2015 American Neuropsychiatric Association Annual Meeting Abstracts

Background: Not all patients referred for evaluation meet criteria required for MS, clinically isolated syndrome (CIS), or radiologically isolated syndrome (RIS). Identification of markers to exclude demyelinating disease may help detect patients whose presenting symptoms are inconsistent with MS. Objectives: Determine whether patients who present a written list of symptoms during an initial visit are less likely to have demyelinating disease and whether this action, which we term the “list sign”, may help exclude demyelinating disease. Methods: All new patients who presented to a neurologist at a tertiary MS referral center were recruited retrospectively, using chart review, for six months. Patients were defined as having demyelinating disease if diagnosed with MS, CIS, or RIS. Results: Of the 107 enrolled subjects, 75 were diagnosed with demyelinating disease, 31 did not meet criteria for demyelinating disease, and one was lost to follow-up. Nine (8.4%) subjects had a positive “list sign”. Of these, none of these had demyelinating disease. The nine subjects described a mean of 10.77 (95% Confidence Interval or CI 8.4 to 13.2) symptoms; all met criteria for somatic symptom disorder as defined by DSM-5. The sensitivity and specificity of the “list sign” for nondemyelinating disease were 0.29 (95% CI 0.15 to 0.48) and 1.0 (95% CI 0.94 to 1.0) respectively. The positive predictive value and negative predictive value of the “list sign” sign were 1.0 (95% CI 0.63 to 1.0) and 0.77 (95% CI 0.67 to 0.85) respectively. Conclusion: A positive “list sign” may be useful to exclude demyelinating disease.

Background: Anton's syndrome is characterized by the denial of loss of vision in the setting of objective visual loss due to bilateral occipital lobe pathology. Although cortical blindness has been reported in some demyelinating conditions, to our knowledge, Anton’s syndrome has not been previously described as a symptom of an acute multiple sclerosis (MS) exacerbation. Case History: A 24 year-old left-handed woman with a history of MS presented with acute onset of right hemiplegia and right homonymous hemianopsia. MRI brain showed a large tumefactive demyelinating lesion in the left parieto-occipital region. She was treated with IV steroids with improvement. Two years later, she presented with acute onset of cortical blindness, global aphasia, and left hemiplegia. Repeat MRI brain showed a large area of active demyelination in the right posterior frontal, temporo-parietal, and anterior occipital lobes in addition to chronic demyelination in the left parieto-occipital region. She was treated with ten days of IV steroids and plasmapharesis. Although her language abilities recovered, she continued to display cortical blindness and visual anosognosia consistent with Anton’s syndrome. Three years later, she exhibited incomplete improvement in visual functioning with persistent symptoms of oculomotor apraxia, optic ataxia, and achromatopsia. Surveillance MRI brain showed confluent areas of chronic demyelination in the bilateral parieto-occipital regions. Conclusions: Our patient’s symptoms were related to dysfunction of the bilateral occipital lobes, which accounts for cortical blindness, and the visual association cortices, which accounts for visual anosognosia. To our knowledge, this is the first case of Anton’s syndrome due to MS.

Background: Psychogenic tremor is a common psychogenic movement disorder yet its diagnosis can be challenging. We present a patient with a distractible tremor-a characteristic feature of psychogenic feature with a concomitant organic cause including chronic kidney disease and alcohol abuse, stressing that psychogenic tremor remains a diagnosis of exclusion. Case History: 68-year-old female with history of stage IV chronic kidney disease, hypertension, rheumatoid arthritis, alcohol abuse, depression and recent job loss presenting with tremor. The onset of tremors in the right upper extremity was months ago with worsening for the past 2 weeks, spreading to the left upper extremity and her legs. On examination, her tremor improved dramatically when she was distracted for example reading a paragraph or while doing the serial sevens, when the tremor disappeared altogether. Her tremors switched easily from extremity to extremity with inconsistent in amplitude and in frequency. Finger to nose beside the tremor was normal. Gait and tandem walking were normal. MRI of the brain showed no acute intracranial lesions. She was treated with lorazepam for possible alcohol withdrawal with improvement in her tremors. We suspect psychogenic as well as organic causes for her tremor given her history of alcohol abuse, kidney disease and recently losing her job with worsening mood symptoms. Conclusions: It is important to rule out organic causes of a tremor despite a strong suspicion for psychogenic causes by history and clinical features including distractibility, variability or suggestibility. This is essential for prompt treatment and improvement of the long-term prognosis.

Background: “Fen-Phen” (fenfluramine/phentermine) was the famous weight loss pill reported to cause Pulmonary Hypertension and valvular heart disease necessitating withdrawal from market in 1997. Although this fatal side effect was attributed to Fenfluramine, Phentermine, which still exists in the market under various brands and combinations with potential serious, under-recognized side effects. We present a case of psychosis as a serious delayed side effect of Phentermine. Case: 38 year old previously healthy female who presented for acute visual and auditory hallucinations and delusions that started 3 days prior to admission. She was started on Phentermine 9 months prior and reported a weight loss of 70 pounds. The patient does not have any family history of psychosis, but she has a remote history of cocaine and alcohol abuse a year prior to presentation. Labs including complete blood count, Comprehensive metabolic profile including liver enzymes, kidney functions and TSH levels were normal. Urine toxicology was positive for amphetamines. The Naranjo algorithm was 6 for our patient which translates into probable causality of psychosis by phentermine. Phentermine was discontinued and the patient was started on Haloperidol with resolution of psychosis. She was discharged home symptom-free after 3 days. Conclusion: Phentermine is an amphetamine similar compound and a TAAR1 agonist that is commonly prescribed for weight loss. Serious adverse reactions such as psychosis are reported scantily in the literature. Our case is unique that the psychosis occurred 9 months after starting the medication.

Background: Tetrabenazine is considered the initial treatment for chorea associated with Huntington disease (HD).However its safety remains questionable especially with concomitant depression. The TETRA-HD study concluded that tetranbenazine was not associated with depressed mood in patients being treated with an antidepressant. We present the case of a patient who became suicidal while on tetrabenazine and antidepressant. Case History: 60 year old lady with HD initially presented with irritability and mood swings treated with a mood stabilizer. Choreiform movements then became apparent along with impaired coordination and gait disturbances. She was treated with an antidepressant with good outcome. Her chorea was then treated with tetrabenazine. After an initial improvement, the chorea continued to progress.CYP2D6 was therefore checked and she was found to be an extreme metabolizer. Hence the dose of tetrabenazine was increased. 3 Years after initiation of tetrabenazine, She reported depressed mood and suicidality while being on her antidepressant. Hence we resorted to quetiapine for her chorea. Conclusions: This case underlies the challenges of treating HD with comorbid depression. We raise the question as to whether it should be avoided altogether in any patient with a history of depression(treated or untreated)given the increased risk of depression as part of the natural course of HD as well as a serious side effect of tetrabenazine itself . Our case demonstrates that despite concurrent antidepressant use the patient still became suicidal contrary to the results of randomized controlled trials showing the contrary.

Background: Lyme disease is an infectious disease that frequently involves the central nervous system, leading to cognitive and/or mood dysfunction. In the chronic stage, many months or years after the initial infection, other neurologic complications may occur and psychiatric disturbances such as depression, catatonia and psychosis may also be seen. Here we present a case of new onset psychosis in a young patient with a prior history of Lyme disease. Case History: Mr. B is a 26 year old male with a previous diagnosis of fibromyalgia and Lyme disease status post treatment with antibiotics. He presented with a chief complaint of hallucinations and frequent headaches for two and half years. He had vivid images of a woman and a man who talked to him and about him. He was started on lithium and risperidone which decreased the frequency of the hallucinations. He was discharged to a partial day program after treatment. Due to worsening of symptoms he was hospitalized again for seventy days and was started on citalopram and clozapine. SPECT scan revealed decreased perfusion in multiple areas of the brain. The patient was seen by a Lyme specialist who started him on hyperbaric oxygen and minocycline. He showed sustained improvement in mood and psychotic symptoms. Conclusion: This case report highlights the diagnostic challenges associated with new onset psychosis in a patient with prior history of Lyme disease. Even though SPECT scans are not specific, they may be helpful in providing objective evidence in support of the clinical diagnosis.

Background: Prior investigations of the predictive value of QEEG for selecting pharmacological treatment have found little or no clinical utility (Crumbley, DeFippis, Dsurney, & Sacco, 2005). Recently, an Event-Related Potential method of QEEG (ERP-QEEG) has been used to select pharmacological treatment for impulsively aggressive juveniles (Matthews, Fisher, & Matthews, 2012; Fisher, Ceballos, Matthews, & Fisher, 2011). Objective: The current investigation is a retrospective study of the clinical utility of the ERP-QEEG for selecting pharmacological treatment, using need for psychiatric rehospitalization as the dependent measure. Methods: Participants were 618 impulsively aggressive juveniles (416 male, 202 female; ages 5–17) treated in a residential treatment center. A neurologist reviewed and localized any abnormalities in the QEEG-ERP’s. Temporal-limbic abnormalities predicted benefit from oxcarbazepine (to stabilize mood dysregulation); frontal-anterior-cingulate abnormalities predicted benefit from amantadine HCl (to improve executive function and impulse control). Participants were discharged on a medication protocol concordant with ERP-QEEG predictors. Results: A mail survey of caregivers, 6 months postdischarge, showed that 190 had changed medication protocols based on physician preference (Discordant-group) and 47 (24.74%) of those required psychiatric rehospitalization, while for the 428 still using the ERP-QEEG predicted protocol (Concordant-group), only 40 (9.25%) required rehospitalization. Using a 2×2 Chi Square, two tailed, Fisher’s Exact Test, there was a significant (p<0.0001) relationship between concordance and rehospitalization. Conclusion: While not a randomized controlled trial, the results suggest that, for this population, using the ERP-QEEG to select pharmacological treatment may have clinical utility.

Background: Neuropsychiatric patients require adequate, standardized, repetitive, rapid, easy, clinical assessments monitoring symptoms and changes diagnostically and therapeutically. Objective: Vernon Neppe’s “DS-10” comprises 10 different structured, standardized questionnaires (227+items), completed by patients in waiting-rooms, in Neuropsychiatric/Psychiatric outpatient settings. Methods: Neppe administered thousands of complete DS-10s on hundreds of patients at the PNI.

—Scoring commonalities: All 10 questionnaires have key item subdivisions. Scoring ranges all 0=normal, variably ordinal 3–10 points in the past week±past month frequency or severity.

—Derivations: Seven questionnaires are modified from previous standardized research (3 MD-ranked, 2 patient-rated); 2 involve significant additions; 3 have no previous equivalents.

— The DS-10 comprises 10 questionnaires:

5 questionnaires partly directly comparable with related modifications of research questionnaires e.g.,

a. MD Ranked:

—depression: “SHADES” (derivation: HamD-21, last week and month),

—anxiety: “SHARMS” (derivation: HamA-14)

b. Patient ranked:

—social anxiety (fears, avoidance): “LSAS-24-SR-MPNI” (24*2=48 items) (derivation: Liebowitz)

—obsessive compulsive: “Y-BOCS” (derivation Yale-Brown-10)

—sleepiness: “ESS-R8” (derivation Epworth)

2 derivative questionnaires have extra additions:

—fatigue: “FISS-R (10+4 items) (derivation Fatigue-Severity-Scale 10)

—attention deficit: “PNI M-CAARS” (14=6=20) (derivation Connors 14)

3 questionnaires fill recognized clinical voids:

—PTSD: “PRICE-20” (derivation DSM4R)

—Stress, Insomnia, Pain, Anger /ictal: “SIPAS” (26+6=32 frequency and severity)

—Extended symptoms: “NESS” (40 items): patient±family-ranked)

Results: Completion takes patients (after familiarity) only ∼15 minutes. Analysis: We analyze examples, clinical utility, diagnostic applications and research. Conclusion: The DS-10 has demonstrated clinical efficacy, research validity, consistent reliability, and universal applicability (PNI, usually 10+years).

Background: Motivation: Whereas frontal lobe dysfunctions can often be measured objectively, most temporal lobe dysfunction involves symptoms: The literature-based INSET (Inventory of Neppe of Symptoms of Epilepsy and the Temporal Lobe 1992 with modifications thereafter) is the only adequate, standardized, brief, historical bedside or waiting-room questionnaire, eliciting pertinent history-taking detail on seizures, peri-ictal symptoms, and temporal lobe features. Diagnostic importance: Whereas 3 to 4-day Ambulatory Electroencephalography (AEEG) objectively measure focal and ictal events, these evaluations are sometimes limited e.g. in mesial temporal dysfunction (particularly absences; smells; rapid mood/ thought fluctuations; explosive irritability), when no pushbutton or nocturnal ictal events occurred, or with some medications (e.g. benzodiazepine). This limits sensitivity of AEEG requiring the routinely used. Objective: Evaluate INSET and SOBIN applications to:

— facilitate more adequate clinical history taking;

—detect potentially abnormal symptoms;

—allow more complete additions to the standardized answers;

—amplify detail to optimize eliciting clinically pertinent symptoms.

Methods: Utilize INSET plus AEEG to identify anticonvulsant responsive patient subpopulations plus mislabeled “seizures” or temporolimbic instability.

Combine with the “SOBIN” (Subtle Organic Brain Inventory of Neppe) to overlap broader neuropsychiatric symptom screens, including higher cortical frontotemporoparietal dysfunction, headache, anger, depression, anxiety, fatigue, sleepiness, flashing lights, and overall functioning.

Results: We evaluate the diagnostic and clinical validity, and reliability of the INSET and SOBIN as adjunct to 3-day AEEG compared with anticonvulsant responsiveness, quantitative clinical improvement and “control” patients.

Conclusion: Even in students, the INSET and SOBIN diagnostically combines with 72-hour AEEG to easily facilitate diagnostic higher cortical and ictal screening.

Background: BROCAS SCAN: Unique, half-hour, comprehensive detailed clinical standardized, validated, Bachelor’s level, bedside screening evaluation clinically test.

Composites: 10 different higher cerebral cortical functions (each 0–10 with overall ranges of 0=perfect to 100=grossly impaired; normal 0–15) and Behavior (MBRS) (Neppe, earliest 1989)

IVA (Sandford, including 1995):

One of several excellent structured objective quarter hour computerized continuous performance test evaluations.

Examines: simple visual and auditory concentration tasks; subtly measures attention and response accuracy and speed (milliseconds); mean=100, SD=10; with report (IVA plus)

Objectives: Are both tests needed?

Can they replace standardized neuropsychological testing in a clinical environment and be more pertinent in neuropsychiatry?

Sample: 1992–2014, PNI: used routinely clinically/ forensically evaluating and monitoring progression in Neuropsychiatric patients.

Utilitizations:

IVA: repeated standardized monitoring

BROCAS SCAN: Measures ten structured higher brain functions.

Both:

Concentration testing useful in both.

useful clinically plus with other structured questionnaires,.

valuable for regular clinical use and forensic applications.

Both useful in malingering, neuropsychiatric diagnosis, repetitive monitoring.

BROCAS SCAN:

Very sensitive.

Particularly useful to differentiate organic and functional illness.

Far better than Folstein’s MMSE.

Follow-up annually to measure changes.

Proven valuable initially and occasional follow-up in all neuropsychiatric patients.

IVA:

Doesn’t measure multitasking.

Added benefits in detecting blank periods in seizure disorders.

Repeated utility even in different times of day.

Applications: attention disorders, seizures, dementia, cognitive disorders, psychopathology.

Conclusions: Together they incompletely replace full-scale Neuropsychological testing (not IQ or memory) in<1 hour of nonspecialized evaluations.

Background: Demand for inpatient geriatric neuropsychiatry far exceeds the supply of available inpatient beds; consequently delays in acute treatment are common. In order to address this clinical need we have developed a program for telephone management of patients on the inpatient waitlist. Objective: To find new ways of managing the health of this population and learn about the needs of patients being referred for care to our unit. Methods: A naturalistic study was done with patients referred for treatment. All patients accepted to our waitlist were offered a telephone consultation with the author. We kept track of the current clinical setting, whether the providers took advantage of this service, exactly what recommendations were offered, and the patient outcome/disposition. Results: After 4 months of the study 48 patients on were offered telephone consultation. Twenty-four consults were done. Four people died while waiting for a bed. Eleven stabilized clinically and admission was declined when offered, and for 4 of these patients the improvement was due to the consultation that was offered. Twenty-two patients remain on the waitlist. Conclusions: When hospitalizations can be avoided due to clinical improvement that is a significant success with important financial and quality of life implications for the patient. It is also of benefit to the system as neuropsychiatric beds are a scarce and expensive resource in high demand. This is one innovative way of effectively managing these patients.

Background: Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA) performances are often interpreted using raw cutoff scores. However, the American Neuropsychiatric Association Committee on Research (Malloy et al. 1997) recommends and the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) requires performance on such measures be normatively interpreted. Population-based normative data are available for the MMSE and MoCA, the characteristics of which informs their clinical use. Objective: To compare the normative distributions of the MMSE and MoCA in adults. Methods: Population-based normative data for the MMSE (Crum et al. 1993; N=18,056) and MoCA (Rosetti et al. 2011; N=2,653) were placed in the same analytic space by calculating weighted means and pooled standard deviations for five 10-year age groups, stratified into two education levels. Results: Mean performance on both measures, and particularly the MoCA, varied as a function of greater age and lower education. MoCA variance was 4.16 times greater (range: 2.47 to 6.19) and 5.26 times greater (range: 3.62 to 7.11) than MMSE variance among those with≤12 and>12 years of education, respectively. On average, the normal distribution of the MoCA is twice as wide as the MMSE normative distribution. Conclusion: Age and education effects on MMSE or MoCA performance render use of raw cutoff scores psychometrically unsound. Loss of nearly twice as many points on the MoCA as on the MMSE is required to engender comparable levels of cognitive impairment. Implications of these findings on clinical use of these measures will be discussed.

Background: Performance validity testing (PVT) has undergone considerable evolution over the past two decades. Baserates for invalid cognitive testing have been relatively high across a number of clinical conditions and evaluation contexts. Providers have struggled to find precise terminology to describe failure on these tests. The purpose of this presentation is to review select topics related to PVT in current practice. Objective: Review terminology in PVT literature; summarize the advantages of administering multiple validity measures; and examine the differing interpretations of failed validity tests. Methods: Recent research and professional consensus papers on PVT are reviewed. Results: Performance validity is the current preferred nomenclature when describing neuropsychological tests that assess the validity of cognitive test performance (e.g. memory, attention, etc.). Performance validity testing (PVT) replaces the vague term “effort” and is not always synonymous with malingering. The standard of practice in neuropsychology is to use multiple validity measures covering several cognitive domains. Accuracy in detecting invalid testing may be improved by utilizing multiple embedded measures and statistical methods which do not rely on a single test or cut score. Recent debates on elevated false-positives when using multiple PVTs are also addressed. Interpretations of invalid cognitive test results are reviewed in the context of confusing and oftentimes misused or overly-broad terminology (e.g. “poor effort,” malingering). Conclusion: It is important to use precision and proper language when discussing the validity of cognitive test results. This review provides an update on current practice of select topics related to validity assessment in neuropsychological evaluation.

Background: In the context of the Atkinson-Shiffrin model of memory, short term memory refers to simple, temporary memory storage. In contrast, the subsequent conceptualization of working memory (WM) involves both temporary storage and mental manipulation of information (e.g. mental arithmetic). Prominent over that past few decades is the Baddeley Model of WM, which includes four major parts: the phonological loop, visuo-spatial sketch pad, central executive, and episodic buffer. Although other WM models exist, the Baddeley Model continues to prevail as a leading theory. Objective: To synthesize research on the cognitive psychology theory, functional neuroanatomy, and clinical relevance of WM, with particular emphasis on the most recent version of the Baddeley Model. Methods: Meta-analyses, reviews, theory papers, imaging literature, and clinical research were reviewed and synthesized. Results: Relevant neuroimaging studies are presented as related to each division of the Baddeley WM model. Functional imaging studies generally support this multicomponent model, with increasing attention on speech and fronto-parietal networks. Current assessment methods common to research and clinical practice for each division are briefly reviewed. Finally, working memory impairments in clinical evaluation are considered. Conclusion: Working memory capacity underlies many cognitive abilities and is essential for adaptive functioning. The Baddeley Model provides a way of conceptualizing this complex cognitive domain, and has generally been supported by cognitive and neuroimaging research. Working memory impairment should be assessed when neuropsychiatric disorders are implicated.

Background: Brain meningiomas are usually benign (noncancerous, slow growing); however, the presence of brain tumors can cause secondary injury related to swelling or effects of neurosurgery. When mass effects are seen in the frontal lobes, a variety of clinical sequelae may arise, including dysexecutive syndromes that can impair socio-emotional functioning but leave cognition relatively intact. In complex cases, evaluation by both neurology and neuropsychology can increase diagnostic understanding and treatment planning. The purpose of this case presentation is to compare evaluations from neurology and neuropsychology, in the context of supporting diagnostic work-up, on a complex post frontal meningioma resection case. Case History: The Veteran is a middle-aged White male with a history of substance dependence, personality pathology, depression, seizures, and “olfactory groove” meningioma removal. He initially presented to VA neurology for treatment of seizure disorder. Neurological examination was positive for disinhibition and irritability, but grossly normal otherwise. Neuropsychological testing revealed average performance in most domains with mild impairments in maintaining set, memory retrieval, and fine motor dexterity. Additional diagnostic work-up including abnormal head MRI, EEG, and sleep study are presented. Conclusions: Mass effect injury to the prefrontal cortex can lead to numerous complications, including dysexecutive syndromes, psychiatric issues, and neurological problems. This case is notable due to the presence of dysexecutive syndrome in the absence of severe cognitive impairments, the complications of psychiatric factors, and the presence of seizure disorder. The Veteran continues to be followed by neurology for seizure management, which has been stabilized with medication.

Background: Studies of handwriting in developmental disorders like Autism Spectrum Disorder (Duane et al, J Neuropsychiatry Clin Neurosci 2014), degenerative neurological disorders like Parkinson's Disease (Letanneux et al, Mov Disord 2014) and psychiatric disorders like Obsessive-Compulsive Disorder (Mavrogiorgou, et al J Neurol Neurosurg Psychiatry 2001), suggest distinctive changes in handwriting. Case History: Although digitized tablets offer the most precise measure of handwriting, we have found that the stop watch timed dictated written sentence “This is my writing” supplemented by the copied Archimedes Spiral with each hand offers a useful baseline of individuals followed longitudinally and between diagnostic groups of subjects. These are supplemented by the Oldfield (Neuropsychologica 1971) Laterality Quotient, a classification and still photo of writing hand and wrist posture (Duane et al, Ann Neurol 1994). In developmental disorders characterized by slow writing speed, the above offers a quantitative means by which students may be qualified for educational accomodation (Pokrajac et al, Ann Neurol 2012). Conclusions: The inclusion of a standardized timed handwriting sample is a useful addition to the neurological examination of children and adults with both neurological (developmental or acquired) and psychiatric disorders.

Background: Neuropsychiatric patients are at relatively high risk for suicide. Therapeutic risk management seeks to optimize patient safety via clinically sound suicide risk assessment and management delivered in a medicolegally informed fashion. But many clinicians working with neuropsychiatric patient populations are neither attuned to the elevated risk for suicide nor well-equipped to engage in suicide risk assessment and management. This situation leaves patients and providers vulnerable to poor outcomes. Objective: To explore methods for achieving therapeutic risk management of the neuropsychiatric patient. Methods: The Veterans Integrated Service Network (VISN) 19 Mental Illness Research, Education and Clinical Center (MIRECC) has developed a model for therapeutic risk management of the suicidal patient. That model is now reconsidered in the context of neuropsychiatric patients and their providers. Results: The model involves three essential components: augmenting clinical risk assessment with structured instruments; stratifying risk in terms of both severity and temporality; and developing and documenting a safety plan. Each of these components can be adapted to the needs of most neuropsychiatric patients. Minimal training will provide clinicians (including psychiatrists, neurologists, neuropsychologists, nurses, social workers, etc.) with the requisite skills and knowledge to deploy this model. Conclusion: The model presented provides concrete guidance on suicide risk assessment and management, involving components that are accessible to clinicians with even modest prior training and/or experience with suicidal patients. We propose that the VISN 19 MIRECC model may help to achieve therapeutic risk management of the neuropsychiatric patient.

Background: The potential for abuse of neuroimaging in brain injury litigation has been explicated in a number of preceding publications and presentations at the annual meeting of the American Neuropsychiatric Association. Unfortunately, such potential has been (and continues to be) realized, as clearly illustrated in the cases presented. Case History: Ongoing involvement in medicolegal consultation has provided ample opportunities to review neuroimaging studies submitted as “proof” of brain injury. However, critical review of such images in many instances clearly reveals grossly inaccurate neuroimaging interpretations and dubious medicolegal opinions attendant to such. Occurrences span various types of brain injury (e.g. traumatic, anoxic, toxic) and multiple neuroimaging modalities (e.g. MRI, DTI, fMRI, SPECT, and PET). The examples presented represent particularly egregious examples of neuroimaging abuse. Conclusion: The clinical and medicolegal utility of various forms of neuroimaging remains a controversial subject, especially in the area of acquired brain injury. Debate surrounding the scientific merit and feasibility of single-subject applications of such techniques to establish a historical brain injury event often detracts attention from an inescapable reality: neuroimaging is sometimes misrepresented to substantiate otherwise untenable medicolegal conclusions. This highlights the importance of ongoing vigilance regarding both the state of the science surrounding such claims more generally, as well as case-by-case analysis to ensure judicious applications on an individual basis.

Background: Cognitive deficits are common across neuropsychiatric disorders, and a primary cause of functional disability. Nevertheless, clinicians have limited therapeutic options to facilitate cognitive enhancement, particularly of executive functions. We present results from a multicenter clinical trial of epidural cortical stimulation in patients with Major Depressive Disorder (MDD). The initial dose determination algorithm revealed acute dose-dependent facilitation of working memory function, suggesting specific therapeutic targets for device-based interventions. Methods: Ten patients with recurrent MDD without psychotic features were enrolled. Electrodes were surgically implanted in the left DLPFC. In order to determine the stimulation parameters, an algorithm was used to assess changes in working memory, mood and anxiety as a function of parametric variations in current amplitude. The Paced Visual Serial Addition Task was used to assess working memory, and Visual Analog Scales for “Sadness” and “Anxiety”. Data were analyzed using repeated measures ANOVAs. Results: Patients tolerated the intervention well without significant side-effects. We observed a statistically significant relationship between current amplitude and working memory performance (p=0.020) and reaction times (p=0.035): higher current led to improved performance and reduced reaction times. We observed a nonsignificant trend for “sadness” and “anxiety”: higher current led to reduced scores for both. Conclusion: These data highlight the relevance of the left DLPFC as a therapeutic target for cognitive enhancement in neuropsychiatric populations. In addition, it confirms the capacity of brain stimulation to improve executive function in compromised patients. Similar strategies may be effective in other clinical populations with compromised cognition, possibly with noninvasive interventions.

Background: Functional neuroimaging of depressed patients who respond to psychotherapy have shown changes within areas of the prefrontal cortex and limbic system. The biological models of depression have implicated these areas in the neuropsychiatric symptoms of depression. Cognitive behavioral therapy and interpersonal psychotherapy are the two commonly studied evidence based psychotherapies in functional neuroimaging studies. Objective: The purpose of this exhibit is to synthesize recent evidence for changes in functional brain areas due to psychotherapy for major depression and to create teaching materials that present color-coded functional neuroanatomic maps of the brain areas involved. The application of this new understanding to the neuropsychiatric symptoms of depression will be emphasized. Methods: The relevant scientific literature was reviewed and synthesized for information related to functional neuroimaging of psychotherapy for major depression. Special focus was placed on evidence-based treatments (cognitive behavioral therapy and interpersonal psychotherapy). Results: Research supports that patients who respond to psychotherapy for major depression show several changes in functional brain imaging in the prefrontal cortex and limbic system. Changes in prefrontal activity have been observed in the dorsolateral and ventrolateral prefrontal cortex (DLPFC and VLPFC), the dorsolateral and ventrolateral medial prefrontal cortex (DMPFC and VMPFC), the orbitofrontal cortex (OFC), and the anterior cingulate cortex (ACC). Changes in the limbic system have been observed in the amygdala, hippocampus, and insula. Conclusions: Response to psychotherapy for major depression is associated with functional brain imaging changes within the prefrontal cortex and limbic system. The understanding of these changes gives insight to the neuropsychiatric symptoms of depression.

Background: There is increasing evidence both explicit and implicit biases can have detrimental effects on healthcare outcomes. Well established is that internalization of societal stigma creates a significant barrier to treatment utilization. Although less studied, clinician held biases can compromise quality of clinical care. Objective: To review and synthesize empirical evidence relevant to the occurrence, regulation and neurobiological correlates of explicit and implicit biases in the clinical context. Methods: The relevant scientific literature related to the cognitive, affective and functional neuroanatomical correlates of occurrence and regulation of bias was reviewed and synthesized, paying particular attention to implicit bias related to the stigma of mental illness and stereotypes. Results: Research indicates that both explicit and implicit biases affect clinical practice and treatment-seeking behavior in patients. Recent literature also supports the hypothesis that the context (e.g. perceived controllability of the stigmatized attribute) alters the regulatory response. For example, different neural networks are involved in the regulation of implicit bias based on whether or not an individual is considered responsible for his/her stigmatized attribute. Intervention strategies such as improving the clinician patient partnership, enhancing emotion regulation skills, and increasing executive control can be beneficial. Conclusions: Implicit and explicit biases affect treatment utilization across medical and psychological domains and may compromise clinical practice. Different neuroanatomical systems are implicated in the formation and regulation of bias depending on the context of the stigmatized attribute. A better understanding of these influences will assist clinicians in recognizing and diminishing negative effects in their clinical practice.

Background: β-amyloid (Aβ) status in older persons is associated with different trajectories of clinical decline. Objective: Determine variable(s) predicting a particular longitudinal trajectory by applying Classification and Regression Tree (CART) analysis to subpopulations identified using Growth Mixture Modeling (GMM). Methods: Healthy controls (N=325), early and late mild cognitive impairment (N=279; N=372 respectively), and Alzheimer’s Disease dementia (N=216) from ADNI-1/GO/2 using first-available Aβ measure- (CSF Aβ_1–42 or [¹¹C]PiB or [¹⁸F]florbetapir PET SUVR) as baseline and up to 24 months follow-up on Alzheimer’s Disease Assessment Scale–Cognitive (ADAS-Cog₁₃) and Functional Activities Questionnaire (FAQ) were analyzed using GMMs to define latent class trajectories. CART analysis discerned among baseline diagnosis, demographics, comorbidities, FAQ, amyloid and APOE4 allele status to best predict trajectory class membership. Results: GMMs found two trajectory classes each (C1/2) for amyloid-positive (P; N=722) and negative (N; N=470) groups. Most (90%) negatives were C2N with mild baseline ADAS-Cog₁₃ and normal FAQ showing essentially flat trajectory, whereas 10% were C1N with moderately impaired baseline FAQ and ADAS-Cog₁₃ with moderately steep trajectory. C1P (26%) had more impaired baseline FAQ and ADAS-Cog₁₃ than C2P (74%) with more steep trajectories in both. CART yielded 4 decision nodes (FAQ≥10.5, FAQ≥6.5, MMSE<26.5, Age≥75.5) in P and 1 node (FAQ≥6.5) in N groups, with 91.4% and 92.8% accuracy for class assignments, respectively. Conclusion: Most amyloid-negative patients did not decline while amyloid-positives did, more steeply with worse baseline function and cognition. CART predicted likely trajectory class with high accuracy using scales easily performed in the office.

Background: The frontotemporal lobar degeneration (FTLD) family of disorders includes a variety of clinical and genetic entities, including language, behavioral and motor variants. Parkinsonism is found in about 20%−30% of patients with FTLD but has received relatively little attention in the literature. Case history: A 23-year-old female began experiencing episodic problems of emotional lability, insomnia, difficulty eating and weight loss. She was treated with paroxetine, but symptoms progressed and she developed tremors, rigidity and slow gait. At age 24, she was admitted to a psychiatric hospital, diagnosed with catatonia and treated with a course of ECT with minor improvement. She progressed to needing 24-hour care at home. She was seen by a neurologist who diagnosed Hashimoto encephalopathy based on mildly elevated anti-TPO and antithyroglobulin antibodies and bilateral medial temporal lobes hyperintensity on MRI. IVIG, steroids, and plasmapheresis were attempted with no improvement. At age 25, the patient was admitted to the University of Chicago after impulsively grabbing a knife to harm herself. She had marked emotional lability, severe axial and appenticular rigidity, brisk reflexes, and choppy saccades. MRI evaluation revealed marked frontotemporal and subcortical atrophy. DaTSCAN showed severe bilateral nigrostriatal dopaminergic deficiency. A diagnosis of frontotemporal dementia with parkinsonism versus progressive supranuclear palsy was made. Conclusion: Our case is an illustration of the importance of considering FTLD spectrum disorders when behavioral disorders become progressive in nature - even in patients in their 20s.

Background: The mechanism of Obsessive Compulsive Disorder (OCD) involves aberration in the circuitry of the orbitofrontal cortex, limbic striatum and thalamus, specifically the mediodorsal nucleus. Here, we present a case of severe, treatment refractory obsessions and compulsions following a left medial thalamic infarct. Case History: A 24 year old male had a history of insulin dependent diabetes since age 14 and bipolar disorder type 1 since age 16 which was stable on ziprasidone. At age 19 he suffered a lacunar infarct of the left thalamus in the paramedian artery territory. A patent foramen ovale was discovered and repaired. Shortly after, the patient began to experience persistent, repetitive unwanted thoughts primarily related to doing unintentional harm or engaging in sexual acts with others. The related compulsions were to seek reassurance from his mother or engage in strenuous exercise. Symptoms escalated to yelling at or hitting strangers as well as seeking reassurance so frequently he could not function outside of the home. Neuropsychological testing demonstrated a dysexecutive and mild amnestic syndrome, consistent with injury to the mediodorsal nucleus and part of the anterior nucleus. His symptoms remain mostly refractory to numerous trials of high dose medication and augmentation strategies, but agitation has improved allowing patient to engage in some activity outside the house. Conclusions: While the role of the mediodorsal nucleus of the thalamus in OCD has been described, to our knowledge this is the first case report of a focal lacunar infarct of this area to induce an OCD-like syndrome.

Background: With an incidence of two to five per 100 million people, Gerstmann-Sträussler-Scheinker Disease is a rare, inherited form of prion disease. The disease commonly presents with ataxia and pyramidal signs followed by dementia. This patient’s presentation is unusual as it had prominent hypo-frontal symptoms and aphasia. Case History: 51-year-old Latino male with a history of hypertension and glaucoma was admitted to neurology for a progressive decline in cognitive functioning and bizarre behaviors. In the months leading up to hospitalization, the patient developed topographical disorientation as well as positive and negative visual hallucinations. He became impulsive and hypersexual eventually developing apraxia and autoprosopagnosia. His family noted his posture became more stooped and he began falling. On exam, the patient was stimulus bound, demonstrated a loss of autobiographical memory, and had frontal release signs. MRI showed generalized atrophy and a small right posterior fossa arachnoid cyst. EEG demonstrated periodic lateralized epileptiform discharges in the right frontal-temporal area. Speech pathology evaluation confirmed transcortical sensory aphasia. Neuropsychological testing showed significant inattention, as well as dysexecutive, perseverative, and stimulus bound behaviors suggestive of marked frontal systems dysfunction. CSF showed significantly elevated tau and normal 14–3-3. Genetic testing later revealed the presence of the A117V mutation in the prion protein gene, linked to Gerstmann-Sträussler-Scheinker disease. Conclusions: This case is significant because it represents an atypical presentation of Gerstmann-Sträussler-Scheinker disease. His most prominent symptoms – impulsivity, hypersexuality and aphasia – are unusual for this particular mutation.

Background: C9orf72 frontotemporal dementia (FTD) is a neurodegenerative disease that causes various neuropsychiatric manifestations. An association between FTD and catatonia as well as between FTD and autoimmune disease has been noted previously, however, improvement in mental status with intravenous immunoglobulin (IVIG) in this setting has not been reported in the literature. Antirecoverin antibody is most commonly associated with cancer-associated retinopathy in patients with small cell lung cancer. There have been no prior reports of association with either catatonia or FTD. Case History: A 55-year-old male with hypertension, diabetes mellitus, and bipolar disorder was transferred for subacute changes in mental status and severe rigidity of unknown etiology. The clinical presentation was consistent with catatonia, for which the etiology was initially unclear. His symptoms persisted despite correction of electrolyte abnormalities and treatment of underlying infections. A trial of intravenous lorazepam was not tolerated due to respiratory depression. MRI of the brain showed ring-enhancing cerebellar mass showing necrosis on biopsy. Genetic testing for FTD was positive for C9orf72 hexaneucleotide expansion. The patient’s serum paraneoplastic panel revealed antirecoverin antibodies. CT of the chest, abdomen, and pelvis did not suggest an underlying malignancy, and neuro-ophthalmological testing did not reveal retinopathy. Following treatment with intravenous immunoglobulin, catatonia resolved and the patient’s mental status improved significantly. Conclusions: The rapid improvement of mental status with IVIG suggests an underlying autoimmune etiology of catatonia. Given the association between FTD and autoimmune disorders, the C9orf72 hexanucleotide expansion may lead to inflammation responsible for auto-antibody production and inflammation induced catatonia.

Background: Correlating clinical phenotype to underlying neuropathology is a necessary but challenging practice in the diagnosis of non-Alzheimer’s disease (AD) dementias. This is particularly challenging in Primary Progressive Aphasia (PPA)/Frontotemporal Dementia (FTD)-spectrum disorders given evolving symptoms, the heterogeneity of possible underlying non-Alzheimer’s pathologies, and the absence of biomarkers that detect these pathologies during life. Case History: Patients with PPA can ultimately show underlying non-Alzheimer’s tauopathy, including Pick’s disease (frontotemporal lobar degeneration; FTLD-tau), Progressive Supranuclear Palsy (PSP), or Corticobasal Degeneration (CBD). In CBD and PSP, motor symptoms consistent with the underlying pathology often emerge. Patients with corticobasal syndrome (CBS) can show a variety of pathologies including CBD, PSP, FTLD, or AD. We present two non-Alzheimer’s cases followed extensively until death. In both cases, CSF AD biomarkers (Aβ42, T-tau, P-tau181) were inconsistent with Alzheimer’s pathology. Case 1 (right-handed, onset=age 66) had a ?5-year history of an atypical form of Wernicke-like PPA with right>left atrophy in lateral temporal cortex, later developing behavioral symptoms, with symmetric parkinsonism emerging one year before death. Autopsy demonstrated CBD pathology. Case 2 (right-handed, onset=age 48) had a ?10-year history of classic CBS, with perirolandic hypometabolism and atrophy. Behavioral symptoms and semantic impairment developed late in course. Autopsy demonstrated Pick’s disease (FTLD-tau). Conclusions: These two well-characterized cases that show postmortem FTLD-tau pathology illustrate currently unclassifiable cases that contradict typical rules-of-thumb when clinicians attempt to predict pathology in patients during life. Sensitive biomarkers that employ tau-PET imaging or CSF may be critical for early detection and treatment of FTLD-tau-spectrum disorders.

Background: Down syndrome (DS), a chromosome 21 trisomy, is associated with early onset Alzheimer’s-type dementia and seizures. The interplay between seizures, cognitive decline and DS remains poorly understood. In Alzheimer’s disease (AD) patients without DS, seizures are associated with more severe cognitive impairment. As of yet, no study has characterized the effect of seizures on cognition, behavior and neuropsychiatric symptoms in DS patients. Objective: To compare the neuropsychiatric, cognitive and behavioral features of DS patients with dementia and seizures to those without seizures. Methods: We identified patients seen at Massachusetts General Hospital (MGH) in Boston, Massachusetts with a diagnosis of DS and dementia over the age of 35. We conducted a retrospective electronic chart review and collected information on premorbid IQ, neuropsychological testing when available, temporal onset of dementia, age of seizure onset and characterization of seizures, mood and anxiety disorders, agitation and psychoactive medication use. Results: We analyzed records for 346 DS patients over the age of 35 with dementia. We dichotomized patients into those with seizures (N=90) and without (N=256). For group comparison, we used independent samples t tests and analyzed neuropsychiatric features between groups. Conclusion: Differentiating the neuropsychiatric features of DS patients with dementia and with and without seizures raises important questions about the genesis and consequence of epileptiform activity in this unique population. This work also provides important prognostic information for patients and families, gaining insight into the complex interaction between DS, seizures and cognitive decline.

Background: The Primary Progressive Aphasias (PPA) are neurodegenerative syndromes that target language networks. While neuropsychiatric symptoms often accompany language impairment in PPA, factors predicting emergence and progression of these symptoms remain elusive. Objective: To identify clinical and imaging predictors of neuropsychiatric symptoms in PPA across the three major variants. Methods: The sample included 44 PPA patients: 15 agrammatic/nonfluent (PPA-G), 13 semantic (PPA-S), 9 logopenic (PPA-L), and 7 other (PPA-O) variants. Baseline cortical thickness measures were available in 37 patients. All patients had serial Neuropsychiatric Inventory Questionnaires (NPI-Q) completed by informants over a 4-year period of follow-up. Results: Mean baseline NPI-Q scores were highest for PPA-S patients (7.5) compared with PPA-G (3.2), PPA-L (2.3) and PPA-O (3.7). Higher baseline NPI-Q scores predicted greater increase in NPI-Q scores over time (p<0.038). Greater baseline cortical atrophy in PPA-vulnerable regions predicted greater increase in NPI-Q scores over time (p<0.003). Conclusion: In our cohort of PPA patients, more prominent baseline neuropsychiatric symptoms and greater cortical atrophy in PPA-vulnerable regions were predictors of a worse neuropsychiatric prognosis.

Background: The SIRS is a clinician-rated structured interview that assesses impairment in daily social interactions. Previous work has shown SIRS ratings relate to atrophy in three distinct neural networks subserving socio-affective function in FTD. Schizophrenia is another disorder characterized by prominent social disturbances, but we do not yet have a clear understanding of the component processes and neural correlates of these impairments. Objective: We asked whether SIRS ratings in schizophrenia relate to atrophy in the same corticolimbic networks as in FTD and whether they are associated with lab-based tasks measuring social impairment. Methods: We administered SIRS to 15 schizophrenia patients, 5 FTD patients, and 9 controls. MRI-derived cortical thickness for the three neural networks was measured. The Faux Pas and Reading the Mind in the Eyes tests were administered. Results: Consistent with prior findings in FTD, atrophy within the aversion and perceptual networks correlated with higher ratings (i.e. more impairment) in the “inappropriate trust or approach behavior” and “lack of attention to social cues” SIRS domains, respectively, across all patients. These relationships were still present when the analysis included only schizophrenia patients. Ratings on these two SIRS domains also correlated with impairment on the Faux Pas test in schizophrenia patients. Conclusion: The association between SIRS ratings and the Faux Pas test further validates SIRS as a measure of component processes of social impairment. SIRS ratings in schizophrenia relate to atrophy in the same corticolimbic networks as in FTD, suggesting that this structural-behavioral relationship is present in a range of neuropsychiatric disorders displaying social impairment.

Background: It is rare for cotwins to suffer discordant neuropsychiatric disorders. Studying such twin pairs may provide a window into genetic and epigenetic mechanisms resulting in the differing phenotypes, and the phenotypes may provide insight into the underlying neurobiology of the respective disorders. This report presents a novel twin pair who as young adults developed catatonia (in the absence of schizophrenia or mood disorder) and bipolar disorder, respectively. Case Report: There are a few reports of cotwins suffering discordant neuropsychiatric conditions. This female twin pair was born prematurely at 33 weeks and by age 3 and 1/2 were suffering EEG-documented temporal lobe seizures requiring anticonvulsant treatment.

Cotwin A: Within a few months of being weaned from her carbamazepine at age 17, this twin suffered a very acute and severe manic episode which promptly resolved with treatment with parenteral aripirazole and subsequent maintenance treatment with carbamazepine. She subsequently suffered syndromal depressive episodes.

Cotwin B: Within a year of her sister’s episode, she developed delirium and catatonia. EEG revealed temporal lobe seizure activity and she was treated with levetiracetam. She was subsequently successfully treated with electroconvulsive therapy which was followed with maintenance valproate. Laboratory data, neurologic exam, cranial MRI and CT, EEG and LP results will be presented.

Conclusions: It is likely that the illnesses described are related to the mesial temporal lobe sclerosis and epilepsy. The illnesses are discordant; the twin with catatonia suffered neither schizophrenia nor a mood disorder. The hypothesis that both illness converge on cortico-striatal-cortico loops is discussed.

Background: Mental disorders are common worldwide and are considered to be of Public Health importance in the United States. Objective: This study aims to identify genes that may be associated with Mental Disorders. Subjects: 1899 patients sampled from a database from 60 Clinical Research Sites in the US were included in this study. Mean age 51.0 (S.D. 31.4), Males 40.8%. Subjects were divided into groups with or without mental disorders as defined by ICD9 codes 290–319. Methods: Subjects were genotyped with the proprietary Proove Narcotic Risk Genetics Profile using TaqMan SNP genotyping assays (Life Technologies, Carlsbad, CA). A panel of 12 SNPs (DRD1 -48A>G, DRD2 A1 allele, DRD4 -521C/T, DAT1, COMT Vall58Met, OPRK1 36G>T, OPRM1 A118G, DBH -1021 C/T, 5-HT2A -1438G/A, 5-HTTLPR, 1519T>C (gamma-aminobutyric acid (GABA)A receptor, gamma 2 GABRG2), and MTHFR C677T). Results: Analyses was done using SNPstats ® and JMP ®11 software. 5-HT2A 1438 G/A (rs7997012) was the only SNP with significant association (p=0.0408, crude model, GG versus GA versus AA). However, the over-dominant model, G/G-A/A versus G/A, was most significant and Correspondence analysis shows that the G/G and A/A variations are more associated with the presence of Mental Disorders compared with the G/A [p=0.013, OR=1.26 (C.I. 1.053–1.515)]. Conclusion: This study aligns with existing literatures that genetics may play a role in the expression of Mental Disorders. From this study, 5HT2a heterozygous disadvantage may play a role in Mental Disorders. This study will hopefully provide useful insight into the role of genes in Mental Disorders.

Background: Several previous studies have found evidence for abnormalities of brain structure in Tourette syndrome (TS), most samples were small. Objective: Study brain structure in children and adolescents with TS in a pilot multicenter MRI study. Methods: Existing and newly-acquired T1-weighted MP-RAGE images were used to create gray matter (GM) and white matter (WM) volume images from 103 children age 7–17 with a chronic tic disorder and 103 control children matched 1:1 for age (within 0.5 year), sex and handedness. General linear models with GM and WM volume as dependent variables were computed at each voxel, with diagnostic group, MRI sequence, and sex as factors, age as a covariate, and group×sex and sex×age interactions, with proportional scaling by each subject’s total brain GM+WM volume. Significance was corrected for multiple comparisons with a cluster-level False Discovery Rate of 0.05. Results: The TS group had greater GM volume in posterior thalamus (p=0.001) and in hypothalamus and midbrain (p=0.011). The TS group had lower WM volume bilaterally in orbital prefrontal cortex and anterior cingulate (left, p=0.001; right, p=0.001; all p values corrected). Internal evidence suggests that these findings are not caused by differences in clinical or MRI methods across sites. Preliminary results show no association of the results with IQ or ADHD. Conclusion: This is one of the largest neuroimaging studies in TS. The WM findings are consistent with a large previous study that found orbital cortex volume was lower by ∼5% in boys with TS.

Background. Tourette syndrome (TS) is a neurodevelopmental disorder characterized by multiple motor and vocal tics. Psychiatric comorbidity is common and includes obsessive-compulsive disorder, attention-deficit and hyperactivity disorder, depression and anxiety. Although TS has been consistently shown to affect quality of life, little is known about the relationship between TS, social status and occupation. Objective. We set out to conduct an exploratory study to investigate the association between TS and socioeconomic class. Methods. A clinical sample of 137 adult patients with TS was assessed for TS-related variables (both tic severity ratings and psychiatric comorbidity) and socioeconomic class (categorised according to the Office for National Statistics classification system). Results. We found no significant difference in socioeconomic class distribution between patients with TS and psychiatric comorbidity (‘TS plus’, N=88) and patients with uncomplicated TS (‘pure TS’, N=49) (P=0.205). Both clinician- and patient-reported tic severity ratings were significantly higher among unemployed patients compared with patients in the highest socioeconomic class (P=0.004 and P<0.001, respectively). Conclusion. These findings suggest that tic severity per se can have a significant impact on the position within social hierarchy and prompt further research into the complex relationship between TS and socioeconomic class.

Background: Urinary incontinence is listed as a sign of catatonia in current psychiatric nosology. However, it is observed in pediatric populations with catatonia, particularly those with neurodevelopmental disorders (1–3). Urinary incontinence occurring in adults with catatonia is not described. Objective: To characterize incontinence occurring in a sample of adult patients with catatonia. Methods: We present a case-series of 12 patients (age≥16y) admitted to a general hospital where they were identified by psychiatry consultants as having catatonia and urinary incontinence. Results: All patients met diagnostic criteria for catatonia, with pretreatment Bush Francis Catatonia Rating Scale scores ranging from 14 to 27 and all patients demonstrating a positive lorazepam challenge. Ten (83%) patients were able to ambulate and void independently. Nine (75%) patients had no active, genitourinary condition. Seven (58%) patients had a comorbid encephalopathy or intellectual disability. Neuropsychiatric diagnoses varied, and all but one patient had recent exposure to antipsychotic medication. In all cases, the catatonia resolved with treatment. In ten (83%) cases the urinary incontinence resolved coincident with resolution of other typical catatonic signs and symptoms. Conclusion: Urinary incontinence is seen in association with catatonia in adult inpatients, including those whose incontinence cannot be attributed to cognitive impairment, immobility, or a primary genitourinary condition. When associated with catatonia, urinary incontinence may resolve with treatments known to be effective for catatonia, an observation supporting the vagal theory of catatonia (4). Delivering safe and effective catatonia treatment may obviate the risks of iatrogenesis associated with urinary catheterization.

Cohen D: Towards a valid nosography and psychopathology of catatonia in children and adolescents. Int Rev Neurobiol 2006; 72:131–147

Dhossche DM, Bouman NH: Catatonia in an adolescent with Prader-Willi syndrome. Ann Clin Psychiatry 1997; 9:247–253

Dhossche D: Autonomic dysfunction in catatonia in autism: implications of a vagal theory. Autism 2012; 2:e114

Wing L, Shah A: Catatonia in autistic spectrum disorders. Br J Psychiatry 2000; 176:357–362

Background: The neuropsychiatric condition Tourette syndrome (TS) frequently involves complex tics with social relevance, including echophenomena (i.e. tics involving imitation) and socially inappropriate behaviors. Recent studies have indicated that these patients can exhibit subtle reasoning differences on tasks involving theory of mind (ToM): the ability to reason about mental states. Objective: We investigated the neural correlates of mentalizing in TS. Methods: Twenty-five adults with TS (but no comorbid disorders) and twenty-five healthy controls underwent fMRI during an established ToM false-belief paradigm. Patients and controls were matched for age and gender and neuropsychological profiles were similar. Tic symptoms, premonitory urges, echophenomena, impulsive and obsessive-compulsive behaviors were assessed for covariate analysis. Results: There were no group differences in behavioral performance on the false-belief task. However, when contrasting neural activation across mentalizing and nonmentalizing conditions and comparing the two groups, patients with TS exhibited abnormalities of up and down-regulation of key nodes within the mentalizing network, including right temporo-parietal junction, right amygdala bordering the temporal pole, and posterior cingulate cortex. Group comparisons collapsed across conditions revealed additional activation differences in the inferior parietal region, part of the human mirror neuron system. In TS, inferior parietal activation covaried with a measure of echophenomena. Conclusion: The observed pattern of altered activation within the mentalizing network may reflect a functional neural biomarker specific to TS, which could underpin the reported differences in reasoning about ToM, and perhaps socially inappropriate behaviors. Furthermore, our findings highlight dysfunction within the mirror neuron system as the likely mechanism driving echophenomena.

Background: Patients with systemic lupus erythematosus commonly develop neuropsychiatric manifestations. Catatonia was not included in the standardized nomenclature of neuropsychiatric lupus syndromes developed by the American College of Rheumatology. Cases of refractory neuropsychiatric lupus and catatonia treated with electroconvulsive therapy have been infrequently reported in the literature. Recommendations as to the indications and frequency of electroconvulsive therapy in these patients are lacking. We present a case of severe malignant catatonia in a patient with neuropsychiatric lupus refractory to high dose benzodiazepines and immunosuppressants that dramatically improved with daily electroconvulsive therapy. Case History: The patient is a 19 year old female with a history of systemic lupus erythematosus and no past psychiatric history who was initially admitted for acute psychosis that resolved with intravenous methylprednisolone. One week later, she presented in an acute confusional state that progressed to severe mutism, rigidity, and dysautonomia requiring intubation in the intensive care unit. Cerebrospinal fluid analysis, magnetic resonance imaging and electroencephalograms were unremarkable. The catatonia and dysautonomia progressed despite a midazolam drip and immunosuppressants. Following a seven day course of daily bilateral electroconvulsive therapy, the dysautonomia and catatonic symptoms improved, allowing for extubation and discontinuation of benzodiazepines. The patient completed a course of physical rehabilitation and did not show signs of catatonia five months post discharge. Conclusion: This case demonstrates that catatonia can be a severe manifestation of neuropsychiatric systemic lupus erythematosus. Daily bilateral electroconvulsive therapy may be considered for patients with life threatening malignant catatonia refractory to high dose benzodiazapines and immunosuppressants.

Background: Cotard’s syndrome is a rare delusion involving the nihilistic denial of the self. It has been reported to occur in multiple neuropsychiatric conditions. The mechanisms of Cotard’s Syndrome are unclear. However, it has been hypothesized to be related to other misidentification syndromes, where the perception of self and familiar persons is altered. Case History: We present a patient with a long history of uncontrolled complex partial seizures with secondary generalization, who has required inpatient psychiatric hospitalizations for nihilistic and Capgras delusions in the context of postictal psychotic depression. She has also been seen as an outpatient for interictal depressive and fluctuating dissociative symptoms. She has been followed for many years, with multiple electrophysiological studies demonstrating generalized slowing and sharp waves in the left anterior temporal areas, temporal slowing on the right, and occasional frontal slowing. Additional MRI, SPECT, and mental status exam findings will be discussed in relation to the patient’s presentation. Conclusion: Cotard’s syndrome has been uncommonly reported in epilepsy, and the mechanisms are currently unknown. It has been postulated to be related to depersonalization and other misidentification syndromes. In this case, denial of the existence of the self, dissociative symptoms, and delusional misidentification may have been a result of abnormalities in the limbic, frontal, and parietal circuitry involved in self monitoring and the perception of familiarity.

Background: Zolpidem, a selective GABA-A agonist, temporarily improves consciousness in about 5% of patients in vegetative and minimally conscious states (VS and MCS, respectively). Two controlled trials failed to identify predictors of this response. GABA-A agonists also are first-line treatments of catatonia, the features of which overlap with those of VS and MCS. ”Catatonic features” (CF) in patients with VS and MCS therefore may predict response to zolpidem. Case History: Three individuals with disorders of consciousness (DOC) were assessed using the 23-item Bush-Francis Catatonia Scale (BFCS) and their zolpidem responses reviewed. Case 1: a teenage patient with severe traumatic brain injury presented with MCS; CF included immobility/stupor, staring, posturing, rigidity, grimacing, dysautonomia (BFCRS=10). Zolpidem produced temporary emergence from MCS and reduced CF. Case 2: a middle-aged man with multiple strokes presented in MCS; CF included immobility/stupor, staring, and stereotypy (BFCRS=5). Zolpidem produced no appreciable changes in MCS or CF. Case 3: a middle-aged man with hypoxic-ischemic brain injury presented in MCS; CF included immobility/stupor, mutism, staring, posturing, grimacing, rigidity, negativism, gegenhalten, grasp, and dysautonomia (BFCRS=23). Zolpidem, and subsequently lorazepam, administration produced temporary improvement in MCS and reduced CF. Conclusions: In this case series, the presence of posturing, rigidity, and dysautonomia distinguished the two GABA-A agonist responders from the nonresponder. This observation suggests the possibility that evaluation of persons with DOC for these CF may enhance identification of zolpidem responders. Further evaluation of CF as predictors of GABA-A agonist response in this population are needed.

Background: Catatonia is a clinical state attributed to a variety of psychiatric and general medical conditions (GMCs). Objective: To investigate the underlying causes and evaluations completed in cases of catatonia. Our hypotheses are that cases of catatonia attributed to psychiatric causes receive significantly less medical workup, and have higher incidence of past psychiatric history. Methods: A retrospective chart review of adult inpatients at the University of Chicago from January 2011 to December 2013 was conducted. 172 charts including the term “catatonia” or “catatonic” were identified and reviewed, and 39 cases of catatonia were found. Results: 19 cases of catatonia were due to GMC. Underlying causes included hyponatremia, infections, intoxications, seizures, normal pressure hydrocephalus, and limbic encephalitis. Z-tests were used to compare proportions. On the medical floor, a GMC was identified in 17/20 cases compared with 2/19 cases in the ER (where most patients were transferred directly to a psychiatric hospital) (p<0.01). Cases of catatonia attributed to psychiatric etiology had more past psychiatric personal (15/20 versus 9/19, p<0.05) and family history (8/12 versus 4/14, p<0.05), and received less workup than GMC cases: brain imaging (10/20 versus 17/19, p<0.01), EEG (3/20 versus 10/19, p<0.01), and CSF evaluation (0/20 versus 3/19, p<0.05). Conclusion: In our sample, a GMC was frequently found to explain catatonia on the medical floors. When catatonia is attributed to a psychiatric cause, it is often in the absence of a medical workup. There is a need for standardization of the medical workup of catatonia.

Background: Disorders of perception comprise some of the most important and complex phenomena encountered in psychiatric assessment. Perceptual disturbances, particularly hallucinations, are usually but not always characteristic of psychiatric disorders such as schizophrenia and delirium.

Charles Bonnet Syndrome is a disorder characterized by complex visual hallucinations with insight, not accompanied by psychotic symptoms, usually observed in elderly patients with an acquired impairment of vision

Case History: This is an 84 year old male with a past medical history of recent stroke who presented to ER with complaints of visual hallucinations. He reported seeing people who are 7–8 feet in height and tiny people running around the house, sticking their heads out of the curtain, seeing old cars flying in front of him. The figures did not talk to him. He reported that he knows that these people did not exist. He did not report auditory hallucinations, delusions, or any other psychotic symptoms. Right lower extremity showed mild weakness and up going plantar reflex. Neurological findings were suggestive of left occipital lobe infarct. CT head was within normal limits. MRI of the brain was not obtained since the patient had a pacemaker.

Psychiatry was consulted for evaluation of Visual Hallucinations and he was diagnosed with Charles Bonnet Syndrome.

Conclusion: Complex Visual Hallucinations has been associated with organic brain disease and our case is consistent with CBS. The consultation liaison Psychiatrist can assist with work up of possible etiologies, thereby preventing the mismanagement of elderly patients presenting with visual hallucinations.

Background: Acute Disseminated Encephalomyelitis (ADEM) is an autoimmune inflammatory disease of the central nervous system (CNS), is characterized by diffuse or multifocal demyelination with corresponding neurological findings localizable to the observed CNS lesions, and is most commonly observed as a sequela of preceding viral infections or vaccinations. ADEM occurs at a rate of 0.4–0.8 per 100,000, with the vast majority of patients under age 10. Adult onset ADEM patients represent a minority of an already rare population, and while the prognosis of ADEM is considered to be generally favorable with the majority of cases achieving full recovery in 1–6 months, prognosis in adults is less favorable with reports of as few as 15% of patients achieving full recovery. Case History: The patient is a 34 y/o male who received a Flumist vaccine and subsequently developed mental status changes with elevated intracranial pressure leading to coma. Upon waking the patient was discovered to have profound deficits in cognition, motor function, and speech. After medical stabilization he underwent intensive inpatient rehabilitation at multiple institutions for continuing residual deficits. At 9 months after initial presentation he continued to demonstrate persistent cognitive and language deficits. Conclusions: This case illustrates not only a rare adult onset case of ADEM, but also is in accordance with a trend in the literature to note both increased severity of illness in adult patients with ADEM and also the lack of complete cognitive recovery after medical stabilization and discharge from the hospital.

Background: Cerebellar cognitive affective syndrome is only more recently recognized in literature. Lesions of the cerebellar vermis have been associated with a primarily affective presentation, and lesions of the posterior lobe have been associated with a primarily cognitive presentation. Case History: We present a case of a 51-year-old Caucasian female with a vague past psychiatric history of unstable mood who initially presented due to a left cerebellar infarct. MRI demonstrated small focal areas of restricted diffusion within the posterior left cerebellar hemisphere. She was discharged on Depakote for headache prophylaxis. She represented 24 hours following her discharge due to altered mental status. The patient displayed new onset disorientation, behavioral disinhibition, and cognitive difficulties, in addition to impaired fine motor coordination. The patient was started on IV methylprednisololone, with some improvement in her disinhibited behaviors and dysexecutive functioning. The patient was discharged on an oral methylprednisolone taper. She was evaluated by neuropsychology fourteen days after discharge. She displayed significant improvement in her disinhibited behaviors. She showed some progress in her neurocognitive function, but continued to display notable deficits in attention and had poor processing speed. Conclusion: The case demonstrates a mixed affective and cognitive syndrome due to a posterior cerebellar stroke. In addition, the case highlights the potentially transient nature of the syndrome, as well as improvement with treatment, with some residual symptoms 2 weeks after the initial effects.

Schmahmann JD, Sherman JC: The cerebellar cognitive affective syndrome. Brain 1998; 121:561–579

Background: Wernicke-Korsakoff syndrome is the result of thiamine deficiency. Wernicke encephalopathy represents the acute presentation of ataxia, confusion, and eye movement abnormalities, and Korsakoff syndrome represents chronic cognitive impairment with anterograde amnesia. This case demonstrates Korsakoff dementia in a patient with no history of alcohol use and only mild preceding Wernicke encephalopathy. Case History: A 55-year-old woman without significant previous psychiatric or substance history developed moderate depression, during which she restricted her diet to liquids which were not nutritionally balanced. She lost 69 pounds; her husband also noted eye movement abnormalities and gait imbalance. Upon admission to the hospital for dehydration, her ambulation, memory, and cognition were reportedly normal. After being started on IV fluids, she became more ataxic and developed significantly impaired cognition. Evaluation in the office demonstrates a dense anterograde amnesia without clear confabulation. Rehabilitation efforts over the past several months have had limited success. MRI of the spine and brain, EEG, EMG and multiple labs do not indicate a clear etiology of symptoms. Neuropsychological assessment is currently pending. Conclusions: This case demonstrates Wernicke-Korsakoff syndrome which has developed independent of alcohol use. This patient’s poor nutritional status was not appreciated prior to refeeding, resulting in catastrophic neurological consequences. Awareness of Wernicke-Korsakoff occurring outside the context of alcohol use is vital for preventing long-term cognitive damage in patients.

Background: Progressive Supranuclear Palsy is a “Parkinson's Plus” syndrome of progressive degeneration of basal ganglia, brainstem, cerebellum, and cortex, typically presenting with balance and gait impairment. Supranuclear ophthalmoplegia is pathognomonic for the disease. Case History: A 72-year-old Caucasian woman presents to movement disorders with 2 year history of imbalance and rigidity following a fall with foot fracture. She had a poorly-characterized history of possible polio as a child and was diagnosed with postpolio syndrome prior to presentation to our clinic. She also reported disabling dizziness. Extraocular movements were intact at that time, with some mild reported short term memory impairments. Patient was referred to Otoneurology; vestibular testing was suggestive of a global cerebral degenerative disorder affecting brainstem and cerebellar pathways. She underwent lumbar puncture which showed no acute inflammation, essentially normal tau, amyloid, and beta results. She was seen by Neuropsychiatry two years after initial presentation and demonstrated reactive depression as well as impaired memory and dysexecutive symptoms. Neuropsychological testing revealed impairments in working memory, visual perception, attention, and executive function, along with decreased blink rate and very limited movement of the eyes and head during the examination. Neuroöphthalmology evaluation contemporaneously showed vertical gaze paresis, upgaze and downgaze, consistent with PSP. Conclusion: This case demonstrates a delayed recognition of PSP initially presenting with imbalance and vertigo. Recognition was complicated by vague history of postpolio syndrome and delayed demonstration of gaze paresis. In retrospect, vestibular test findings could have given more weight to a PSP diagnosis.

Background: Neurological insults may lead to psychiatric, behavioral and physical sequelae. Careful neuropsychiatric examination is imperative to identify reversible causes. Case History: The patient is a 55 year-old married, self-employed, Hispanic man with a history of hypertension, alcohol use, and unspecified anxiety, who underwent a transphenoidal resection of a pituitary adenoma, with complications of CSF leakage, Klebsiella UTI, and S. pneumoniae meningitis. Evident neurosequelae included agitation, confusion, bilateral hearing loss, aphasic speech, and unsteady gait. A psychiatry consultation was requested 2 weeks after surgery to assist with agitation management.

Upon initial presentation, the patient was in restraints, inattentive, shouting random words, and was unable to cooperate with interview. The diagnosis was acute delirium. Multiple etiologies were identified: status-post surgery, infections (meningitis, recurrent UTIs), sensory deprivation, and polypharmacy (concomitant use of multiple antipsychotics, opioids, benzodiazepines, steroids, and anticholinergic medications). EEG showed generalized diffuse slowing. Brain CT scan showed a hypodensity at the medial aspect of bilateral anterior temporal lobes, while brain MRI suggested diffuse meningeal disease affecting left frontal lobe and bilateral cerebellar hemispheres.

After 2 months follow-up, successful treatment ultimately involved monotherapy trial with an atypical antipsychotic, quetiapine, combined with valproic acid. Sedation and dizziness were prominent side effects. Akathisia responded to propranolol.

Conclusions: This case widens the clinical spectrum of delirium in complicated neurosurgical patients. Atypical antipsychotics were effective to manage multifactorial delirium, although side effects were prominent, requiring careful monitoring. It is critical to early identify and treat delirium to minimize poor outcomes and prolonged hospital stay.

Background: Susac Syndrome is characterized by the clinical triad of encephalopathy, branch retinal artery occlusion, and sensorineural hearing loss. An autoimmune endotheliopathy affecting microvessels of the brain, retina, and cochlea has been implicated. Neuropsychiatric symptoms include confusion, memory loss, dysarthria, mood and personality change, and bizarre behavior. These symptoms may dominate the clinical presentation, and obscure severe headaches which may be a major presenting feature of encephalopathy. We illustrate a patient with Susac Syndrome treated in the hospital setting with severe neuropsychosis intractable to antipsychotics. After recognition and treatment of his headache, his agitation subsided and was able to be discharged. Case History: A 34 year old male with Susac Syndrome was readmitted to the hospital with worsening encephalopathy. Medications on admission included Seroquel, Trazadone, Ativan, and Cellcept. His agitation, combativeness, and episodes of shouting and moaning prevented adequate communication. Psychiatry was consulted and recommended increasing Seroquel and adding Haldol, which did not improve his symptoms. Recognizing he would often hold his head, untreated headaches were thought to be the cause of his neuropsychosis. Subsequently, Toradol was administered and his agitation improved. He was ultimately discharged on Seroquel 50mg TID for agitation. Conclusion: Untreated headache should be considered in Susac patients with persistent neuropsychosis. Early recognition and treatment of headache in the hospital setting may prevent the use of unneeded medications. Although immunosuppressive therapy remains the mainstay for treatment, these medications may take time for a clinical response. Treatment guidelines for the acute neuropsychiatric manifestations of Susac Syndrome may be warranted.

Background: Lyme disease affects greater than 20,000 people every year in the United States. Up to 40% of patients with Lyme disease develop disorders of the peripheral or central nervous system (CNS), the latter causing both neurological and psychiatric manifestations.

A varied range of psychiatric conditions have been associated with Lyme disease including paranoia, dementia, schizophrenia, bipolar disorder, panic attacks, major depression, anorexia nervosa, and obsessive-compulsive disorder. The authors present the case of a man with delusional disorder in the aftermath of a diagnosis of Lyme disease.

Case Report: A 55 year old Caucasian male with past history of Lyme disease was admitted to the neurology unit with seizures. Psychiatry was consulted for his delusional and paranoid behavior. On psychiatric evaluation the patient stated that he was the victim of a conspiracy by the US government, who had created the serum for Lyme disease to eradicate enemies. He reported that his brain was destroyed by the spirochetes resulting in seizures. He refused treatment stating that he only needed to be treated with the antidote to the Lyme serum. Collateral history from the family revealed that the patient had been obsessed with his Lyme disease since it was detected and became delusional after developing seizure episodes. He responded to treatment with low dose antipsychotic and antiepileptic medication. Conclusion: Our case illustrates that late stage Lyme disease can present as a delusional disorder.Studies on Lyme disease have described a staging of psychiatric symptoms, with depression occurring in early CNS disease and mood and psychotic disorders occurring in late-stage of the disease. Neurologist and psychiatrist should work as a team to aid early diagnosis and efficacious treatment of patients suffering from the disease.

1. Fallon BA, Nields JA: Lyme disease: a neuropsychiatric illness. Am J Psychiatry 1994; 151:1571–1583

2. Hájek T, Pasková B, Janovská D, et al: Higher prevalence of antibodies to Borrelia burgdorferi in psychiatric patients than in healthy subjects. Am J Psychiatry 2002; 159:297–301

Background: Depression is common after stroke and is associated with suboptimal rehabilitation outcomes and reduced quality of life. Early studies suggested a greater prevalence of poststroke depression (PSD) with left-sided and left anterior lesions, though more recent studies have not supported this finding beyond 3 months poststroke. Poststroke mania and bipolar disorder are distinctly less common than PSD and are typically associated with right-sided lesions. Unlike the findings of left laterality and PSD, the association of poststroke mania with right-sided lesions remains largely consistent in the case report literature. We report here a case of enduring mania-hypomania after a right-sided basal ganglia stroke. Case Report: A 55 yo man with a past medical history of COPD presented with new onset left-sided weakness. Exam demonstrated left facial droop, left upper and lower extremity weakness, and right gaze preference. Initial brain CT noted an old right parietal lobe infarct, hyperdensity of the M1 segment of the right MCA, and otherwise normal parenchyma. MRI of the brain noted acute infarcts involving the right caudate and lentiform nuclei and right superior temporal gyrus, and smaller foci in the right middle frontal and precentral gyri. He underwent successful right M1 thrombectomy. He subsequently developed persistent elevation in mood, pressured thought, psychomotor activation, engagement in behaviors with a high risk for adverse consequences, and vegetative changes consistent with enduring mania-hypomania. Conclusion: The roles of hemispheric lateralization of emotion and “hypo-frontality” resulting from disruption of frontal-subcortical loops subserving behavioral regulation are discussed.

Background: Poisons are classically divided into five categories: heavy metals, gases, organophosphates/solvents, complex metal ions, and drugs of abuse with each having differing effects on the CNS. An exposure should be viewed in terms of length and amount of exposure, predisposing comorbidities, and healthcare received. Exposure to hydrocarbon solvents can occur in occupational, accidental, or abuse settings (“huffing” or in “cooking meth”). Objective: Create new teaching materials with color carrying a significant portion of the information, so that large volumes of data on functional neuroanatomy and clinical presentation can be combined without overwhelming learners. Methods: New scientific and clinical research relevant to hydrocarbons’ effects on CY-P450 enzymes, injury to the lipid-rich CNS, and resultant clinical conditions were reviewed, synthesized, and summarized into graphic rich original teaching materials (e.g. diagrams, charts, models). Results: Evaluations from previous ANPA presentations in this series (2009, 2012, 2014), were very positive and indicated the need for more teaching products of this type. Incorporating feedback has allowed further refinement and adaption of these materials for use in additional clinical conditions. Use of graphic-rich materials that connect functional neuroanatomy 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 the development of the active, integrated knowledge of functional anatomy required for the practice of neuropsychiatry as it relates to the assessment and treatment of solvent-exposed patients.

Background: Attention Deficit/Hyperactivity Disorder (ADHD) was previously viewed as a behavioral disorder of childhood. It is now known that a large portion of those diagnosed as children with ADHD continue to experience clinically significant symptoms that impair functioning as adults. Objective: To review and synthesize current research on adults with ADHD. Methods: The results of meta-analyses, reviews, neuroimaging studies, and clinical research relevant to adult ADHD were reviewed. Areas of focus include: factors that differ from childhood ADHD, structural and functional neuroimaging findings, neuropsychological deficits, and treatment. Results: Research indicates that some symptoms of ADHD persist into adulthood for 50%−80% of individuals who experienced ADHD as children. However, the presentation of the disorder may change; inattention is the more enduring subset of symptoms in adults. Structural and functional neuroimaging studies show marked differences between adults with ADHD and healthy controls, particularly in frontal regions that underlie executive functioning. Both psychotherapeutic (robust findings using Cognitive Behavioral Therapy) and pharmacological (medium-to-high effect size estimates compared with placebo) approaches are effective at reducing symptoms in adults with ADHD. Structural MRI studies suggest that treatment naïve individuals might have greater neuroanatomical deficits than individuals treated with medication. Conclusion: ADHD is a disorder that persists into adulthood for a subset of those diagnosed as children, and has a distinct symptom presentation and neuroanatomical findings. Nevertheless, treatment has been shown to be effective. Research suggests the possibility that early psychopharmacological treatment may act as a protective factor, although additional studies are needed.

Background: We offer a case report describing the clinical, neuropsychological, and neuroimaging findings in a 49-year-old male who experienced an onset of cognitive and emotional deficits following a series of cerebellar strokes and eventual diagnosis of neurosarcoidosis, with resolution of his emotional dysregulation after treatment with escitalopram, followed by a course of intravenous prednisone. Case History: The patient is a 49-year-old right-handed male with a history of behavioral changes that emerged after multiple bilateral posterior circulation strokes and development of neurosarcoidosis. The patient developed deficits in executive functioning, memory, and impulse control, including emotional dysregulation, irritability, and aggression. These behaviors were a significant departure from his premorbid personality.

After his second stroke, a brain MRI revealed old right superior cerebellar artery territorial infarction with associated encephalomalacia with more evident vermis and bilateral cerebellar hemisphere atrophy. Neuropsychological testing revealed deficits in executive functioning and memory. Further collateral information revealed increased irritability and aggression. The patient was first treated with escitalopram, which led to significant reduction in impulsivity, irritability, and aggression. After a month of his successful treatment with escitalopram, he was treated for his neurosarcoidosis with a course of intravenous prednisone.

Conclusions: It is possible that the patient's cognitive and affective symptoms are the result of disruption of specific neural networks (frontal-cerebellar) by his series of strokes. The particular constellation of symptoms that he exhibits has been reported in the literature as part of the Cerebellar Cognitive Affective Syndrome. There may also be contribution from his neurosarcoidosis, which has been shown to be associated with dementia and depression. To our knowledge, this is the first case to describe the benefits of escitalopram for treatment of the emotional deficits associated with these syndromes.

Background: Frontal-striatal circuitry provides a framework for understanding behavioral changes in neuropsychiatric disorders. A set of parallel, segregated circuits are known to link specific regions of the frontal cortex to the striatum, globus pallidus, substantia nigra, and thalamus – constituting important computational mechanisms that allow the organism to interact with the environment. Impairments through anatomical lesions or physiological/chemical changes manifest in impaired executive function, apathy and impulsivity. Calcium is known to be involved in the control of neuronal excitability. Hypocalcemia secondary to hypoparathyroidism commonly results in neuropsychiatric features such as emotional instability, bizarre behavior that are reversible with correction of hypocalcemia. Case Report: The patient is a 25 y/o AAM brought to the ED by his wife after becoming increasingly irritable and violent, punching his wife in the face several times, resulting in a black eye. The patient has a PMH of TBI s/p left frontal contusion five years prior, basal ganglia calcifications on head CT, and autoimmune hypoparathyrodism. Both the patient and family report that irritability and aggression increased after the TBI, but symptoms worsen with hypocalcemia and improve with calcium correction. In two years, the patient has had numerous admissions for behavior change in the context of hypocalcemia. His symptoms have been successfully treated with haloperidol, but he does not comply as an outpatient. On exam, the patient exhibits agitation, rapid speech, utilization behavior, and tangential thought process. He endorses intermittent AH. MOCA testing reveals deficits in executive functioning, visuospatial skills, abstraction, and delayed recall with score of 24/30. Head CT shows calcifications in the head of the caudate nucleus on the left along with chronic extra-axial left frontal hematoma, all stable in comparison to previous studies. Labs were notable for total Ca 6.2mg/dL, ionized Ca 3.3, Mg 1.7 mg/dL, P 7.6mg/dL, VitD (25-OH) 26 ng/mL, and PTH 8 pg/mL. After Ca replacement, he was started on aripiprazole 5mg and valproic acid ER 1000mg. His mood and behavior improved markedly over several days. He was discharged home on both medications in addition to Ca, Mg, and VitD supplements. Conclusion: This case illustrates the importance of frontal-striatal circuitry dysfunction in neuropsychiatric disorders. The patient has caudate nucleus lesions, known to disrupt behaviorally circuitry leading to deficits in executive function and disinhibition. During episodes of hypocalcemia, the patient becomes acutely symptomatic. These findings imply interaction of anatomic, physiological and chemical mechanisms in this brain circuitry and the importance of calcium-phosphate balance in patients with TBI and basal ganglia calcification. Baseline imaging following TBI and during behavioral episodes may point to underlying etiology and help guide management.

Background: Pyruvate Dehydrogenase (PDH) Deficiency is a genetic disorder that prevents appropriate conversion of Pyruvate into Acetyl-CoA in the mitochondria. One presentation can be Leigh Syndrome, characterized by hypotonia, dystonia, and ataxia, with bilateral T2 hyperintensities of the basal ganglia. Most patients do not live longer than childhood or adolescence, so very little is known about progression into adulthood. In this case, classic symptoms appeared as a toddler and neuropsychiatric symptoms appeared in adulthood. The description, treatment, and implications are discussed. Case History: This patient had a normal development until he was 18-months, at which point he developed paralysis after feeds. A work-up revealed lactic acidosis, bilateral globus pallidi T2 hyperintensities, and PDH E1-alpha subunit Deficiency on skin biopsy and western blot. Treatment started with lipoic acid, potassium citrate, carnitine, high fat then ketogenic diet, cocktail of B vitamins, coenzyme Q10, Vitamin E, Vitamin C. Medications for diplopia, dystonia, and ataxia have included diphenhydramine, trihexyphenidyl, carbidopa/levodopa, baclofen, clonazepam, Botox injections, ankle braces, and occupational/physical therapy. At age 29, he developed depression with multiple suicide attempts and psychosis with delusions of reference and persecution. Treatment with quetiapine then olanzapine, venlafaxine, and psychotherapy led to lessened symptom severity. Supportive data including MRI brain, MR spectroscopy, neuropsychological testing, laboratory results (lactate, serum amino acids, acylcarnitine profile, urinary organic acids), visual evoked potentials, EEG, and EMG are provided about this interesting case. Conclusions: Although Leigh Syndrome is typically rapidly progressive leading to death, milder cases with proper treatment may prolong life into adulthood.

Background: For over one hundred years it has been known that the thyroid hormone plays an integral role in the development of the central nervous system. More recent investigations have elucidated the regulatory function of the thyroid and it is now widely understood that thyroid status exerts a strong influence on both cognition and affective state. The association between thyroid and psychosis is probably less well known. Therefore, it may be surprising to note that the documented relationship between hypothyroidism and psychosis dates back to 1888, when the Committee on Myxedema of the Clinical Society of London noted psychotic symptoms in nearly half of 109 patients presented in a case series (Heinrich and Grahm, 2003). Later, in 1949, Asher coined the term “myxedema madness” to describe 14 edematous, cognitively dull, and “mad” patients in his seminal case series published in the British Medical Journal (Asher, 1949). As improvements in laboratory techniques and access to care have rendered overt myxedema rare in the developed world, the term myxedema madness has become anachronistic and misleading, implying the importance of myxedema, rather than thyroid status, in the pathogenesis of psychosis. In fact, as our literature review shows, many patients with this condition lack the typical symptoms or physical exam findings usually attributed to a state of hypothyroidism. Therefore, we propose the new term Hypothyroid Associated Behavioral Disturbance (HABD) to replace the term myxedema madness. In this report, we describe a case of HABD with rapid and complete response to thyroid supplementation. In order to better understand the clinical presentation and treatment outcomes associated with this condition, we also performed a systematic review of the literature for cases reported since 1980. Case History: The case involves a 39-year-old Native American female who experienced the abrupt onset of manic and psychotic symptoms. Her medical history was significant for untreated hypothyroidism. TSH on admission was 116.9 uIU/mL. She was admitted to an inpatient psychiatric unit where she received thyroid replacement. After three days she had complete resolution of symptoms and has remained well for the past year. Neurodiagnostic data includes laboratory values only.

The following section includes a comprehensive review of reported cases of hypothyroid-induced psychosis since 1980. This section includes a table outlining demographic and presenting characteristics of the 54 cases reviewed, a table summarizing the thyroid profile of these cases, and a table summarizing treatment and outcome data from these cases.

In the discussion section, we briefly review the animal literature regarding the changes seen in the dopamine system following periods of induced hypothyroidism. Based on this literature we propose a model of increased dopamine receptor sensitivity as the cause of behavioral changes due to hypothyroidism.

Conclusions: Myxedema madness as Archer described it in 1948, may no longer be an appropriate description in the contemporary medical environment. We propose the term, Hypothyroid Associated Behavioral Disturbance (HABD) as we believe it better captures the clinical picture of patients with this condition. HABD is a secondary cause of psychosis and mania. Many patients with this disease lack the overt signs and symptoms typically associated with hypothyroidism. Therefore, it should be considered in any patient presenting with psychosis or mania. Patients with HABD should be treated with careful thyroid replacement. Animal studies have revealed that the underlying pathophysiologic mechanism is probably due to increased dopamine receptor sensitivity.

Background: Recent neuroimaging studies implicate affective regulatory circuits as important contributors to symptoms in patients with Functional Neurological Symptom Disorder (FND). Improved emotion regulation correlates with amygdala changes during psychotherapy in some non-FND populations. To date no study has measured emotion regulation using standardized scales in FND patients.

• Measure emotion regulation in FND patients receiving group Dialectical Behavior Therapy (DBT) over 2 years.

• Test the hypothesis that improved emotion regulation predicts improved symptom outcome.

Methods: 25 subjects participated in a modified form of group DBT over two years. The treatment involved modules on mindfulness, interpersonal effectiveness, emotion regulation, and distress tolerance. Measures collected included symptom frequency, Beck Depression Index, Positive and Negative Affect Scale (PANAS), and Difficulties in Emotional Regulation Scale (DERS). Results: The study’s results will be discussed with respect to changes in emotion regulation and symptom frequency over two years of DBT. Self-reported symptom rates greater than 100 will be winsorized and used in analysis of change over time in a mixed effect model to determine the effect of emotion regulation measures, PANAS and DERS, on symptom rate. Symptom rate estimates have a positively skewed distribution, typical of count data, so a log link (Poisson regression) will be used in analysis. Conclusion: This study will examine the effect of emotion regulation on symptom outcome in DBT treatment of FND. Further research on emotion regulation skills training and DBT may lead to a new treatment modality and therapeutic conceptualization to guide clinicians treating FND.

Background: Schizophrenia patients have difficulties in social functioning, a landmark of the condition linked to neurocognitive abnormalities and to treatment outcomes. Social functioning and interactions critically demand coordinated and contrasted assessment of emotions and intentions in self and others. Yet these cognitive elements have rarely been concurrently studied, even less at the neurofunctional level. Objective: We studied whether the appraisal of emotions or intentions in self or in others was associated to specific brain dysfunctions in schizophrenia. Methods: We used fMRI to characterize brain function in 30 schizophrenia patients and 30 age-, gender-, and parental education-matched healthy controls during performance of a battery of tasks that required assessing emotions (observed or expected) or intentions, both in self or in others. The design allowed for the individual analysis of and multiple comparisons between processing situations (e.g. emotions versus intentions, self versus others, emotions and/or intentions in self versus others, etc) as well as contrasts between patients and controls for each particular situation or comparison. Imaging data (3T Siemens Trio) were analyzed using SPM12 and conservatively applied random effect models. Results: Significant differences in areas known to be involved in empathy, self-awareness, self-reflection, understanding of others, and assessment of facial affect processes were found between controls and schizophrenia patients. Conclusion: The results provide further support to the hypothesis that social dysfunction in schizophrenia is associated with abnormalities in brain function supporting social cognitive processes. These abnormalities might be primary, secondary (compensatory), or even the result of chronic or developmental “lack of use”.

Background: Behavioral and Psychological Symptoms of Dementia (BPSD) are integral to dementing disorders. Consensus guidelines for the management of BPSD emphasize environmental, behavioral, and pharmacological approaches to treatment yet a significant proportion of patients do not respond to these interventions. Objective: To determine the efficacy of ECT in treatment-refractory BPSD using a prospective, open-label, observational design in the setting of a multidisciplinary inpatient dementia service. Method: Inclusion criteria consisted of: 1. BPSD of sufficient severity to preclude discharge to any nonhospital environment; 2. BPSD unresponsive to multiple pharmacologic and nonpharmacologic treatments; 3. Medical clearance for ECT; and 4. Informed, written consent from patient or substitute decision maker. ECT was administered twice weekly for up to ten weeks. The primary outcome measure was change in the Neuropsychiatric Inventory (NPI) at baseline compared with the end of treatment. Results: Five subjects with BPSD were enrolled thus far. Mean age was 74 (range: 64–84) and three were female. Three subjects had a diagnosis of Alzheimer’s disease, one had vascular dementia, and one had mixed dementia. Three patients had a prior history of depression and one had received ECT in the past. NPI scores improved significantly after treatment (Wilcoxon signed-rank test, z=−1.99, p=0.046) with a large effect size (r=−0.63). Conclusion: These early data add to the small literature devoted to ECT for BPSD. Larger, well-designed treatment studies are required to more definitively ascertain the safety and effectiveness of this intervention for BPSD.

Background: Repetitive transcranial magnetic stimulation (rTMS) of the dorsolateral prefrontal cortex (dlPFC) is an established treatment for depression. The dlPFC is involved in working memory, executive control and response inhibition. Objective: To monitor cognitive changes throughout rTMS treatment for depression, and test whether cognitive performance can be predictive of treatment response. Methods: Eight patients with treatment resistant depression participated in this study. Patients received 30 sessions of 10 Hz rTMS over the left dlPFC. Patients completed a battery of computerized neurocognitive tasks including Stroop, Task-Switching and 3-Back after 0, 6, 12, and 30 sessions of treatment. Depression scores were rated using the Hamilton Depression (Ham-D) scale. Clinical response was defined as a greater than 50% reduction in Ham-D score. Results: Five patients showed a clinical response to rTMS treatment.

Response times (RT) for responders were faster than for nonresponders in the Task-Switching test (p<0.01). There was a trend toward this same pattern in the Stroop task but it was not significant.

There was also a positive correlation between RT and Ham-D score across sessions for both the Task-Switching and Stroop tasks (p<0.01). There were no significant differences between responders and nonresponders at baseline or across sessions for Stroop effect, switch-cost, or error rates.

Conclusions: Depressed patients who were successfully treated with rTMS showed overall faster response times before treatment. Lower Ham-D scores were associated with faster responses. We speculate that baseline processing speed in mental tasks such as Task-Switching might be an indicator of a future favorable response to rTMS.

Background: Transcranial magnetic stimulation (TMS) is an increasingly common treatment for major depressive disorder (MDD). Though TMS has been shown to be effective for many treatment-resistant MDD patients, it is not clear which patients may benefit. It would be helpful to have a biomarker assay to predict response to TMS. We hypothesized that the MDDScore panel, a commercially available compendium of 9 serum biomarkers, may be such an assay. Objective: To assess if the MDDScore assay could help predict TMS outcomes in patients with MDD. Methods: This study retrospectively looked at data from patients who had an MDDScore result and who did TMS treatment (N=9). Patients were classified as TMS responders if they had at least a 50% reduction in HAM-D or QIDS scores by the end of treatment. Results: 6/7 of the responders had a positive MDDScore result, while 2/2 of the nonresponders had a negative MDDScore result; this was a significant difference (X²=5.1429, p=0.0233). If a patient had a positive result, there was an 85.71% chance that they would respond to TMS. If a patient had a negative result, there was a 100% chance that they would not respond to TMS. Put another way, the MDDScore assay had a sensitivity of 1.0 and specificity of 0.67. Conclusion: Although TMS can be very effective for MDD, it is not clear who will be a good candidate for this treatment. In this study, we found that the MDDScore assay may help predict responsiveness to TMS.

Background: The subthalamic nucleus (STN) in a new target for deep brain stimulation (DBS) in OCD. The STN can be divided into functional regions: sensorimotor, emotional and cognitive areas. Objective: We hypothesize that subareas of the STN can be differentiated by electrophysiological activity. Methods: We report an OCD patient implanted with a novel DBS system with long-term local field potential (LFP) sensing capability. During electrode implantation surgery, functional electrophysiological recordings (single unit) of the STN were performed to evaluate the neural activity during rest and in response to specific emotional stimuli, cognitive test and a visual OCD provocation test. During the first months postoperatively, using the novel DBS system, we repeated the emotional, cognitive and OCD provocation stimuli during LFP electrophysiological recordings of the STN. We compared the recordings in the “on” versus “off” states of the electrical stimulation. Results: We found beta oscillations (12–30Hz) restricted to the dorsolateral part of the STN that corresponds to the sensorimotor STN and theta oscillations (4–7Hz) in the ventromedial part of the STN that corresponds to the emotional-cognitive STN. Different electrical activity was recorded in the dorsolateral and ventromedial areas in response to emotional, cognitive and OCD tests. Electrical stimulation was found to change the neural activity. Conclusions: Our preliminary results suggest that neurons in the STN of OCD patients may display a distinct neural signature. Future location for electrode implantation might be guided by electrophysiological recordings and parameters of the DBS will be manipulated both according to clinical assessment and electrophysiological findings.

Background: The subthalamic nucleus (STN) can be divided into three functional regions: sensorimotor, emotional and cognitive areas. Although many studies have investigated the sensorimotor area of the STN, the nonmotor (emotional-cognitive) areas are far less studied. Objective: We hypothesize that the cognitive and emotional areas of the STN are lateralized to a dominant and nondominant hemisphere, respectively. Methods: In this study, during surgery for deep brain stimulation (DBS) in human Parkinson's disease patients (N=27), electrophysiological recording of the STN were performed. Microelectrodes were utilized to record the STN spontaneous spiking activity and responses to vocal nonverbal emotional stimuli and Go-No-Go cognitive task. Results: The oscillation properties of the STN neurons were used to map the dorsal oscillatory and the ventral nonoscillatory regions of the STN. Beta oscillations (12–30Hz) are restricted to the dorsolateral part of the STN that corresponds to the sensorimotor STN. Emotive auditory stimulation evoked activity in the ventral nonoscillatory region of the right STN whereas cognitive tasks evoked activity in the ventral nonoscillatory region of the left STN. Conclusions: Our results suggest that the ventral nonoscillatory regions are asymmetrically associated with nonmotor functions, with the right ventral STN associated with emotional processing and the left ventral STN associated with cognitive processing. These results suggest that DBS of the right or left ventral STN may be associated with beneficial or adverse emotional and cognitive effects observed in PD patients. DBS of the right ventral STN should be considered in order to relieve mental symptoms in other neuropsychiatric diseases.

Background: The American Academy of Neurology (AAN) driving safety questionnaire evaluates caregiver concerns about driving ability in dementia patients. The Frontal Systems Behavior Scale (FrSBe) measures behaviors associated with frontal-subcortical circuits (specifically apathy, disinhibition, and executive dysfunction). Cognitively, visual attention, executive functioning, and visuoperception are most strongly associated with driving safety risk in older adults. While research supports associations between behavioral and cognitive deficits and driving impairment, no studies have examined the predictors of caregiver concerns. Objective: The current study explored whether objective cognition (Judgment of Line Orientation; Trail Making Test B; and Rey Osterreith Complex Figure Organization) and/or behavioral dysfunction (as measured by the three FrSBe subscales) predict caregiver concerns about patient driving safety on the AAN Caregiver Driving Safety Questionnaire. Methods: Participants were 80 caregivers of patients with Mild Cognitive Impairment (N=46) or early Alzheimer's disease (N=34) who completed the FrSBe and AAN Driving Questionnaire. All patients completed a comprehensive neuropsychological evaluation. Results: Linear regressions revealed that after controlling for patient age and education, and including the above mentioned cognitive and behavioral variables in the model, only FrSBe Apathy (p=0.005) predicted caregiver concerns about patient driving (as measured by total score on the AAN driving safety questionnaire). No other cognitive or behavioral variables were significant predictors. Conclusion: Caregiver concerns about driving safety are more influenced by patient behavioral deficits, particularly decreased motivation, than by objective cognitive changes in the patient. Caregivers may benefit from psychoeducation about cognitive factors that may negatively impact driving safety.

Background: Neuropsychiatric symptoms (NPS) associated with brain injury occur frequently and are the most common cause of poor quality of life and caregiver burden. They can disrupt rehabilitation therapies and contribute to functional impairment if not appropriately treated. Although some of these patients can be treated adequately in an outpatient brain injury clinic or rehabilitation clinic, others may need a more specialized structured program. Behavioral problems in particular are challenging and often lead to discharge of patients from traditional rehabilitation programs as their behaviors can be disruptive and/or unsafe to themselves and others. These patients are often admitted to inpatient general psychiatric units where they do not receive the comprehensive care they need. Case History/Program Description: In an effort to prevent unnecessary hospitalizations and to provide comprehensive treatment we have developed a community-based multidisciplinary program to address the physical, cognitive and psychiatric needs of those with brain injury. We will provide a short description of two patients who have benefitted from the program: 1) 31 year old man with severe traumatic brain injury with subsequent cognitive and behavioral symptoms who had improvement in symptoms and quality of life. 2) 38 year old female with cognitive and mood symptoms after left temporal lobe resection due to medication-refractory epilepsy who had improved mood symptoms and functionality. Conclusion: Brain injury is commonly associated with myriad of neuropsychiatric symptoms which wax and wane. There is an urgent need to develop comprehensive programs that can address their multiple needs in a community setting.

Background: There are several challenges in diagnosing and treating neuropsychiatric symptoms after brain injury. Often times, formulation of symptoms cannot adequately be accomplished strictly using a biopsychosocial model. The cultural components play an imperative role in etiology and treatment. Culture can include ethnic groups and encompass organized units and affiliations such as sports and the military. With the expanding incidence of brain injuries in the sports and military worlds as well as an increase in immigrant populations, it is critical to determine the cultural psychology of various groups to determine its role in symptomatology and efficacy of guiding treatment. Case History: To exemplify the importance of using culture to comprehensively assess psychiatric brain injury symptomatology, the authors describe the case of a 34 year old South Asian female who developed depression after a severe traumatic brain injury. Her role failure as the matriarch of her household was attributed solely to her brain injury. Reluctance to engage in psychiatric treatment due to stigma of mental illness and culture-specific underreporting of symptoms proved a barrier to successful treatment. Conclusions: This case highlights how cultural values can contribute to and incite psychiatric symptoms. Just as ethnic values complicate diagnosis and drive treatment outcomes, military and sports cultures similarly impact evaluation and management secondary to misattribution of symptoms and/or failure of disclosure. Cultural factors can contribute significantly to the etiopathogenesis of neuropsychiatric symptoms. It is important for clinicians to assess the role of culture and determine its strengths and weaknesses.

Background: Patients with psychogenic nonepileptic seizures (PNES) are known to have difficulty engaging in treatment. Little is known about the risk factors that signal nonadherence to follow-up. Objective: Determine adherence to first follow-up appointment and factors that may predict adherence. Methods: 59 PNES patients were retrospectively divided in two groups based on their attendance to their first follow-up appointment, which took place 1–4 weeks after diagnosis confirmation by video-EEG. Demographic, clinical, social and psychopathological factors were compared between groups. Results: 48 patients attended their first follow-up appointment (81%) and 11 did not (19%). Ethnicity differed between groups, with Blacks showing a higher proportion of nonattendance (p=0.007). Reported event symptoms that differed between the groups included head (p=0.03) and pelvic movements (p=0.008), and sound production (p=0.03), all more common in the not-attended group. Past (but not active) posttraumatic stress disorder (PTSD) (p=0.04), past (but not current) psychosis (p=0.01), current substance abuse (p=0.01), and lifetime history of IV drug (p=0.04) or benzodiazepine abuse (p=0.04) were more common in the not-attended group. Somatic complaints were also more frequent in the not-attended group (p=0.04). Other demographic, clinical, social and psychopathological measures did not differ between groups. Conclusions: After formal presentation of a PNES diagnosis, most patients attended the first follow-up appointment. Specific ethnicities, symptoms, and psychiatric comorbidities were more frequent among nonadherent patients. Predicting likelihood of nonadherence to follow up may help focus resources at time of diagnosis and develop formal interventions to improve treatment engagement in PNES.

Background: Needs remain in our community to provide Neuropsychiatric services to patients with concussion/traumatic brain injury with varying combinations of emotional, cognitive and physical problems. Our Neuropsychiatry Program was poised to create a Concussion Clinic, with subspecialty trained staff. Funding sources to support our clinic’s mission have been imperative to preserve an expert approach to patient care and secure financial viability for our transformed clinic model. Objective: To characterize the clinic’s evolution administratively and clinically, highlighting successes and challenges that have driven clinic change. Methods: Retrospective chart review of patient characteristics and administrative processes. Results: Since mid-2010, > 225 patient referrals have been triaged resulting in 129 TBI-related evaluations. One-time consultations were provided for 30 patients (23%), 16 patients (12%) had≤5 visits, and the majority (83 patients or 64%) had more≥6 visits. Workers compensation handled 18 (14%) of cases. Patients saw both a psychotherapist and a neuropsychiatrist in most cases (95 or 74%), some only a neuropsychiatrist (33 or 26%) and 1 (<1%) a psychotherapist only. Most patients (83 or 65%) were found to have 1 TBI, whereas 45 patients (35%) had>1 TBI, of varying severities. Conclusion: Our Concussion Clinic has evolved with flexibility to best match both patient and service needs. Some imperative changes developed to troubleshoot problems and accommodate for repeated challenges, both administrative and clinical. Overall, individuals with multiple concussions/head injuries and those that depended upon workers compensation had longer treatment courses and more complex and time-demanding administrative requirements.

Background: To date, there is yet no established effective treatment (medication or cognitive intervention) for posttraumatic brain injury (TBI) patients with chronic sequelae. Objective: Enriched Environment (EE) has been recognized of importance in brain regulation, behavior and physiology. Rodents reared in, or pre-exposed to EE, recovered better from brain insults. Methods: Using the concussive head trauma model of minimal TBI in mice, we evaluated the effect of transition to EE following a weight-drop (30 gr or 50 gr) induced mTBI on behavioral and cognitive parameters in mice in the Novel Object Recognition task, the Y- and the Elevated Plus mazes. Results: In all assays, both mTBI groups (30 gr, 50 gr) housed in normal conditions were equally and significantly impaired 6 weeks post injury in comparison with the no-mTBI (p<0.001and p<0.03 respectively) and the mTBI+EE groups (p<0.001for the 30g, and p<0.017for the 50g). No differences were found between the control and the EE mice. Conclusions: Two separate finding emerge: (1) the significantly positive effects of the placement in EE following mTBI, on the rehabilitative process of the tested behaviors in the affected mice; (2) the lack of difference between the groups of mice affected by 30 gr or by 50 gr. Further studies are needed in order to characterize the exact pathways involved in the positive effects of the EE on mice recovery from mTBI. Possible clinical implications indicate the importance of adapting correlates of EE to humans, i.e. prolonged and intensive physical activity – possibly combined with juggling training and intensive cognitive stimulation.

Background: Poststroke depression (PSD) is common and early recognition of depressive symptoms and identification of patients at risk for PSD has significant potential benefit because PSD negatively affects stroke outcome and costs of medical care. The frequency of PSD has been established by multiple studies, and ranges from 16% to 65%. Objective: To correlate stroke location with poststroke depression. Methods: This was a retrospective chart review done on patients whom were diagnosed with a single, first ever ischemic or hemorrhagic stroke at Good Samaritan Regional Medical Center between January of 2010 and December of 2012. Results: Multivariate logistic regression was used to analyze study findings. Females are more likely to suffer from depressive symptoms following stroke than males [OR=2.38 95% CI 1.134–5.006 unadjusted]. Age has an inverse relationship with depression risk; for every year increase in age, risk of depression in patients with stroke decreases by 1.7% [OR 0.983, 95% CI 0.9260–1.007]. Patients with parietal lobe strokes were more likely to suffer depressive symptoms when compared with all other lesion locations [OR 2.29 95% CI 1.038–5.069 unadjusted]. When controlling for hemisphere, it appears that specifically right-sided parietal lobe strokes resulted in higher depression risk [OR 3.231 95% CI 1.103–9.464]. Conclusion: The principle findings of the study are that females are more likely to suffer from depressive symptoms following stroke than males, age appears to have an inverse relationship with depression, and right-sided parietal lobe strokes resulted in higher depression risk. This study presents compelling evidence that sex, age, and parietal lobe stroke location are significant predictors for future depression following stroke.

Background: Moyamoya disease is characterized by progressive bilateral internal carotid artery stenosis. Previous research revealed cerebral hypoperfusion that related to impaired intellectual development in pediatric patients. Objective: The current study aimed to further investigate the dynamic relationship between brain perfusion in particular regions and specific domains of cognitive functions following surgical treatment. Methods: Pre- and postencephaloduroarteriosynangiosis (EDAS) cognitive functions and perfusion computed tomography (CT) results were collected in seven children diagnosed with moyamoya disease. Cognitive measures included intelligence, verbal learning, and semantic fluency tests. Spearman sign rank correlations were performed to explore relationships between changes of cognitive performances and parametric time-to-peak (TTP) at bilateral temporal and frontal areas after EDAS. Results: There was no significant relationship between changes of intelligence quotient (IQ) and brain perfusion at any regions of interest. However, a positive correlation was found between performance improvement on the semantic fluency test and increased perfusion at the left temporal area. Conclusion: This preliminary analysis supported a promising surgical effect of EDAS on improvement of specific cognitive function evidenced by changes of correlational neurosubstrates. Further studies with a larger sample size and sophisticated methodology were suggested.

Background: Synthetic cannabis (SC) has become well-known as a drug of abuse. It is reported that approximately 12% of U.S. high school students have used SC in the past year. Although the use of SC is growing, treating SC intoxication and withdrawal continues to be difficult. A recent survey of emergency room physicians practicing in urban areas revealed that only 20% felt prepared to take care of a patient with acute SC intoxication. Here we present a case that highlights the medical, neurological, and psychiatric sequelae from acute SC intoxication, as well as the psychiatrist's role in treating SC withdrawal. Case History: A 28-year-old man with a prior history of cannabis and nicotine abuse was found obtunded and witnessed to have a seizure. After transport to the emergency room, two subsequent seizures were witnessed; postictally, the patient was agitated. Neurology ordered imaging and a lumbar puncture, but all results were normal. Soon after admission, the patient developed acute kidney failure requiring dialysis. As the patient recovered, he began experiencing insomnia and panic attacks. Psychiatric evaluation revealed extensive SC use over 4 years. The patient was placed on a benzodiazepine and clonidine to treat his prolonged SC withdrawal. Conclusions: Unlike 9-THC, which is a partial agonist at cannabinoid receptors, SC is a full agonist and binds with higher affinity than 9-THC at endogenous cannabinoid receptors in the left caudate and hippocampus. This may explain SC's increased risk of psychosis, seizures, renal insults and its prolonged anxiogenic effects.