Article AbstractBecause this piece does not have an abstract, we have provided for your benefit the first 3 sentences of the full text.The short- and long-term psychological sequelae resulting from exposure to trauma can vary from complete recovery to various psychiatric conditions of various severities. Why do some persons appear not to have clinically significant long-term effects from trauma, while others do? The text reviews the normal responses to traumatic events and what factors increase the likelihood of developing significant long-term psychopathology.†‹

Article AbstractFrom our regular book review column. Disorders of Brain and Mind is an excellent resource text for students, clinicians, and researchers in the fields of psychology, neurology, and psychiatry. The text begins by reviewing the normal neurophysiology of the frontal lobes. After this background, there is a comprehensive discussion of the potential neuropsychological sequelae of frontal lobe damage. Overall, the discussion of frontal lobe functioning and how symptoms consistent with frontal lobe dysfunction are seen in patients with schizophrenia is excellent. The authors acknowledge, however, that frontal lobe dysfunction, in and of itself, cannot explain the full spectrum of schizophrenic symptoms.

In the past several years, there has been an increased appreciation for the importance of including cultural and ethnic factors in the evaluation and treatment of patients in psychiatry. Most of the focus has been on understanding the patients' psychosocial milieu and how these factors contribute to the patient's overall clinical presentation. Few studies have addressed the significance of pharmacogenetic heterogeneity among various cultural, ethnic, and racial groups. This article reviews the pharmacogenetic data and summarizes the sparse pharmacokinetic and pharmacodynamic data that pertain to the treatment of mood disorders in different ethnic and racial groups.

The authors hypothesized that patients who develop gross EEG abnormalities during clozapine treatment would have a less favorable outcome than patients who did not develop abnormal EEGs. The clinical EEGs and the Brief Psychiatric Rating Scale (BPRS) scores of 12 patients with schizophrenia and 4 patients with schizoaffective disorder were compared before and during treatment with clozapine. Eight patients developed significant EEG abnormalities on clozapine; 1 showed worsening of an abnormal pre-clozapine EEG; none of these subjects had clinical seizures. BPRS scores improved significantly in the group of patients who developed abnormal EEGs but not in the group who did not. Findings are consistent with previous reports of a high incidence of clozapine-induced EEG abnormalities and a positive association between these abnormalities and clinical improvement.

The BE(2)‐M17 and BE(2)‐C human neuroblastoma cell lines have been shown to synthesize and secrete corticotropin‐releasing factor (CRF) following retinoic acid treatment. It has been demonstrated that CRF secretion and intracellular synthesis increases in response to forskolin treatment. In this report, we have further characterized these cells in response to protein kinase C activators, dexamethasone, interleukin—1x, as well as various neurotransmitters and peptides. Nanomolar concentrations of the phorbol ester—phorbol 12 myristate 13—acetate (TPA), increased intracellular CRF content in both cell lines while increasing secretion only in the BE(2)‐M17 cell. Nanomolar concentrations of dexamethasone were not able to alter basal levels of secretion and content in either cell type. However, in the BE(2)‐Ml7 cell but not the BE(2)‐C cell, the same concentrations of dexamethasone added to 30 μM forskolin augmented levels of CRF secretion and content. Likewise, the same augmented response in CRF secretion and content was seen only in the BE(2)‐M17 cell line when nanomolar concentrations of dexamethasone were added to 20 nM TPA. Furthermore, only in the BE(2)‐M17 cell line were micromolar levels of the biogenic amine serotonin able to increase levels of CRF secretion and content. No effects on CRF in both cell lines were demonstrable with picomolar levels of interleukin‐10: as well as micromolar levels of acetylcholine, norepinephrine, arginine‐vasopressin, oxytocin, and angiotensin‐II. The potential usefulness of these cells as models of central nervous system or placental CRF‐containing neurons is discussed.

AnxietyVolume 1, Issue 4 p. 192-195 Brief Report Natural killer cell activity in patients with panic disorder J. Stephen McDaniel M.D., Corresponding Author J. Stephen McDaniel M.D. Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GeorgiaEmory Clinic-Psychiatry, 1365 Clifton Road, NE, Atlanta, GA 30322Search for more papers by this authorEmile D. Risby, Emile D. Risby Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GeorgiaSearch for more papers by this authorMark Stipetic, Mark Stipetic Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GeorgiaSearch for more papers by this authorRita D. Jewart, Rita D. Jewart Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GeorgiaSearch for more papers by this authorJane Caudle, Jane Caudle Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GeorgiaSearch for more papers by this author J. Stephen McDaniel M.D., Corresponding Author J. Stephen McDaniel M.D. Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GeorgiaEmory Clinic-Psychiatry, 1365 Clifton Road, NE, Atlanta, GA 30322Search for more papers by this authorEmile D. Risby, Emile D. Risby Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GeorgiaSearch for more papers by this authorMark Stipetic, Mark Stipetic Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GeorgiaSearch for more papers by this authorRita D. Jewart, Rita D. Jewart Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GeorgiaSearch for more papers by this authorJane Caudle, Jane Caudle Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GeorgiaSearch for more papers by this author First published: 1994 https://doi.org/10.1002/anxi.3070010408Citations: 8AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume1, Issue41994Pages 192-195 RelatedInformation

To highlight some problems that may occur when investigating clozapine-associated deaths including (i) that death may be related to gastrointestinal hypomotility and (ii) that post-mortem blood clozapine and norclozapine concentrations may not reflect ante-mortem concentrations.A 41-year-old male died 40 min after admission to hospital as a result of aspiration complicating severe, clozapine-induced constipation. At post-mortem the small bowel was dilated and contained bloodstained mucus, particularly within the jejunum. The large bowel was considerably dilated and contained large quantities of foul-smelling, bloodstained fluid and a small amount of stool. Its lining was focally congested, but there was no other obvious abnormality. Analysis of serum obtained on admission revealed clozapine and norclozapine concentrations of 0.56 and 0.43 mg/L, respectively, whereas post-mortem femoral whole blood obtained <34 h after death showed clozapine and norclozapine concentrations of 3.73 and 1.75 mg/L, respectively. In 6 out of a further 12 clozapine-associated deaths investigated 2002–9 there were reports of gastrointestinal tract problems of varying severity.Severe constipation or paralytic ileus in clozapine-treated patients may lead to intestinal necrosis and/or perforation, or pulmonary aspiration. In some such cases the immediate cause of death may be obvious, but in others only careful assessment of the clinical course of the terminal illness may reveal gastrointestinal hypomotility as a likely underlying cause of death.

There has been much speculation as to the role of dopamine in the etiology and/or manifestation of positive and negative symptoms. Traditionally, cerebrospinal fluid (CSP) concentrations of homovanillic acid (HVA) has been used as an index of central dopaminergic activity. Relea~l dopamine is metabolized to HVA, by catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO) (Cooper et al 1991). A review of the CSF HVA literature, however, reveals no consistent correlations between HVA and schizophrenic symptomatoiogy (reviewed by Pickax et al ! 9907. Yet there is sufficient data to suggest that dopamine activity is abnormal in schizophrenia (Davis et al 19917. Therefore the evaluation of other putative measures of dopamine release or metabolism seems warranted. Released dopamine is also converted to dopamine sulfate (DASO47 by the enzyme phenolsulphotransferase (PST7 (Jenner and Rose, 1973). in the brain, it appears that the sulfoconjugation of dopamine occurs primarily outside of dopaminergic neurons (Tyce et al 1988). Therefore CSF DASO~ concentrations may reflect an important alternate route of dopamine metabolism. Assessment of PST-dependent DASO4 independently, or in re-

The family of G proteins play a key role in transmembrane signal transduction. A review of the literature suggests that there is sufficient data to consider abnormalities in G-protein coupling or content in many neuropsychiatric disorders. Whether such changes are primary or secondary remains to be elucidated.

Natural killer cell activity was prospectively studied in 15 patients with chronic schizophrenia and in seven patients with schizoaffective disorder, depressed type. These patients were compared to individually matched normal controls. No mean differences in natural killer cell activity between the patient groups and their controls were observed.

Some investigators have speculated that structural brain alterations observed in some psychiatric patients might be related to increased limbic-hypothalamic-pituitary-adrenal axis (LHPA) activity. To explore this hypothesis, we prospectively studied 166 research volunteers (19 patients with research diagnostic criteria (RDC) major depression, 9 patients with RDC bipolar depression, 45 patients with RDC schizophrenia, and 94 RDC normal controls), examining the relationship between magnetic resonance image-determined ventricular-to-brain ratio (VBR) and indices of LHPA axis function (cerebrospinal fluid (CSF) corticotropin-releasing factor (CRF), CSF adrenocorticotropic hormone (ACTH), and 24-hour urinary-free cortisol secretion). We observed no significant differences in mean VBR among the three patient groups and the normal control volunteers. Of the indices of LHPA activity, only CSF CRF concentrations distinguished the four subject groups, with CSF CRF being significantly elevated in the more severely depressed major depression patients. Indices of LHPA activity were not significantly correlated with VBR in any of the three patient groups or in the normal volunteers. These preliminary results suggest that VBR is not highly associated with alterations in LHPA activity, at least as determined cross-sectionally. Further longitudinal studies with reference to diagnostic subtypes, severity, symptom profiles, and more specific neuroanatomic regions may allow the elucidation of possible relationships between LHPA pathology and structural brain alterations.