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<title>Journal of Neuropsychiatry</title>
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<title><![CDATA[[WINDOWS TO THE BRAIN] Astroglia: Not Just Glue]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/2/iv?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Taber, K. H., Hurley, R. A.]]></dc:creator>
<dc:date>2008-05-01</dc:date>
<dc:subject><![CDATA[Molecular Biology, Other Neuroanatomy]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.2.iv</dc:identifier>
<dc:title><![CDATA[[WINDOWS TO THE BRAIN] Astroglia: Not Just Glue]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>2</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>129</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>iv</prism:startingPage>
<prism:section>WINDOWS TO THE BRAIN</prism:section>
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<title><![CDATA[[SPECIAL ARTICLES] An Evidence-Based Review of the Psychopathology of Frontotemporal Dementia: A Report of the ANPA Committee on Research]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/2/130?rss=1</link>
<description><![CDATA[
<p>The Committee on Research of the American Neuropsychiatric Association conducted a review of the noncognitive neuropsychiatric manifestations of frontotemporal dementia. The Committee on Research searched reviews and several online databases for all pertinent publications. Single case reports without pathology were excluded, except for psychosis, where single cases made up much of the literature. The strongest evidence supports an association of frontotemporal dementia with the following behaviors: apathy-abulia; disinhibition-impulsivity; loss of insight and self-referential behavior; decreased emotion and empathy; violation of social and moral norms; changes in dietary or eating behavior; and repetitive behaviors. Frontotemporal dementia is less frequently associated with anxiety and mood disorders, which may be a prodrome or risk factor, and rarely presents with delusions or hallucinations. The results of this review highlight the distinct neuropsychiatric manifestations of frontotemporal dementia and the need to reconsider the current diagnostic criteria for this disorder.</p>
]]></description>
<dc:creator><![CDATA[Mendez, M. F., Lauterbach, E. C., Sampson, S. M., ANPA Committee on Research]]></dc:creator>
<dc:date>2008-05-01</dc:date>
<dc:subject><![CDATA[Dementias (General), Symptoms/Dimensions]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.2.130</dc:identifier>
<dc:title><![CDATA[[SPECIAL ARTICLES] An Evidence-Based Review of the Psychopathology of Frontotemporal Dementia: A Report of the ANPA Committee on Research]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>2</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>149</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>130</prism:startingPage>
<prism:section>SPECIAL ARTICLES</prism:section>
</item>

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<title><![CDATA[[SPECIAL ARTICLES] Comparability of the Clinical Diagnostic Criteria for Vascular Dementia: A Critical Review. Part I]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/2/150?rss=1</link>
<description><![CDATA[
<p>This review is the first of a two-part series focusing on the comparability of eight clinical criteria used for the diagnosis of vascular dementia: the Hachinski Ischemic Scale; the Ischemic Scale of Rosen; the criteria proposed by the Diagnostic and Statistical Manual of Mental Disorder&ndash;Third Edition (DSM-III), DSM-III-R, DSM-IV; International Classification of Diseases, 10th Revision (ICD-10); State of California Alzheimer&rsquo;s Disease Diagnostic and Treatment Centers (ADDTC); and the National Institute of Neurological Disorders and Stroke-Association Internationale pour la Recherche et l&rsquo;Enseignement en Neurosciences (NINDS-AIREN). The authors discuss the critical issues related to the definition of the cognitive syndromes as well as the vascular causes and associated heterogeneity of symptomatology across these criteria.</p>
]]></description>
<dc:creator><![CDATA[Wiederkehr, S., Simard, M., Fortin, C., van Reekum, R.]]></dc:creator>
<dc:date>2008-05-01</dc:date>
<dc:subject><![CDATA[Dementias (General), Diagnostic Criteria]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.2.150</dc:identifier>
<dc:title><![CDATA[[SPECIAL ARTICLES] Comparability of the Clinical Diagnostic Criteria for Vascular Dementia: A Critical Review. Part I]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>2</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>161</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>150</prism:startingPage>
<prism:section>SPECIAL ARTICLES</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/2/162?rss=1">
<title><![CDATA[[SPECIAL ARTICLES] Validity of the Clinical Diagnostic Criteria for Vascular Dementia: A Critical Review. Part II]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/2/162?rss=1</link>
<description><![CDATA[
<p>This review is the second of a two-part series focusing on the validity of eight clinical criteria for vascular dementia. Sixteen studies were selected according to their purposes and quality of experimental design. The analysis revealed that criteria for vascular dementia are not interchangeable; the eight criteria sets yielded different sensitivity and specificity results, as well as marked variability in incidence, prevalence, and frequency rates. Although the State of California Alzheimer&rsquo;s Disease Diagnostic and Treatment Centers (ADDTC) were the most sensitive and useful criteria in clinical settings and the National Institute of Neurological Disorders and Stroke-Association Internationale pour la Recherche et l&rsquo;Enseignement en Neurosciences (NINDS-AIREN) were the most specific and useful criteria in research, all criteria shared similar flaws. A definition of the cognitive syndrome, associated vascular causes or lesions, and methods of assessment should be clearly specified in the future. Suggestions for improvement are made.</p>
]]></description>
<dc:creator><![CDATA[Wiederkehr, S., Simard, M., Fortin, C., van Reekum, R.]]></dc:creator>
<dc:date>2008-05-01</dc:date>
<dc:subject><![CDATA[Dementias (General), Diagnostic Criteria]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.2.162</dc:identifier>
<dc:title><![CDATA[[SPECIAL ARTICLES] Validity of the Clinical Diagnostic Criteria for Vascular Dementia: A Critical Review. Part II]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>2</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>177</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>162</prism:startingPage>
<prism:section>SPECIAL ARTICLES</prism:section>
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<title><![CDATA[[REGULAR ARTICLES] Double-Blind Randomized Treatment of Poststroke Depression Using Nefiracetam]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/2/178?rss=1</link>
<description><![CDATA[
<p>In preliminary trials, nefiracetam, a gamma aminobutyric compound, enhanced blood flow and improved mood following stroke. Within 3 months following stroke with major depression, 159 patients were enrolled in a double-blind trial of nefiracetam or placebo. Repeated measures analysis of covariance failed to show a significant time-by-treatment interaction. Response rates were greater than 70% and remission rates were greater than 40% for nefiracetam and placebo. The top quintile of Hamilton Depression Rating Scale scores showed significant effect after 900 mg of nefiracetam versus 600 mg or placebo. Nefiracetam was not an effective treatment for poststroke depression but produced significant improvement in the most severely depressed patients.</p>
]]></description>
<dc:creator><![CDATA[Robinson, R. G., Jorge, R. E., Clarence-Smith, K.]]></dc:creator>
<dc:date>2008-05-01</dc:date>
<dc:subject><![CDATA[Depression, Stroke]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.2.178</dc:identifier>
<dc:title><![CDATA[[REGULAR ARTICLES] Double-Blind Randomized Treatment of Poststroke Depression Using Nefiracetam]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>2</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>184</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>178</prism:startingPage>
<prism:section>REGULAR ARTICLES</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/2/185?rss=1">
<title><![CDATA[[REGULAR ARTICLES] A New Data-Based Motor Subtype Schema for Delirium]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/2/185?rss=1</link>
<description><![CDATA[
<p>The authors sought to validate a new approach to motor subtyping in delirium based on data from a controlled comparison of items from three existing psychomotor schema combined into the Delirium Motoric Checklist. Principal components analysis of the Delirium Motoric Checklist identified two factors that correlated significantly with independently assessed motor agitation and retardation. Symptoms loading at &gt;0.65 were extracted to form subtype criteria composed of four hyperactive items and seven hypoactive items which, when applied to the delirious population, suggested a cutoff of two items for subtypes. This new scale is derived from existing approaches but is more concise, focused on motor disturbances, and validated against nondelirious comparison subjects and independently rated motor disturbance. </p>
]]></description>
<dc:creator><![CDATA[Meagher, D., Moran, M., Raju, B., Leonard, M., Donnelly, S., Saunders, J., Trzepacz, P.]]></dc:creator>
<dc:date>2008-05-01</dc:date>
<dc:subject><![CDATA[Delirium]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.2.185</dc:identifier>
<dc:title><![CDATA[[REGULAR ARTICLES] A New Data-Based Motor Subtype Schema for Delirium]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>2</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>193</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>185</prism:startingPage>
<prism:section>REGULAR ARTICLES</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/2/194?rss=1">
<title><![CDATA[[REGULAR ARTICLES] Prediction of Clinical Outcomes From rTMS in Depressed Patients With Lateral Visual Field Stimulation: A Replication]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/2/194?rss=1</link>
<description><![CDATA[
<p>The authors sought to replicate an earlier finding that baseline lateral visual field stimulation, a procedure shown to activate the contralateral hemisphere and induce affective changes, predicted the clinical outcomes of a 10-day course of left-sided rapid transcranial magnetic stimulation (rTMS). For 23 patients there was a significant 1-tailed Pearson correlation between the percent improvement in response to rTMS and their lateralized affective responses to lateral visual field stimulation. These correlations, across the whole group and within genders, were almost identical to those previously reported from 37 patients studied at a different site.</p>
]]></description>
<dc:creator><![CDATA[Schiffer, F., Glass, I., Lord, J., Teicher, M. H.]]></dc:creator>
<dc:date>2008-05-01</dc:date>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.2.194</dc:identifier>
<dc:title><![CDATA[[REGULAR ARTICLES] Prediction of Clinical Outcomes From rTMS in Depressed Patients With Lateral Visual Field Stimulation: A Replication]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>2</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>200</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>194</prism:startingPage>
<prism:section>REGULAR ARTICLES</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/2/201?rss=1">
<title><![CDATA[[REGULAR ARTICLES] A Clinical Electrophysiological Study of Emotional Lability in Patients With Systemic Lupus Erythematosus]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/2/201?rss=1</link>
<description><![CDATA[
<p>Neuropsychiatric symptoms are well recognized in systemic lupus erythematosus (SLE), with depression and anxiety often reported. The authors&rsquo; clinical observations suggested emotional lability might also be a noteworthy symptom. In a consecutive series of systemic lupus erythematosus clinic attendees the authors therefore measured depression, anxiety, and emotional lability. Additionally, based on reports linking emotional reactivity and transient mood changes to alterations in early attentional processes, the authors investigated event-related potential indices of preattentive and early orienting responses to auditory stimuli (N1, MMN, P3a and P3b). The authors observed that 15 of 32 participants with systemic lupus erythematosus had high lability scores and, comparing event-related potential measures between the high and low lability subgroups, noted that those with greater emotional lability demonstrated reduced response latencies in N1 and MMN paradigms.</p>
]]></description>
<dc:creator><![CDATA[Langosch, J., Rand, S., Ghosh, B., Sharma, S., Tench, C., Stratton, R., D'Cruz, D., Trimble, M., Barrett, G., Ring, H.]]></dc:creator>
<dc:date>2008-05-01</dc:date>
<dc:subject><![CDATA[General Topics in Psychiatry, Other Mood Disorders]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.2.201</dc:identifier>
<dc:title><![CDATA[[REGULAR ARTICLES] A Clinical Electrophysiological Study of Emotional Lability in Patients With Systemic Lupus Erythematosus]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>2</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>209</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>201</prism:startingPage>
<prism:section>REGULAR ARTICLES</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/2/210?rss=1">
<title><![CDATA[[REGULAR ARTICLES] Reversal Learning as a Neuropsychological Indicator for the Neuropathology of Obsessive Compulsive Disorder? A Behavioral Study]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/2/210?rss=1</link>
<description><![CDATA[
<p>A dysfunction of the fronto-striatal loop has been associated with obsessive-compulsive disorder (OCD). Functional imaging studies suggest that reversal learning is affected by deficits in fronto-striatal brain areas and thus should be impaired in patients with OCD. The authors compared patients with OCD and healthy comparison subjects on a reversal learning task. Correlation analyses and group comparisons showing prolonged reaction times of different response parameters are associated with increasing severity of compulsions. The reversal learning task has been shown to be associated with ventral fronto-striatal brain activation by functional magnetic resonance imaging (fMRI) in healthy comparison subjects. The purpose of this article is to suggest that the reversal learning task can be used as a neuropsychiatric measurement of the ventral fronto-striatal dysfunction in OCD.</p>
]]></description>
<dc:creator><![CDATA[Valerius, G., Lumpp, A., Kuelz, A.-K., Freyer, T., Voderholzer, U.]]></dc:creator>
<dc:date>2008-05-01</dc:date>
<dc:subject><![CDATA[Obsessive-Compulsive Disorder, Behavior Therapy]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.2.210</dc:identifier>
<dc:title><![CDATA[[REGULAR ARTICLES] Reversal Learning as a Neuropsychological Indicator for the Neuropathology of Obsessive Compulsive Disorder? A Behavioral Study]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>2</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>218</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>210</prism:startingPage>
<prism:section>REGULAR ARTICLES</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/2/219?rss=1">
<title><![CDATA[[CLINICAL AND RESEARCH REPORTS] "Denkfaulheit" in Frontotemporal Dementia: A Preliminary Analysis]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/2/219?rss=1</link>
<description><![CDATA[
<p>The initial recognition of frontotemporal dementia is often difficult. Frontotemporal dementia presents with subtle personality changes in the absence of a definitive biomarker. The authors report an analysis of cognitive shallowness, or "Denkfaulheit," in patients with frontotemporal dementia early in its course.</p>
]]></description>
<dc:creator><![CDATA[Mendez, M. F., Shapira, J. S., Licht, E. A.]]></dc:creator>
<dc:date>2008-05-01</dc:date>
<dc:subject><![CDATA[Dementias (General)]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.2.219</dc:identifier>
<dc:title><![CDATA[[CLINICAL AND RESEARCH REPORTS] "Denkfaulheit" in Frontotemporal Dementia: A Preliminary Analysis]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>2</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>222</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>219</prism:startingPage>
<prism:section>CLINICAL AND RESEARCH REPORTS</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/2/222?rss=1">
<title><![CDATA[[CALENDAR] CME Calendar]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/2/222?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>2008-05-01</dc:date>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.2.222</dc:identifier>
<dc:title><![CDATA[[CALENDAR] CME Calendar]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>2</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>222</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>222</prism:startingPage>
<prism:section>CALENDAR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/2/223?rss=1">
<title><![CDATA[[CLINICAL AND RESEARCH REPORTS] Phenomenology of Obsessive Compulsive Disorder in Patients with Temporal Lobe Epilepsy or Tourette Syndrome]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/2/223?rss=1</link>
<description><![CDATA[
<p>Phenomenology of comorbid obsessive-compulsive disorder was compared in nine patients with temporal lobe epilepsy and 15 with Tourette syndrome. Content of obsessive-compulsive themes focuses on sexuality and impulsiveness in Tourette syndrome and existential thoughts in temporal lobe epilepsy.</p>
]]></description>
<dc:creator><![CDATA[Mula, M., Cavanna, A. E., Critchley, H., Robertson, M. M., Monaco, F.]]></dc:creator>
<dc:date>2008-05-01</dc:date>
<dc:subject><![CDATA[Tourette's, Epilepsy, Obsessive-Compulsive Disorder]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.2.223</dc:identifier>
<dc:title><![CDATA[[CLINICAL AND RESEARCH REPORTS] Phenomenology of Obsessive Compulsive Disorder in Patients with Temporal Lobe Epilepsy or Tourette Syndrome]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>2</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>226</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>223</prism:startingPage>
<prism:section>CLINICAL AND RESEARCH REPORTS</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/2/227?rss=1">
<title><![CDATA[[CLINICAL AND RESEARCH REPORTS] Sex-Dependent Hippocampal Volume Reductions in Schizophrenia Relate to Episodic Memory Deficits]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/2/227?rss=1</link>
<description><![CDATA[
<p>Morphological abnormalities of the hippocampus might form the neurobiological basis of memory dysfunction in schizophrenia. Hippocampal volume was found to be bilaterally reduced in male, but not in female, subjects with schizophrenia. Right hippocampal volume was significantly related to impaired visual learning.</p>
]]></description>
<dc:creator><![CDATA[Exner, C., Nehrkorn, B., Martin, V., Huber, M., Shiratori, K., Rief, W.]]></dc:creator>
<dc:date>2008-05-01</dc:date>
<dc:subject><![CDATA[Schizophrenia Spectrum Disorders]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.2.227</dc:identifier>
<dc:title><![CDATA[[CLINICAL AND RESEARCH REPORTS] Sex-Dependent Hippocampal Volume Reductions in Schizophrenia Relate to Episodic Memory Deficits]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>2</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>230</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>227</prism:startingPage>
<prism:section>CLINICAL AND RESEARCH REPORTS</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/2/232?rss=1">
<title><![CDATA[[PROCEEDINGS] ]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/2/232?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>2008-05-01</dc:date>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.2.232</dc:identifier>
<dc:title><![CDATA[[PROCEEDINGS] ]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>2</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>234</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>232</prism:startingPage>
<prism:section>PROCEEDINGS</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/2/235?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] A Case of Temporary Finger Tremors Due to Amantadine Withdrawal]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/2/235?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Shinohara, Y., Hayakawa, N.]]></dc:creator>
<dc:date>2008-05-01</dc:date>
<dc:subject><![CDATA[Symptoms/Dimensions, Other Neuroscience]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.2.235</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] A Case of Temporary Finger Tremors Due to Amantadine Withdrawal]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>2</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>235</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>235</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/2/235-a?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] Multiple Embolic Phenomenon in the Brain Associated With Parenteral Buprenorphine Abuse]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/2/235-a?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Lee, T.-S., Ng, B. Y.]]></dc:creator>
<dc:date>2008-05-01</dc:date>
<dc:subject><![CDATA[Opioids]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.2.235-a</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] Multiple Embolic Phenomenon in the Brain Associated With Parenteral Buprenorphine Abuse]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>2</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>237</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>235</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/2/237?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] Paroxysmal Kinesigenic Dyskinesia and Cervical Disc Prolapse With Cord Compression: More Than a Coincidence?]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/2/237?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Yulug, B., Bakar, M., Ozer H, H., Yilmaz, M., Unlu, B.]]></dc:creator>
<dc:date>2008-05-01</dc:date>
<dc:subject><![CDATA[Symptoms/Dimensions, Other Neuroanatomy]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.2.237</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] Paroxysmal Kinesigenic Dyskinesia and Cervical Disc Prolapse With Cord Compression: More Than a Coincidence?]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>2</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>239</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>237</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/2/239?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] Clozapine-Induced Delirium]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/2/239?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Shankar, B. R.]]></dc:creator>
<dc:date>2008-05-01</dc:date>
<dc:subject><![CDATA[Delirium, Other Somatic Therapy]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.2.239</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] Clozapine-Induced Delirium]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>2</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>240</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>239</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/2/240?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] A Diffuse Brain Injury Leading to a Complex Neurobehavioral Syndrome]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/2/240?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Arauco, A. R., Grados, M. A., Vizcarra, D.]]></dc:creator>
<dc:date>2008-05-01</dc:date>
<dc:subject><![CDATA[Other Neuropsychiatric Disorders]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.2.240</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] A Diffuse Brain Injury Leading to a Complex Neurobehavioral Syndrome]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>2</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>241</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>240</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/2/241?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] Neuroleptic Induced Laryngo-Pharyngeal Dystonia]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/2/241?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Alappan, N., Shyam Sundar, A., Varghese, S. T.]]></dc:creator>
<dc:date>2008-05-01</dc:date>
<dc:subject><![CDATA[Crisis and Emergency Treatment]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.2.241</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] Neuroleptic Induced Laryngo-Pharyngeal Dystonia]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>2</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>242</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>241</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/2/242?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] Electroconvulsive Therapy of a Depressed Patient with Septo-Optic Dysplasia]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/2/242?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Ni, H.-C., Liu, H.-M., Tseng, M. M.]]></dc:creator>
<dc:date>2008-05-01</dc:date>
<dc:subject><![CDATA[Depression, ECT]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.2.242</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] Electroconvulsive Therapy of a Depressed Patient with Septo-Optic Dysplasia]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>2</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>243</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>242</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/2/244?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] Frontal Lobe Syndrome in a Patient without Structural Brain Abnormalities]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/2/244?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Hennings, J. M.H., Wetter, T. C., Zihl, J.]]></dc:creator>
<dc:date>2008-05-01</dc:date>
<dc:subject><![CDATA[Other Neuropsychiatric Disorders, Other Neuroanatomy]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.2.244</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] Frontal Lobe Syndrome in a Patient without Structural Brain Abnormalities]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>2</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>245</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>244</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/2/245?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] Neuroimaging Correlates of Chronic Delusional Jealousy after Right Cerebral Infarction]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/2/245?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Luaute, J-P, Saladini, O, Luaute, J]]></dc:creator>
<dc:date>2008-05-01</dc:date>
<dc:subject><![CDATA[SPECT]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.2.245</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] Neuroimaging Correlates of Chronic Delusional Jealousy after Right Cerebral Infarction]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>2</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>247</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>245</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/2/247?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] Risperidone and Valproate for Mania Following Stroke]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/2/247?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Dervaux, A., Levasseur, M.]]></dc:creator>
<dc:date>2008-05-01</dc:date>
<dc:subject><![CDATA[Other Mood Disorders, Stroke, Miscellaneous Somatic Therapies]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.2.247</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] Risperidone and Valproate for Mania Following Stroke]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>2</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>247</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>247</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/2/247-a?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] Depression Preceding the Onset of Progressive Supranuclear Paralysis: A Case Report]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/2/247-a?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Quante, A., Jakob, F., Wolf, J.]]></dc:creator>
<dc:date>2008-05-01</dc:date>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.2.247-a</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] Depression Preceding the Onset of Progressive Supranuclear Paralysis: A Case Report]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>2</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>248</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>247</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/2/248?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] Marked Hyperphagia Associated With Total Loss of Satiety in Alzheimer's Disease]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/2/248?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Bhagavati, S.]]></dc:creator>
<dc:date>2008-05-01</dc:date>
<dc:subject><![CDATA[Alzheimer's Disease, Dementias (General)]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.2.248</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] Marked Hyperphagia Associated With Total Loss of Satiety in Alzheimer's Disease]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>2</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>249</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>248</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/2/249?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] Topiramate-Induced Palinopsia]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/2/249?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Fontenelle, L. F.]]></dc:creator>
<dc:date>2008-05-01</dc:date>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.2.249</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] Topiramate-Induced Palinopsia]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>2</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>250</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>249</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/1/iv?rss=1">
<title><![CDATA[[WINDOWS TO THE BRAIN] Acute and Chronic Lyme Disease: Controversies for Neuropsychiatry]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/1/iv?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Hurley, R. A., Taber, K. H.]]></dc:creator>
<dc:date>2008-02-27</dc:date>
<dc:subject><![CDATA[Other Neuropsychiatric Disorders, Other Somatic Therapy]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.1.iv</dc:identifier>
<dc:title><![CDATA[[WINDOWS TO THE BRAIN] Acute and Chronic Lyme Disease: Controversies for Neuropsychiatry]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>6</prism:endingPage>
<prism:publicationDate>2008-02-01</prism:publicationDate>
<prism:startingPage>iv</prism:startingPage>
<prism:section>WINDOWS TO THE BRAIN</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/1/7?rss=1">
<title><![CDATA[[SPECIAL ARTICLES] Electroencephalographic Cerebral Dysrhythmic Abnormalities in the Trinity of Nonepileptic General Population, Neuropsychiatric, and Neurobehavioral Disorders]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/1/7?rss=1</link>
<description><![CDATA[
<p>Subclinical electroencephalographic epileptiform discharges in neurobehavioral disorders are not uncommon. The clinical significance and behavioral, diagnostic, and therapeutic implications of this EEG cerebral dysrhythmia have not been fully examined. Currently the only connotation for distinctive epileptiform electroencephalographic patterns is epileptic seizures. Given the prevailing dogma of not treating EEGs, these potential aberrations are either disregarded as irrelevant or are misattributed to indicate epilepsy. This article reappraises the literature on paroxysmal EEG dysrhythmia in normative studies of the "healthy" nonepileptic general populations, neuropsychiatry, and in neurobehavioral disorders. These EEG aberrations may be reflective of underlying morpho-functional brain abnormalities that underpin various neurobehavioral disturbances.</p>
]]></description>
<dc:creator><![CDATA[Shelley, B. P., Trimble, M. R., Boutros, N. N.]]></dc:creator>
<dc:date>2008-02-27</dc:date>
<dc:subject><![CDATA[Other Neuropsychiatric Disorders, Other Neuroscience]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.1.7</dc:identifier>
<dc:title><![CDATA[[SPECIAL ARTICLES] Electroencephalographic Cerebral Dysrhythmic Abnormalities in the Trinity of Nonepileptic General Population, Neuropsychiatric, and Neurobehavioral Disorders]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>22</prism:endingPage>
<prism:publicationDate>2008-02-01</prism:publicationDate>
<prism:startingPage>7</prism:startingPage>
<prism:section>SPECIAL ARTICLES</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/1/23?rss=1">
<title><![CDATA[[SPECIAL ARTICLES] Behavioral Reactivity and Addiction: The Adaptation of Behavioral Response to Reward Opportunities]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/1/23?rss=1</link>
<description><![CDATA[
<p>Persons recovering from addiction must refrain from drug use even when the opportunity to use exists. Understanding how behavioral response to drug reward opportunities is modified is key to treating addiction. Most effective behavioral therapies encourage patients to increase reinforcement opportunities by engaging unidentified sources of nondrug reward. The authors integrate transdisciplinary research on the brain and behavioral effects of increasing reward availability to demonstrate one neurobiological mechanism by which behavioral therapies help patients abstain. Explicating neurobiological processes underlying psychotherapy provides predictions about the interaction between dopaminergic medications and therapy and the  impact of individual differences in dopamine receptor expression on addiction vulnerability.</p>
]]></description>
<dc:creator><![CDATA[Trafton, J. A., Gifford, E. V.]]></dc:creator>
<dc:date>2008-02-27</dc:date>
<dc:subject><![CDATA[Addictive Disorders (General), Behavior Therapy]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.1.23</dc:identifier>
<dc:title><![CDATA[[SPECIAL ARTICLES] Behavioral Reactivity and Addiction: The Adaptation of Behavioral Response to Reward Opportunities]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>35</prism:endingPage>
<prism:publicationDate>2008-02-01</prism:publicationDate>
<prism:startingPage>23</prism:startingPage>
<prism:section>SPECIAL ARTICLES</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/1/36?rss=1">
<title><![CDATA[[SPECIAL ARTICLES] Multiple Sclerosis, Cannabinoids, and Cognition]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/1/36?rss=1</link>
<description><![CDATA[
<p>There is increasing interest in the therapeutic potential of cannabis-based medicinal extracts in multiple sclerosis. Cognitive deficits that have been attributed to long-term heavy recreational use of cannabis are not necessarily extended to controlled pharmaceutical use of cannabis-based medicinal extracts. Available data indicate that after relatively short-term administration of cannabis-based medicinal extracts no significant cognitive decline occurs. Due to the absence of large scale long-term systematic clinical trials of cannabis-based medicinal extracts in multiple sclerosis therapeutics, however, many issues remain unresolved, including the possible adverse effects of cannabis-based medicinal extracts on cognition. This article critically reviews the current literature and considers the potential for cognitive adverse effects of long-term cannabinoid use in multiple sclerosis therapeutics.</p>
]]></description>
<dc:creator><![CDATA[Papathanasopoulos, P., Messinis, L., Lyros, E., Kastellakis, A., Panagis, G.]]></dc:creator>
<dc:date>2008-02-27</dc:date>
<dc:subject><![CDATA[Other Neuropsychiatric Disorders]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.1.36</dc:identifier>
<dc:title><![CDATA[[SPECIAL ARTICLES] Multiple Sclerosis, Cannabinoids, and Cognition]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>51</prism:endingPage>
<prism:publicationDate>2008-02-01</prism:publicationDate>
<prism:startingPage>36</prism:startingPage>
<prism:section>SPECIAL ARTICLES</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/1/52?rss=1">
<title><![CDATA[[REGULAR ARTICLES] Nondysphoric Depression Following Stroke]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/1/52?rss=1</link>
<description><![CDATA[
<p>Right hemisphere damage may influence the presentation of depressive disorders ensuing after stroke by disrupting emotion processing mechanisms. Three-hundred and one consecutive admissions for acute stroke were examined and subjects meeting previously validated criteria for nondysphoric depression (i.e., depressive ideation without endorsement of sad emotions) were compared to dysphoric depression, and to nondepressed patients. Compared to dysphoric depression, nondysphoric depression showed more frequent right anterior hemisphere lesions and more psychomotor slowing, self-depreciation, and severe sad affect. Psychopathological features and location of damage suggest that nondysphoric depression may be a special presentation of depressive disorder following stroke in which right hemisphere damage limits the apprehension of personal emotional changes.</p>
]]></description>
<dc:creator><![CDATA[Paradiso, S., Vaidya, J., Tranel, D., Kosier, T., Robinson, R. G.]]></dc:creator>
<dc:date>2008-02-27</dc:date>
<dc:subject><![CDATA[Depression, Stroke]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.1.52</dc:identifier>
<dc:title><![CDATA[[REGULAR ARTICLES] Nondysphoric Depression Following Stroke]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>61</prism:endingPage>
<prism:publicationDate>2008-02-01</prism:publicationDate>
<prism:startingPage>52</prism:startingPage>
<prism:section>REGULAR ARTICLES</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/1/62?rss=1">
<title><![CDATA[[REGULAR ARTICLES] Content-Specific Delusions From Right Caudate Lacunar Stroke: Association with Prefrontal Hypometabolism]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/1/62?rss=1</link>
<description><![CDATA[
<p>Patients with caudate lesions can present with content-specific delusions, possibly due to disruption of frontosubcortical circuits connecting the frontal lobes with the basal ganglia. This study included eight patients who presented with content-specific delusions after right caudate stroke and an equal number of matched controls, without stroke or delusions. Compared to controls, patients with caudate lesions performed less well on tests of memory, abstract reasoning, and frontal executive functions, and had significantly reduced metabolism in the inferior prefrontal cortex. These patients suggest an etiological relationship between alterations in inferior prefrontal functions and the development of content-specific delusions.</p>
]]></description>
<dc:creator><![CDATA[McMurtray, A. M., Sultzer, D. L., Monserratt, L., Yeo, T., Mendez, M. F.]]></dc:creator>
<dc:date>2008-02-27</dc:date>
<dc:subject><![CDATA[Stroke, Symptoms/Dimensions]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.1.62</dc:identifier>
<dc:title><![CDATA[[REGULAR ARTICLES] Content-Specific Delusions From Right Caudate Lacunar Stroke: Association with Prefrontal Hypometabolism]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>67</prism:endingPage>
<prism:publicationDate>2008-02-01</prism:publicationDate>
<prism:startingPage>62</prism:startingPage>
<prism:section>REGULAR ARTICLES</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/1/68?rss=1">
<title><![CDATA[[REGULAR ARTICLES] Traumatic Brain Injury, Apolipoprotein E-{epsilon}4, and Cognition in Older Adults: A Two-Year Longitudinal Study]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/1/68?rss=1</link>
<description><![CDATA[
<p>Patients with mild-to-moderate traumatic brain injury (TBI) (N=69) were compared with age-, gender-, and education-matched healthy control group subjects (N=79) on performance of neuropsychological tests at one and 2 years following injury, and informant-rated functional abilities. All subjects were assessed for the presence of the Apolipoprotein E-4 (APOE-4) allele and rated for "mild cognitive impairment" (MCI) or dementia. Traumatic brain injury patients were no different from the comparison group on measures of cognition or functional impairment. Traumatic brain injury was not associated with higher rates of amnestic mild cognitive impairment or dementia, and APOE-4 was not associated with cognition.</p>
]]></description>
<dc:creator><![CDATA[Rapoport, M., Wolf, U., Herrmann, N., Kiss, A., Shammi, P., Reis, M., Phillips, A., Feinstein, A.]]></dc:creator>
<dc:date>2008-02-27</dc:date>
<dc:subject><![CDATA[Geriatric Psychiatry, Traumatic Brain Injury]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.1.68</dc:identifier>
<dc:title><![CDATA[[REGULAR ARTICLES] Traumatic Brain Injury, Apolipoprotein E-{epsilon}4, and Cognition in Older Adults: A Two-Year Longitudinal Study]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>73</prism:endingPage>
<prism:publicationDate>2008-02-01</prism:publicationDate>
<prism:startingPage>68</prism:startingPage>
<prism:section>REGULAR ARTICLES</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/1/74?rss=1">
<title><![CDATA[[REGULAR ARTICLES] Changes in Regional Cerebral Blood Flow After Repetitive Transcranial Magnetic Stimulation of the Left Dorsolateral Prefrontal Cortex in Treatment-Resistant Depression]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/1/74?rss=1</link>
<description><![CDATA[
<p>High-frequency repetitive transcranial magnetic stimulation (rTMS) of the left dorsolateral prefrontal cortex is effective in treatment-resistant depression, although its mechanism is still not completely elucidated. To clarify the neuroanatomical alteration of function elicited by rTMS, single photon emission computed tomography (SPECT) with <sup>99m</sup>Tc-ECD was performed on 12 male inpatients with treatment-resistant unipolar depression before and after high-frequency rTMS of the left dorsolateral prefrontal cortex. These results suggest that the manifestation of the antidepressant effect of high-frequency rTMS is associated with changes in the neuroanatomical function of the left dorsolateral prefrontal cortex as well as of the limbic-paralimbic region, including the ipsilateral subgenual cingulate, and the basal ganglia.</p>
]]></description>
<dc:creator><![CDATA[Kito, S., Fujita, K., Koga, Y.]]></dc:creator>
<dc:date>2008-02-27</dc:date>
<dc:subject><![CDATA[Depression, Other Somatic Therapy]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.1.74</dc:identifier>
<dc:title><![CDATA[[REGULAR ARTICLES] Changes in Regional Cerebral Blood Flow After Repetitive Transcranial Magnetic Stimulation of the Left Dorsolateral Prefrontal Cortex in Treatment-Resistant Depression]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>80</prism:endingPage>
<prism:publicationDate>2008-02-01</prism:publicationDate>
<prism:startingPage>74</prism:startingPage>
<prism:section>REGULAR ARTICLES</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/1/81?rss=1">
<title><![CDATA[[REGULAR ARTICLES] Psychiatric Manifestations in Wilson's Disease: A Cross-Sectional Analysis]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/1/81?rss=1</link>
<description><![CDATA[
<p>Behavioral and psychiatric abnormalities in Wilson&rsquo;s disease (WD) have a variable frequency and spectrum. This study involved evaluation of the psychiatric comorbidities in patients of Wilson&rsquo;s disease, using structured clinical interview for DSM-IV Axis-I disorders (SCID). Among the 50 confirmed patients with Wilson&rsquo;s disease recruited for this study, 12 patients (24%) fulfilled the diagnostic criteria for syndromic psychiatric diagnosis: bipolar affective disorder (18%), major depression (4%), and dysthymia (2%). Formal assessment of psychopathology in all patients with Wilson&rsquo;s disease may have therapeutic significance.</p>
]]></description>
<dc:creator><![CDATA[Shanmugiah, A., Sinha, S., Taly, A.B., Prashanth, L.K., Tomar, M., Arunodaya, G.R., Reddy, J. Y.C., Khanna, S.]]></dc:creator>
<dc:date>2008-02-27</dc:date>
<dc:subject><![CDATA[Syndromes Secondary to General Medical Disorders, Other Neuroscience]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.1.81</dc:identifier>
<dc:title><![CDATA[[REGULAR ARTICLES] Psychiatric Manifestations in Wilson's Disease: A Cross-Sectional Analysis]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>85</prism:endingPage>
<prism:publicationDate>2008-02-01</prism:publicationDate>
<prism:startingPage>81</prism:startingPage>
<prism:section>REGULAR ARTICLES</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/1/86?rss=1">
<title><![CDATA[[REGULAR ARTICLES] The Neuropsychiatry and Neuropsychology Of Lipoid Proteinosis]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/1/86?rss=1</link>
<description><![CDATA[
<p>Lipoid proteinosis is a rare hereditary disease which often results in bilateral calcifications in the medial temporal region. Thirty-four adults living with lipoid proteinosis (&gt;10% of the world population) were extensively assessed with standardized neuropsychiatric and neuropsychological measures. Of these, 27 patients representing a homogenous group living in the Northern Cape were matched with 47 controls. Subjects with lipoid proteinosis had a high incidence of neuropsychiatric disorders and performed poorly on facial recognition of positive and negative emotions and on many neuropsychological measures. These findings are consistent with involvement of the medial temporal areas in cognitive and emotive processing.</p>
]]></description>
<dc:creator><![CDATA[Thornton, H. B., Nel, D., Thornton, D., van Honk, J., Baker, G. A., Stein, D. J.]]></dc:creator>
<dc:date>2008-02-27</dc:date>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.1.86</dc:identifier>
<dc:title><![CDATA[[REGULAR ARTICLES] The Neuropsychiatry and Neuropsychology Of Lipoid Proteinosis]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>92</prism:endingPage>
<prism:publicationDate>2008-02-01</prism:publicationDate>
<prism:startingPage>86</prism:startingPage>
<prism:section>REGULAR ARTICLES</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/1/93?rss=1">
<title><![CDATA[[CLINICAL AND RESEARCH REPORTS] Treatment of Akinetic Mutism with Intramuscular Olanzapine: A Case Series]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/1/93?rss=1</link>
<description><![CDATA[
<p>Akinetic mutism is a wakeful state of severe apathy and paucity of volitional movement. Evidence indicates a possible dopaminergic hypofunction within the anterior cingulate cortex. The authors present three cases of acute onset akinetic mutism successfully treated with intramuscular olanzapine.</p>
]]></description>
<dc:creator><![CDATA[Spiegel, D. R., Casella, D. P., Callender, D. M., Dhadwal, N.]]></dc:creator>
<dc:date>2008-02-27</dc:date>
<dc:subject><![CDATA[Other Neuropsychiatric Disorders]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.1.93</dc:identifier>
<dc:title><![CDATA[[CLINICAL AND RESEARCH REPORTS] Treatment of Akinetic Mutism with Intramuscular Olanzapine: A Case Series]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>95</prism:endingPage>
<prism:publicationDate>2008-02-01</prism:publicationDate>
<prism:startingPage>93</prism:startingPage>
<prism:section>CLINICAL AND RESEARCH REPORTS</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/1/96?rss=1">
<title><![CDATA[[CLINICAL AND RESEARCH REPORTS] Correlation Between Denial of Illness and Executive Function Following Stroke: A Pilot Study]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/1/96?rss=1</link>
<description><![CDATA[
<p>Executive function and denial of illness were examined among 24 patients who received double-blind antidepressant treatment following stroke. Between end-of-treatment at 3 months and follow-up at 2 years, significant correlation was found between improvement in executive function and decrease in denial of illness.</p>
]]></description>
<dc:creator><![CDATA[Narushima, K., Moser, D. J., Robinson, R. G.]]></dc:creator>
<dc:date>2008-02-27</dc:date>
<dc:subject><![CDATA[Stroke]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.1.96</dc:identifier>
<dc:title><![CDATA[[CLINICAL AND RESEARCH REPORTS] Correlation Between Denial of Illness and Executive Function Following Stroke: A Pilot Study]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>100</prism:endingPage>
<prism:publicationDate>2008-02-01</prism:publicationDate>
<prism:startingPage>96</prism:startingPage>
<prism:section>CLINICAL AND RESEARCH REPORTS</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/1/101?rss=1">
<title><![CDATA[[CLINICAL AND RESEARCH REPORTS] Restless Legs Syndrome is Associated with DSM-IV Major Depressive Disorder and Panic Disorder in the Community]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/1/101?rss=1</link>
<description><![CDATA[
<p>The authors examined the association between restless legs syndrome (RLS) and DSM-IV major depressive disorder and panic disorder based on Wave III and IV of the Baltimore ECA follow-up study. Of 1071 participants, 1024 completed the RLS Questionnaire and Diagnostic Interview Schedule. Adjusted odds ratio for diagnosis of major depressive disorder (4.7, 95% confidence interval [1.6, 14.5]) and panic disorder (12.9 [3.6, 46.0]) and comorbidity of major depressive disorder and panic disorder (9.7 [1.4, 69.0]) in the past 12 months suggested a strong association between restless legs syndrome and major depressive disorder and/or panic disorder.</p>
]]></description>
<dc:creator><![CDATA[Lee, H. B., Hening, W. A., Allen, R. P., Kalaydjian, A. E., Earley, C. J., Eaton, W. W., Lyketsos, C. G.]]></dc:creator>
<dc:date>2008-02-27</dc:date>
<dc:subject><![CDATA[Depression, Panic Disorder]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.1.101</dc:identifier>
<dc:title><![CDATA[[CLINICAL AND RESEARCH REPORTS] Restless Legs Syndrome is Associated with DSM-IV Major Depressive Disorder and Panic Disorder in the Community]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>105</prism:endingPage>
<prism:publicationDate>2008-02-01</prism:publicationDate>
<prism:startingPage>101</prism:startingPage>
<prism:section>CLINICAL AND RESEARCH REPORTS</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/1/106?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] Use of Donepezil in the Treatment of Cognitive Impairments of Moderate Traumatic Brain Injury]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/1/106?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Foster, M., Spiegel, D. R.]]></dc:creator>
<dc:date>2008-02-27</dc:date>
<dc:subject><![CDATA[Traumatic Brain Injury, Other Somatic Therapy]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.1.106</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] Use of Donepezil in the Treatment of Cognitive Impairments of Moderate Traumatic Brain Injury]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>106</prism:endingPage>
<prism:publicationDate>2008-02-01</prism:publicationDate>
<prism:startingPage>106</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/1/107?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] Donepezil Induced Hypomania]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/1/107?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Rao, V., Ovitt, L., Robbins, B.]]></dc:creator>
<dc:date>2008-02-27</dc:date>
<dc:subject><![CDATA[Other Neuropsychiatric Disorders]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.1.107</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] Donepezil Induced Hypomania]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>107</prism:endingPage>
<prism:publicationDate>2008-02-01</prism:publicationDate>
<prism:startingPage>107</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/1/107-a?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] The Neuroprotective Effect of Olanzapine]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/1/107-a?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Yulug, B., Bakar, M., Ozan, E.]]></dc:creator>
<dc:date>2008-02-27</dc:date>
<dc:subject><![CDATA[Other Somatic Therapy]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.1.107-a</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] The Neuroprotective Effect of Olanzapine]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>108</prism:endingPage>
<prism:publicationDate>2008-02-01</prism:publicationDate>
<prism:startingPage>107</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/1/108?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] Acute Pisa Syndrome and Pharnygolaryngeal Dystonia Due to Ziprasidone]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/1/108?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Duggal, H. S.]]></dc:creator>
<dc:date>2008-02-27</dc:date>
<dc:subject><![CDATA[Other Somatic Therapy]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.1.108</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] Acute Pisa Syndrome and Pharnygolaryngeal Dystonia Due to Ziprasidone]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>109</prism:endingPage>
<prism:publicationDate>2008-02-01</prism:publicationDate>
<prism:startingPage>108</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/1/109?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] A Squint of Brain: A Capgras Syndrome Variant]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/1/109?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Carota, A., Mishra, N., Allaoua, M., Ghika, J.]]></dc:creator>
<dc:date>2008-02-27</dc:date>
<dc:subject><![CDATA[Other Neuropsychiatric Disorders]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.1.109</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] A Squint of Brain: A Capgras Syndrome Variant]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>110</prism:endingPage>
<prism:publicationDate>2008-02-01</prism:publicationDate>
<prism:startingPage>109</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/1/110?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] Pseudobulbar Palsy and Affect in a Case of Progressive Multifocal Leukoencephalopathy]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/1/110?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Graham, K. C., Spiegel, D. R.]]></dc:creator>
<dc:date>2008-02-27</dc:date>
<dc:subject><![CDATA[Other Neuropsychiatric Disorders]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.1.110</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] Pseudobulbar Palsy and Affect in a Case of Progressive Multifocal Leukoencephalopathy]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>111</prism:endingPage>
<prism:publicationDate>2008-02-01</prism:publicationDate>
<prism:startingPage>110</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/1/111?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] Valproate-Induced Subclinical Hypothyroidism]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/1/111?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Rao, P., Madhav Natu, S., Mati Goel, M., Ali, B.]]></dc:creator>
<dc:date>2008-02-27</dc:date>
<dc:subject><![CDATA[Other Treatment]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.1.111</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] Valproate-Induced Subclinical Hypothyroidism]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>112</prism:endingPage>
<prism:publicationDate>2008-02-01</prism:publicationDate>
<prism:startingPage>111</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/1/112?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] Successful Treatment of Delusion of Parasitosis with Risperidone]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/1/112?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Mahgoub, N. A.]]></dc:creator>
<dc:date>2008-02-27</dc:date>
<dc:subject><![CDATA[Other Neuropsychiatric Disorders]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.1.112</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] Successful Treatment of Delusion of Parasitosis with Risperidone]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>113</prism:endingPage>
<prism:publicationDate>2008-02-01</prism:publicationDate>
<prism:startingPage>112</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/1/113?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] Reduction in Salivary Cortisol Concentration Correlates with Resolution of Psychosis in Cushing's Syndrome]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/1/113?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Myhill, P. C., Sillars, B. A., Starkstein, S., Annus, T., Yeap, B. B.]]></dc:creator>
<dc:date>2008-02-27</dc:date>
<dc:subject><![CDATA[Other Somatic Therapy]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.1.113</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] Reduction in Salivary Cortisol Concentration Correlates with Resolution of Psychosis in Cushing's Syndrome]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>115</prism:endingPage>
<prism:publicationDate>2008-02-01</prism:publicationDate>
<prism:startingPage>113</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/1/115?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] Transient Amnestic Syndrome in the Setting of Recurrent Partial Elementary Seizures]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/1/115?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Weiss, G. M., Spiegel, D. R.]]></dc:creator>
<dc:date>2008-02-27</dc:date>
<dc:subject><![CDATA[Other Neuropsychiatric Disorders, Symptoms/Dimensions]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.1.115</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] Transient Amnestic Syndrome in the Setting of Recurrent Partial Elementary Seizures]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>116</prism:endingPage>
<prism:publicationDate>2008-02-01</prism:publicationDate>
<prism:startingPage>115</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/1/116?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] Poststroke Hallucination Delusion Syndrome]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/1/116?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Mishra, N. K., Hastak, S.]]></dc:creator>
<dc:date>2008-02-27</dc:date>
<dc:subject><![CDATA[Stroke, Other Neuropsychiatric Disorders, Symptoms/Dimensions]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.1.116</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] Poststroke Hallucination Delusion Syndrome]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>116</prism:endingPage>
<prism:publicationDate>2008-02-01</prism:publicationDate>
<prism:startingPage>116</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/1/116-a?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] Late-Life Anxiety]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/1/116-a?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Mahgoub, N. A., Saifollahi, J., Lantz, M.]]></dc:creator>
<dc:date>2008-02-27</dc:date>
<dc:subject><![CDATA[Geriatric Psychiatry, Anxiety Disorders (General)]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.1.116-a</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] Late-Life Anxiety]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>117</prism:endingPage>
<prism:publicationDate>2008-02-01</prism:publicationDate>
<prism:startingPage>116</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/1/117?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] Aripiprazole Diminishes Cannabis Use in Schizophrenia]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/1/117?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Desseilles, M., Mathot, F., Desseilles, M.]]></dc:creator>
<dc:date>2008-02-27</dc:date>
<dc:subject><![CDATA[Schizophrenia Spectrum Disorders]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.1.117</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] Aripiprazole Diminishes Cannabis Use in Schizophrenia]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>118</prism:endingPage>
<prism:publicationDate>2008-02-01</prism:publicationDate>
<prism:startingPage>117</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/1/118?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] Clinical Correlates of Personality Changes Associated With Traumatic Brain Injury]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/1/118?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Rao, V., Spiro, J. R., Handel, S., Onyike, C. U.]]></dc:creator>
<dc:date>2008-02-27</dc:date>
<dc:subject><![CDATA[Traumatic Brain Injury, Other Personality Disorders]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.1.118</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] Clinical Correlates of Personality Changes Associated With Traumatic Brain Injury]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>119</prism:endingPage>
<prism:publicationDate>2008-02-01</prism:publicationDate>
<prism:startingPage>118</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/1/119?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] Memantine in Major Depression with Catatonic Features]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/1/119?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Munoz, C., Yulan, N., Achaval, V., Appiani, F., Carroll, B. T.]]></dc:creator>
<dc:date>2008-02-27</dc:date>
<dc:subject><![CDATA[Depression, Other Neuropsychiatric Disorders, Other Somatic Therapy]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.1.119</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] Memantine in Major Depression with Catatonic Features]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>120</prism:endingPage>
<prism:publicationDate>2008-02-01</prism:publicationDate>
<prism:startingPage>119</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/1/120?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] Ethnicity and Cognition: Dangers of Biological Determinism]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/1/120?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Benning, T. B]]></dc:creator>
<dc:date>2008-02-27</dc:date>
<dc:subject><![CDATA[Cross-Cultural Psychiatry, Stigma, Discrimination]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.1.120</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] Ethnicity and Cognition: Dangers of Biological Determinism]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>121</prism:endingPage>
<prism:publicationDate>2008-02-01</prism:publicationDate>
<prism:startingPage>120</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/1/121?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] Lamotrigine for the Treatment of Impulsive Aggression and Affective Symptoms in a Patient with Borderline Personality Disorder Comorbid with Body Dysmorphic Disorder]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/1/121?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Pavlovic, Z. M.]]></dc:creator>
<dc:date>2008-02-27</dc:date>
<dc:subject><![CDATA[Borderline Personality Disorders]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.1.121</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] Lamotrigine for the Treatment of Impulsive Aggression and Affective Symptoms in a Patient with Borderline Personality Disorder Comorbid with Body Dysmorphic Disorder]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>122</prism:endingPage>
<prism:publicationDate>2008-02-01</prism:publicationDate>
<prism:startingPage>121</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/1/122?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] Persistent Neurobehavioral Signs and Symptoms Following West Nile Fever]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/1/122?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Hall, D. A., Tyler, K. L., Frey, K. L., Kozora, E., Arciniegas, D. B.]]></dc:creator>
<dc:date>2008-02-27</dc:date>
<dc:subject><![CDATA[Other Health Services Issues, Other Neuropsychiatric Disorders, Other Neuroscience]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.1.122</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] Persistent Neurobehavioral Signs and Symptoms Following West Nile Fever]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>123</prism:endingPage>
<prism:publicationDate>2008-02-01</prism:publicationDate>
<prism:startingPage>122</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/20/1/123?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] Brain Damage After Preischemic Locomotor Activity]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/20/1/123?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Yulug, B., Bakar, M., Ozan, E.]]></dc:creator>
<dc:date>2008-02-27</dc:date>
<dc:subject><![CDATA[Other Neuroscience]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.20.1.123</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] Brain Damage After Preischemic Locomotor Activity]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>20</prism:volume>
<prism:endingPage>124</prism:endingPage>
<prism:publicationDate>2008-02-01</prism:publicationDate>
<prism:startingPage>123</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/19/4/358?rss=1">
<title><![CDATA[[WINDOWS TO THE BRAIN] Functional Anatomy of Humor: Positive Affect and Chronic Mental Illness]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/19/4/358?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Taber, K. H., Redden, M., Hurley, R. A.]]></dc:creator>
<dc:date>2007-12-10</dc:date>
<dc:identifier>info:doi/10.1176/appi.neuropsych.19.4.358</dc:identifier>
<dc:title><![CDATA[[WINDOWS TO THE BRAIN] Functional Anatomy of Humor: Positive Affect and Chronic Mental Illness]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>19</prism:volume>
<prism:endingPage>362</prism:endingPage>
<prism:publicationDate>2007-11-01</prism:publicationDate>
<prism:startingPage>358</prism:startingPage>
<prism:section>WINDOWS TO THE BRAIN</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/19/4/363?rss=1">
<title><![CDATA[[SPECIAL ARTICLES] The Neuroendocrine Effects of Traumatic Brain Injury]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/19/4/363?rss=1</link>
<description><![CDATA[
<p>Neuroendocrine dysfunction after traumatic brain injury (TBI) is under-diagnosed, under-treated, and may adversely affect the rate of recovery. Single or multiple pituitary-target hormone disruption occurs in up to two-thirds of persons with TBI, most commonly affecting the gonadal and growth hormone axes. The time course of decline in and recovery of pituitary function in relation to cognitive dysfunction and rehabilitation progress are not well described. This article reviews the clinical spectrum of neuroendocrine deficits after TBI and their underlying mechanisms. Future studies of the effects of hormonal replacement on recovery are recommended.</p>
]]></description>
<dc:creator><![CDATA[Rothman, M. S., Arciniegas, D. B., Filley, C. M., Wierman, M. E.]]></dc:creator>
<dc:date>2007-12-10</dc:date>
<dc:subject><![CDATA[Traumatic Brain Injury]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.19.4.363</dc:identifier>
<dc:title><![CDATA[[SPECIAL ARTICLES] The Neuroendocrine Effects of Traumatic Brain Injury]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>19</prism:volume>
<prism:endingPage>372</prism:endingPage>
<prism:publicationDate>2007-11-01</prism:publicationDate>
<prism:startingPage>363</prism:startingPage>
<prism:section>SPECIAL ARTICLES</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/19/4/373?rss=1">
<title><![CDATA[[SPECIAL ARTICLES] Neurocognitive Impairment and Dementia in Mood Disorders]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/19/4/373?rss=1</link>
<description><![CDATA[
<p>In a substantial percentage of patients, mood disorders are accompanied by persistent neurocognitive impairment. Elderly patients with dementia often suffer from depression. Neurocognitive tests and imaging are increasingly used to complement diagnostics. Tests assessing memory, attention, executive functions, and visuospatial abilities might help to distinguish mood disorder patients who can be expected to develop dementia from those who will not. This review presents a summary of knowledge on neurocognitive profiles differentiating impairment in mood disorders and dementia. Ideas on pathophysiological causation and progression are translated into recommendations for patient management.</p>
]]></description>
<dc:creator><![CDATA[Pfennig, A., Littmann, E., Bauer, M.]]></dc:creator>
<dc:date>2007-12-10</dc:date>
<dc:subject><![CDATA[Mood Disorders (General), Dementias (General)]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.19.4.373</dc:identifier>
<dc:title><![CDATA[[SPECIAL ARTICLES] Neurocognitive Impairment and Dementia in Mood Disorders]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>19</prism:volume>
<prism:endingPage>382</prism:endingPage>
<prism:publicationDate>2007-11-01</prism:publicationDate>
<prism:startingPage>373</prism:startingPage>
<prism:section>SPECIAL ARTICLES</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/19/4/383?rss=1">
<title><![CDATA[[REGULAR ARTICLES] Frontal White Matter Integrity in Borderline Personality Disorder With Self-Injurious Behavior]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/19/4/383?rss=1</link>
<description><![CDATA[
<p>Self-injurious behavior in borderline personality disorder is a frequent cause of morbidity and mortality, but neurobiological studies examining this behavior are few. Nine women with borderline personality disorder self-injurious behavior and seven comparison subjects underwent diffusion tensor imaging (DTI). Trace and fractional anisotropy (FA) were calculated for frontal and posterior regions. Borderline personality disorder-self-injurious behavior subjects also underwent a battery of neuropsychological tests that emphasized executive functions. They had significantly higher trace and lower FA in inferior frontal but not posterior regions. Correlational analyses between DTI and cognitive variables showed a pattern of results that was contrary to expectations with posterior white matter integrity correlating with isolated measures of executive function and anterior white matter integrity correlating with a component of verbal memory test performance. Women with borderline personality disorder-self-injurious behavior exhibit decreased white matter microstructural integrity in inferior frontal brain regions that may include components of orbito-frontal circuitry.</p>
]]></description>
<dc:creator><![CDATA[Grant, J. E., Correia, S., Brennan-Krohn, T., Malloy, P. F., Laidlaw, D. H., Schulz, S. C.]]></dc:creator>
<dc:date>2007-12-10</dc:date>
<dc:subject><![CDATA[Borderline Personality Disorders, Other Violence/Aggression, MRI]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.19.4.383</dc:identifier>
<dc:title><![CDATA[[REGULAR ARTICLES] Frontal White Matter Integrity in Borderline Personality Disorder With Self-Injurious Behavior]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>19</prism:volume>
<prism:endingPage>390</prism:endingPage>
<prism:publicationDate>2007-11-01</prism:publicationDate>
<prism:startingPage>383</prism:startingPage>
<prism:section>REGULAR ARTICLES</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/19/4/391?rss=1">
<title><![CDATA[[REGULAR ARTICLES] Methodological Issues in Conducting Treatment Trials for Psychological Nonepileptic Seizures]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/19/4/391?rss=1</link>
<description><![CDATA[
<p>A randomized, placebo-controlled trial has yet to be completed in patients with psychological nonepileptic seizures (NES). Treatment publications for NES are limited to class III trials and class IV reports. Little is written on the methodology of treatment trials in NES. The authors describe the procedures and limitations of such a trial to inform future NES treatment trials, based on their prospective, open-label pharmacological, feasibility trial. The authors review the recruitment, enrollment, completion of surveys, compliance, and follow-up of patients with NES. The majority of patients who enrolled, readily completed surveys and took the medication during the trial. Twelve patients were screened, eight enrolled, and six completed the trial. The authors discuss the use of outcomes and the various symptoms scales in the trial. A comprehensive neuropsychiatric initial assessment and assessing cognitive, emotional, behavioral, and psychosocial measures are important for monitoring the outcomes in NES treatment RCTs.</p>
]]></description>
<dc:creator><![CDATA[LaFrance, W. C., Blum, A. S., Miller, I. W., Ryan, C. E., Keitner, G. I.]]></dc:creator>
<dc:date>2007-12-10</dc:date>
<dc:subject><![CDATA[Research Design, Methodology, Epilepsy]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.19.4.391</dc:identifier>
<dc:title><![CDATA[[REGULAR ARTICLES] Methodological Issues in Conducting Treatment Trials for Psychological Nonepileptic Seizures]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>19</prism:volume>
<prism:endingPage>398</prism:endingPage>
<prism:publicationDate>2007-11-01</prism:publicationDate>
<prism:startingPage>391</prism:startingPage>
<prism:section>REGULAR ARTICLES</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/19/4/399?rss=1">
<title><![CDATA[[REGULAR ARTICLES] Risk Factors for and Correlates of Poststroke Depression Following Discontinuation of Antidepressants]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/19/4/399?rss=1</link>
<description><![CDATA[
<p>The authors randomly assigned nondepressed patients at least 3 months poststroke to receive nortriptyline, fluoxetine, or placebo for 3 months using double-blind methodology. Patients were followed at 3, 6, 9, and 21 months for new onset of depression. In patients treated with antidepressants, lesion volume and degree of social impairment were associated with subsequent late-onset of poststroke depression at 6 and 9 months. In the placebo group, severity of impairment in activities of daily living, at 3 and 9 months, was associated with late onset poststroke depression. Differences in the clinical/pathological correlates may reflect subtle differences in the pathophysiology of poststroke depression following prophylactic antidepressants.</p>
]]></description>
<dc:creator><![CDATA[Fiedorowicz, J. G., Takezawa, K., Robinson, R. G.]]></dc:creator>
<dc:date>2007-12-10</dc:date>
<dc:subject><![CDATA[Depression, Stroke]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.19.4.399</dc:identifier>
<dc:title><![CDATA[[REGULAR ARTICLES] Risk Factors for and Correlates of Poststroke Depression Following Discontinuation of Antidepressants]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>19</prism:volume>
<prism:endingPage>405</prism:endingPage>
<prism:publicationDate>2007-11-01</prism:publicationDate>
<prism:startingPage>399</prism:startingPage>
<prism:section>REGULAR ARTICLES</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/19/4/406?rss=1">
<title><![CDATA[[REGULAR ARTICLES] Review of Adjunctive Glutamate Antagonist Therapy in the Treatment of Catatonic Syndromes]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/19/4/406?rss=1</link>
<description><![CDATA[
<p>Catatonia is a common neuropsychiatric syndrome which may arise from GABA-A hypoactivity, dopamine (D2) hypoactivity,and possibly glutamate NMDA hyperactivity. Amantadine and memantine have been reported as effective treatments for catatonia in selected cases, and probably mediate the presence of catatonic signs and symptoms through complex pathways involving glutamate antagonism. The authors identified 25 cases of catatonia treated with either agent. This article provides indirect evidence that glutamate antagonists may improve catatonic signs in some patients who fail to respond to established treatment, including lorazepam or electroconvulsive therapy. Further study of glutamate antagonists in the treatment of catatonia is needed.</p>
]]></description>
<dc:creator><![CDATA[Carroll, B. T., Goforth, H. W., Thomas, C., Ahuja, N., McDaniel, W. W., Kraus, M. F., Spiegel, D. R., Franco, K. N., Pozuelo, L., Munoz, C.]]></dc:creator>
<dc:date>2007-12-10</dc:date>
<dc:subject><![CDATA[Other Neuropsychiatric Disorders]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.19.4.406</dc:identifier>
<dc:title><![CDATA[[REGULAR ARTICLES] Review of Adjunctive Glutamate Antagonist Therapy in the Treatment of Catatonic Syndromes]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>19</prism:volume>
<prism:endingPage>412</prism:endingPage>
<prism:publicationDate>2007-11-01</prism:publicationDate>
<prism:startingPage>406</prism:startingPage>
<prism:section>REGULAR ARTICLES</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/19/4/413?rss=1">
<title><![CDATA[[REGULAR ARTICLES] Hypocretin/Orexin: A Molecular Link Between Sleep, Energy Regulation, and Pleasure]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/19/4/413?rss=1</link>
<description><![CDATA[
<p>Hypocretin (Hcrt) is a neurotransmitter of the dorsal and lateral hypothalamus that regulates sleep, appetite, and energy consumption. Recent evidence indicates that it is also involved in pleasure/reward-seeking. Mutation of the Hcrt-receptor gene causes narcolepsy in canines, and Hcrt knockout mice exhibit narcolepsy-like symptoms. Human narcoleptics do not commonly have mutations in the ligand or receptor but do have degeneration of Hcrt-containing neurons, possibly through an autoimmune mechanism. When Hcrt neurons degenerate in mice, hypophagia and obesity are observed, symptoms that are also present in some human narcoleptics. This article reviews the recent literature with regard to the many functions of this single molecule. The authors suggest that eating habits and impulsivity may be topics worth exploring in the evaluation of narcoleptic patients.</p>
]]></description>
<dc:creator><![CDATA[Ganjavi, H., Shapiro, C. M.]]></dc:creator>
<dc:date>2007-12-10</dc:date>
<dc:identifier>info:doi/10.1176/appi.neuropsych.19.4.413</dc:identifier>
<dc:title><![CDATA[[REGULAR ARTICLES] Hypocretin/Orexin: A Molecular Link Between Sleep, Energy Regulation, and Pleasure]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>19</prism:volume>
<prism:endingPage>419</prism:endingPage>
<prism:publicationDate>2007-11-01</prism:publicationDate>
<prism:startingPage>413</prism:startingPage>
<prism:section>REGULAR ARTICLES</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/19/4/420?rss=1">
<title><![CDATA[[REGULAR ARTICLES] Neurological Soft Signs in Mentally Disordered Offenders]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/19/4/420?rss=1</link>
<description><![CDATA[
<p>The study used the Neurological Evaluation Scale to assess neurological soft signs in 351 offenders and 80 healthy comparison subjects. Offenders were also interviewed using the Structured Clinical Interview for DSM-IV and the Hare Psychopathy Checklist. Neurological signs were significantly increased in offenders compared with healthy subjects. Offenders with repeated misdemeanors had higher rates of neurological signs than those with a single felony. Neurological scores were significantly predicted by lifetime diagnoses of psychotic, anxiety, and substance use disorders. Each diagnostic category was associated with a distinct pattern of neurological abnormalities.</p>
]]></description>
<dc:creator><![CDATA[Assadi, S. M., Noroozian, M., Shariat, S. V., Yahyazadeh, O., Pakravannejad, M., Aghayan, S.]]></dc:creator>
<dc:date>2007-12-10</dc:date>
<dc:subject><![CDATA[Other Neuropsychiatric Disorders, DSM]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.19.4.420</dc:identifier>
<dc:title><![CDATA[[REGULAR ARTICLES] Neurological Soft Signs in Mentally Disordered Offenders]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>19</prism:volume>
<prism:endingPage>427</prism:endingPage>
<prism:publicationDate>2007-11-01</prism:publicationDate>
<prism:startingPage>420</prism:startingPage>
<prism:section>REGULAR ARTICLES</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/19/4/428?rss=1">
<title><![CDATA[[REGULAR ARTICLES] Does the Presentation of Creutzfeldt-Jakob Disease Vary by Age or Presumed Etiology? A Meta-Analysis of the Past 10 Years]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/19/4/428?rss=1</link>
<description><![CDATA[
<p>It is not clear whether differences in symptom presentation vary by age or etiological subtype in Creutzfeldt-Jakob disease. A PubMed search was conducted using the keyword "Creutzfeldt-Jakob" and results within the last 10 years were sorted by the English language. We found that certain characteristics, such as affective illness (28.8%), present more commonly in younger patients irrespective of disease type. Young age of onset predicts presenting symptoms of affective illness, sleep disturbance, and poor concentration, as well as certain neurological symptoms, including cerebellar/gait disturbance, visual/oculomotor disturbance, sensory disorder, vertigo/dizziness, and headache.</p>
]]></description>
<dc:creator><![CDATA[Appleby, B. S., Appleby, K. K., Rabins, P. V.]]></dc:creator>
<dc:date>2007-12-10</dc:date>
<dc:identifier>info:doi/10.1176/appi.neuropsych.19.4.428</dc:identifier>
<dc:title><![CDATA[[REGULAR ARTICLES] Does the Presentation of Creutzfeldt-Jakob Disease Vary by Age or Presumed Etiology? A Meta-Analysis of the Past 10 Years]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>19</prism:volume>
<prism:endingPage>435</prism:endingPage>
<prism:publicationDate>2007-11-01</prism:publicationDate>
<prism:startingPage>428</prism:startingPage>
<prism:section>REGULAR ARTICLES</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/19/4/436?rss=1">
<title><![CDATA[[REGULAR ARTICLES] Impaired Perception of Affective Prosody in Remitted Patients With Bipolar Disorder]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/19/4/436?rss=1</link>
<description><![CDATA[
<p>Patients with bipolar disorder present deficits in facial emotion perception, both during a manic episode as well as upon recovery. Our goal in the present study was to investigate the ability of remitted patients with bipolar disorder to perceive affective prosody and to explore potential differences in the specific emotions that are troublesome for them. Participants included 19 patients with bipolar disorder I, currently in remission, and 22 healthy comparison subjects, matched on age, education, and gender. An affective prosody test (APT) was administered to all participants. Bipolar patients had significantly lower overall scores on the APT than healthy individuals. This impairment was specific to female patients and certain emotions (e.g., fear and surprise).</p>
]]></description>
<dc:creator><![CDATA[Bozikas, V. P., Kosmidis, M. H., Tonia, T., Andreou, C., Focas, K., Karavatos, A.]]></dc:creator>
<dc:date>2007-12-10</dc:date>
<dc:subject><![CDATA[Bipolar Disorder]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.19.4.436</dc:identifier>
<dc:title><![CDATA[[REGULAR ARTICLES] Impaired Perception of Affective Prosody in Remitted Patients With Bipolar Disorder]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>19</prism:volume>
<prism:endingPage>440</prism:endingPage>
<prism:publicationDate>2007-11-01</prism:publicationDate>
<prism:startingPage>436</prism:startingPage>
<prism:section>REGULAR ARTICLES</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/19/4/441?rss=1">
<title><![CDATA[[REGULAR ARTICLES] Psychopathology in Verified Huntington's Disease Gene Carriers]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/19/4/441?rss=1</link>
<description><![CDATA[
<p>Huntington&rsquo;s disease is characterized by motor, cognitive, and neuropsychiatric symptoms. This study reviews original research on psychopathology in Huntington&rsquo;s disease that uses standardized instruments in verified gene carriers. Frequently reported neuropsychiatric symptoms are depressed mood, anxiety, irritability, and apathy, with prevalences of 33% to 76%. Obsessive-compulsive symptoms and psychosis occur less often with prevalences of 10% to 52% and 3% to 11%, respectively. Available research provides little insight into the true prevalences of psychopathology in Huntington&rsquo;s disease due to small sample sizes, use of different methodologies, and lack of comparison groups. Future research requires larger cohorts stratified to disease stage, consistent methodologies, and adequate comparison groups.</p>
]]></description>
<dc:creator><![CDATA[van Duijn, E., Kingma, E.M., van der Mast, R.C.]]></dc:creator>
<dc:date>2007-12-10</dc:date>
<dc:subject><![CDATA[Huntington's Disease]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.19.4.441</dc:identifier>
<dc:title><![CDATA[[REGULAR ARTICLES] Psychopathology in Verified Huntington's Disease Gene Carriers]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>19</prism:volume>
<prism:endingPage>448</prism:endingPage>
<prism:publicationDate>2007-11-01</prism:publicationDate>
<prism:startingPage>441</prism:startingPage>
<prism:section>REGULAR ARTICLES</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/19/4/449?rss=1">
<title><![CDATA[[CLINICAL AND RESEARCH REPORTS] Mood-Elevating Effects of Opioid Analgesics in Patients With Bipolar Disorder]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/19/4/449?rss=1</link>
<description><![CDATA[
<p>Opioids can have mood-elevating effects in healthy subjects and have been used successfully to treat refractory depressed patients. A few case reports indicate that opioid analgesics can induce mania. The authors investigated the mood reaction of opioid analgesics in patients with bipolar disorder. Nine (27%) of 33 patients who took opioid analgesics for medical reasons experienced a significant hypomanic/manic reaction, and two other patients reported an antidepressant effect. None of the comparison subjects reported a significant mood reaction from opioid analgesics. These results indicate that opioid analgesics can have an important mood-altering effect on patients with known bipolar disorder.</p>
]]></description>
<dc:creator><![CDATA[Schaffer, C. B., Nordahl, T. E., Schaffer, L. C., Howe, J.]]></dc:creator>
<dc:date>2007-12-10</dc:date>
<dc:subject><![CDATA[Opioids, Bipolar Disorder]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.19.4.449</dc:identifier>
<dc:title><![CDATA[[CLINICAL AND RESEARCH REPORTS] Mood-Elevating Effects of Opioid Analgesics in Patients With Bipolar Disorder]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>19</prism:volume>
<prism:endingPage>452</prism:endingPage>
<prism:publicationDate>2007-11-01</prism:publicationDate>
<prism:startingPage>449</prism:startingPage>
<prism:section>CLINICAL AND RESEARCH REPORTS</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/19/4/453?rss=1">
<title><![CDATA[[CLINICAL AND RESEARCH REPORTS] Electrode Placement and Ictal EEG Indices in Electroconvulsive Therapy]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/19/4/453?rss=1</link>
<description><![CDATA[
<p>The authors determine whether quantitative electroencephalography (EEG) indices in electroconvulsive therapy (ECT) seizures correlate with stimulus electrode placement. The authors analyzed data from ECT seizures involving three electrode placements on 37 different quantitative EEG measures. Though there were a few statistically significant comparisons, no consistent pattern of differences was discerned among the three electrode placements. Though many different EEG analytical indices are available on modern ECT machines, the clinical or neurophysiologic relevance has yet to be established. These data provide a groundwork for future research on the neurophysiological aspects of ECT.</p>
]]></description>
<dc:creator><![CDATA[Rasmussen, K. G., Varghese, R., Stevens, S. R., Ryan, D. A.]]></dc:creator>
<dc:date>2007-12-10</dc:date>
<dc:subject><![CDATA[Other Treatment, ECT]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.19.4.453</dc:identifier>
<dc:title><![CDATA[[CLINICAL AND RESEARCH REPORTS] Electrode Placement and Ictal EEG Indices in Electroconvulsive Therapy]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>19</prism:volume>
<prism:endingPage>457</prism:endingPage>
<prism:publicationDate>2007-11-01</prism:publicationDate>
<prism:startingPage>453</prism:startingPage>
<prism:section>CLINICAL AND RESEARCH REPORTS</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/19/4/458?rss=1">
<title><![CDATA[[CLINICAL AND RESEARCH REPORTS] Within-Session Mood Changes From TMS in Depressed Patients]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/19/4/458?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Dang, T., Avery, D. H., Russo, J.]]></dc:creator>
<dc:date>2007-12-10</dc:date>
<dc:subject><![CDATA[Depression, Other Neuroimaging]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.19.4.458</dc:identifier>
<dc:title><![CDATA[[CLINICAL AND RESEARCH REPORTS] Within-Session Mood Changes From TMS in Depressed Patients]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>19</prism:volume>
<prism:endingPage>463</prism:endingPage>
<prism:publicationDate>2007-11-01</prism:publicationDate>
<prism:startingPage>458</prism:startingPage>
<prism:section>CLINICAL AND RESEARCH REPORTS</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/19/4/464?rss=1">
<title><![CDATA[[CLINICAL AND RESEARCH REPORTS] Efficacy of Adjuvant High Frequency Repetitive Transcranial Magnetic Stimulation on Negative and Positive Symptoms of Schizophrenia: Preliminary Results of a Double-Blind Sham-Controlled Study]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/19/4/464?rss=1</link>
<description><![CDATA[
<p>The potential effect of repetitive transcranial magnetic stimulation (rTMS) on core positive and negative symptoms in schizophrenia has not yet been clearly established. The aim of this study was to examine the efficacy of adjuvant 10 Hz, suprathreshold left prefrontal rTMS in negative symptoms of schizophrenia in a double-blind sham-controlled design. Additionally, our study also investigated the suitability of applying the same stimulus condition on positive symptoms. Ten right-handed schizophrenia patients received sham or active 10 Hz suprathreshold rTMS to the left dorsolateral prefrontal cortex with psychopathology, depression and global improvement ratings before and after rTMS sessions. Compared to sham, active rTMS significantly improved negative symptoms, irrespective of change in depressive symptoms.</p>
]]></description>
<dc:creator><![CDATA[Goyal, N., Nizamie, S. H., Desarkar, P.]]></dc:creator>
<dc:date>2007-12-10</dc:date>
<dc:subject><![CDATA[Schizophrenia Spectrum Disorders, Other Neuroimaging]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.19.4.464</dc:identifier>
<dc:title><![CDATA[[CLINICAL AND RESEARCH REPORTS] Efficacy of Adjuvant High Frequency Repetitive Transcranial Magnetic Stimulation on Negative and Positive Symptoms of Schizophrenia: Preliminary Results of a Double-Blind Sham-Controlled Study]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>19</prism:volume>
<prism:endingPage>467</prism:endingPage>
<prism:publicationDate>2007-11-01</prism:publicationDate>
<prism:startingPage>464</prism:startingPage>
<prism:section>CLINICAL AND RESEARCH REPORTS</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/19/4/468?rss=1">
<title><![CDATA[[NEUROPSYCHIATRIC PRACTICE AND OPINION] Phenomenological Distinctions Needed in DSM-V: Delirium, Subsyndromal Delirium, and Dementias]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/19/4/468?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Meagher, D., Trzepacz, P. T.]]></dc:creator>
<dc:date>2007-12-10</dc:date>
<dc:subject><![CDATA[Alzheimer's Disease, Delirium, Dementias (General), DSM]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.neuropsych.19.4.468</dc:identifier>
<dc:title><![CDATA[[NEUROPSYCHIATRIC PRACTICE AND OPINION] Phenomenological Distinctions Needed in DSM-V: Delirium, Subsyndromal Delirium, and Dementias]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>19</prism:volume>
<prism:endingPage>470</prism:endingPage>
<prism:publicationDate>2007-11-01</prism:publicationDate>
<prism:startingPage>468</prism:startingPage>
<prism:section>NEUROPSYCHIATRIC PRACTICE AND OPINION</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/19/4/471?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] Cilostazol, a cAMP Phosphodiesterase 3 Inhibitor, in the Treatment of Poststroke Depression]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/19/4/471?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Nishimura, K., Ishigooka, J., Imamura, Y., Ihara, S.]]></dc:creator>
<dc:date>2007-12-10</dc:date>
<dc:identifier>info:doi/10.1176/appi.neuropsych.19.4.471</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] Cilostazol, a cAMP Phosphodiesterase 3 Inhibitor, in the Treatment of Poststroke Depression]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>19</prism:volume>
<prism:endingPage>472</prism:endingPage>
<prism:publicationDate>2007-11-01</prism:publicationDate>
<prism:startingPage>471</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/19/4/472?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] Potential Drugs for Improving Chronic Fatigue Syndrome]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/19/4/472?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Hoseini, S. S., Gharibzadeh, S.]]></dc:creator>
<dc:date>2007-12-10</dc:date>
<dc:identifier>info:doi/10.1176/appi.neuropsych.19.4.472</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] Potential Drugs for Improving Chronic Fatigue Syndrome]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>19</prism:volume>
<prism:endingPage>472</prism:endingPage>
<prism:publicationDate>2007-11-01</prism:publicationDate>
<prism:startingPage>472</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/19/4/472-a?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] Basal Ganglia Calcification and Pulmonary Embolism in Catatonia]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/19/4/472-a?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Woo, B. K. P.]]></dc:creator>
<dc:date>2007-12-10</dc:date>
<dc:identifier>info:doi/10.1176/appi.neuropsych.19.4.472-a</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] Basal Ganglia Calcification and Pulmonary Embolism in Catatonia]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>19</prism:volume>
<prism:endingPage>473</prism:endingPage>
<prism:publicationDate>2007-11-01</prism:publicationDate>
<prism:startingPage>472</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/19/4/473?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] Pathological Gambling Associated With Cabergoline Therapy in a Patient With a Pituitary prolactinoma.]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/19/4/473?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Davie, M.]]></dc:creator>
<dc:date>2007-12-10</dc:date>
<dc:identifier>info:doi/10.1176/appi.neuropsych.19.4.473</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] Pathological Gambling Associated With Cabergoline Therapy in a Patient With a Pituitary prolactinoma.]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>19</prism:volume>
<prism:endingPage>474</prism:endingPage>
<prism:publicationDate>2007-11-01</prism:publicationDate>
<prism:startingPage>473</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/19/4/474?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] Acquired Variant of Rett's Disorder and Response to Lamotrigine]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/19/4/474?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Mendhekar, D. N., Duggal, H. S.]]></dc:creator>
<dc:date>2007-12-10</dc:date>
<dc:identifier>info:doi/10.1176/appi.neuropsych.19.4.474</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] Acquired Variant of Rett's Disorder and Response to Lamotrigine]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>19</prism:volume>
<prism:endingPage>475</prism:endingPage>
<prism:publicationDate>2007-11-01</prism:publicationDate>
<prism:startingPage>474</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/19/4/475?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] Neuroanatomical Changes After Eye Movement Desensitization and Reprocessing (EMDR) Treatment in Posttraumatic Stress Disorder]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/19/4/475?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Letizia, B., Andrea, F., Paolo, C.]]></dc:creator>
<dc:date>2007-12-10</dc:date>
<dc:identifier>info:doi/10.1176/appi.neuropsych.19.4.475</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] Neuroanatomical Changes After Eye Movement Desensitization and Reprocessing (EMDR) Treatment in Posttraumatic Stress Disorder]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>19</prism:volume>
<prism:endingPage>476</prism:endingPage>
<prism:publicationDate>2007-11-01</prism:publicationDate>
<prism:startingPage>475</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/19/4/476?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] A Case Report With Ziprasidone-Induced Catatonic Symptoms]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/19/4/476?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Markham-Abedi, C., McNeely, C., de Leon, J.]]></dc:creator>
<dc:date>2007-12-10</dc:date>
<dc:identifier>info:doi/10.1176/appi.neuropsych.19.4.476</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] A Case Report With Ziprasidone-Induced Catatonic Symptoms]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>19</prism:volume>
<prism:endingPage>477</prism:endingPage>
<prism:publicationDate>2007-11-01</prism:publicationDate>
<prism:startingPage>476</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/19/4/477?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] Possible Neuroleptic Malignant Syndrome Associated With Paliperidone]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/19/4/477?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Duggal, H. S.]]></dc:creator>
<dc:date>2007-12-10</dc:date>
<dc:identifier>info:doi/10.1176/appi.neuropsych.19.4.477</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] Possible Neuroleptic Malignant Syndrome Associated With Paliperidone]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>19</prism:volume>
<prism:endingPage>478</prism:endingPage>
<prism:publicationDate>2007-11-01</prism:publicationDate>
<prism:startingPage>477</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/19/4/478?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] Differential Cerebral Cortical Responsiveness Examination in Minimally Conscious Versus Persistent Vegetative States: A New Role for Neuropsychiatry and Behavioral Neurology]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/19/4/478?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Neppe, V. M.]]></dc:creator>
<dc:date>2007-12-10</dc:date>
<dc:identifier>info:doi/10.1176/appi.neuropsych.19.4.478</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] Differential Cerebral Cortical Responsiveness Examination in Minimally Conscious Versus Persistent Vegetative States: A New Role for Neuropsychiatry and Behavioral Neurology]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>19</prism:volume>
<prism:endingPage>479</prism:endingPage>
<prism:publicationDate>2007-11-01</prism:publicationDate>
<prism:startingPage>478</prism:startingPage>
<prism:section>LETTERS TO THE EDITOR</prism:section>
</item>

<item rdf:about="http://neuro.psychiatryonline.org/cgi/content/short/19/4/479?rss=1">
<title><![CDATA[[LETTERS TO THE EDITOR] The Schizophrenic Disguise of Complex Partial Seizures]]></title>
<link>http://neuro.psychiatryonline.org/cgi/content/short/19/4/479?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Palaniyappan, L.]]></dc:creator>
<dc:date>2007-12-10</dc:date>
<dc:identifier>info:doi/10.1176/appi.neuropsych.19.4.479</dc:identifier>
<dc:title><![CDATA[[LETTERS TO THE EDITOR] The Schizophrenic Disguise of Complex Partial Seizures]]></dc:title>
<dc:publisher>American Neuropsychiatric Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>19</prism:volume>
<prism:endingPage>480</prism:endingPage>
<prism