Internalized Stigma of Mental Illness (ISMI) Scale: A multinational review

The Internalized Stigma of Mental Illness (ISMI) scale is a 29-item questionnaire measuring self-stigma among persons with psychiatric disorders. It was developed with substantial consumer input and has been widely used, but its psychometric qualities have not been comprehensively evaluated across multiple versions. Here we review the 55 known versions, and provide the 47 available versions, including: Arabic, Armenian, Bengali, Bulgarian, Chinese (Mainland, Taiwan, Hong Kong), Croatian, Dutch, English (USA, South Africa), Estonian, Farsi, Finnish, French, German, Greek, Hebrew, Hindi, Japanese, Khmer, Korean, Lithuanian, Lugandan, Maltese, Polish, Portuguese (Portugal, Brazil), Romanian, Russian, Samoan, Slovenian, Spanish (Spain), Swahili, Swedish, Tongan, Turkish, Urdu, and Yoruba, and qualitative English and Swahili versions, as well as versions for depression, schizophrenia, substance abuse, eating disorders, epilepsy, inflammatory bowel disease, leprosy, smoking, parents and caregivers of people with mental illness, and ethnicity. The various versions show reliability and validity across a wide range of languages, cultures, and writing systems. The most commonly reported findings of studies using the ISMI are that internalized stigma correlates with higher depression, lower self esteem, and higher symptom severity. Initial studies of ways to reduce internalized stigma are promising and warrant further investigation.     

Genetics of psychiatric disorders in the GWAS era: an update on schizophrenia

The influence of genetic factors in the development of schizophrenia has been convincingly demonstrated by family, twin, and adoption studies. The statistical construct of heritability is generally used for estimating the liability due to genetic factors. Heritability estimates for schizophrenia are reported to be between 60 and 80 %. Due to the technical achievements in whole genome-wide association studies, dissection of the underlying genetic factors was intensified recently, resulting in the conclusion that schizophrenia is essentially a polygenic, complex disorder. Most likely more than 100 genes, each with small effect size, contribute to disease risk. A most recent multi-stage genome-wide association study (Ripke et al. in Nat Genet 2013) identified 22 risk loci and estimated that 8,300 independent single-nucleotide polymorphisms contributed to the risk accounting collectively for 32 % in liability. In addition to this polygenic, complex inheritance, there is also strong indication that in some patients a deletion or insertion of a larger chromosomal region [so-called copy number variation (CNV)] might play a crucial role in pathogenesis. This could be specifically important in sporadic cases with schizophrenia, since a higher frequency of de novo mutations has been associated with these CNVs. Further studies, combining much larger sample sizes as well as application of newer technology, such as deep sequencing technologies will be necessary in order to obtain a more comprehensive understanding of the genetic foundations of schizophrenia.

     

Insular cortex and neuropsychiatric disorders: a review of recent literature.

The insular cortex is located in the centre of the cerebral hemisphere, having connections with the primary and secondary somatosensory areas, anterior cingulate cortex, amygdaloid body, prefrontal cortex, superior temporal gyrus, temporal pole, orbitofrontal cortex, frontal and parietal opercula, primary and association auditory cortices, visual association cortex, olfactory bulb, hippocampus, entorhinal cortex, and motor cortex. Accordingly, dense connections exist among insular cortex neurons. The insular cortex is involved in the processing of visceral sensory, visceral motor, vestibular, attention, pain, emotion, verbal, motor information, inputs related to music and eating, in addition to gustatory, olfactory, visual, auditory, and tactile data. In this article, the literature on the relationship between the insular cortex and neuropsychiatric disorders was summarized following a computer search of the Pub-Med database. Recent neuroimaging data, including voxel based morphometry, PET and fMRI, revealed that the insular cortex was involved in various neuropsychiatric diseases such as mood disorders, panic disorders, PTSD, obsessive-compulsive disorders, eating disorders, and schizophrenia. Investigations of functions and connections of the insular cortex suggest that sensory information including gustatory, olfactory, visual, auditory, and tactile inputs converge on the insular cortex, and that these multimodal sensory information may be integrated there.     

出血性卒中与缺血性卒中危险因素比较

目的探讨不同危险因素对缺血性和出血性卒中发病的影响。方法收集3 102例脑卒中患者的个人疾病史、生活方式、临床检查及生化指标结果等资料,运用Epidata软件建立数据库,采用SAS 9.2进行统计分析。结果脑梗死组发病到入院时间、住院时间、高胆固醇血症、糖尿病史、心脏病史、房颤史、脑卒中史,吸烟的OR值分别是3.36、4.953、3.375、2.224、2.394、2.362、3.573、2.076、2.885。脑出血组呼吸、体温、心率、血压、高血糖、Tbil、高血压史OR值分别是0.824、0.390、0.673、0.425、0.594、0.598、0.934。结论发病到入院时间、住院时间、高胆固醇血症、糖尿病史、心脏病史、房颤史、脑卒中史、吸烟等对脑梗死的影响更大,而呼吸、体温、心率、高血压、高血糖、Tbil、高血压史对脑出血的影响更大。     

Book Reviews

Exacting Beauty: Theory, Assessment, and Treatment of Body Image Disturbance, J. Kevin Thompson, Leslie J. Heinberg, Madeline Al-tabe, & Stacey Tantleff-Dunn, Washington, DC, American Psychological Association, 1999, 396 pages, $39.95

The Don't Diet, Live-It! Workbook: Healing Food, Weight, and Body Issues, by Andrea LoBue and Marsea Marcus, Carlsbad, California: Gurze Books, 1999, 255 pages, $17.95     

Retrograde transport of brain-derived neurotrophic factor (BDNF) following infusion in neo-and limbic cortex in rat: Relationship to BDNF mRNA expressing neurons

Brain-derived neurotrophic factor (BDNF) was the second member of the nerve growth factor (NGF) family to be isolated. The ability of BDNF to be retrogradely transported following intraparenchymal infusion represents a unique neurobiological tool to determine the location of putative neuron-specific BDNF-responsive neuronal systems. In the present study, we infused recombinant human (rh) BDNF into the rodent neo- and limbic cortex and used a turkey anti-BDNF antibody to determine specific populations of neurons which retrogradely transport this neurotrophin. Frontal cortex infusion retrogradely labeled neurons within the ipsilateral and contralateral frontal cortex, basal forebrain, lateral hypothalamus, centrolateral, mediodorsal, ventrolateral, ventromedial, ventral posterior, rhomboid, reuniens, and medial geniculate thalamic nuclei, and locus coeruleus. Occipital cortex infusion retrogradely labeled neurons in the frontal, temporal, occipital, and perirhinal cortices as well as the claustrum, basal forebrain, thalamus, epithalamus, hypothalamus, and raphe nuclei. Dorsal hippocampal infusion retrogradely labeled neurons within the septal diagonal band, supramammillary nucleus, and entorhinal cortex and was also transported within various hippocampal subfields. Entorhinal cortex infusion retrogradely labeled neurons within the perirhinal cortex, endopiriform nucleus, piriform cortex, dentate gyrus, presubiculum, parasubiculum, CA1-CA4 fields, amygdaloid nuclei, basal forebrain, thalamus, hypothalamus, periaqueductal gray, raphe nuclei, and locus coeruleus. Amygdala infusion labeled neurons in the endopiriform nucleus, temporal cortex, piriform cortex, paralimbic cortex, hippocampus, subiculum, entorhinal cortex, amygdala, basal forebrain, thalamus, hypothalamus, substantia nigra, pars compacta, raphe, and pontine parabrachial-nuclei. In situ hybridization experiments demonstrated that virtually all areas which retrogradely transport BDNF also express its message. Neuroanatomical distributional studies of BDNF will unravel specific central nervous system neurotrophic-responsive systems. © 1996 Wiley-Liss, Inc.     

Clinical aspects of abnormal eye movements]

This paper reviews a variety of abnormal eye movements which include abnormal ocular positions, restricted eye motions, impairment of conjugated eye movements, abnormal smooth pursuit, abnormal saccade, gaze-evoked nystagmus, down-beat nystagmus, internuclear ophthalmoplegia, supranuclear ophthalmoplegia, square wave jerks, roving eye movement, ocular bobbing, ocular dipping, reverse ocular bobbing, and ping-pong gaze. Abnormal eye movements occur from stroke, spinocerebellar degeneration, Parkinson disease, multiple system atrophy, progressive supranuclear palsy, multiple sclerosis, Miller Fisher syndrome, myasthenia gravis, opsoclonus-polymyoclonia syndrome, and Creutzfeldt-Jakob disease. In neurological practice, it is important to observe abnormal eye movements accurately and enthusiastically, to make appropriate anatomical and etiological diagnosis.     

Aberrant inflammatory profile in acute but not recovered anorexia nervosa

Anorexia nervosa (AN) is a severe psychiatric disorder with high mortality and relapse rates. Even though changes in inflammatory markers and cytokines are known to accompany cachexia associated with somatic disorders such as cancer and chronic kidney disorder, studies on inflammatory markers in AN are rare and typically include few individuals. Here, we utilize an Olink Proteomics inflammatory panel to explore the concentrations of 92 preselected inflammation-related proteins in plasma samples from women with active AN (N = 113), recovered from AN (AN-REC, N = 113), and normal weight healthy controls (N = 114). After correction for multiple testing, twenty-five proteins differed significantly between the AN group and controls (lower levels: ADA, CCL19, CD40, CD5, CD8A, CSF1, CXCL1, CXCL5, HGF, IL10RB, IL12B, 1L18R1, LAP TGFß1, MCP3, OSM, TGFα, TNFRSF9, TNFS14 and TRANCE; higher levels: CCL11, CCL25, CST5, DNER, LIFR and OPG). Although more than half of these differences (N = 15) were present in the comparison between AN and AN-REC, no significant differences were seen between AN-REC and controls. Furthermore, twenty-five proteins correlated positively with BMI (ADA, AXIN1, CASP8, CD5, CD40, CSF1, CXCL1, CXCL5, EN-RAGE, HGF, IL6, IL10RB, IL12B, IL18, IL18R1, LAP TGFß1, OSM, SIRT2, STAMBP, TGFα, TNFRSF9, TNFS14, TRANCE, TRAIL and VEGFA) and four proteins correlated negatively with BMI (CCL11, CCL25, CCL28 and DNER).These results suggest that a dysregulated inflammatory status is associated with AN, but, importantly, seem to be confined to the acute illness state.     

Structures of telencephalic projection in the pigeon. Identification by marking with horseradish peroxidase

The sites of origin of afferents to the telencephalon in the pigeon were investigated using the HRP technique (TMB). Following large multiple injections of the enzyme into the cerebral hemisphere, peroxidase-positive neurons were identified at diencephalic levels: ipsilaterally in DLM, DMA, DLP, DIP, DMP, Rt, Ov, SRt and SCE/SCI; bilaterally in DLA and SPC. At mesencephalic and posterior brainstem levels, HRP-labeled neurons were found: ipsilaterally in AVT, ZpNIII, ICo, FRM, FRL, TP and SCv; bilaterally in GCt, ZpFLM, neurons were found: ipsilaterally in AVT, ZpNIII, ICo, FRM, FRL, TP and SCv; bilaterally in GCt, ZpFLM, Annul, LoC, LC and PrV. Smaller injections of HRP into different regions of the telencephalon demonstrated, for some of the latter structures, either single or multiple projections upon topographically distinct subdivisions.     

Afferent and efferent connections of the medial preoptic area in the rat: A WGA-HRP study

Afferent and efferent connections of the medial preoptic area including medial preoptic nucleus (MP) and periventricular area at the MP level were examined using WGA-HRP as a marker. Injections were performed by insertion of micropipette containing (1) small amount of HRP powder or (2) dryed HRP solution for 24 to 48 hr until the fixation or for 5 min respectively. Dorsal and ventral approaches of injection micropipettes were performed and the results were compared. Previously reported reciprocal connections with lateral septum, bed nucleus of the stria terminalis, medial amygdaloid nucleus, lateral hypothalamic nucleus, paraventricular hypothalamic nucleus, ventromedial hypothalamic nucleus, arcuate nucleus, supramammillary nucleus, central gray at the mesencephalon, raphe dorsalis, raphe medianus, and lateral parabrachial nucleus have been confirmed. In addition, we found reciprocal connections with septo-hypothalamic nucleus, amygdalo-hipocampal nucleus, subiculum, parafascicular thalamic nucleus, posterior thalamic nucleus at the caudo-ventral subdivision, median preoptic nucleus, lateral preoptic nucleus, anterior hypothalamic nucleus, periventricular area at the caudal hypothalamic level, dorsomedial hypothalamic nucleus, posterior hypothalamic nucleus, dorsal and ventral premammillary nucleus, lateral mammillary nucleus, peripeduncular nucleus, periventricular gray, ventral tegmental area, interpeduncular nucleus, nucleus raphe pontis, nucleus raphe magnus, pedunculo-pontine tegmental nucleus, gigantocellular reticular nucleus and solitary tract nucleus. The areas which had only efferent connections from MP were accumbens, caudate putamen, ventral pallidum, substantia innominata, lateral habenular nucleus, paratenial thalamic nucleus, paraventricular thalamic nucleus, mediodorsal thalamic nucleus, reuniens thalamic nucleus, median eminence, medial mammillary nucleus, subthalamic nucleus, pars compacta of substantia nigra, oculomotor nucleus, red nucleus, laterodorsal tegmental nucleus, reticular tegmental nucleus, cuneiform nucleus, nucleus locus coeruleus, and dorsal motor nucleus of vagus among which substantia innominata and median eminence were previously reported. Efferent connections to the nucleus of Darkschewitsch, interstitial nucleus of Cajal, dorsal tegmental nucleus, ventral tegmental nucleus, vestibular nuclei, nucleus raphe obsculus were very weak or abscent in the ventral approach while they were observed in dorsal approach. Previously reported afferent connections from dorsal tegmental nucleus, cuneiform nucleus, and nucleus locus ceruleus were not detected in this study.(ABSTRACT TRUNCATED AT 400 WORDS)     

Neurotransmitter alterations in PTSD: catecholamines and serotonin.

In this chapter we review trauma-related studies involving epinephrine (E), norepinephrine (NE), and serotonin (5-HT). Central catecholamine neurons seem to play a critical role in level of alertness, vigilance, orienting, selective attention, memory, fear conditioning, and cardiovascular responses to life-threatening stimuli. Evidence of catecholamine dysregulation in post-traumatic stress disorder (PTSD) includes exaggerated increases in heart rate and blood pressure when exposed to visual and auditory reminders of trauma, elevated 24-hour urine catecholamine excretion, decreased platelet alpha-2 adrenergic receptor number, exaggerated behavioral, cardiovascular, and biochemical responses to IY yohimbine, decreased cortical brain metabolism secondary to IV yohimbine, and clinical efficacy of adrenergic blocking agents. Serotonin seems to play numerous roles in the central nervous system, including regulation of sleep, aggression, appetite, cardiovascular and respiratory activity, motor output, anxiety, mood, neuroendocrine secretion, and analgesia. Evidence of serotonergic dysregulation in PTSD includes frequent symptoms of aggression, impulsivity, depression and suicidality, decreased platelet paroxetine binding, blunted prolactin response to fenfluramine, exaggerated reactivity to m-chloro-phenyl-piperazine, and clinical efficacy of serotonin reuptake inhibitors. It has been suggested that alterations in NE, E, and 5-HT may have relevance for symptoms commonly seen in survivors with PTSD, including hypervigilance, exaggerated startle, irritability, impulsivity, aggression, intrusive memories, depressed mood, and suicidality.     

Leigh and Leigh-like syndrome in children and adults

Leigh syndrome (also termed subacute, necrotizing encephalopathy) is a devastating neurodegenerative disorder, characterized by almost identical brain changes, e.g., focal, bilaterally symmetric lesions, particularly in the basal ganglia, thalamus, and brainstem, but with considerable clinical and genetic heterogeneity. Clinically, Leigh syndrome is characterized by a wide variety of abnormalities, from severe neurologic problems to a near absence of abnormalities. Most frequently the central nervous system is affected, with psychomotor retardation, seizures, nystagmus, ophthalmoparesis, optic atrophy, ataxia, dystonia, or respiratory failure. Some patients also present with peripheral nervous system involvement, including polyneuropathy or myopathy, or non-neurologic abnormalities, e.g., diabetes, short stature, hypertrichosis, cardiomyopathy, anemia, renal failure, vomiting, or diarrhea (Leigh-like syndrome). In the majority of cases, onset is in early childhood, but in a small number of cases, adults are affected. In the majority of cases, dysfunction of the respiratory chain (particularly complexes I, II, IV, or V), of coenzyme Q, or of the pyruvate dehydrogenase complex are responsible for the disease. Associated mutations affect genes of the mitochondrial or nuclear genome. Leigh syndrome and Leigh-like syndrome are the mitochondrial disorders with the largest genetic heterogeneity.     

Neck and back pain: musculoskeletal disorders

In this article, non-neurologic causes of neck and back pain are reviewed. Musculoskeletal pain generators include muscle, tendon, ligament, intervertebral disc, articular cartilage, and bone. Disorders that can produce neck and back pain include muscle strain, ligament sprain, myofascial pain, fibromyalgia, facet joint pain, internal disc disruption, somatic dysfunction, spinal fracture, vertebral osteomyelitis, and polymyalgia rheumatica. Atlantoaxial instability and atlanto-occipital joint pain are additional causes of neck pain. Back pain resulting from vertebral compression fracture, Scheuermann's disease, spondylolysis and spondylolisthesis, pregnancy, Baastrup's disease, sacroiliac joint dysfunction, and sacral stress fracture is discussed.     

Brainstem neurons with descending projections to the spinal cord of two elasmobranch fishes: Thornback guitarfish,Platyrhinoidis triseriata,and horn shark,Heterodontus francisci

We studied two cartilaginous fishes and described their brainstem supraspinal projections because most nuclei in the reticular formation can be identified that way. A retrogradely transported tracer, horseradish peroxidase or Fluoro-Gold, was injected into the spinal cord of Platyrhinoidis triseriata (thornback guitarfish) or Heterodontus fransisci (horn shark). We described labeled reticular cells by their position, morpohology, somatic orientation, dendritic processes, and laterality of spinal projections. Nineteen reticular nuclei have spinal projections: reticularis (r.) dorsalis, r. ventralis pars α and β, r. gigantocellularis, r. magnocellularis, r. parvocellularis, r. paragigantocellularis lateralis and dorsalis, r. pontis caudalis pars α and β, r. pontis oralis pars medialis and lateralis, r. subcuneiformis, r. peduncularis pars compacta, r. subcoeruleus pars α, raphe obscurus, raphe pallidus, raphe magnus, and locus coeruleus. Twenty nonreticular nuclei have spinal projections: descending trigeminal, retroambiguus, solitarius, posterior octaval, descending octaval, magnocellular octaval, ruber, Edinger-Westphal, nucleus of the medial longitudinal fasciculus, interstitial nucleus of Cajal, latral mesencephalic complex, periventricularis pretectalis pars dorsalis, central pretectal, ventromedial thalamic, posterior central thalamic, posterior dorsal thalamic, the posterior tuberculum, and nuclei B, F, and J. The large number of distinct reticular nuclei with spinal projections corroborates the hypothesis that the reticular formation of elasmobranches is complexly organized into many of the same nuclei that are found in frogs, reptiles, birds, and mammals. J. Comp. Neurol. 403:534–560, 1999. © 1999 Wiley-Liss, Inc.     

Books Received

Mc. Alpine, D., C. E. Lumsden, E. D. Acheson , A re-appraisal.
Smith, B. H. , Principles of Clinical Neurology
M. Mumenthaler, H. Schliack, Torben Fog , Läsionen periphärer Nerven
E. Ettlinger , Functions of the Corpus Callosum
J. C. Scotto , L'hyperostose frontale interne
D. Ingvar, N. Lassen , Regional Cerebral Blood Flow
Michaelis, L. , Orthopaedic surgery of the limbs in paraplegia
Adolf Juba , Pathologie des Ballismus
I. Taylor , The neurological mechanisms of hearing and speech in Children
F. Mellerio , L'electroencéphalographie dans les intoxications aigués
T. W. Farmer , Pediatric Neurology
P. Bourret, R. Louis , Anatomie du systéme nerveux central
M. Brazier , Brain Function. Vol. II. RNA and brain function; memory and learning
E. Gutmann, P. Hnik , The effect of use and disuse on neuromuscular functions
R. G. Siekert, J. P. Whisnant , Cerebral Vascular Disease
Excerpta Medica Foundation , Third International Congress of Neurological Surgery, Copenhagen, August 1965
H. W. Delank , Das Eiweissbild des Liquor cerebrospinalis und seine klinische Bedeutung
Schadé, J. P., D. H. Ford , Basic Neurology
C. Bernhard, E. Bohm , Local Anaesthetics as Anticonvulsants
M. Singer, J. Schadé , Degeneration Patterns in the Nervous System
K. Akert, C. Bally, J. Schadé, H. Pakkenberg , Sleep Mechanisms     

Rehabilitation challenges in multiple sclerosis

While current immunomodulating drugs aim to reduce multiple sclerosis (MS) exacerbations and slow disease progression, rehabilitation aims to improve and maintain the functional abilities of patients in the face of disease progression. An increasing number of journal articles are describing the value of the many rehabilitation interventions that can be used throughout the course of the disease, from the initial symptoms to the advanced stages. An integrated team of healthcare professionals is necessary to address a myriad of problems to reduce impairments, disabilities, and handicaps. The problems may be related to fatigue, weakness, spasticity, mobility, balance, pain, cognition, mood, relationships, bowel, bladder, sexual function, swallowing, speech, transportation, employment, recreation, and activities of daily living (ADL) such as dressing, eating, bathing, and household chores. The team can help prevent complications and secondary disabilities, while increasing patient safety. Improving neurologically related function, maintaining good relationships, and feeling productive and creative adds enormously to the quality of life of people with MS and their families. Rehabilitation is more than an ‘extra’ service that is given after medical therapies; it is an integral part of the management of the diverse set of problems encountered throughout the course of the disease. An interdisciplinary team may have many members, including physicians, nurses, physical therapists, occupational therapists, speech and language pathologists, psychotherapists, social workers, recreational therapists, vocational rehabilitation therapists, patients, families, and other caregivers.     

Comparison of sublingual and oral prazepam in normal subjects. I. Clinical data

Five normal volunteers received at a 2-week interval a single dose of sublingual or oral prazepam in double-blind and cross-over conditions. All subjects completed a battery of 15 visual analogue scales before drug intake and 7.5, 15, 22.5, 30, 45, 60, 90 min, 2, 3, 5, 6, 7, 8, 9, 10 and 24 h following intake whereas a computerized assessment of vigilance (reaction time) was performed before intake, 15, 30, 60 min, 2, 3, 6, 8, 10 h following intake. Subjects rated themselves significantly more feeble, clumsy, lethargic, and incompetent following sublingual as compared to oral prazepam while a trend in the same direction was noted for the adjectives muzzy and mentally slow. In contrast, reaction time did not exhibit significantly different changes over time between the two forms. These results suggest a subjectively more rapid onset of activity following sublingual compared to oral prazepam.     

Some hormones secretion and personality in anorexia nervosa syndrome

The relationship between plasma leptin, some hormones (GH, IRI, IGF-1, DHEA-S, LH, FSH, T, E2, TSH, fT3, fT4), glucose level, personality dispositions and adipose tissue content in 22 women with anorexia nervosa were evaluated. Some personality features as: defensiveness, domination and aggression necessities, high self-control, bad self-estimation, retiring, expectation of custody--correlated with some hormones (LH, E2, IGF-1, fT3, F, T) and leptin level. The ascertained relationships suggest that still unexplained causes generate simultaneous disturbances in the endocrine and psychic processes in central nervous system of anorexia nervosa patients. Probably hormonal and neurotransmitter derangement are the adaptive changes allowing longer survival, as the low leptin secretion in the severest undernutrition states is.     

Antipsychotic metabolic effects: weight gain, diabetes mellitus, and lipid abnormalities.

OBJECTIVE: To review published and nonpublished literature describing changes in weight, glucose homeostasis, and lipid milieu with antipsychotics. METHODS: A Medline search was completed using the words weight gain, diabetes mellitus, cholesterol, triglycerides, risperidone, clozapine, olanzapine, quetiapine, ziprasidone, predictors, prolactin, obesity, and conventional antipsychotics. Publications, including original articles, review articles, letters to the editor, abstracts or posters presented at professional meetings in the last 4 years, and references from published articles, were collected. Manufacturers, including Eli Lilly Canada Inc, JanssenOrtho Inc, Pfizer Canada Inc, AstraZeneca Inc, and Novartis Pharmaceuticals, were contacted to retrieve additional medical information. RESULTS: The topic of antipsychotic-induced weight gain is understudied, and there are relatively few well-controlled studies. Weight gain as a side effect has been described with both conventional and atypical antipsychotics. Moreover, some atypical antipsychotics are associated with de novo diabetes mellitus and increased serum triglyceride levels. Predictors of weight gain may be age, baseline body mass index, appetite stimulation, previous antipsychotic exposure, and antipsychotic treatment duration. CONCLUSION: Significant weight gain is reported with the existing atypical antipsychotics. The weight gain described is highly distressing to patients, may reduce treatment adherence, and may increase the relative risk for diabetes mellitus and hypertriglyceridemia. Physicians employing these agents should routinely monitor weight, fasting blood glucose, and lipid profiles.     

What event-related potentials (ERPs) bring to social neuroscience?

Social cognitive neuroscience is a recent interdisciplinary field that studies the neural basis of the social mind. Event-related potentials (ERPs) provide precise information about the time dynamics of the brain. In this study, we assess the role of ERPs in cognitive neuroscience, particularly in the emerging area of social neuroscience. First, we briefly introduce the technique of ERPs. Subsequently, we describe several ERP components (P1, N1, N170, vertex positive potential, early posterior negativity, N2, P2, P3, N400, N400-like, late positive complex, late positive potential, P600, error-related negativity, feedback error-related negativity, contingent negative variation, readiness potential, lateralized readiness potential, motor potential, re-afferent potential) that assess perceptual, cognitive, and motor processing. Then, we introduce ERP studies in social neuroscience on contextual effects on speech, emotional processing, empathy, and decision making. We provide an outline of ERPs' relevance and applications in the field of social cognitive neuroscience. We also introduce important methodological issues that extend classical ERP research, such as intracranial recordings (iERP) and source location in dense arrays and simultaneous functional magnetic resonance imaging recordings. Further, this review discusses possible caveats of the ERP question assessment on neuroanatomical areas, biophysical origin, and methodological problems, and their relevance to explanatory pluralism and multilevel, contextual, and situated approaches to social neuroscience.