The Journal of Neuropsychiatry and Clinical Neurosciences最新文献

{"title":"Clonazepam needs to be taken care for refractory epilepsy: a rare case and review.","authors":"Kai Fu, Dong Zhou, Xiangdong Tang, Lei Chen","doi":"10.1176/appi.neuropsych.13120361","DOIUrl":"https://doi.org/10.1176/appi.neuropsych.13120361","url":null,"abstract":"To the Editor: Clonazepam is rarely used as a primary antiepileptic drug because of a higher incidence of side effects and potential tolerance. Here the authors report a patient whowas diagnosedwith refractory epilepsy and clonazepam was added. However, this young patient’s seizures during sleep increased due to lengthening of non-REM sleep stage 2, which is rare. The authors remind neurologists to pay attention to the distribution of ictal discharges in nocturnal polysomnography as well as the effects of antiepileptic drugs on sleep when analogous drugs are added.","PeriodicalId":514751,"journal":{"name":"The Journal of Neuropsychiatry and Clinical Neurosciences","volume":" ","pages":"e143-5"},"PeriodicalIF":2.9,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1176/appi.neuropsych.13120361","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33135189","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acute pisa syndrome as a neurological emergency.","authors":"Vladimir Miletić, Boris Radić, Maja Relja","doi":"10.1176/appi.neuropsych.14050105","DOIUrl":"https://doi.org/10.1176/appi.neuropsych.14050105","url":null,"abstract":"To the Editor: Pisa syndrome is a rare clinical entity usually associated with underlying neurodegenerative diseases such as Parkinson’s disease and multiple system atrophy. However, it can also occur as an adverse effect of treatment with antipsychotics, especially in patients with predefined risk factors. Pisa syndrome is defined as sustained lateral flexion of the trunk.When observed in practice, it denotes an incapacitating symptom of underlying neurodegenerative diseases such as Parkinson’s disease and multiple system atrophy. Pisa syndrome can also occur as an adverse effect of prolonged treatment with antipsychotics, especially typical agents. However, reports describing acute drug-induced Pisa syndrome with possible treatment modalities are lacking. Here we report a patient with Alzheimer’s disease with severe risperidoneinduced acute Pisa syndrome in the neurological emergency room,whowas successfully treatedwith low-dose quetiapine.","PeriodicalId":514751,"journal":{"name":"The Journal of Neuropsychiatry and Clinical Neurosciences","volume":" ","pages":"e159-60"},"PeriodicalIF":2.9,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1176/appi.neuropsych.14050105","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33135197","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Catatonia and klüver-bucy syndrome in a patient with acute disseminated encephalomyelitis.","authors":"Jose Fernando Muñoz Zúñiga, Jesus Ramirez-Bermudez, José de Jesús Flores Rivera, Teresa Corona","doi":"10.1176/appi.neuropsych.14060120","DOIUrl":"https://doi.org/10.1176/appi.neuropsych.14060120","url":null,"abstract":"","PeriodicalId":514751,"journal":{"name":"The Journal of Neuropsychiatry and Clinical Neurosciences","volume":" ","pages":"e161-2"},"PeriodicalIF":2.9,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1176/appi.neuropsych.14060120","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33135198","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Confirmatory Factor Analysis of the Delirium Rating Scale Revised-98 (DRS-R98).","authors":"Steven Thurber,&nbsp;Yasuhiro Kishi,&nbsp;Paula T Trzepacz,&nbsp;Jose G Franco,&nbsp;David J Meagher,&nbsp;Yanghyun Lee,&nbsp;Jeong-Lan Kim,&nbsp;Leticia M Furlanetto,&nbsp;Daniel Negreiros,&nbsp;Ming-Chyi Huang,&nbsp;Chun-Hsin Chen,&nbsp;Jacob Kean,&nbsp;Maeve Leonard","doi":"10.1176/appi.neuropsych.13110345","DOIUrl":"https://doi.org/10.1176/appi.neuropsych.13110345","url":null,"abstract":"<p><p>Principal components analysis applied to the Delirium Rating Scale-Revised-98 contributes to understanding the delirium construct. Using a multisite pooled international delirium database, the authors applied confirmatory factor analysis to Delirium Rating Scale-Revised-98 scores from 859 adult patients evaluated by delirium experts (delirium, N=516; nondelirium, N=343). Confirmatory factor analysis found all diagnostic features and core symptoms (cognitive, language, thought process, sleep-wake cycle, motor retardation), except motor agitation, loaded onto factor 1. Motor agitation loaded onto factor 2 with noncore symptoms (delusions, affective lability, and perceptual disturbances). Factor 1 loading supports delirium as a single construct, but when accompanied by psychosis, motor agitation's role may not be solely as a circadian activity indicator. </p>","PeriodicalId":514751,"journal":{"name":"The Journal of Neuropsychiatry and Clinical Neurosciences","volume":" ","pages":"e122-7"},"PeriodicalIF":2.9,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1176/appi.neuropsych.13110345","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33135184","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Poststroke subcortical aphasia and neurobehavioral disturbances without motor or sensory deficits.","authors":"Elias D Granadillo,&nbsp;David B Arciniegas","doi":"10.1176/appi.neuropsych.14060138","DOIUrl":"https://doi.org/10.1176/appi.neuropsych.14060138","url":null,"abstract":"To the Editor: Subcortical aphasia may result from lesions of the basal ganglia, anterolateral nuclei of the thalamus, and capsular/pericapsular whitematter of the language-dominant hemisphere. Subcortical aphasia associated with lesions of the posterior limb of the internal capsule (ICp) and adjacent subcortical structures typically involves impaired picture naming (letters better than objects), rapid fluent speechwith paraphasias and extended jargon, poor comprehension, and impaired repetition. Contralateral disturbances of elementary motor and sensory function typically occur; with posterior extension of the capsular lesion, these disturbances may be accompanied by visual field deficits and auditory dysfunction. Subcortical aphasia associated with lesions of the anterior limb of the internal capsule (ICa) and adjacent structures (often including the genu of the internal capsule [ICg]) typically involves impaired picture naming (objects better than letters), grammatical but slow dysarthric speech output, good semantic comprehension with impaired syntactic comprehension, and repetition impairments primarily for low-probability sentences (with articulatory distortions and word omissions); impaired articulatory agility, buccofacial apraxia, and contralateral hemiparesis also are typically present. Subcortical aphasia associated with lesions involving the ICa, ICp, and adjacent subcortical structures features more severe language disturbances (i.e., global aphasia) and contralateral motor, sensory, and visual field deficits. The neuropsychiatric, motor, and sensory concomitants of subcortical aphasia follow capsular anatomy (Figure 1 [A]). The frontopontine, thalamofrontal, and thalamostriate fibers in the ICa subserve circuits regulating emotion, comportment, motivation, and executive function. The ICg comprises fibers of the corticonuclear tract, connecting the motor cortex to contralateral cranial nerve nuclei. The ICp comprises fibers of the corticospinal (pyramidal or voluntary motor) tract, as well as sensory fibers originating from the thalamus and, to a lesser extent, from the medial lemniscus; the distal one-third of the ICp includes fibers of the optic and acoustic radiations, as well as temporopontine, parietopontine, and occipitopontine fibers. Concomitant neuropsychiatric disturbances (especially executive dysfunction, disordered comportment, diminished motivation, and/or emotional dysregulation) would be expected among persons with subcortical aphasia involving lesions of the ICa and adjacent subcortical structures. By contrast, elementary motor impairments are expected concomitants of subcortical aphasia associated with lesions involving the ICg and/or ICp, and sensory impairments are expected accompaniments of lesions involving the ICp. Contrary to these expectations, we present a case of acute subcortical stroke involving the ICg and ICp as well as adjacent subcortical structures (with caudal extension) associated with subcortical ","PeriodicalId":514751,"journal":{"name":"The Journal of Neuropsychiatry and Clinical Neurosciences","volume":" ","pages":"e165-7"},"PeriodicalIF":2.9,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1176/appi.neuropsych.14060138","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33135200","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Number of Cysteine Residues per Mole in Apolipoprotein E Is Associated With the Severity of PTSD Re-Experiencing Symptoms.","authors":"Carly K Peterson,&nbsp;Lisa M James,&nbsp;Samantha L Anders,&nbsp;Brian E Engdahl,&nbsp;Apostolos P Georgopoulos","doi":"10.1176/appi.neuropsych.13090205","DOIUrl":"https://doi.org/10.1176/appi.neuropsych.13090205","url":null,"abstract":"<p><p>Apolipoprotien E (ApoE) is involved in critical neural functions and is associated with various neuropsychiatric disorders. ApoE exists in three isoforms that differ in the number of cysteine residues per mole (CysR/mole). This study evaluated associations between this informative ordinal biochemical scale (CysR/mole) and symptom severity in veterans with posttraumatic stress disorder (PTSD) or subthreshold PTSD. Results demonstrated a significant negative relationship between the CysR/mole and severity of PTSD re-experiencing symptoms, adjusted for trauma. The findings suggest a genetic influence on PTSD symptomatology and dovetail with recent advances regarding the molecular mechanisms underlying the differential effects of ApoE in the brain. </p>","PeriodicalId":514751,"journal":{"name":"The Journal of Neuropsychiatry and Clinical Neurosciences","volume":" ","pages":"157-61"},"PeriodicalIF":2.9,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1176/appi.neuropsych.13090205","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33113309","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Negative symptoms in neuropsychiatric systemic lupus erythematosus.","authors":"Chein-Heng Lin,&nbsp;Chih-Min Liu,&nbsp;Meg Mei-Chih Tseng,&nbsp;Wei-Lieh Huang","doi":"10.1176/appi.neuropsych.13110342","DOIUrl":"https://doi.org/10.1176/appi.neuropsych.13110342","url":null,"abstract":"","PeriodicalId":514751,"journal":{"name":"The Journal of Neuropsychiatry and Clinical Neurosciences","volume":" ","pages":"e142"},"PeriodicalIF":2.9,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1176/appi.neuropsych.13110342","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33135188","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Low doses of benzodiazepines for catatonia associated with systemic lupus erythematosus.","authors":"Caleb P Canders,&nbsp;Garth E Terry,&nbsp;Guiselle Clark","doi":"10.1176/appi.neuropsych.14030057","DOIUrl":"https://doi.org/10.1176/appi.neuropsych.14030057","url":null,"abstract":"","PeriodicalId":514751,"journal":{"name":"The Journal of Neuropsychiatry and Clinical Neurosciences","volume":" ","pages":"e146-8"},"PeriodicalIF":2.9,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1176/appi.neuropsych.14030057","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33135190","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Enhanced Olfactory Cortex Connectivity in a Patient With PTSD With Olfactory Hallucinations.","authors":"Caitlin Ridgewell,&nbsp;Allison Bray,&nbsp;Kaylah Curtis,&nbsp;Kenia Velasquez,&nbsp;Philip R Baldwin,&nbsp;J Christopher Fowler,&nbsp;Sanjay J Mathew,&nbsp;Ramiro Salas","doi":"10.1176/appi.neuropsych.14070156","DOIUrl":"https://doi.org/10.1176/appi.neuropsych.14070156","url":null,"abstract":"","PeriodicalId":514751,"journal":{"name":"The Journal of Neuropsychiatry and Clinical Neurosciences","volume":" ","pages":"e170-1"},"PeriodicalIF":2.9,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1176/appi.neuropsych.14070156","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33140921","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A season of change for the journal of neuropsychiatry and clinical neurosciences.","authors":"David B Arciniegas,&nbsp;Robert E Hales,&nbsp;Stuart C Yudofsky","doi":"10.1176/appi.neuropsych.270301","DOIUrl":"https://doi.org/10.1176/appi.neuropsych.270301","url":null,"abstract":"","PeriodicalId":514751,"journal":{"name":"The Journal of Neuropsychiatry and Clinical Neurosciences","volume":" ","pages":"80"},"PeriodicalIF":2.9,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1176/appi.neuropsych.270301","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33261870","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}