa/levodopa with an equivocal motor response. Dopamine transporter (DaT) scan showed normal dopamine uptake in the striatum. MRI brain showed old lacunar infarcts in the right cerebellum and left cingulate gyrus with mild volume loss. His depression was treated with high dose SSRI, augmented with methylphenidate and aripiprazole. Subsequently, mood, gait, and parkinsonism improved. Conclusions: Up to 80% of patients with PD have comorbid depression. Psychomotor slowing is well described in depression in the elderly. We describe a case of refractory depression presenting with parkinsonism but with negative DaT scan. We believe his parkinsonism is secondary to depression. DaT scans aid in diagnosis of dopaminergic disorders. Providers should screen for depression in patients with parkinsonism.

Background: Functional neurological symptoms are common, occurring in up to one third of neurology outpatients, yet remain inadequately understood within the healthcare community. The lack of a widely-accepted explanatory model leads many clinicians to feel uncomfortable assessing and treating these patients, further contributing to the significant morbidity associated with FND. However, considerable progress has been made in recent years in clarifying the psychological and neurobiological underpinnings of FND. Objective: In the current study we aimed to evaluate the effectiveness of an FND training module for healthcare providers that incorporates recent research findings in pathophysiology, assessment, and treatment. Methods: Clinicians participated in a one-hour seminar, completing questionnaires assessing their perceptions of the disorder before and after training. The settings of the seminars included an in-patient psychiatry unit, psychiatry residency didactics, and a community educational night between 2014–2016. Participants (N=18) included psychiatry residents, medical students, psychologists, occupational and physical therapists, and nurses. A questionnaire assessing attitude and knowledge regarding FND was developed in-house, based on previously published research. Results: Preliminary results reveal highly significant improvements in provider attitude (p=0.0009) and knowledge (p=0.00004) following training (paired t tests, one-tailed). Conclusions: The results of this pilot study show that a brief, cost-effective training module can significantly improve the knowledge and attitude of healthcare providers regarding this stigmatized group of patients.

Background: Gilles de la Tourette syndrome (GTS) is a neurodevelopmental condition characterized by the presence of multiple motor and phonic tics, often associated with co-morbid behavioral problems bearing an impact on patients’ health-related quality of life. The number of scientific publications on GTS has increased considerably in recent years, making it difficult for clinicians and researchers to keep up to date with research developments. Objective: This review aimed to identify and critically evaluate the most important research articles on GTS published over the last five years (2010 to 2015). Methods: A systematic search of original scientific articles in Medline, EMBASE and PsycInfo, complemented by manual screening of journal archives, yielded 490 relevant publications within the reference period. Results: The majority of the identified studies were categorized as belonging to Class III and IV according to the American Academy of Neurology grading system. Following quality appraisal 50 studies were selected for inclusion in the final list of most important articles, and were critically appraised according to methodological design, main focus and wider impact. Conclusion: Analysis of original research publications on GTS shows that our knowledge of the condition has expanded significantly in recent years, yielding new insights on the aetiology, treatment and impact on patients’ health-related quality of life. This body of research has in turn guided the development of new hypotheses and research questions to continue expanding our understanding of GTS and improving care provision.

Background: Toxic leukoencephalopathy (TL) is a white matter disorder due to exposure to leukotoxic agents. Diagnosis can be challenging because of TL mimickers, and the range of leukotoxins is expanding. Case History: A 51-year old woman was admitted in coma 12 hours after suicide attempt (SA) with clonazepam, hydrocodone/acetaminophen, zolpidem, and acetaminophen. Head CT was normal. Recovery was rapid, with Mini-Mental State Examination score of 23 after 5 days, and she was discharged 10 days later. Eight days after discharge her husband described “catatonia.” Examination documented cognitive slowing, bradykinesia, and parkinsonian gait. MRI showed widespread leukoencephalopathy 27 days after SA. Extensive blood and CSF testing, including urinary toxicology screen, serum toluene, tests for CADASIL and leukodystrophy, was unremarkable. Trials of steroids and IVIG were ineffective. Thirty-five days after SA, she was inattentive, with little speech and spontaneous movement, diffuse rigidity, and slowed gait. Elevated TPO and TGO antibodies suggested Hashimoto’s encephalopathy (HE). Forty-five days after SA, she was fully oriented, could recite the days of the week, and had no parkinsonism. Montreal Cognitive Assessment scores were 22 at 2 and 5 months after SA, and 26 after 10 months, paralleled by improvement in MRI leukoencephalopathy. Conclusions: Delayed posthypoxic leukoencephalopathy after SA produced TL in this case, and the absence of response to steroids and IVIG, combined with the presence of TPO and TGO antibodies in 10% of normal adults, render HE unlikely. Diagnosis of TL can be complicated by the expanding variety of autoimmune, genetic, and toxic white matter insults.

Background: Psychiatric disorders, including depression and anxiety, are prevalent in epilepsy. However, very little is known regarding associated obsessive compulsive(OC) and phobic symptoms. Objective: To assess for independent association of demographic and epilepsy-related factors with obsessive compulsive and phobic symptoms, as well as how these symptoms affect quality of life. Methods: In a cohort of 422 patients from a tertiary epilepsy center (Columbia University), multiple logistic regression analysis was used to assess the association of demographic and epilepsy-related factors with high self-reported OC or phobic symptoms. This was assessed using the respective subscales from the SCL-90R instrument (T score ≥60 considered high group). Quality of life was measured by the QOLIE-89 scale. Results: Using simple logistic regression, lower education (without college degree), lower IQ, non-Caucasian race/ethnicity, Spanish native language, lack of seizure freedom, higher number of antiseizure medications and history of head trauma were associated with high phobic symptoms. Only lower education (adjusted OR 3.38) and non-Caucasian race/ethnicity (adjusted OR 2.34) were independently associated with high phobic symptoms (p<0.005). None of the demographic or epilepsy-related variables were independently associated with high OC symptoms. Quality of life was significantly worse in the high OC group and high phobic group versus respective low groups (p<0.001). Conclusion: Not surprisingly, obsessive compulsive and phobic symptoms in patients with epilepsy are associated with poor quality of life. Clinicians should consider assessing for these symptoms, especially in patients with lower education and minority populations, who may be at particularly high risk.

Background: Blood-brain barrier (BBB) breakdown allows plasma components (including amyloid-β₄₂ and autoantibodies) to enter into the brain interstitium and interact with cell surfaces, disturbing neuronal function and contributing to progression of Alzheimer’s disease (AD). Objective: To reveal the synergistic roles of BBB breakdown and autoantibodies in AD pathogenesis and their utility in early blood-based diagnosis and disease monitoring. Method: Immunohistochemistry (IHC) was used to monitor BBB breakdown in AD brains as well as the interactions of amyloid-β₄₂ and autoantibodies with AD-vulnerable neurons. A cell culture model was used to test the mechanistic role of autoantibodies in intraneuronal amyloid deposition. Lastly, human protein microarrays were employed to explore the utility of autoantibodies as diagnostic biomarkers for early-stage AD detection and disease staging. Results: IHC experiments showed that brain-reactive autoantibodies bind selectively to pyramidal neurons in regions of BBB compromise and trigger pathological changes, including intraneuronal accumulation of amyloid-β₄₂, a hallmark feature of AD, and lysosomal compartment expansion. An array of serum autoantibodies from controls and AD patients dramatically increased rate and extent of intraneuronal amyloid-β₄₂ deposition in the cell culture model. Conclusion: Results suggest brain-reactive autoantibodies have diagnostic utility and can gain access to the brain interstitium via a defective BBB. The latter allows them to bind selectively to neuronal surfaces and enhance intraneuronal deposition of amyloid-β₄₂ in AD brains, proposing that in the context of BBB compromise, brain-reactive autoantibodies may be an important risk factor for the initiation and progression of AD as well as other neurodegenerative diseases.

Background: Pick coined “reduplicative paramnesia” (RP) in 1903 to describe a patient’s belief that the clinic in which they were located was a duplicate of one in her hometown. RP is considered a delusional misidentification syndrome (DMS); these delusions center on an experience of hyper- or hypofamiliarity and occur disproportionately following right frontal lobe pathology. While RP is described most often in the spatial realm, it can occur in the spheres of person and time, with the latter being the least well described. Case History: We present two patients with right frontal lesions experiencing isolated RP for events. In the first, a 58-year-old man with traumatic brain injury (TBI) believes that the accident causing his TBI was the second of two major accidents; in the second, a 54-year-old woman with a right frontal metastasis describes a police encounter that did occur, along with a second one that did not. Both agree that these duplicated events could not have occurred; yet both report a strong “memory” for them. We show magnetic resonance imaging (MRI) for both and discuss anatomic networks which may play a role in confabulation and delusion including dorsolateral prefrontal cortex, ventromedial prefrontal cortex, and hippocampal connections. Conclusions: Erroneous belief after brain injury may be related to impaired “filtering” of memories and autonomic data, with uncertainty arising as to what is occurring now; what already occurred; and what is imagined. Future work is needed to clarify specific anatomic networks underlying the linked phenomena of confabulation and delusion.

Background: Loss of taste of liquids with relative preservation of taste of solids, in the presence of chemosensory dysfunction, has not heretofore been described. Case History: Case study: A 53-year-old male two years prior to presentation suffered head trauma with loss of consciousness resulted, followed by total loss of smell and taste, which partially returned. He admitted flavorful eructations and first taste phenomenon. He was able to taste all foods (though less intensely) with the exception of dark chocolate, which had no taste. His ability to detect taste was far greater when food was in solid versus liquid form. For example, a milk chocolate bar had greater flavor than a chocolate milkshake. Chemosensory testing: Olfaction: Brief Smell Identification Test: 11 (normosmia). Pocket Smell Test: 3 (normosmia). Alcohol Sniff Test: 17 (hyposmia). Retronasal olfactory testing: Retronasal Smell Index: 1 (abnormal). Gustation: Normogeusia to Propylthiouracil Disk Taste Test: (9). Taste threshold (2) to sodium chloride, sucrose, hydrochloric acid, urea, and phenythiocarbamol. Conclusions: The abnormality in the Retronasal Smell Index, may explain the preserved taste to solids, since mastication increases salivary flow and retronasal smell. The increased oral transit time for solid food molecules may have allowed greater interaction with oral taste receptors and thus preserved taste of solids. Investigations into mechanisms causing differences in taste to solid versus liquid foods may provide insight; further query of this phenomenon in those with chemosensory dysfunction is warranted.

Christensen CM, Navazesh M: Anticipatory salivary flow to the sight of different foods. Appetite 1984; 5:307–315. Available at doi: 10.1016/S0195-6663(84)80003-3

Cook DJ, Hollowood TA, Linforth RST, et al: Oral shear stress predicts flavour perception in viscous solutions. Chem Senses 2002; 28:11–23. Available at doi: 10.1093/chemse/28.1.11

Dietrich AM: The sense of smell: contributions of orthonasal and retronasal perception applied to metallic flavor of drinking water. J Water Supply 2009; 58:562–570 Retrieved from http://web.a.ebscohost.com.ezp.waldenulibrary.org/ehost/pdfviewer/pdfviewer?sid=eeedfae7-4239-49dd-866b-7cad23d9e4c0%40sessionmgr4005&vid=1&hid=4209

Ekstrom J, Khosravani N, Castagnola M, et al: Saliva and the control of its secretion. Dysphagia, Medical Radiology. Diagn Imaging (San Franc) 2012. Available at doi: 10.1007/174_2011_481

Kanwar S, Chand MR, Hirsch AR: When Matter Matters: Taste of Solids Versus Liquids. Manuscript submitted for publication. (2016).

Shatzman AR, Henkin R: Gustin concentration changes relative to salivary zinc and taste in humans. Proc Natl Acad Sci USA 1981; 78:3867–3871 Retrieved from http://www.pnas.org/content/78/6/3867.short

Sullivan JF, Lankford HG: Zinc metabolism and chronic alcoholism. American Society for Clinical Nutrition, 1965; 17(2):57–63. Retrieved from http://ajcn.nutrition.org/content/17/2/57.short

Taste and Smell Clinic: Role of Gustin (Carbonic Anhydrase VI) in Sensory Perception. Center for Molecular Nutrition and Sensory Disorders. July 2003. Retrieved from http://www.tasteandsmell.com/jul03.htm

Watanabe S, Dawes C: A comparison of the effects of tasting and chewing foods on the flow rate of whole saliva in man. Arch Oral Biol 1988; 33:761–764. Available at doi: 10.1016/0003-9969(88)90010-6

Background: Brexpiprazole has not heretofore been reported to cause parkinsonism. Such a case is presented. Case History: A 53-year-old right handed female, with bipolar illness, without a history of movement disorders, has lifelong episodic depression. Four months prior to presentation she was started on lurasidone, without improvement or side effect. Two months later brexpiprazole was added. The next day she observed massive shaking and tremors with no change in gait. She stopped brexpiprazole and the tremors substantially reduced. Six days prior to presentation she stopped lurasidone and the tremors resolved. Physical examination: Affect, sad, nonreactive, facial akinesia, decreased blink frequency. Cranial nerve (CN) examination: CNI Alcohol Sniff Test 5 cm (anosmia) CN III, IV, VI: bilateral ptosis, saccaddization of horizontal eye movements. CN IX, X: Gag: absent. Uvula deviated to left. Motor examination: Bradykinesia. 1+cogwheel rigidity right upper extremity. 3 per second pill rolling tremor at rest, bilateral upper extremities. Right pronator drift. Left holmes sign. Gait examination: 1+retropulsion. Sensory examination: Positive romberg sign. Reflexes: 1+throughout except 0 triceps and ankle jerks bilaterally. Neuropsychiatry testing: Beck Depression Inventory: 26 (Moderate Depression). Patient Health Questionnaire-9: 17 (moderately severe depression). Conclusion: The mechanism for brexpiprazole induced Parkinsonism may be there as a dopamine depleter and blockade of dopamine in the striatum. The resolution of her symptoms a week after discontinuation of this agent, conforms with brexpiprazole’s half- life of 91 hours. It may be worthwhile to examine patients on brexpiprazole to assess for presence of drug induced parkinsonism.

Background: Multiple Sclerosis (MS) is characterized by demyelinating lesions and symptomatology separated in both space and time. It is frequently polysymptomatic, with neurologic findings on presentation. Infrequently, initial presentations can include psychiatric and cognitive manifestations. Case History: A 54-year-old Caucasian female with a remote history of dysthymia was brought to the ED by family for a three-day course of rapidly developing paranoia, erratic behavior, depressed mood, cognitive impairment, and decreased sleep. Initial workup was negative for common causes of delirium or acute intracranial process on CT. Discussion between neurology and psychiatry led to an MRI which demonstrated non-contrast-enhancing white matter lesions throughout the brain including subcortical, periventricular, mesial temporal, and pericallosal regions suggestive of demyelination. Without clear neurologic findings this was considered a radiologically isolated syndrome. LP was positive for elevated CSF oligoclonal bands. The patient’s mood and psychotic symptoms were stabilized on medical therapy by discharge, and she has followed with both neuropsychiatry and MS clinics. Further questioning has demonstrated no history of any traditionally defined neurologic symptoms of MS. The literature however yields several reports of patients with isolated neuropsychiatric manifestations of temporal lobe demyelinating lesions, and given her temporal lobe MRI findings she has been offered disease-modifying therapy for a presumed diagnosis of MS. Conclusion: This case demonstrates an atypical presentation of presumed MS, which was determined after close collaboration between both neurology and psychiatry departments. Increased recognition of neuropsychiatric manifestations of MS may lead to expedited diagnosis and workup with access to appropriate specialists.

Background: Poisons are classically divided into five categories: heavy metals, gases, organophosphates/solvents, complex metal ions, and drugs of abuse. Effects on CNS differ with each class. An exposure should be viewed in terms of length/amount of exposure, pre-exposure risk factors, and postexposure healthcare. Toxic gas exposures can occur in occupational (included war-related), accidental, or abuse settings. Evaluations from a previous ANPA presentation in this poison/toxin series (2015) were very positive, and indicated the need for more teaching products of this type. Incorporating feedback has allowed 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, allowing 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 toxic gasses, particularly with reference to comorbid war-related TBI, burn pit exposure, and blast physics 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 toxic gas exposures, particularly with comorbid war-related TBI.

Background: The direct impact of olanpzapine on chemosensory hedonics has not heretofore been described. Case History: A 27-year-old, pathological left handed male presented with one year of declining olfactory ability to 10% of normal, but with multiple olfactory windows each day, which were not hedonically imbued. For two weeks, while undergoing treatment with 10 mg of olanzapine for obsessive compulsive disorder, he observed transformation in the hedonics of olfactory windows: the odors would be markedly pleasant or unpleasant. For instance barbeque, donuts, coffee, and hamburgers would be incredibly pleasant and appetizing, whereas, fecal matter would be horribly disgusting. Within two days of reduction of olanzapine to 7.5 mg, the hyperhedonics of the olfactory windows disappeared, Neurological examination: bradyphrenia. Monotoned speech. Poor eye contact. Slow thought processes with tangentiality. Reflexes: 3+throughout with pendular quadriceps femoris bilaterally. Positive jaw jerk. Chemosensory testing: Olfaction: Quick Smell Identification: 3 (normosmia). Pocket Smell Test: 2 (hyposmia), Brief Smell Identification 11 (normosmia). Alcohol Sniff Test: 4 (anosmia). University of Pennsylvania Smell Identification Test: L 35, R 36 (normosmia). Phenylethyl Alcohol Threshold Test: L: −4.0, R: −4.0 (hyposmia). Olfactometer Identification Test: L: 18 (normosmia), R: 18 (normosmia). Retronasal Smell Index: 6 (normal). Other: MRI of the brain with and without contrast: normal. Conclusion: It is possible that chemosensory hyperhedonics intensifies the reward value of food, and thus facilitates olanzapine-associated weight gain. Exploration of olanzapine’s use to enhance chemosensory experience for treatment in hedonically inhibited states is warranted.

Background: Existing literature addresses subjective feelings of cognitive impairment and higher incidence of some psychiatric disorders in postural orthostatic tachycardia syndrome (POTS) patients. However the potential effects of POTS as a mediating factor in treatments for psychiatric illness, including possible influence on ECT-induced-mania in a depressed patient with no history of mania, have not been well characterized. We present a case which embodies all of these components, and illustrates the need to further evaluate treatment options for this unique group of patients. Case History: The patient is a 40-year-old female with PTSD, alcohol use disorder in remission, major depressive disorder, disordered eating, history of borderline personality traits, and POTS, whom the author met during an inpatient admission planned for ECT. She endorsed debilitating depression, chronic suicidal thoughts with multiple attempts, and extensive medication trials without relief. There was no history of mania. The first round of ECT was discontinued due to cognitive impairment with bilateral treatments and she was discharged to outpatient medication management. ECT was reattempted during a subsequent admission, which went well until manic symptoms appeared. These subsided after ECT discontinuation. The patient has consistently reported that providers underappreciate how much POTS affects her mental illness, which she believes is a decisive factor in her sensitivity to many medications, her cognitive fluctuations, and her ECT-induced mania. Conclusions: A comorbid diagnosis of POTS in psychiatric patients warrants heightened awareness of the effect of pharmacologic and nonpharmacologic treatments on symptomatology and cognitive functioning.

Background: Aphasic status epilepticus is a rare phenomenon characterized by language disturbance, electrographic seizure activity, and relative preservation of sensorium. The authors present a case of a patient with an isolated global aphasia associated with left hemisphere epileptiform activity. Over the course of a prolonged hospitalization, the patient’s language disturbance covaried with aspects of the electroencephalographic signal. Case History: Patient is a 45-year-old right-handed female with a history of severe alcohol abuse, remote traumatic brain injury, and suspected posttraumatic epilepsy who was admitted for presumed altered mental status. On presentation, patient was alert but demonstrated sparse, perseverative speech and an inability to follow simple commands. An extensive work-up for possible ischemic, metabolic, paraneoplastic, and autoimmune etiologies was unrevealing. MRI Brain showed encephalomalacic changes, siderosis, and blood products bifrontally, biparietally, along the interhemispheric fissure, and in the subcortical areas of the temporal lobes without evidence of mesial temporal sclerosis. Continuous EEG showed activity ranging from frequent sharp waves to periodic lateralized epileptiform discharges maximal in the left anterior and posterior temporal lobes. Her electroclinical state ultimately proved refractory to both antiepileptic polytherapy and anesthetic-induced burst suppression. Discussion: The patient’s fluctuating aphasic symptoms were found to correlate with certain characteristics of the electroencephalographic record, most notably, spike frequency. The case demonstrates the utility of examining the EEG record for particular signal variables, including spike frequency, localization, and degree of spread. These electrographic characteristics, among others not examined here, might constitute biomarkers of symptom burden in aphasic status epilepticus.

Background: Our patient developed drug-induced parkinsonism and concurrent hypothyroidism with lithium used without adverse effects for more than 10 years. It is rare to see concurrent drug-induced parkinsonism and hypothyroidism especially within a normal therapeutic serum level of Lithium. Case History: Out patient is a 76-year-old white female with bipolar disorder. She has been on lithium and adjunctive psychotropic medications for more than 10 years. Lithium level was regularly monitored and was in the target therapeutic range. The patient presented to our outpatient clinic with a complaint of frequent falls over the past 5 to 6 years, a month history of parkinsonism-like movements, and dizziness upon standing from sitting position. Neurological examination was significant for fine tremor of bilateral upper extremities both at rest and with action, slight rigidity in all four extremities, and mild slowing on movement. Laboratory work up showed normal lithium level of 0.9 mmol/L, elevated TSH of 76.5 UIU/ml, low Free T3 1.38 pg/ml, and low T4 0.55 ng/ml. Given the findings, the suspicion for lithium-induced hypothyroidism and lithium-induced parkinsonism was raised. Lithium was gradually discontinued under supervision following which the patient’s abnormal movements had improved. Also, DAT scan was negative, which rule out Parkinson’s disease. She showed dramatic significant improvement in 4 months after the discontinuation of lithium. Conclusions: This case suggests physicians who take care of elderly patients should give close attention to those side effects on clinical neurologic and mental examination while continuing dose adjustment and regular monitoring of serum lithium concentrations.

Background: Catatonia is a neuropsychiatric syndrome with a 70% response rate to lorazepam. Some studies suggest that patients with catatonia and known structural brain disease might have lower response rates to treatments for catatonia. Objective: To analyze if presence of abnormalities on EEG or neuroimaging tests in patients with catatonia are related to worse outcomes. Methods: A retrospective chart review was conducted and 54 cases were diagnosed with catatonia between 2011 and 2013 at the University of Chicago. Clinical variables, EEGs and neuroimaging were systematically studied. Chi square, Barnard’s and T tests were used to find differences between groups with abnormal and normal findings. Results: Length of stay was longer in patients with abnormal EEGs (mean 23 days abnormal; 11.9 days normal; p=0.04) or abnormal neuroimaging (mean 17 days abnormal; 6 days normal; p=0.006). Rates of response to lorazepam were lower in patients with EEG abnormalities (60% vs. 100%; p=0.09) and neuroimaging abnormalities (67% vs. 100%; p=0.06). Neuroimaging abnormalities, but not EEG abnormalities, correlated with presence of suspected comorbid delirium during the episode (20 out of 24 with abnormal neuroimaging compared to 8 out of 16 with normal imaging; 83% vs. 50%; p=0.024). Conclusions: Presence of EEG or neuroimaging abnormalities might be associated with negative outcome measures in patients with catatonia. Further studies are needed to investigate the clinical utility of such tests in predicting outcomes.

Background: Posttraumatic stress disorder (PTSD) and sleep problems are significant behavioral health concerns in the veteran population. To date, there is mixed evidence about the effects of traumatic brain injury (TBI) on sleep quality. In addition, the effects of blast exposure have not been assessed. Objective: Determine if the association between PTSD symptoms and sleep quality was contingent upon degrees of blast exposure in Iraq and Afghanistan combat veterans. Methods: Participants were Iraq and Afghanistan veterans between the ages of 26–68. Veterans completed a full day assessment, including the Clinician Administered PTSD Scale (CAPS-5), Pittsburgh Sleep Quality Index (PSQI), and an in-depth TBI and blast exposure assessment. Moderation analysis was conducted to test the hypothesis. Results: PTSD symptoms were significantly associated with sleep quality, β=0.22, CI [0.11, 0.33]. Blast exposure was not associated with sleep quality after adjusting for the effects of PTSD symptoms, β=0.63, CI [–1.91, 3.17]. Additionally, there were no interaction effects, ΔR²=0.02, p=0.29, for the blast exposed, β=–0.13, CI [–0.29, 0.03], or mild TBI (blunt or multiple mechanism) groups, β=–0.11, CI [–0.27, 0.06], as sleep quality deteriorated similarly for all groups as PTSD symptoms increased, regardless of blast exposure status. Conclusion: PTSD symptoms accounted for a significant portion of variance in sleep quality that was not conditional upon blast exposure status. Clinicians treating veterans with sleep problems may not be able to attribute these issues to blast exposure in veterans regardless of PTSD symptoms.

Background: Patients with functional neurological disorder (FND)/conversion disorder, a neglected yet common neuropsychiatric population, present diagnostic and therapeutic challenges. The many overlapping features of individuals with psychogenic nonepileptic seizures, functional weakness and functional movement disorders highlight the necessity for an integrated approach to clinical and research efforts in this population. Objective: This cohort study investigated associations between neuropsychiatric characteristics and gender, prolonged illness duration and work disability status in an FND clinic population. Methods: We retrospectively reviewed charts for 100 consecutive new patients (79 women; 21 men) with motor FND and used univariate tests followed by multivariate logistic regression to perform analyses. Results: Men compared to women reported increased frequency of cognitive complaints (odds ratio=5.6; p=0.009), higher prevalence of functional weakness (odds ratio=3.3; p=0.045) and lower rates of physical/sexual trauma (odds ratio=0.2; p=0.034). Across the entire cohort, an illness duration of greater than one year was predicted by prior head trauma (odds ratio=3.0; p=0.030), number of medication allergies (odds ratio=1.5; p=0.037) and unemployment (odds ratio=2.8; p=0.033). Work disability status was predicted by past psychiatric hospitalization (odds ratio=3.0; p=0.030). 30 of 100 patients exhibited mixed functional motor symptoms. Conclusion: This study reveals demographic and neuropsychiatric factors associated with gender, prolonged illness duration and work disability across the spectrum of motor FND. The transdiagnostic nature of this study further supports the feasibility of an integrated approach to FND research across the motor spectrum.

Background: Postoperative psychiatric symptoms like depression, emotional lability, and psychosis have been associated with standard temporal lobe resection. However, psychiatric outcomes have not been evaluated for epilepsy patients undergoing stereotactic laser ablation. We present the case of a patient with left temporal lobe epilepsy who developed exacerbation of psychiatric symptoms following ablation. Case History: A 38-year-old man with a history of left temporal lobe epilepsy as well as mood disorder and cannabis use disorder presented for management of refractory seizures. Presurgical workup revealed normal MRI brain. PET brain showed hypometabolism of the left mesial anterior temporal lobe, and EEGs were consistent with seizure onset in this region. Neuropsychological testing showed bitemporal dysfunction and a high level of depression on self-report scales. He underwent laser ablation of the left mesial temporal structures. About 2 months postoperatively, he reported worsened anxiety, depression, and word-finding problems, as well as new-onset headache, gait instability, and tremor. On exam, he exhibited labile affect, stuttering speech, paranoid ideation and religious preoccupations. Workup suggested a functional movement disorder in addition to likely exacerbation of underlying mood disorder. Of note, his seizure control had significantly improved after ablation. He was started on olanzapine and was noted to have improvement of psychiatric symptoms at 9-month follow-up. Conclusions: This case raises intriguing questions regarding the differential diagnosis for neuropsychiatric symptoms following laser ablation, as well as the epidemiology, pathogenesis, and treatment decisions.

Background: Loss of slow wave activity (SWA) during non-rapid-eye-movement (NREM) sleep is known to occur during the physiologic process of aging and is hypothesized to contribute to the progression of Mild Cognitive Impairment (MCI) to Alzheimer’s disease. Transcranial alternating current stimulation (tACS) has been demonstrated to enhance SWA in healthy adults, but has relied on the use of a dedicated sleep facility and technician for delivery, thus limiting development of clinical applications. Objective: Our goal is to develop an automated system for delivery of tACS at-home during NREM sleep for SWA enhancement. Our hypothesis is that automated tACS during sleep can be achieved with real-time analysis of electroencephalography (EEG) data. Methods: We utilized an automated system to record EEG during sleep at-home in our pilot subject, and to detect SWA in data obtained during NREM sleep. Our system identifies SWA using a modified zero crossing function of MATLAB to analyze EEG data. Results: Our system generated consistent at-home EEG overnight recording data during sleep. With this sleep data, we have performed automated analysis of EEG and successful identification of SWA during NREM sleep. Conclusion: Development of automated tACS during NREM sleep is a critical step in further clinical trial implementation. Our next steps are to apply this system to operate tACS stimulation during NREM for modulation of SWA. We plan to apply this technique for enhancement of sleep and restoration of SWA in MCI patients, with the long-term goal of developing a therapeutic intervention for impairments of sleep and cognition.

Background: Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is a rare autoimmune disorder with a prominent neuropsychiatric presentation including catatonia. ECT has demonstrated improvement in psychotic and catatonic symptoms in NMDAR encephalitis. The clock drawing test (CDT) is a useful tool for longitudinal qualitative and quantitative assessment of many cognitive functions. Case History: A 27-year-old highly educated female began experiencing insomnia, emotional lability, delusions, and hallucinations over a 2-month period. She was admitted to a psychiatric hospital and treated with antipsychotics and mood stabilizers. Her symptoms progressed to abnormal movements, memory deficits, and catatonia. She was treated with lorazepam up to 36 mg/day with only partial response. A lumbar puncture revealed antibodies to NMDAR. Neuroimaging was normal. Pelvic imaging for teratoma and whole body PET showed no underlying malignancy. Further treatment with IVIG and corticosteroids provided minimal improvement. The patient subsequently received ECT. Pre-ECT CDT showed severe perseveration and conceptual deficits resulting in an inability to make any reasonable representation of a clock. After the second ECT, CDT showed moderate visuospatial disorganization of numbers and planning deficits. After the sixth treatment, CDT showed a stimulus bound response error seen during time setting instructions but overall significant improvement in planning and visuospatial organization. The improvement in CDT correlated with improvement in cognition and resolution of catatonic symptoms and psychosis. Conclusions: To our knowledge, this is the first case report of the clock drawing test being used to monitor improvement of cognitive function parallel to resolution of psychotic and catatonic symptoms.

Background: There are 5 million visits to US emergency departments (ED)/year for migraine/headache. Though many of these patients would benefit from preventive therapy these teachable moments are usually lost. Objective: We examined whether migraineurs would agree to try progressive muscle relaxation (PMR), a proven behavioral preventive therapy, while in the ED, and for how long they would engage in an introductory session. Methods: Research assistants in our urban academic ED introduced the study concept to eligible migraineurs in the ED. Patients completed a survey about their headache history and were asked to listen to a 20-minute audio recording of PMR. Results: We approached 11 patients and 8 agreed to participate (73%). Mean age of participants was 35.5 (13.17) years and 63% were female. Headaches occurred on 10.7 days/month on average and were usually severe (63%) or moderate (25%). No one had previously done PMR though two had previously tried biofeedback. All had previously visited an ED for their headaches; mean number of prior ED visits was 2.38 (range 1–5). Half had seen a neurologist for treatment of their headaches. One did not do the PMR session in the ED. Of the remaining seven who did the PMR, mean time spent doing it was 7.6 minutes (range 1–20). Conclusions: Migraineurs presenting to the ED have severe and frequent migraines which make them candidates for preventive behavioral treatments. PMR can be introduced in the ED setting. Follow-up studies should examine whether patients will continue to use these behavioral techniques at home.

Background: Veterans with PTSD frequently endorse distressing psychological or cognitive symptoms that affect functioning, and they may seek compensation/pension. In clinical, forensic, and research settings it is important to include both performance and symptom validity testing (PVT and SVT, respectively). Objective: Examine the relationship between PTSD and performance on PVTs and SVTs. We hypothesized that the relationship between PTSD diagnosis and performance on SVT and PVTs would be mediated by distress tolerance and PTSD symptom severity. Methods: Sixty-three Iraq and Afghanistan veterans (mean age 41 years, 89% male) completed testing. Dichotomous variables were created for PTSD diagnosis (using CAPS-5), Medical Symptom Validity Test (MSVT) failure, and b-Test failure. Continuous variables were created for the Structured Inventory of Malingered Symptomatology (SIMS), distress tolerance (DTS), and symptom distress (PCL-5). Hypothesis testing was conducted using serial mediation analysis, with distress tolerance and symptom distress as mediators, respectively. Results: Models predicting b Test and MSVT failure were not significant. The model predicting SIMS score was significant, β=2.22, CI [1.07, 4.75]. Post hoc analyses of SIMS subscales indicated that the serial mediation model predicted the Neurologic Impairment, β=0.54, CI [0.19, 1.41], Amnestic Disorders, β=0.64, CI [0.26, 1.49], and Affective Disorders subscales, β=0.64, CI [0.25, 1.54], but not Psychosis or Low Intelligence. Conclusion: Results suggest that difficulty tolerating negative affect may contribute to elevated PTSD symptom distress and result in over-reporting symptoms. Distress tolerance and symptom burden were not associated with failure on PVTs, further supporting the independence of PVTs and SVTs.

Background: Novel expensive diagnostic tests are rapidly emerging. However, the answer to the most complex presentations is sometimes closely tied to knowledge of the founding roots of clinical neuropsychiatry. Case History: A 33-year-old male presented with confusion, weakness, and tremors. His symptoms started six months prior to presentation, initially with memory problems. He progressively became confused and developed speech difficulties, unsteady gait, and left sided tremors and weakness. On exam, he was predominantly abulic but with intermittent and extreme mood lability. He lacked insight, was not oriented, and his attention was poor. He had bilateral ptosis and a mydriatic right pupil, poorly reactive to light. He also had mild left lower facial weakness, subtle left spastic hemiparesis, and left hemibody action tremor. His reflexes were brisker on the left and his left toes up-going. He had spastic hemiparetic gait. MRI of the brain demonstrated nonspecific diffuse parenchymal volume loss. Serum and CSF studies were positive for RPR and VDRL respectively. Conclusions: This is a case of a young patient with neurosyphilis who presented with progressive subacute cognitive decline, associated with focal neurological signs but no focal lesions on brain imaging. We discuss a systematic differential diagnosis of similar neuropsychiatric presentations and highlight the fundamental principle in clinical medicine, “when you hear hoofbeats, think of horses not zebras.”

Background: Cognitive assessment in acute stroke can be challenging. Common vascular cognitive impairment screenings have largely not been validated in acute stroke and may not detect subtle cognitive impairments in all stroke presentations. Measure accessibility may also be limited by stroke-related factors (e.g. hemiparesis). Thus, the LASS-I (Lexington Acute Stroke Scale–Inpatient) was developed for acute stroke use. Objective: To examine the LASS-I’s validity against standard ratings of stroke severity and disability (NIHSS, Barthel Index, and Modified Rankin Scale). Methods: 222 acute stroke inpatients were administered the LASS-I, NIHSS, Barthel Index, and Modified Rankin Scale. Individual analyses included different numbers of patients based on testing tolerance and score availability in admission records. Results: LASS-I total score correlations were significant in the expected directions and magnitudes (NIHSS r=–0.35, p<0.01; Barthel Index r=0.48, p<0.01, Modified Rankin Scale r=–0.44, p<0.01). All LASS-I subscale cognitive domains were significantly related to all outcome measures. By regression, LASS-I score was significantly predictive of disability on the Modified Rankin Scale, Barthel Index, and NIHSS. Conclusion: Initial analysis suggests appropriate validity of the LASS-I for cognitive assessment in acute stroke, with analyses suggesting relationships with established measures in the expected directions (construct validity) and strengths (divergent validity). However, further effort will be necessary to assess validity more fully, to identify those patients for whom comprehensive screening is most fitting, and to identify standardized methods for addressing acute stroke patients’ common barriers to completing cognitive screening measures.

Background: Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus (PANDAS) is a subgroup of children with obsessive compulsive disorder whose onset is abrupt and severe and is associated with streptococcus infection. The primary symptoms are severe anxiety, tics and mood lability. Murphy et al. (2014) found 28% of children with PANS experienced symptoms of psychosis, and 14% had low IgA, indicative of immune deficiency. Intravenous immunoglobulin (IVIG) and antibiotic therapy has been found to be effective in reducing symptoms in 35%−45% in patients with infection triggered OCD and tics. The current case is unique in that the patient has a PANDAS-like presentation with psychosis and remits completely with one course of IVIG and treatment dosing of azithromycin. Case History: A 5-year-old previously healthy male presents with a 5-month history of severe symptoms including significant weight loss secondary to fear of choking, vomiting, and decreased appetite, tics, somatic symptoms, and psychosis (auditory and visual hallucinations). Laboratory results revealed low IgA and elevated ASO and antiDNAse B titers. The patient remitted one week after the initiation of azithromycin and one course of CNS autoimmune dosing of IVIG. Patient’s remission was maintained at one year follow up. Conclusions: The prevalence of psychosis in the PANDAS population is not fully understood but IVIG may be an effective treatment for children with a PANDAS-like presentation who have psychosis and low IgA, however more research is needed. This case highlights the benefit of considering nontraditional approaches to psychiatric care.

Background: Psychosis is considered an infrequent psychiatric symptom of MS (4.3%; 0–10.3%) and thought to occur only after neurological disability is well-established. We present 3 cases of MS with refractory psychosis as the initial neuropsychiatric symptom, and atypically large lesion loads. Case History: Case 1: 55-year-old woman with first-break psychosis one year prior. Non-compliant with outpatient treatment. Presented with gait disturbance, urinary incontinence and delusions. MRI with numerous T2 hyper-intensities in the pons, Dawson’s fingers, T1 hypo-intensities, atrophic left optic nerve and left periventricular contrast enhancing lesion. Case 2: 19-year-old woman with first-break psychosis at age 16. MS diagnosed then, following incidental findings on MRI. Presented with refractory suicidality due to florid persecutory delusions, and first physical symptoms (left pronator drift, dysdiadochokinesia, dysmetria, Hoffman’s reflex). MRI revealed contrast-enhancing tumefactive right frontal periventricular lesion involving the corpus callosum. Case 3: 34-year-old woman with first-break psychosis at age 24. Physical symptoms (bilateral leg weakness, numbness, incoordination) began at age 27. MRI with T2 hyper-intensities in right medulla, right posterior limb of internal capsule and Dawson’s fingers. Conclusions: These cases highlight the need to consider MS on the differential of first-break psychosis, particularly in women of child-bearing age. Each case had atypically large lesion loads upon onset of physical symptoms and time of diagnosis. Additionally, psychosis was relatively treatment refractory. Therapeutic benefit (physically and psychiatrically) may occur with earlier initiation of disease modifying agents. Also, we recommend further study of efficacy of anti-psychotics specific to psychosis in MS.

Background: Attention deficit hyperactivity disorder (ADHD) is a common psychiatric disorder frequently characterized by inattention, impulsivity and hyperactivity. In an absence of adequate treatments, ADHD could severely impede both academic and social performance. Although ADHD is generally well responsive to medications, its potent comorbidities such as oppositional or conduct, mood and developmental disorders often impair patients’ adherences. We here describe the case of ADHD that risperidone long-acting injection (RLAI) was effective to control impulsivity. Case History: The patient was a Japanese 12 years old girl, whose chief compliant were inattentiveness and impulsivity. She had a history of repeated exposure to alcohol during prenatal period and domestic violence since early childhood. Both parents were diagnosed to bipolar disorder and alcoholism while her only sister had depression. Through clinical assessments, we found that she met the diagnostic criterion, according to the 5th American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders (DSM-5), of ADHD and comorbid disorders including oppositional defiant disorder, reactive attachment disorder and Tourette syndrome. Atomoxetine showed insufficient effectiveness to control impulsivity, although we observed the clear improvement when risperidone was medicated. However, her inattentiveness and behavioral difficulties were the major limitation for the continuation of oral medications. Conclusion: We observed that the use of RLAI for 12-year-old ADHD patient with complex comorbidities overcame the limitation in adherence and resulted in the improvement of hardly controlled impulsivity. This case shows that LAI would make an alternative candidate for medications especially when patients have difficulties in maintaining reliable adherence.

Background: Endocannabinoid, dopaminergic, neuromodulatory interactions in a young adult with a history of posttraumatic stress disorder, polydrug use disorder, comorbidities, and traumatic brain injury presenting with auditory hallucinations and a circumscribed delusional disorder focused on a silica chip device implanted in lateral upper neck subauricular region. Complex pharmacotherapy inclusive of strain-specific medical cannabis resulted in sustained positive clinical course. Case History: John Doe is a young adult male who has had multiple hospitalizations for anxiety and depression centered around a recurring delusion that a microchip was injected into his neck during a traumatic incident. Patient likely suffered mild to moderate traumatic brain injury in a fall. His anxiety and depression inhibited him from engaging in employment and social interactions. Patient was treated with complex pharmacotherapy including diazepam, quetiapine, buprenorphine, amphetamine/dextroamphetamine, paliperidone, armodafinil, and opiates. Nutraceuticals, neurofeedback, and mindfulness techniques were also employed. This course yielded mild improvement. When strain-specific medical cannabis was introduced, physician noted major positive change in behavioral evaluation and QEEG data analysis. Patient has found two sources of employment, and has begun increased social activity. Clinical improvement will be illustrated by QEEG data from three separate scans in addition to clinical evaluations. Conclusion: When managing acute mental illness with complex pharmacotherapy, existing literature is inconclusive regarding the clinical value of introducing strain-specific medical cannabis. The sustained positive clinical course of this patient warrants further investigation into the use of strain-specific medical cannabis in conjunction with other treatment modalities in treatment of acute mental illness.

Background: Adverse early-life events are etiological factors for functional neurological disorder (FND) and posttraumatic stress disorder (PTSD). Cingulo-insular alterations are implicated in both conditions, and are well-documented sites of stress-mediated neuroplasticity. Objective: The aim of this study is to investigate cingulo-insular structural reductions associated with FND symptoms, adverse life events and PTSD symptoms in FND. We hypothesized that FND symptom severity and childhood abuse would be associated with anterior cingulate cortex (ACC) and insula volumetric reductions, and that FND and PTSD symptoms would map onto distinct cingulo-insular areas. Methods: This within-group Voxel-Based Morphometry study probed gray matter associations with self-report measures of FND, adverse life events and PTSD symptoms in 23 mixed-gender patients with FND. Results: In women with FND (N=18), parallel inverse associations were observed between left anterior insula volume and FND symptoms as measured by the Patient Health Questionnaire-15 (p_{small-volume-corrected(svc)}=0.032) and the Screening for Somatoform Symptoms Conversion Disorder subscale (p_svc=0.038). Similar inverse relationships were appreciated between Childhood Trauma Questionnaire-abuse scores (p_svc=0.021) and left anterior insula volume. When investigating the intersection of functional symptoms and childhood abuse, associations with reduced left anterior insula volume reached whole-brain-corrected statistical significance (p=0.42) and remained significant controlling for depression and anxiety. Across all subjects, PTSD symptom severity was inversely associated with ACC volume, and cumulative adverse life event burden was inversely associated with left hippocampal volume. Conclusion: These observations reveal distinct cingulo-insular alterations for FND and PTSD symptoms, and suggest biological convergence between stress-related neuroplasticity, FND symptoms and reduced anterior insula gray matter.

Background: Traumatic brain injury (TBI) in older adults is understudied. Established criteria for obtaining head computerized tomography (CT) in the setting of suspected TBI includes older age as a criterion. Objective: We hypothesized that (1) fewer older individuals (≥65 years) receiving head CT in the ED for suspected TBI would meet American Congress of Rehabilitation Medicine (ACRM) criteria for TBI and therefore (2) older individuals would have better one-month outcomes than younger. However, when restricting the study population to just those meeting ACRM criteria for TBI, we hypothesized that older would have worse outcomes. Methods: The Head Injury Serum Markers for Assessing Response to Trauma study (HeadSMART) was a prospective cohort study examining blood-based biomarkers in TBI. Differences in demographics, injury characteristics, and one-month outcomes were analyzed with age dichotomized at 65 years. Results: Older more likely to be female, white, married, and unemployed and less likely to have prior concussion. Older most commonly injured by falls and younger by motor vehicle collision. More younger met ACRM criteria for TBI (79.3% versus 66.1%, p=0.005). Within the entire study population, at one-month, older were less likely to have postconcussive or depressive symptoms. Among those meeting ACRM criteria, older individuals were more likely to have upper/lower good functional recovery (71.0% versus 58.7%, p=0.013) and less likely to have postconcussive (34.4% versus 54.0%, p=0.004) or depressive symptoms (30.5% versus 46.2%, p=0.030). Conclusions: Surprisingly, when constrained to those meeting ACRM criteria for TBI, older participants had better outcomes on all three outcomes measures.

Background: Patients with Functional Neurological Disorders (FND), particularly those with Psychogenic Nonepileptic Seizures (PNES), are highly prevalent and difficult to treat. Up to 20% of patients presenting to epilepsy units for video-electroencephalogram (vEEG) monitoring are diagnosed with PNES. Recent neuroimaging studies have emphasized the role of temporoparietal junction (TPJ) in deficits of self-agency in FND. Despite growing awareness of the neurobiological networks involved in this condition, there are currently few effective treatments to offer patients with PNES. Objective: The aim of this study is to conduct an open label pilot study to investigate the feasibility and efficacy of repetitive Transcranial Magnetic Stimulation (rTMS) over the right TPJ to decrease the frequency of nonepileptic events in PNES. Methods: Four patients (2 female; mean age=46.3±6.0) with PNES (confirmed by vEEG) underwent 30 sessions of 10Hz TMS at 110% resting motor threshold over the right TPJ (3000 pulses per session). Patients received two sessions per day separated by a 10-minute break over 15 consecutive working days. Weekly nonepileptic event logs were completed pre, post, and throughout the three weeks of treatment. Medications were held stable throughout this period. Results: Three out of four patients showed a considerable decrease in their nonepileptic event frequency post-TMS (mean baseline event frequency = 10.3/week; mean post-rTMS frequency=1.3/week). No adverse events were observed as a result of rTMS. Conclusion: High-frequency rTMS over the right TPJ represents a novel, feasible, and potentially efficacious treatment in individuals with PNES. Future prospective controlled clinical research trials are needed.

Background: Suicide risk assessment and management are often predicated upon comprehensive neuropsychiatric assessment, which involve formal assessment of performance and symptom validity. While there are no instruments for examining the validity of subjective suicidal ideation or self-reported history of self-directed violence, diffuse problematic results across measures of performance and symptom validity necessarily raise concern regarding the veracity of subjective complaints more generally, and self-report regarding suicidality specifically. There remains a dearth of literature guiding suicide risk assessment and management in the context of validity concerns, and clinicians are left with balancing the potentially competing duties of mitigating suicide risk while also attending to validity concerns. Case History: A male veteran with history of PTSD, major depression with psychotic features, traumatic brain injury, and migraines was referred for consultation regarding suicide risk assessment and management. Clinical evaluation revealed atypical neuropsychiatric symptoms and prominent suicidal ideation with self-report of numerous prior attempts, while measures of performance and symptom validity consistently yielded grossly invalid results. Conclusions: The existing literature features little research and limited guidance to clinicians having to reconcile subjective reports of suicidal ideation and self-directed violence with problematic validity results. Despite the lack of empirical guidance, suicide risk assessment and management mandates clinical attention to self-report, even when validity concerns may be present. Genuine distress and related suicide risk may coexist with otherwise invalid neuropsychiatric presentations. Recommendations for recognizing and articulating the limitations imposed by invalid presentation upon clinical assessment and risk stratification, while simultaneously mitigating genuine suicide risk, are offered.

Background: Cenesthopathy is a syndrome in which patients complain of bizarre descriptions of abnormal body sensations that are medically inexplicable. Somatic misperceptions and delusions occur in a variety of pathologies, though there is limited understanding of the associated pathophysiology. The author presents a case of cenesthopathic anxiety and a brief discussion of neurobiological mechanisms in other disorders of somatic misperception and somatic delusional content. Case History: A 15-year-old girl presented with concerns that her spine is missing or not her own, that her legs may not be attached to her body, and that her internal organs are being blackened and contaminated by the loudness of voices around her. The patient’s symptoms progressed in the setting of increasing academic pressures and significant depression and anxiety when unable to meet her desired goals. Conclusions: Cenesthopathic symptoms may have origins in psychosis, somatic anxiety, and/or hypochondriasis. Frontal-thalamic structural perturbation has been demonstrated in schizophrenic patients with somatic hallucinations. Somatization disorders have also been theorized to be secondary to a somatosensory amplification involving anterior cingulate, insula, amygdala, hippocampal formation, and striatum. Misinterpretations of normal bodily sensations in semantic dementia may lead to delusional disorder through an inability to read and name these sensations, termed alexisomia. Investigating neurobiological mechanisms from a variety of somatic misperception disorders provides context for the inquiry into the pathophysiology of cenesthopathy.

Introduction: Dysgeusia as a precondition for cacogeusia. A patient with cacogeusia without dysgeusia due to texture is described. Method: Case Study: Six years prior to presentation, a 52-year-old, right handed female developed severe upper respiratory infection followed by a loss of smell and taste. She finds steak disgusting to her, despite having no taste, because of its gritty texture. Attempts to eat steak or other meat induce immediate nausea with the first bite, before even swallowing. Results: Abnormalities in Neurological Examination: Pyramidal drift with left cerebellar spooning. Finger-to-nose: bilateral dysmetria, slow rapid alternating movements of left upper extremity. Reflexes: 3+ quadriceps femoris bilaterally. Delayed return of ankle jerks bilaterally. Chemosensory Testing: Olfaction: Dirhinous University of Pennsylvania Smell Identification Test: 22 (hyposmia). Alcohol Sniff Test: 1 (anosmia). Brief Smell Identification: 8 (hyposmia). Retronasal Olfactory: Retronasal Smell Index 1, Olfactometer Identification: Left 8, Right 7 (anosmia). Brief Smell Identification Test: 8 (hyposmia). Gustation: Propylthiouracil Disk Taste: 9 (normogeusia). Other: MRI of the brain with or without infusion: Normal. Tongue Candida Culture: Candida Albicans positive. Discussion: Discordance between expected flavor and perceived flavor may lead to negative hedonics. The absence of flavor may psychologically convert the food to be perceived as a tasteless non-food item, which has been overlearned to be excluded from the oral cavity, and thus disgusting. Psychodynamically, such non-food items may evoke psychosexual images, disinhibiting repressed memories, associated with disgust. Query as to perception of food hedonics in those who complain of chemosensory dysfunction is warranted.

Hart HH: Bad taste (cacogeusia). Arch Neurol Psych 1938; 39(4):771

Kaveh K, Hirsch AR: Cacogeusia sans dysgeusia. Manuscript submitted for publication. 2016

Miller SM, Naylor GJ: Unpleasant taste—a neglected symptom in depression. J Affective Disorders 1989; 17(3):291–293

Introduction: Vortioxetine induced craving for sweets has not heretofore been described. Method: Case Study: A 52-year-old right handed female presented with a seven year history of head trauma with reduced ability to smell and impaired taste with ability to taste only sweet and salty foods. She also suffered from depression for which she was treated with 5 mg vortioxetine every night. The next day, and continuing for the month she was taking vortioxetine she experienced an insatiable sweet tooth occurring ten times a day. For instance, in one day she ate an entire chocolate cake, a smoothie, five Mexican wedding cookies, five sugar crapes, a chocolate mousse, five marzipan cookies, and 50 jellybeans. Such appetite for sugar caused her to gain 6 pounds during the course of treatment. On discontinuation of the vortioxetine the craving for sweets resolved. Results: Chemosensory Testing: Olfaction all anosmic including, Brief Smell Identification: 6, Alcohol Sniff: 0, Pocket Smell: 1, Olfactometer Identification: left 6, right 6, Phenylethyl Alcohol Snap Threshold: left 2.0, right 2.0, and Suprathreshold Amylacetate Odor Intensity Test: flat line. Retronasal Smell Index: 1 (abnormal). Gustation: Propythiouracil Disk: 5 (normogeusia). Discussion: Drug-induced exacerbation of anxiety may have provoked her to search for sweet food as a way of self-medicating (Wurtman and Wurtman 1995). Improvement in her depression may have enhanced her desire to indulge in hedonic pleasures (Macht 1999). Glycolimia may be the origin for vortioxetine weight gain and it may be worthwhile to query about sweet cravings and monitor weight.

Hirsch AR: Sweet taste preference and alcohol dependence. Am J Psychiatry 2002; 159:497–498

Hirsch AR: High sucrose preference in alcoholic men. Am J Psychiatry 1997; 154:1631–1632

Macht M: Characteristics of eating in anger, fears, sadness and joy. Institute of Psychology 1999; 199:129–139

Wurtman RJ, Wurtman JJ: Brain serotonin, carbohydrate-craving, obesity and depression. Obes Res 1995; 3:477S–480S

Background: Psychogenic speech and voice disorders (PSVDs) are characterized by abnormal speech and voice patterns that are incongruent with organic neurologic disorders. PSVDs are common in patients with other psychogenic disorders and significantly contribute to morbidity. Treatment for PSVDs includes speech therapy, psychotherapy, and pharmacotherapy in some cases. Hypnosis for treating PSVDs has sparse representation in the literature. Emerging evidence identifying possible physiological commonality between hypnosis and psychogenic disorders may help explain the utility of hypnosis in PSVDs. Case History: Here we present Patient M, a 36-year-old woman admitted to the Epilepsy Monitoring Unit for diagnosis of her seizures. During admission, events were confirmed to be psychogenic nonepileptic seizures (PNES) and she was also diagnosed with PSVD. When engaged in hypnosis, her speech and voice abnormalities temporarily improved and she was able to sing several lines from a favorite childhood song. She was also taught self-hypnosis for continued treatment of PNES and PSVD. We will present video sample of this patient during hypnosis; patient consent obtained. Conclusions: The use of hypnosis appears to be effective for treating PSVDs and is theoretically supported by overlapping physiological mechanisms of hypnosis and psychogenic disorders. Given the relative frequency of PSVDs in other psychogenic disorders as well as their marked impact on morbidity, it is important for clinicians to be aware of these disorders to guide treatment. Hypnosis should particularly be considered as it is a low-cost treatment for this patient population that usually does not have access to adequate treatment resources.

Background: Alzheimer’s dementia in the elderly adult is the most frequent neurodegenerative disease, usually with memory dysfunction behavioral symptoms are present at the moment of the diagnosis and represent one of the main complaints during the course of the disease. Objective: To determinate the main behavioral and psychological symptoms in elderly patients with dementia and its correlation with stage disease and caregiver burden. Design/Methods: We conducted population-based study in Havana, Cuba, where the diagnosis of dementia was established in those over 65 years of age. Dementia diagnosis was made using 10/66 dementia and DSM-IV criteria. Patients (323) and controls (N=2 621) were followed up during 5 years in order to determine the pattern of behavioral and psychological symptoms in patients with dementia syndrome and its relation with the caregiver burden. Results: The prevalence of DSM-IV dementia was 6.4% and 10.8% according to the 10/66. Of the patients with dementia, 61.2% were patients with Alzheimer’s disease, 18.6% had mixed dementia and 10,1% vascular dementia. Dementia associated with Parkinson’s disease and fronto-temporal dementia syndrome was detected in a 5.3% and 4.3% of cases, respectively. Behavioral and psychological symptoms were identified in 75.7% (OR 4.26) of patients studied, and of those 85.7% (95% CI, 81.4–89.1) had more than one symptom during the course of the disease. The most common behavioral symptoms associated with dementia were: activity disorder (60.4%), physical or verbal aggression (52.7%) and sleep disorders (43.4%); the latter predominate in women as well as paranoid hallucinations, anxiety and phobias (33.8%). Aggressiveness (86.9%) and hallucinations (49.2%) were more frequent in men. Conclusions: Most of the patients studied had psychological and behavioral symptoms that were predominately activity disorders, aggression and sleep disorders. The caregiver burden was correlated more strongly with the presence of behavioral and psychological than with the cognitive issues.

Background: Validity testing is a routine aspect of neuropsychological evaluations. It has been proposed that performance validity tests (PVT) and symptom validity tests (SVT) relate to different domains of function and practitioners are encouraged to examine validity across all modes and domains of evaluation. Objective: To evaluate the relationship between PVTs, SVTs and performance on symptom reports and cognitive testing. Methods: Combat veterans (N=74) from an ongoing study completed a cognitive battery and symptom report measures, in addition to PVTs [Medical Symptom Validity Test (MSVT), b-Test] and SVTs [Structured Inventory of Malingered Symptoms (SIMS)]. PVT and SVT failure rates were compared using chi-square tests. Participants passing or failing each validity test were compared on symptom reports and cognitive testing using one-way ANOVA with False Discovery Rate correction. Results: Failing the MSVT significantly increased the likelihood of failing the SIMS, χ²=7.44, p=0.029. Performance on the b-Test was not related to the MSVT or SIMS. The b-test was related to WAIS-IV Cancellation, but not symptom reports. The MSVT was related to posttraumatic stress symptoms, pain interference, and postconcussive symptoms; as well as Trail Making Test Parts A & B and WAIS-IV Coding. The SIMS was related to all symptom measures except alcohol problems, but not cognitive performance. Conclusion: Results confirm that PVTs and SVTs measure different constructs. Additionally, these results support the use of multiple validity tests across domains as performance on the MSVT and b-Test were unrelated, and differentially related to outcomes.

Background: Age, depressive symptoms, gender and the apolipoprotein E (APOE) e4 allele are independently associated with δ (for dementia)¹. Resistin was identified as a depression serum biomarker². In this analysis, we studied Resistin as a possible mediator of Depression’s specific association with δ. We used longitudinal mediation models in a structural equation model (SEM) framework to examine the mediation effect in longitudinal data from the Texas Alzheimer’s Research and Care Consortium (TARCC). Methods: Structural equation models (SEM) was used in the Texas Alzheimer’s Research and Care Consortium (TARCC) cohort (n=3358) and conducted in Analysis of Moment Structures (AMOS). Resistin levels were determined at baseline. We used an ethnicity equivalent δ homolog wave 2 [dEQ(w2)]. Thus, the model is longitudinal and arguable causal. Results: Model fit was excellent [e.g., Resistin: χ²=53.28 (17), p<0.001; CFI=0.992; RMSEA=0.025]. Serum Resistin was found to mediate 33.2% of depression’s association with Wave 2 dEQ scores (p<0.001) [Table 1]. The effect generalized across random subsets of TARCC’s sample. Conclusions: Our findings suggest that depression’s specific association with δ is partially mediated by the serum Resistin level. That may offer a target for the treatment of depression specific effects on dementia severity and conversion risk.

1. Royall DR, Palmer RF: Thrombopoietin is associated with δ’s intercept, and only in non-Hispanic whites. Alzheimers Dement (Amst) 2016; 3:35–42. doi:10.1016/j.dadm.2016.02.003.

2. Bilello JA, Thurmond LM, Smith KM, et al: MDDScore: Confirmation of a blood test to aid in the diagnosis of major depressive disorder. J Clin Psychiatry 2015;76(2):e199–e206. doi:10.4088/JCP.14m09029.

Background: ANPA is a unique professional organization filling an interdisciplinary niche where psychiatry and neurology overlap. A brief cross-sectional questionnaire survey was designed to examine the interests and characteristics of the membership. Objective: To learn characteristics and preferences of ANPA members and perceived value of membership. Methods: A 5-minute, 12-question survey, was developed with an online platform. Active members of the American Neuropsychiatric Association were invited to participate via email solicitation. The survey response window was 3 weeks, with one reminder email sent at the midpoint. No personally identifying information was collected and no responses were tagged in any way. Partial responses were allowed for some items. The project is classifiable as a quality improvement, non-human subject, (exempt) research activity. Results: 65 respondents initiated the survey with 59 completed. Gender and age were not recorded. 6 reported trainee status. 29/65 (44%) joined ANPA during training. Top 3 practice settings were academic medical center (44%), solo private practice (17%) and psychiatric hospital (17%). Over half of respondents identified themselves as primarily neuropsychiatrists (55%) and 37% as primarily psychiatrists. 37% reported regularly attending the annual meeting. 55% reported being in practice for over 20 years since training. 70% agree or strongly agree with welcoming opportunities to collaborate with other members on academic projects. 31% were interested in utilizing ANPA focused social media. The main benefit perceived from membership was identification with an organization consistent with professional identity (90%). Conclusion: ANPA members place high value in aspects of professional identification and tend towards academic interests and involvement.

Background: ANPA is a unique professional organization catering to clinicians and researchers interested in brain and behavior relationships. Details of professional interests and preferences of membership are largely unknown given the wide variety of disciplines represented and diverse experience level among members. Objective: To learn details of the professional interests of ANPA members. Methods: A brief, cross-sectional, online survey of ANPA members was recently conducted via e-mail for an organizational quality improvement effort. Perceived value of aspects of ANPA membership and professional interests were rated on a 5-point scale. 65 members participated; partial responses were permitted. Comparisons were made between groups based upon seniority (under or over 20 years posttraining) and whether a member joined during training or afterward. Rating averages and variances were compared. Results: Of the respondents, 29/65 (44%) joined ANPA during training. The remainder joined after training was complete. 29/59 (49%) have been in practice 20 years or less posttraining. All groups highly valued programming and professional identity offered by the organization. Trainee joiners placed a somewhat higher value upon networking opportunities (mean 3.92, variance 0.71 versus mean 3.58, variance 1.64). Interest in social networking also differed (mean 3.04, variance 1.88 versus mean 2.5, variance 1.84). Those in practice less than 20 years were more interested in academic collaborations (mean 4.21, variance 0.72 versus mean 3.43, variance 1.71). Conclusion: ANPA members had varying interest levels in academic collaboration, professional networking, and social media, but uniformly valued programming identification with ANPA.

Background: There might be a common neurobiological basis underlying dementia and affective disorders. We describe two cases with affective disorders and developed frontotemporal dementia (FTD) at their mid-forties. Case History: Both cases had no history of familiar or personal medical and psychiatric diseases. Case 1 is a 45-year-old male with past history of depressive symptoms for 7 years that led to impaired work and social functioning, with partial improvement after treatment. Later on, the patient began with executive dysfunction. MRI showed bilateral frontotemporal (FT) atrophy. Brain SPECT showed bilateral FT hypoperfusion. Case 2 is a 48-year-old female diagnosed with bipolar disorder type 1 since 24 years old. In the last year she began having word finding difficulties, her speech became effortful as she started producing fewer words, some naming and comprehension difficulties. MRI showed bilateral FT atrophy, with predominance on the ventral left side. Brain SPECT showed bilateral FT hypoperfusion being severe in the left side. Conclusions: In both cases, an affective spectrum was diagnosed previously to FTD. It is well known, an affective disorder could be both a prodrome and a risk factor for dementia. Several data demonstrate a link between the two conditions probably due to common diathesis, or to specific brain changes emerging during affective episodes. A diagnosis of FTD should therefore be taken into account, in case of unexpected cognitive and behavioral decline in patients with a long history of affective disorders.

Background: CTE is a neurodegenerative disease clinically characterized by impairment in cognition, behavior and mood. Neuropathological examination reveals a phosphorylated-taupathy with deposition of neurofibrillary tangles, astrocytic tangles and neuritis around cortical blood vessels. It can be associated with beta-amyloid (43%), Lewy bodies (22%) and TDP-43. We describe a patient with a history of multiple TBI who presented with a mental status examination consistent with multiple distinct neurodegenerative disorders. Case History: A 55-year-old man presented following suicide attempt via carbon monoxide poisoning. He had a 5-year history of progressively worsening irritability, paranoia and executive dysfunction. He suffered multiple concussions dating to high school, most recent being 11 years ago. Mental status exam revealed impairment in bilateral frontal (executive dysfunction, echopraxia, disinhibition), parietal (Gerstmann’s syndrome, ideomotor apraxia, right hemi-neglect), temporal (anomia, paraphasic errors, amnesia), and parieto-occipital (Balint’s syndrome, visual hallucinations, constructional apraxia) function and mild Parkinsonism. MRI shows diffuse cortical atrophy with corpus callosal thinning. Conclusion: This case highlights the utility of a thorough mental status examination in considering CTE as a possible diagnosis. CTE can only be diagnosed with certainty by neuropathological examination. There are potential useful imaging techniques and biomarkers e.g., PET ligands for p-Tau, MRS and CSF markers, however, these in-vivo diagnostic techniques are not readily accessible. Furthermore, this patient’s mental status exam with features of AD, bvFTD and LBD suggests that CTE may be viewed as a spectrum disorder that can present with manifestations of multiple distinct neurodegenerative disorders consistent with its neuropathology.

Background: Evidence suggests that both low IQ and ADHD are risk factors for PTSD. However, this line of research is limited by methodological issues, and little is known regarding these neurodevelopmentally-mediated factors and PTSD in veterans. Objective: To evaluate relations between neurodevelopmental factors and adult PTSD, we hypothesized that PTSD diagnosis would be associated with lower IQ estimates, and that veterans with PTSD would screen positive for adult ADHD more often than those without PTSD. Methods: Combat veterans (N=66) from an ongoing study completed several intelligence estimates (WAIS-IV GAI and TOPF), a self-report ADHD screen (ASRS Part A), and a structured PTSD interview (CAPS-5). Independent t tests and chi square analyses were conducted both before and after accounting for overreporting and invalid performance. Results: Using the full sample, there were no significant differences in any intelligence estimate in participants with PTSD compared with those without. There was a significantly higher rate of possible ADHD in participants with PTSD compared with those without (χ²=10.55, Cramér’s V=0.41). However, after eliminating participants with invalid presentations (using SIMS, MSVT, and b Test), the difference became nonsignificant (χ²=3.46, Cramér’s V=0.28). Follow-up analyses indicated that ADHD status was related to overreporting of symptoms (SIMS) but not underperformance. Conclusion: This study did not support a relationship among intelligence and PTSD nor ADHD and PTSD after adjusting for validity. Inappropriate selection of intelligence measures and failure to consider validity may account for those positive findings in previous literature.

Background: While prednisone helps some forms of smell loss, its effects on olfactory windows have not heretofore been described. Case History: A 42-year-old right-handed male with chronic sinus infections, one year prior to presentation underwent cardiac ablation for atrial fibrillation. One week later he noticed a sudden persistent loss of taste and smell. He has no smell and taste is 70% of normal. After a 3-week course of prednisone, 60 mg, olfactory windows of one-second duration increased from monthly to weekly and were correct representations of odors. Olfactory ability between olfactory windows remained unchanged. Results: Chemosensory testing: olfactory testing: Anosmia on: phenylethyl alcohol threshold: R>−2.0, L>−2.0, Quick Smell Identification: 0. Brief Smell Identification: 3. Olfactometer N-butanol threshold: R 1.0, L 0.0. Alcohol Sniff: 0. University of Pennsylvania Smell Identification: L 11, R 8. Pocket Smell Identification: 1. Sniff magnitude ratio: 0.92. Sniff-n-Sticks threshold: L<1, R<1. Odorant discrimination: 6. Odorant Identification: 6. Odor Memory: 10 sec: 1, 30 sec: 1, 60 sec: 1, total: 3. Suprathreshold Amylacetate Odor Intensity: horizontal line. Retronasal Smell Index: 1 (abnormal). Other: MRI of Brain with and without infusion: normal. Fiberoptic endoscopy: normal. Conclusion: Possible mechanisms of steroid effect include increase in Na-K-ATPase activity of olfactory receptor neurons, improving their efficacy (Rydzewski, 2000). Possibly, olfactory windows are most responsive to steroids, and in pathologic situations show first signs of improvement. Investigation into the prevalence and natural variation of olfactory windows in those undergoing treatment for chemosensory dysfunction is warranted.

Background: In 1899, Hughlings Jackson noted phantosmia of uncinate fits in those with temporal lobe epilepsy (Chen 2003). However, the perception of smell is a combination of olfactory and chemesthetic (trigeminal) sensations (Hudson 2015). Isolated phantochemesthesia in temporal lobe epilepsy has not heretofore been described. Case History: An 81-year-old, presented with 8 months of epochs taking place on daily basis. These began with hemicephalgia followed by tongue grittiness, anxiety and variety of phantosmia. She described olfactory hallucinations which over time changed to purely chemesthatic sensations in nature—no smell and no taste, but rather just a burning sensation, commencing at the throat, progressing up to the mouth and ending at the nose, lasted for 15s. The earlier olfactory seizures had resolved and transformed into chemesthetic seizures. Conclusions: Neurological Examination: Mental status examination: recent recall: 0/4 objects in three minutes & 2/4 with reinforcement. Motor examination: drift testing: right cerebellar spooning. Reflexes: 0–1+throughout. Other: Chemosensory testing: olfactory testing: Brief Smell Identification Test: 12. Alcohol Sniff Test: 22. Retronasal Olfactory Testing: Retronasal Smell Index: 4. Gustatory Testing: Propylthiouracil Disc Taste Test: 10. MRI of brain with & without infusion: periventricular & subcortical microangiopathic disease.EEG: Polymorphic slowing with theta waves in the left TL. Confusion between olfaction, gustation and chemesthatic sensation is ubiquitous. Oft described burning phantosmias of temporal lobe epilepsy can be chemesthetic sensation. The patient’s description is a classic example (Thomas CS 2010). In those who present with phantosmia, additional inquiry as to phantochemesthesia is warranted.

Background: In contrast to temporal desensitization to olfactory stimuli (first taste syndrome), the temporal sensitization to olfactory stimuli, as manifested by flavor, has not heretofore been described. Case History: Case Report: A 50-year-old male, after an upper RTI noted over 9 months a gradual reduction in his ability to smell and taste, to the point of total loss of smell and taste upon initial consumption. He noted that after 20 to 30 minutes of leisurely consumption the food gradually became imbued with flavor. Initially he had no taste when eating popcorn, but after 20 minutes of relaxed mastication, he was able to taste the popcorn and the flavor persisted till the end. Similar phenomena occurred when eating chocolate cookies. He’s also complained of water smelling different and chemical-like, and tastes are distorted whereby olives taste fecal, pickles taste like vinegar, cottage cheese tastes unpleasant, Oreos taste like flowers, and sour cream is no longer sour. Conclusion: Chemosensory testing: olfactory: all abnormal: brief smell identification test: 6, olfactometer identification: l 9, r 9, pocket smell test: 1/3, alcohol sniff test: 0. Retronasal smell: jellybean difference test: 0 (abnl). Gustatory: 6-n-propythiouracil disc test: 10/10 (nl). MRI: moderate pansinusitis. Possibly this phenomena is due to a temporal summation in olfactory (Hummel 2002), gustatory (Bagla 1997), trigeminal (Viereck 1997), or retronasal smell (Mialon 1997). This could be a chemosensory equivalent of somesthetic/tactile illusion combined with expectation affect. The phenomena of temporal summation may be of utility in treatment of those with chemosensory dysfunction.

Background: Therapeutic effects of deep brain stimulation (DBS) of the subthalamic nucleus (STN) may depend on specific placement of DBS electrodes within the STN, but direct evidence for this is sparse. We previously used a novel 3D statistical mapping method to show that unlike motor response, cognitive and affective response varies according to precise location of clinically-optimized DBS contacts. This may be related to anatomically-distinct motor, affective, and associative STN tracts. Objective: To use 3D statistical mapping to determine the acute cognitive, affective, and motor effects of standardized stimulation at various precise points in/near the STN. Methods: Thirty-six subjects with STN DBS were evaluated on separate days with right-and left-sided stimulation activated at contacts near the dorsal and ventral aspects of the STN. Measures included Spielberger state-trait anxiety inventory, visual analog scale (anxiety, emotional valence, arousal, and apathy), probability estimation, affective go-no-go, and motor scales. Voxel-wise weighted t-tests produced composite images demonstrating the expected effect of stimulation at each voxel within the STN. A permutation test computed the probability that the effect depended on stimulation location. Results: Voxel-wise weighted t-tests identified specific stimulation points where cognitive and affective responses were greatest. After stringent correction for multiple comparisons, these changes were not found to be statistically significant. Conclusions: Unlike clinically-optimized stimulation, precise location of standardized stimulation at pre-determined sites was not significantly associated with improvement in cognitive and affective response. Future directions will include finite element modeling of volume of tissue activated, thereby allowing comparison between subjects with varying stimulation parameters.

Background: Repetitive transcranial magnetic stimulation (rTMS) has demonstrated antidepressant efficacy, but has not been tested in depression associated with traumatic brain injury (TBI). While resting-state fMRI (rsfMRI) has been proposed as a method for targeting rTMS, it is limited by reliance on group-mean connectivity maps from healthy control subjects, which may not generalize to individual patients with neuropsychiatric disorders. Objectives: To investigate the use rTMS treatment targeted with individualized mapping of dorsal attention network (DAN) and default mode network (DMN) in subjects with treatment-resistant depression (TRD) associated with TBI. Methods: Subjects with TRD and TBI received rsfMRI scans with individual-level connectome mapping based on a machine-learning algorithm which classifies networks based on known interindividual variability. Subjects were randomized to 20 sessions of bilateral rTMS treatment (4000 left-sided excitatory pulses, 1000 right-sided inhibitory pulses) or sham. Treatment was targeted to the prefrontal location maximally correlated with DAN and anticorrelated with DMN. Pre- and posttreatment testing included Montgomery-Asberg Depression Rating Scale (MADRS) and rsfMRI. Results: Preliminary data from six subjects showed MADRS improvement of 72%, 71%, 61%, and 50% with active treatment compared with 38% and 22% with sham. Treatment was associated with increased size/connectivity of DAN (including dorsolateral prefrontal cortex), increased connectivity within DMN, increased anticorrelation between DAN and DMN, and increased orbitofrontal-limbic-striatal connectivity. Conclusions: rTMS targeted based on individual-level connectome mapping appears to cause mood effects and neural network dynamics reflecting the expected changes based on the stimulated networks. We are currently collecting additional data in a larger sample.

Background: Gilles de la Tourette syndrome (GTS) is a childhood-onset neuropsychiatric disorder characterized by multiple tics and often associated with behavioral problems. Although there is evidence of significantly reduced self-esteem in children and adolescents with GTS, little is known about perceived self-concept and its clinical determinants at the transition age between adolescence and adulthood, a crucial age for personal development. Objective: This original study aimed to investigate self-concept in a clinical sample of young patients with GTS at the transition age between adolescence and adulthood. Methods: In addition to standard demographic and clinical data, we collected self-ratings using a standardized battery of psychometric instruments, as well as the Multidimensional Self Concept Scale, a comprehensive questionnaire developed to assess self-concept in subjects aged 9 to 19 years, tapping into the social, competence, affect, academic, family, and physical domains. Results: We found that patients diagnosed with at least one comorbid psychiatric disorder (“GTS-plus” phenotype) reported significantly lower self-concept than patients with “pure GTS,” whereas tic-related variables had no impact on self-concept. Anxiety symptoms were the main determinants of self-concept, especially trait anxiety with regard to social and affective domains. Affective symptoms could also have a negative impact on the physical, affective, competence, and social domains of self-concept. Conclusion: Routine screening for comorbid conditions, especially anxiety and affective symptoms, should be recommended in all patients with GTS seen at transition clinics from pediatric to adult care, in order to implement effective treatment interventions to improve self-concept whenever possible.

Background: Developing interventions to reduce age-related cognitive decline is a critical public health goal. Computerized cognitive training (CCT) has been marketed increasingly to older adults, but its efficacy remains unclear. Working memory (WM), a key determinant of higher cognitive abilities, is susceptible to age-related decline, which makes WM a relevant target for CCT in elders. Objective: To evaluate the efficacy of CCT focused on WM compared with an active control condition in healthy older adults. Methods: Seventy-six cognitively normal elders from two sites (US and Sweden) were randomly assigned to Cogmed Adaptive or Non-Adaptive (active control) CCT groups. Training was performed in participants’ homes during sessions lasting ∼ 40 minutes, 5 days per week over 5 weeks. In the Adaptive CCT, difficulty level was continually adjusted, while for the Non-Adaptive group, difficulty level remained the same. The outcome measures included performance on Trails A and B, Digit Symbol, Phonemic and Semantic Fluency. Results: The intervention groups were comparable at baseline, although the Adaptive group tended to have slightly higher estimated IQs. ANOVA demonstrated a group-by-time interaction for Trails B and Digit Symbol, with significant improvement only following Adaptive training. After controlling for IQ, the interactions remained significant. In addition, the magnitude of the intervention effect was similar at both sites. Conclusions: Adaptive WM training effectively improved executive functioning and processing speed in elders from different cultural backgrounds. The benefits over the active control group suggest that the Adaptive CCT gains were linked to providing a continuously challenging level of WM difficulty.

Background: Poor regulation of stimulus-driven preconscious orienting responses (OR) may predispose to impulsivity, a complex construct consisting of trait impulsivity, impulsive action (response inhibition), and impulsive choice (delay discounting). An electrophysiological measure of OR is the mismatch negativity (MMN). Prior studies showed higher trait impulsivity but lower impulsive action with a larger MMN, suggesting opposite relationships with OR. Objective: Evaluate relationships between OR and facets of impulsivity across healthy volunteers and patients with a psychiatric disorder marked by pathological impulsivity. All subjects completed all measures. Methods: Recruited were patients with bipolar disorder (N=11), antisocial personality disorder, (N=9) and healthy volunteers (N=11). Univariate general linear models and correlation analyses were used to demonstrate a relationship between auditory duration MMN and (i) trait impulsivity measured by the Barrat Impulsiveness scale (BIS-11), (ii) impulsive action reflected by commission errors (CE) corrected for correct detections (CD) (CE/CD ratio) on the Immediate Memory Task (IMT), (iii) impulsive choice reflected by short-delay choices on the Two Choice Impulsiveness Paradigm (TCIP). Results: A smaller MMN amplitude correlated with higher IMT CE/CD ratio (r=0.52, p=0.005), which was driven by CE (r=0.52, p=0.007; CD: r=−0.07, p=0.75), and diminished signal-noise discriminability (IMT A’, r=−46, p=0.016). No significant associations were found with BIS-11 or TCIP. Conclusion: Partially consistent with prior studies, our outcomes suggest that weaker stimulus-driven preconscious OR measured by MMN amplitude may predispose to impulsive action, perhaps due to insufficient discrimination between signal and noise.

Background: Occlusion of the artery of Percheron, off of the posterior cerebral artery, can lead to bilateral thalamic infarcts, which cause amnesia and confusion. We describe a patient with schizophrenia and profound memory dysfunction secondary to bilateral thalamic infarcts who required a significantly reduced antipsychotic dosage poststroke. Case History: A 40-year-old man with schizophrenia was admitted with bizarre behavior and profound amnesia, following a cerebrovascular accident. Despite being hospitalized for over 3 months, on initial neuropsychiatric interview, he was only oriented to self. He could not remember events leading to hospitalization and he required guidance to find his room and classes. Despite intact attention and concentration, his short-term recall was negligible. He had naming deficits, perseverative retracing of letters and numbers, difficulty discriminating past, present, and future, mild right-sided dysmetria, upgoing toes, left foot drop, and right hand posturing on prolonged gait. Brain MRI showed bilateral thalamic infarcts and a right superior cerebellar infarct. Hippocampi where robust. CT Angiogram revealed a right vertebral dissection (C4-C5). Antipsychotic requirement poststroke was one-fourth of his premorbid dose. Conclusions This patient’s severe anterograde and retrograde amnesia was a result of bilateral thalamic infarcts from an occlusion of the artery of Percheron. His difficulties with comprehending time, perseveration, and up-going toes are consistent with a prefrontal disconnect secondary to bithalamic infarcts. Reduction of psychotic symptoms poststroke raises the question of memory’s role in psychosis.

Background: Confusion and agitation in the setting of frontal lesions can be caused by the lesions themselves or secondary to a superimposed delirium. We present the case of a patient with frontal lobe glioblastoma and presenting symptoms of paranoia and cognitive impairment who subsequently developed delirium. Case History: The patient was a 72-year-old man with history of colon cancer treated with sigmoidectomy and chronic back pain on opioids, who presented to the emergency department complaining of two months of intermittent urinary incontinence, accompanied by subacute cognitive decline, with the patient getting lost driving familiar routes and missing several medical appointments. His wife noted significant new-onset paranoia and irritability over the same period, with the patient concerned his activities were being monitored, and staying up to read voraciously at night about esoteric topics. MRI revealed a large right-of-midline frontal mass, glioblastoma WHO grade IV on biopsy. The patient was admitted to neurology and started on dexamethasone for cerebral edema. He subsequently became agitated at night, for which psychiatry was consulted. The patient’s delirium improved with the minimization of polypharmacy, including discontinuation of outpatient amphetamines, and institution of low-dose antidopaminergic treatment. Conclusions: Distinguishing delirium from frontal mass sequelae is of clinical import because it can guide clinical goals in the treatment of delirium. Improvement of the underlying symptoms of a frontal tumor is dependent on definitive or palliative treatment of the brain mass, whereas the episodic symptoms of delirium respond to preventative and symptomatic interventions.

Background: Psychiatric symptoms like depression have a broad differential diagnosis which includes intracranial processes. We present a case of an intracranial hemorrhage that could have been missed in favor of an idiopathic psychiatric diagnosis. Case History: A 56-year-old woman with past medical history of peripheral vascular disease was brought in by police after coworkers called for a wellness check. Psychiatry was consulted in the emergency department for evaluation of “extended bereavement”/depression given concern for flat affect in the setting of daughter’s death 3 months earlier. History revealed a sudden change in mental status 5 days earlier and memory impairment. Blood pressure was 188/94. On examination, she had restricted affect, cognitive deficits in language and attention with severe visuospatial disorganization on clock drawing, weakness in left upper and lower extremities, and left hyperreflexia. Head CT revealed acute 1.7×2.6 cm parenchymal right thalamic hematoma likely hypertensive in nature and mild obstructive hydrocephalus. She was admitted to medicine for blood pressure control. Workup revealed right renal artery stenosis. With blood pressure control, patient’s mental status improved. Conclusions: Thalamic lesions, especially on the right, have been associated with amnesia and cognitive impairment. Thalamic and basal ganglia lesions can be associated with emotional blunting and mood symptoms. We report a case in which an acute-subacute hemorrhagic stroke presented with primarily affective symptoms. The case underscores the importance of maintaining a broad differential diagnosis and performing a neurological exam when presented with acute psychiatric symptoms, particularly when they are accompanied by cognitive impairments.

Background: Current literature suggests that right hemisphere lesions produce predominant hemispatial-related dyslexic error in English speakers. However, little is known regarding such lesions in Chinese speakers. Case History: In this paper, we describe the dyslexic characteristics of a Chinese-English bilingual patient with a right posterior cortical lesion. He was found to have profound hemispatial-related errors during his English word reading, in both real and nonwords. During Chinese word reading, there was significantly less error compared with English, probably due to the ideographic nature of the Chinese language. He was also found to commit ‘phonological’ errors in English, characterized by error responses that were visually similar to the actual word. There was no significant difference in ‘visual’ errors during English word reading compared with Chinese. In Chinese word reading, he committed errors mostly in vertically oriented characters, consistent with evidence that the right hemisphere is likely involved in radical analysis. Conclusions: In general, our patient’s performance in both languages appears to be consistent with the current literature on right posterior hemisphere lesions. Additionally, his performance also likely suggests that the right posterior cortical region participates in the visual analysis of orthographical word representation, both in ideographical and alphabetic languages, at least from a bilingual perspective. Future studies should further examine the role of the right posterior region in initial visual analysis of both languages.

Background: Deep brain stimulation (DBS) of the subthalamic nuclei (STN) is an effective treatment for motor symptoms of Parkinson’s disease (PD). Emergence of cognitive, affective, and behavioral disinhibition occurs in one to fifteen percent of cases following DBS surgery. Legal and ethical issues that arise when patients develop neuropsychiatric sequelae following DBS surgery have been described. The study of legal and ethical issues associated with patients adjusting their own stimulator settings has been less robust. Case History: A 52-year-old Asian-American male with PD and no prior psychiatric or legal history underwent DBS surgery. Two weeks later stimulation was turned on, and the patient became acutely euphoric and disoriented. Good motor control without cognitive or affective side effects was achieved with lower voltage stimulation. The patient was taught to adjust the stimulator settings himself, and he was subsequently lost to outpatient follow-up. Four months later he presented to the emergency department with mania, psychosis, and altered mental status while in police custody. Interval history revealed that the patient had increased his DBS stimulation dose to four times his baseline settings, and that he had been charged with assault. Inpatient management included decreasing DBS stimulation to the original dose and revoking the patient’s ability to adjust his own stimulator settings. Conclusions: Legal and ethical issues arose in this case regarding whether or not the patient was culpable for his criminal actions, and regarding his autonomy to adjust stimulator settings himself. Further research is needed to guide clinicians’ decision-making in such cases.

Voltage gated potassium channel (VGKC) antibody limbic encephalitis is a rare, usually nonparaneoplastic limbic encephalitis that has mainly been described in the literature in case reports. Neuropsychiatric abnormalities that have been described include memory problems, confusion, obsessive-compulsive symptoms, altered behavior, and impaired naming abilities. Here we report on a case of VGKC antibody limbic encephalitis in a patient with pre-existing cognitive deficits (anterograde and retrograde amnesia and expressive aphasia) related to temporal lobe epilepsy s/p right anterior temporal lobectomy. He developed progressive difficulties with verbal learning, memory, and language. Laboratory evaluation, including LP with CSF analysis and paraneoplastic panel, showed positive serum VGKC antibody on two occasions as well as an elevated IgG index and oligoclonal bands. Patient had a positive response to corticosteroids, with improvement in cognitive deficits. We describe the results of neuropsychological testing both immediately after treatment for encephalitis and 2 years later to illustrate his cognitive profile, which shows significantly impaired expressive language abilities and verbal memory but preserved nonverbal memory.

Background: Rapid decision making and delay discounting are forms of decisional impulsivity. The subthalamic nucleus (STN) is implicated in inhibitory function but its role in decisional impulsivity is less well-understood. Deep brain stimulation (DBS) of the limbic-associative STN is effective for obsessive-compulsive disorder (OCD). We investigate decisional impulsivity in OCD subjects who have undergone STN DBS and also the relationship with functional connectivity in healthy controls. Methods: We test OCD subjects on and off DBS in a randomized counterbalanced double blind manner on evidence accumulation during probabilistic uncertainty (Beads task) and delay discounting. We use resting state functional connectivity in healthy controls to parcellate limbic-associative and motor cortical connectivity with STN. Results: STN DBS in OCD (N=12) increases decisional impulsivity with less evidence accumulation and greater delay discounting. In healthy controls (N=154) we show peak connectivity of anterior limbic-associative (ventral striatal, dorsolateral prefrontal cortex, dorsal cingulate) and posterior motor STN (supplementary motor area and M1). Optimal DBS contacts converge in anterior STN in OCD patients. In healthy controls (N=54), evidence accumulation correlates with anterior associative-limbic STN and right dorsolateral prefrontal functional connectivity. Conclusion: We highlight specificity of the anterior associative-limbic STN in increasing decisional impulsivity suggesting impaired action outcome mapping in the context of uncertainty. STN stimulation shifts evidence accumulation in OCD toward a functional less cautious adaptive style closer to healthy controls. We replicate in humans, tracing studies conducted in primates dissociating limbic-associative and motor hyper-direct cortical connectivity with STN subregions. Localization of STN stimulation may have clinical implications for behavioral symptoms.

Background/Objective: We hypothesized that the presence of psychiatric symptoms would predict the progression from normal cognition (NC) to mild cognitive impairment (MCI) in an elderly population. Methods: 386 participants (mean age 69, SD 8) with NC from the Texas Alzheimer Research and Care Consortium were studied. Each subject completed up to five yearly assessments. Kaplan Meier method and Cox proportional hazards regression models were used to determine effects of baseline variables on progression to MCI. To test for ethnic specific results, we also analyzed data separately for Hispanic and Non-Hispanic subjects. NC and MCI were diagnosed using Mayo Clinic and Petersen criteria. Clinical and sociodemographic variables, Neuropsychiatric Inventory Questionnaire (NPI-Q), Geriatric Depression Scale-30 item (GDS), CDR-SUM, and MMSE were collected. Results: 76 of the 386 subjects (19.69%) progressed to MCI during the follow up period. Progression to MCI was significantly associated with GDS score, having one or more positive item on the NPI, Hispanic ancestry, age, BMI, education and MMSE (unadjusted analyses). In adjusted analyses, only age and Hispanic ancestry were significantly associated with progression to MCI. In separate, adjusted analyses of Hispanics and non-Hispanics, age was significantly associated with progression to MCI in both groups. GDS score was associated with progression to MCI in the non-Hispanic group only. Conclusion: Our findings support our previous report (Salazar et al., 2016) suggesting that psychiatric symptoms at baseline (as seen in the NPI or GDS) and Hispanic ethnicity are risk factors for progression from NC to MCI in an elderly population.

Background: Individuals with developmental disorders, such as intellectual disability (ID) and autism spectrum disorder (ASD), can engage in severe behaviors that place themselves and others at dire risk. Many of these patients are refractory to pharmacological and behavioral interventions and are expelled from conventional treatment programs with no recourse. Graduated electronic deceleration (GED) is an aversive conditioning approach that has been shown to be effective in eliminating dangerous behaviors, but no mechanism has been offered for its efficacy. Objective: Here we present evidence using case histories, and we synthesize a hypothesis for the neuroanatomical basis for the success of GED. Methods: Students enrolled at the Judge Rotenberg Center (JRC) with severe behaviors who had not responded to behavioral and pharmacological interventions were evaluated before and after introduction of GED. All subjects continued to undergo positive behavioral analysis throughout the evaluation period. Self-injurious and assaultive behaviors were quantified daily and depicted graphically. We also conducted a literature review of imaging data for patients with ID and ASD and formulated a potential neuroanatomical explanation for failure of positive-only behavioral treatments and success of GED. Conclusions: GED has repeatedly proven effective in eliminating high-risk, dangerous behaviors for individuals with developmental disorders who are otherwise treatment refractory. The neuroanatomical abnormalities seen in these patients are consistent with the failure of conventional behavioral interventions and the success of GED.

Background: Strong evidence suggests that mild cognitive impairment (MCI) starts years before functional decline. Similarly, neuropsychiatric symptoms (NPS) in cognitively normal (CN) older adults, may be an early sign and a risk factor for progression to MCI. Objective: We explored the role of apolipoprotein E ε4 (APO ε4) allele and its interaction with NPS at baseline in the development of MCI. Methods: 94 of 386 CN individuals from Texas Alzheimer's Research and Care Consortium who carried the APOE ε4 genotype, were followed. Clinical and socio-demographic variables, Neuropsychiatric Inventory Questionnaire (NPI-Q), Geriatric Depression Scale-30 item (GDS), CDR-SUM, and Mini Mental State Exam (MMSE) were collected. Each subject completed up to five yearly assessments. Kaplan Meier method and Cox proportional hazards regression models were the statistical methods used. Results: 20 of the 94 CN subjects with APOE ε4 allele (mean age 71.45, SD 7.78) progressed to MCI during follow-up visits. In stratified analysis, we found that the presence of one APO ε4 allele is associated with an increased risk of MCI in non-Hispanics (p=0.002), while in Hispanics, APOE ε4 allele was not found to be associated with conversion to MCI. Among individuals with APOE ε4, only age, MMSE and Hispanic ethnicity were significantly associated with conversion to MCI (Adjusted). Conclusion: In CN individuals carrying APOE ε4 allele, the presence of≥1 NPI symptom did not increase the risk of progression to MCI, while age, MMSE and Hispanic ethnicity were found to be significantly associated with progression to MCI.

Background: While disorders leading to nasal congestion have been described as an origin of phantosmia, nasal congestion induced alleviation of phantosmia has not heretofore been described. Case History: A 63-year-old female, one month after exposure to chemicals involving mold remediation noted 30 second epochs of pleasant phantosmias of wood, occurring 15 times a day, level 3/10 in intensity. When real odors were present, the phantom smell would mix with them, which would be unpleasant. She denied smell defect, but complained of reduced ability to taste and dysgeusia. On two separate occasions, she developed severe upper respiratory infection (URI) causing her nose to be congested. Coincident with these URIs, her phantosmia resolved for the duration of the congestion, returning with resolution of the URIs. Conclusion: Results: Chemosensory testing: Olfactory: Brief Smell Identification Test: 11 (normosmia). Alcohol sniff Test: 2 (anosmia). Retronasal Smell Index: 6/9. (normal). Gustatory testing: 6 Propylthiouracil Disc Taste Test: 10 (normogeusia). Cognitive testing: Clock drawing test: 4. (normal). Semantic fluency test: 34. (normal). EEG: normal. CT scan with and without infusion of head and sinuses: normal. Discussion: The mechanism may be due to congestion-induced obstruction of the airways preventing synesthesia. Alternatively, the nasal congestion may have decreased the ability to smell an olfactory nidus which otherwise may serve to initiate the phantosmia. This implies occlusion of the nostrils (with nose plugs) or the use of pharmacological agents that cause nasal congestion (i.e. sildenafil) may have efficacy in treatment of phantosmia. Investigation of this is warranted.

Background: Clinicians have noted many similarities between schizophrenia and multiple sclerosis (MS) including onset in young adulthood, relapsing-remitting course, cytokine abnormalities, neurodegeneration, cognitive impairment, heterogeneity of clinical presentation, increased comorbidity with autoimmune disease, and shared genetic susceptibility in the major histocompatibility (MHC) region. While the treatment of MS has undergone a renaissance, the treatment of schizophrenia has remained focused on dopaminergic therapies despite a vast body of evidence linking schizophrenia to inflammation and immune dysfunction. Objectives: Identify potential new therapies to treat schizophrenia. Methods: Literature review focused on identifying overlap between mechanisms of MS treatments and their applicability in schizophrenia. Results: Two drugs show immediate promise: glatiramer acetate (GA) and dalfampridine. GA has both widespread effects on the immune system and neuroprotective actions including attenuation of key proinflammatory cytokines (TNF-alpha, IL-12, and INF-gamma), increased production of anti-inflammatory cytokines (IL-10 and TGF-beta), preservation of brain tissue integrity on MRI, and increased proliferation and recruitment of neuronal progenitor cells to areas of neuronal injury. All of which are relevant to schizophrenia. Additionally, pretreatment with GA has been shown to prevent the onset of cognitive and behavioral abnormalities in mice treated with psychotomimetic agents. Dalfampridine is thought to improve walking in MS by increasing conduction of action potentials along demyelinated white matter tracts. There is increasing evidence that it improves cognition as well. Conclusion: GA and dalfampridine may have potential benefit to treat clinical symptoms of schizophrenia, including cognitive deficits. Clinical trials to study these two medications in this patient population are warranted.