5 Serum glucose levels were determined using glucose-oxidase method. The intra- and interassay variances were 2% and 4%, respectively. Fifty µl of serum was used for the measurement of insulin by immunoradiometric assay (Biosource INS-IRMA Kit). The

intra- and interassay variances were 4% and 8%, respectively. Lipid profile, FIRI, alanin transaminase (ALT), and alkaline phosphatase (ALP) were determined by commercial kits and enzymic ways.11 Statistical Analysis The data were expressed as mean±SEM. Data http://www.selleckchem.com/products/Erlotinib-Hydrochloride.html distribution was assessed by Shapiro-Wilk’s test. The data were analyzed by one-way ANOVA and post hoc least significant different (LSD) tests. A P value Inhibitors,research,lifescience,medical of ≤ 0.05 was considered as significant. Results Effect of Fructose Administration Compared to control group, daily administration of fructose for eight weeks was associated with significant increase in blood glucose (P<0.05), insulin (P<0.001), and FIRI (P<0.001) (figures 1-3). Effect of Urtica Dioica Extract Compared to vehicle, Urtica dioica

extract Inhibitors,research,lifescience,medical at 100 mg/kg (P<0.01) and 200 mg/kg (P<0.001) significantly decreased serum glucose (figure 1). Moreover, compared to the vehicle, Urtica dioica at 50, 100 and 200 mg/kg significantly (P<0.001) decreased serum Inhibitors,research,lifescience,medical insulin and FIRI (figures 2 and ​and33). Figure 1: Serum glucose concentration (mean±SEM n=8 each) of control, fructose-treated Inhibitors,research,lifescience,medical and Urtica dioica extract-treated rats at 50, 100 or 200 mg/kg/day. *Indicates significant difference from the control group; ΔIndicates significant difference ... Figure 2: Serum insulin concentration (mean±SEM, n=8 each) of control, fructose-treated and Urtica dioica extract-treated rats at 50, 100 or 200 mg/kg/day). *Indicates significant difference from the control group; ΔIndicates significant difference ... Figure 3: The values (mean±SEM, n=8 each) of fasting insulin resistance index (FIRI) of control, fructose-treated Inhibitors,research,lifescience,medical and Urtica dioica extract-treated (50, 100, 200 mg/kg/day) rats. *Indicates significant difference from the control group; ΔIndicates ... Effect of Urtica Dioica Extract on Lipid

Profile Daily administration of fructose for eight weeks did not change serum TG, total cholesterol, VLDL, LDL-cholesterol, HDL-cholesterol, isothipendyl LDL/HDL ratio compared to those of the control group (table 1). Table 1: The values (mean ±SEM, n=8 each) of serum lipid profile, hepatic enzymes, and leptin of control, fructose-treated and Urtica dioica extract-treated (50, 100, 200 mg/kg/day) rats Compared to the fructose group, Urtica dioica extract at 50 mg/kg significantly (P<0.05) increased serum TG and VLDL-cholesterol, and significantly (P<0.05) decreased serum LDL and LDL/HDL ratio (table 1). Moreover, compared to fructose group, the extract at 100 and 200 mg/kg/day significantly (P<0.05) increased TG, and significantly (P<0.05) decreased LDL and LDL/HDL ratio.

However, in reality we were able to do much more. By sequencing this family and other families, we were able to use family genome sequencing to eliminate more than 70% of the sequencing selleck inhibitor errors in a family of four, and 90% of the errors in a family of six. In addition, we were able to immediately identify rare variants because they were present in two or more members of the family and hence were very unlikely to be sequencing errors. This is important

since it is the rare variants that are the origins of many diseases. Moreover, we could actually delineate the haplotypes of all the members of the family with enormous precision.17 The importance of the family genomics tool is in its ability to reduce significantly Inhibitors,research,lifescience,medical Inhibitors,research,lifescience,medical the dimensionality of chromosomal search space for disease genes. When searching for the disease genes, we can simply detect the haplotype blocks that the diseased individuals share which differ from the normal individuals and know that the disease genes must reside in these regions. In one such family we reduced the search space to 0.1% (J. Roach, personal communication). This vast reduction allows researchers to sort through the genes in the remaining DNA. In the previously mentioned family of four, we were Inhibitors,research,lifescience,medical able to identify four

diseased gene candidates, and it was relatively easy to identify the disease genes encoding each of Inhibitors,research,lifescience,medical the two diseases (Figure 9). Figure 9. A chromosomal map of one of the offspring with a genetic disease, showing possible candidate genes for the disease. In the near future, family sequencing will provide a fundamental medical record for each of us. The cost of sequencing is steadily decreasing, and within 5 years it will be well under $1,000. Third-generation sequencing technologies, using single-molecule physical measurements, will allow us to read sequences in lengths of 10,000 to 100,000 base-pairs at a time.18 Consequently, the speed of sequencing a human genome will be very rapid (e.g. 15 minutes), Inhibitors,research,lifescience,medical and the cost will be under $500. All individuals will benefit from sequencing their genome. The benefit is in the isothipendyl identification of actionable

gene variants. Actionable gene variants are defective genes which cause negative health effects, and medical intervention is available for reversing these effects. For example, if sequencing reveals a defect in a vitamin D transporter which has caused early onset of osteoporosis, an available solution would be taking megadoses of vitamin D to reverse the osteoporosis. We have identified almost 300 highly penetrant variants that fall into the actionable gene variants category. Sequencing the genome is a one-time investment, and once a genome is sequenced it can be searched every year for newly identified actionable genes. Sequencing is a smart investment in improving and optimizing wellness and avoiding disease.

107 It therefore appears that spine morphology is modulated by stress, although other factors such as sex hormones may also have an effect, on their formation. Chronic stress and neuronal

death? There have been reports that social stress leads to cell death in the hippocampal formation.108 PH-797804 ic50 However, recent studies using the optical dissector technique, a. reliable method for quantification of neurons within an entire brain region, showed that stress does not affect neuron numbers in the CA1 and CA3 areas of the hippocampus.109 Moreover, experiments using Inhibitors,research,lifescience,medical an in situ end-labeling technique to identify apoptotic (dying) cells showed a significant decrease in the number of apoptotic cells when all hippocampal areas were analyzed.110 Although stress-induced death of principal neurons in the hippocampus is questionable, it is clear that stress profoundly affects these neurons. Their nuclear ultrastructure Inhibitors,research,lifescience,medical changes as shown in the significant intensification in Nissl staining.111 An electron microscopic analysis indicated that this effect is due to increased heterochromatin formation in the neuronal nuclei.112 The physiological role of these

changes is unknown, but one may speculate that they are accompanied by alterations in gene transcription. Inhibitors,research,lifescience,medical Recent tree shrew studies showed that chronic psychosocial stress reduced the expression of certain genes that, are related to the shape of neurons and other Inhibitors,research,lifescience,medical brain cells.113 In the brains of adult rats that had been prenatally stressed through

the stressful treatment of the pregnant dams, expression of genes associated with excitatory neurotransmission and mechanisms ofneurotransmitt.errelea.se were significantly altered.114 Furthermore, a large group of genes in the hippocampus has been shown to be differentially expressed after glucocorticoid treatment.76 Conclusions and further directions Despite extensive preclinical and clinical investigations, the exact neurobiological processes leading to depression and the mechanisms Inhibitors,research,lifescience,medical responsible for the therapeutic effects of antidepressant drugs are still CYTH4 not completely understood. Antidepressants are presently believed to exert their primary biochemical effects by readjusting aberrant intrasynaptic concentrations of neuromodulators such as 5-HT However, the limitations of current antidepressant medications, such as the time delay for a full therapeutic response, the substantial number of nonresponders, and bothersome side effects merit, a full exploration of all plausible agents with novel antidepressant mechanisms of action. Recent preclinical and clinical studies suggest that major depressive disorders are associated with cellular resilience and an impairment of synaptic and structural plasticity, and that antidepressant medications may act by correcting this dysfunction.

Since the earliest publications on the subject, the excellent therapeutic effectiveness of this method in the treatment of depression and other psychiatric disorders has been described in a variety of reviews and meta-analyses.2-4 However, although the technique and practice of ECT has improved considerably in the last decades, the crucial ncurobiological mechanisms contributing to the therapeutic efficacy in distinct, psychiatric disorders are still under investigation. Putative mechanisms of action of ECT Although decades of research and clinical experience have improved the technique and

practice of ECT, the underlying crucial mechanisms which contribute to the superior therapeutic effects of ECT are still under Inhibitors,research,lifescience,medical investigation. Most research investigating the neurobiological effects of ECT focused on the antidepressant potential of ECT, and revealed Inhibitors,research,lifescience,medical that. ECT particularly affects neurotransmitter systems which may be involved in the pathophysiology of depression.5 In accordance with the monoamine deficiency hypothesis in depression, several studies indicated that. ECT attenuates serotonergic and noradrenergic neurotransmission. However, animal studies revealed conflicting results, such as an enhanced sensitivity of presynaptic

hippocampal serotonin (5-HT)1Areceptors,6 but. also a decreased sensitivity of hippocampal 5-HT1Areceptors,7 have been described after electroconvulsive Inhibitors,research,lifescience,medical shocks (ECS) in rats. However, in patients suffering from major depression, ECT Inhibitors,research,lifescience,medical has been shown to increase tryptophan plasma click here levels8,9 suggesting that an increased availability of the serotonin precursor may contribute to the therapeutic

effects of ECT.9 Table I. The administration of ECT according to WHO recommendations. In addition, a compensatory increase in y-aminobutyric acid (GABA) neurotransmission has been suggested as a. possible mechanism of ECT. In line with the anticonvulsant effects of ECT and Inhibitors,research,lifescience,medical the GABA-dcficit hypothesis of depression,10 a proton magnetic resonance spectroscopy study showed that occipital cortex GABA concentrations“ are increased in depressed patients treated with ECT. Furthermore, an iomazcnil-single-photon emission computer because tomography (SPECT) study suggested an enhanced GABAergic neurotransmission as a possible mechanism of ECT12 Recently, ECT has been shown to enhance activity of inhibitory circuits in human motor cortex, further indicating that. ECT has marked effects on GABAergic neurotransmission.13 Due to the fact that ECT increased glutamate plasma levels9 and normalized reduced glutamate/glutaminc levels in the left, cingulum in depressed patients responding to ECT,14 effects on glutamate, an excitatory neurotransmitter, may also play a role. In addition to effects on neurotransmitter systems, therapeutic effects of ECT have also been attributed to its influence on the hypothalamic-pituitary-adrenal (HPA) axis.

30 Decreases in astrocytic immunoreactivity for cellular GFAP and the neuron-specific phosphoprotein B50 (or GAP-45) were detected in CA1 and CA2 in depression.31 The authors suggest that apoptosis may only be a minor contributor to volume www.selleckchem.com/products/gw-4064.html changes in the hippocampus in depression, while patterns of reactive astrogliosis and synaptic

reorganization proteins are significantly Inhibitors,research,lifescience,medical altered in only some hippocampal regions in depression. Other reports of hippocampal changes in mood disorders identify a significant decrease in the density of nonpyramidal neurons in the CA2 region and a reduction in reelin-positive cell density in the hilus in subjects with BPD.32,33 Two other studies conducted on the postmortem hippocampal formation in a small sample of subjects with

BPD reveal a decrease in the density and size Inhibitors,research,lifescience,medical of nonpyramidal neurons in the CA2 region and some disorganization in neuronal clusters in layers II and III of the entorhinal cortex.34,35 Neuronal and glial cell packing density and soma size were estimated recently in Nissl-stained sections including the hippocampal subfields in 16 subjects with MDD and 16 age-matched normal control subjects.36 Representative photomicrographs are presented in Figure 2. Prominent abnormalities in the CA regions and dentate gyrus are found in subjects with MDD. There Inhibitors,research,lifescience,medical is a significant increase in the mean density of pyramidal neurons in depressed subjects, as compared with normal control subjects. In the granule cell layer of the dentate gyrus, cell density is significantly increased in MDD. In addition, there is a significant decrease in the mean soma size Inhibitors,research,lifescience,medical of pyramidal neurons in depressed subjects, as compared with normal control subjects. On the basis of covariate analyses, the main findings of increased neuronal density

and decreased neuron Inhibitors,research,lifescience,medical soma size in depression are not significantly altered when taking into consideration such factors as gender, age, postmortem interval, tissue pH, brain weight, smoking, antidepressant, drug prescription in the last month of life, or suicide. The substantial increases noted in neuronal packing density and decrease in neuronal Fossariinae soma size detected in postmortem tissue may be related to the decrease in hippocampal volume noted by some in MDD. Figure 2. Brightfield photomicrographs of coronal sections of the postmortem human hippocampal formation. A. Cresyl violet-stained coronal section from a 54-year-old male (23-h postmortem interval). B. An adjacent coronal section processed byTimm staining. Note … Glial pathology in depression appears to extend beyond the frontal cortex to the hippocampus. A recent study of the hippocampus in a large number of subjects with MDD and aged-matched normal control subjects reports a significant increase in the density of glial cells in all hippocampal CA subfields and the granule cell layer of the dentate gyrus.

4 Spedding and colleagues have cogently argued that a systems-level approach using animal models will lead to more effective Gedatolisib treatment for psychiatric diseases.4 Based on a model which involves specific alterations in hippocampal-cortical circuitry, they propose testing compounds in animals in which these circuits are disrupted by phenycyclidinc (PCP). In support of this systems-level approach, nearly every approved antipsychotic drug will ameliorate PCPinduced alterations in neuronal functioning.37 However, it is also true that drug classes with demonstrated ability

Inhibitors,research,lifescience,medical to ameliorate PCP-induced deficits (eg, 5-HT2A antagonists38) are only marginally effective in treating schizophrenia.39-40 Thus, in vivo systems-level screens can be highly effective tools to verify in vivo actions of putative atypical antipsychotic drugs. It Inhibitors,research,lifescience,medical does not appear that any of the available in vivo screening models are able to predict relative efficacy at treating schizophrenia, however. In addition, none of the available models appears to adequately recapitulate the entirety of the human phenotype.37 One can easily provide the counterargument that a “suitable animal model will eventually be found which recapitulates the schizophrenia phenotype,” although it is also plausible that “no suitable preclinical model will ever be found which adequately recapitulates schizophrenia,

Inhibitors,research,lifescience,medical pathology.” Clearly, despite decades of research we have not yet discovered an adequate preclinical model, and it is within the Inhibitors,research,lifescience,medical realm of possibility that “schizophrenia is a uniquely human disease which cannot be adequately modeled in rodents.” In large measure, this is likely to be due to the fact that a number of genetic “hits” as well as nongenomic factors converge Inhibitors,research,lifescience,medical to produce the final phenotype in humans.41 At present, we have no way to predict either way, and continued research in this arena will be based more on untested assumptions than on data. Is schizophrenia similar to hypertension in being complex, polygenic, and epigenetic? Another possibility is that schizophrenia represents a complex disease with genetic and epigenetic factors

and which is both chronic and progressive, resulting in irreversible end-organ of damage – similar to hypertension. Indeed, there is accumulating evidence for epigenetic factors involved in the etiology of schizophrenia – particularly relating to reelin.42-45 There has also been abundant evidence accumulated over the past several decades that schizophrenia is associated with subtle but reproducibly documented neurodegeneration (reviewed in refs 46,47). Accordingly, optimal treatment of schizophrenia would be similar to that for other progressive and complex diseases such as hypertension, where individuals at risk would be identified and then treated to avoid end-organ damage. Such an approach has already been attempted, with a mixed degree of success.

In addition, bothersome side effects such as somnolence or sexual dysfunction, even when they do not lead to

premature drug discontinuation or inadequate dosing, clearly compromise quality of life. Methodological issues There are considerable methodological challenges related to the study and clinical management of side effects. When evaluating side-effect data, it is important to consider Inhibitors,research,lifescience,medical whether the information was obtained by spontaneous report, self-report checklists, or responses to direct, questioning. Spontaneous reporting of side effects following an open-ended question (eg, “any change since last, visit?”) typically yields a lower incidence of adverse events than itemized self-report checklists Inhibitors,research,lifescience,medical (eg, the Frequency, Intensity, and Burden of Side Effects Rating (FIBSER) Scale4) or direct questioning about specific side effects (The Systematic Assessment for Treatment Emergent Events-Specific Inquiry [SAFTEE-SI]5).The reporting of certain side effects, particularly sexual dysfunction, may also be influenced by the degree of comfort the patient/subject has with the subject area and

with the questioner; this may be affected by gender, culture, and other factors. Side-effect rates presented for an antidepressant in isolation tend to be of somewhat Inhibitors,research,lifescience,medical limited benefit, as common experiences such as headache or rhinitis inevitably figure prominently, even if they bear Inhibitors,research,lifescience,medical no specific relationship to the agent. Hence, side effects presented as placebo-adjusted rates are often more informative. So too arc comparative rates of specific side effects buy Ki16425 across a number of antidepressant agents, which allow clinicians and patients to make informed choices about the relative

risks of side effects of greatest concern to the patient. In both research and clinical contexts, an important challenge is presented by the Inhibitors,research,lifescience,medical phenomenological overlap between side effects and residual symptoms of depression. Thus, fatigue, cognitive impairment, apathy, jitteriness and irritability, and sleep and appetite changes are core features of depression, but may also be related to antidepressant, treatment. In a small study of 43 depressed inpatients,6 which investigated the Phosphoprotein phosphatase rate of somatic symptoms and complaints that were present before and after treatment, many symptoms often considered to be side effects of drugs were also present prior to treatment, including dry mouth, lightheadedness, sweating, tremors, and constipation. The distinction between residual symptoms and side effects is crucial, as they call for very different responses. In the latter case, a dose increase or pharmacological or other augmentation of treatment may be required. In the former case, a dose reduction or use of a pharmacological antidote would be important initial considerations.

Results from studies of androgen levels have been similarly inconsistent demonstrating both normal and decreased testosterone levels137-139 and elevated and decreased free testosterone levels.138,139 In conclusion, there is no consistent or convincing evidence that PMS is characterized by abnormal circulating plasma levels of gonadal steroids or gonadotropins or by hypothalamic-pituitary-ovarian axis dysfunction. Several studies do, however, suggest that levels of estradiol, progesterone,

or neurosteroids Inhibitors,research,lifescience,medical (eg, pregnenolone sulfate) may be correlated with symptom severity in women with PMS.134,140,141 (See references 142 and 143 for summaries of hormonal studies of P.M.S.) If PMS is not due to a deficiency or excess of reproductive steroids (or of any other hormone studied to date), do these steroids play any role at all in the precipitation of the syndrome? We attempted to answer this question by posing four questions. Is the luteal phase necessary Inhibitors,research,lifescience,medical for the appearance

of PMS? If there was no Inhibitors,research,lifescience,medical obvious abnormality in the activity of the reproductive axis, was PMS in fact dependent on the menstrual cycle for its expression, or could it be dissociated from the luteal phase? We blinded women to their position in the menstrual cycle by administering the progesterone receptor antagonist RU-486 (which both precipitates menses and ends corpus luteum activity), alone or with human chorionic gonadotropin (hCG) (which preserves corpus luteum activity).144 Thus, after receiving the RU-486 (6 days after the LH surge), subjects did not know whether they were in the RAD001 clinical trial follicular phase of the next cycle Inhibitors,research,lifescience,medical (RU-486 alone) or in the preserved luteal phase of the initial cycle (RU-486 + hCG). Subjects in all three groups (a placebo-only group was included) experienced highly comparable symptoms

that were significantly greater than those seen in the follicular Inhibitors,research,lifescience,medical phase; ie, women receiving RU-486 alone developed characteristic symptoms of PMS in the experimentally produced follicular phase of the next cycle. P.M.S, therefore, was not dependent on reproductive endocrine changes occurring in the mid-late luteal phase, as we were able to eliminate those changes without influencing subsequent symptom Idoxuridine development. This left open the question of whether events occurring earlier than the mid-late luteal phase might, nonetheless, be influencing subsequent symptom development. If you suppress ovarian activity, can you prevent the symptoms of PMS? As the RU-486 study eliminated only the mid-late luteal phase, PMS symptoms might have appeared consequent to reproductive endocrine events occurring earlier in the menstrual cycle. To test this possibility, we performed “medical oophorectomies” by administering the gonadotropin-releasing hormone (GnRH) agonist leuprolide acetate (3.

6,7 It remains to be determined whether a family history influences SA characteristics in schizophrenia. The goals of the present study were twofold: To determine and compare the this website frequency of a family history of suicide in patients with schizophrenia and in normal controls. To determine the influence of a family history of suicide on the frequency Inhibitors,research,lifescience,medical of SA in patients with schizophrenia and on SA characteristics. Methods Subjects were over 18 years old and gave informed consent;

all subjects had information on both parents. A total of 160 schizophrenic inpatients and 102 normal controls participated in the study. Information on history of personal and familial suicidal behaviors was obtained with the use of a structured interview. Suicide methods were classified as low and high lethality as defined in a previous study.8 Subjects were classified in the

high-lethality group if they had made at least one high -lethality SA in Inhibitors,research,lifescience,medical their life. Normal controls were healthy volunteers recruited for phase 1 drug studies. Results The results of this study arc summarized in Tables Inhibitors,research,lifescience,medical I to IV. Table I Demographics of the study population. Table II Characteristics of suicide attempters (for the 80 schizophrenics who had a history of suicide attempts [SA]). Table III Effect of a family history of suicide. SA: suicide attempt; NS: nonsignificant. Table IV Association Inhibitors,research,lifescience,medical between family history of suicide and suicide attempt (SA) lethality and repeated SA in the group of schizophrenic patients (Mantel-Haenszel X 2 test for 3 groups): number and proportion of patients with a positive family history of suicide. … Conclusion Half of the schizophrenic inpatients had a personal

history of SA: they made their first attempt at an early age, and 44% of the suicide attempters made repeated attempts. The frequency of having Inhibitors,research,lifescience,medical a blood relative who has committed suicide did not differ between schizophrenic subjects and normal controls, but schizophrenic subjects have a higher frequency of suicide in their first-degree relatives. This is in accord with the current conception of suicidally: suicidal behavior and psychiatric disorders have different origins, unless but suicidality needs the presence of a psychiatric disorder to be expressed as a suicidal behavior. A higher frequency of suicide in first-degree relatives in the schizophrenia group can be interpreted in two ways: Having a first-degree relative who committed suicide may worsen the course of schizophrenia in the probands and thus increases the risk of being an inpatient. Having a schizophrenic child or sibling can be a stress factor in first-degree relatives, who could subsequently develop a psychiatric disorder and suicidal behavior if they are prone to it. In our study, a family history of suicide was associated with an increased risk of personal history of SA, higherlethality SA, and multiple SAs.

43 It integrates elements of psychoanalytic object relations theory and cognitive psychology by focusing on understanding the individual’s problematic relationships patterns and the resulting thoughts, feelings, and behavioral responses.

Routinely, 24 CAT sessions are offered with four post-therapy SCH727965 order follow-ups. The patient also benefits from general psychiatric care for assessment and treatment of comorbidity and use of eventual Inhibitors,research,lifescience,medical pharmacotherapy, plus crisis team and occasional brief and goal-directed inpatient care. The HYPE program also engages families with psychoeducation and up to four sessions of family intervention. The HYPE intervention is supported by effectiveness data and can be adapted to existing services in other settings.42 Pharmacotherapy There is very little empirical evidence supporting the use of pharmacotherapy with adolescents struggling with BPD. This discussion will be derived from what is suggested in adults and from our clinical experience Inhibitors,research,lifescience,medical with adolescents (the reader may refer to the article by Luis

H. Ripoll [p 213] in this issue for a review of the pharmacologic treatment of BPD). In BPD, medication should only be used as an adjunct to a multidimensional psychosocial approach and its limitations should be made clear for the patient. If two different persons are involved as the psychotherapist and the prescribing doctor, communication is very important. The pharmacological Inhibitors,research,lifescience,medical treatment will be symptom-oriented and will address impulsivity,

affective instability, suicidal behaviors, and non-suicidal self-injury. No medication has received an official indication in the treatment of BPD, and long-term use of pharmacotherapy has not been studied in BPD. A good Inhibitors,research,lifescience,medical strategy could be to maintain a medication that works until psychotherapy Inhibitors,research,lifescience,medical has led to the development of new strategies. Selective serotonin reuptake inhibitors In BPD, most studies suggest that selective serotonin reuptake inhibitors (SSRIs) are most effective in reducing anger and impulsive symptoms; a reduction in mood swings is also mentioned.44,45 Other Mannose-binding protein-associated serine protease antidepressants are also studied (tricyclics and MAO inhibitors) but SSRIs are preferred, since they are better tolerated in regard to side effects and also they appear safer in case of overdose, which is a particular concern with BPD patients. Bulimia nervosa, a form of behavioral dyscontrol that usually develops in adolescents, is frequently associated with BPD and tends to respond to SSRIs.46 Regarding antidepressants, which are widely prescribed to patients with BPD, one has to keep in mind that they do not treat the disorder and do not produce remission.44 Antipsychotics The literature concerning antipsychotics in BPD is sparse and the samples are small.44,45 Cognitive-perceptual symptoms (reference and paranoid ideas, illusions and hallucinations, derealization) arise mainly in periods of intense emotional stress.