Efficacy and safety of chloral hydrate in auditory brainstem response test: A systematic review and single-arm meta-analysis.

OBJECTIVES: To evaluate the safety and efficacy of chloral hydrate in auditory brainstem response (ABR) tests. SETTING AND DESIGN: In this study, the authors systematically searched both English (Embase, PubMed, and Web of Science) and Chinese (Chinese National Knowledge Infrastructure, Wanfang Data, and VIP Chinese Science) databases. Two authors independently performed data extraction and quality assessment. The pooled sedation failure rate and the pooled incidence of adverse events were calculated via a random-effects model. Sensitivity and subgroup analyses were performed to explore the sources of heterogeneity, and the PRISMA guideline was followed. PARTICIPANTS: Patients with ABR tests receiving chloral hydrate sedation. MAIN OUTCOME MEASURES: The pooled sedation failure rate and the pooled incidence of adverse events. RESULTS: A total of 23 clinical studies were included in the final analysis. The pooled sedation failure rate of patients who received chloral hydrate sedation before ABR examination was 10.0% [95% confidence interval (CI) (6.7%, 15.0%), I2 = 95%, p < .01]. There were significant differences in the prevalence of sedation failure between sample sizes greater than 200 and those less than or equal to 200 (5.6% vs. 19.6%, p < .01) and between the studies that reported sleep deprivation and those that did not report sleep deprivation (7.1% vs. 18.9%, p < .01). The pooled incidence of adverse events was 10.32% [95% CI (5.83%, 14.82%), I2 = 98.1%, p < .01]. CONCLUSIONS: Chloral hydrate has a high rate of sedation failure, adverse events, and potential carcinogenicity. Therefore, replacing its use in ABR tests with safer and more effective sedatives is warranted.

Sleep Patterns and Risk of Prostate Cancer: A Population-Based Case Control Study in France (EPICAP).

BACKGROUND: Sleep disturbances have been singled out for their implication in the risk of several cancer sites. However, results for prostate cancer are still inconsistent. METHODS: We used data from the EPICAP study, a French population-based case-control study including 819 incident prostate cancer cases and 879 controls frequency matched by age. Detailed information on sleep duration on work/free days, and sleep medication over lifetime was collected. RESULTS: Sleep duration and sleep deprivation were not associated with prostate cancer, whatever the aggressiveness of prostate cancer. However, sleep deprivation was associated with an increased prostate cancer risk among men with an evening chronotype [OR, 1.96; 95% confidence interval (CI), 1.04-3.70]. We also observed an increased risk of prostate cancer with higher duration of sleep medication use (Ptrend = 0.008). This association with long duration of sleep medication use (≥10 years) was more pronounced among men who worked at night 15 years or more (OR, 3.84; 95% CI, 1.30-11.4) and among nonusers of NSAID (OR, 2.08; 95% CI, 1.15-3.75). CONCLUSIONS: Our results suggested that chronotype, night work, or NSAID use could modify the association between sleep disorders and prostate cancer occurrence needing further investigations to go further. IMPACT: EPICAP is the first study, which investigates several sleep indicators taking into account potential effect modifiers. If our findings were confirmed, we could identify subgroups of men at higher risk of prostate cancer that may be accessible to preventive measures.

Sleep Deprivation & Amphetamine Induced Psychosis.

Objectives: To explore the relationship between sleep deprivation and amphetamine-induced psychosis. Methods: The patient group included 78 patients with a diagnosis of amphetamine (Captagon)-induced psychosis. The control group included 49 patients with no current or past history of amphetamine (Captagon)-induced psychosis. All study subjects underwent the following: a demographic sheet, a structured clinical interview for SM-IV (SCID 1), a drug use questionnaire, a questionnaire to explore any relationship between sleep deprivation and Captagon-induced psychosis, routine medical investigation, and urine screening for detection of drugs. Results: The patient group showed significantly higher both regular and maximum daily doses of Captagon. Patients showed more periods of sleep deprivation with the use of Captagon in comparison to controls, especially with the increase of the Captagon dose. Patients believed that the occurrence and termination of sleep deprivation were the cause of the start and end of psychotic experiences (more so than the increase and decrease or stoppage of Captagon doses). Conclusion: sleep deprivation plays an essential role in the development of psychotic symptoms in patients who are using Captagon.

Analysis of Risk Factors for Chloral Hydrate Sedative Failure with Initial Dose in Pediatric Patients: a Retrospective Analysis.

BACKGROUND: Although chloral hydrate has been used as a sedative for more than 100 years, dozens of studies have reported that it has inconsistent sedative effects and high sedation failure rates with initial dose. The high failure rates may lead to repeated administration of sedatives, guardians' dissatisfaction, parental anxiety, increasing medical workload as well as leading to an increase of adverse events. Our aim is to identify the risk factors associated with chloral hydrate sedative failure with initial dose in children undergoing noninvasive diagnostic procedures. METHODS: Pediatric patients who underwent chloral hydrate sedation for noninvasive diagnostic procedures at our institution between 1 December 2019 and 1 January 2021 were retrospectively analyzed. Data collected included patients' age, gender, weight, sedation history, sedation failure history, type of procedures, initial dose of choral hydrate, sleep deprivation, sedation failure with initial dose, and sedative duration. The initial dose was classified into three levels: reduced dose (< 40 mg/kg), standard dose (40-60 mg/kg), and high dose (> 60 mg/kg). The patients were divided into three cohorts according to the different initial doses. RESULTS: A total of 15,922 patients were included in the analysis; 1928 (12.1%) were not well-sedated after administering the initial dose of chloral hydrate. The highest sedative failure was observed in the reduced dose group. By multivariate regression, we identified that heavier weight, patients with a history of sedation or a history of sedation failure, and patients who received magnetic resonance imaging (MRI) or more than one procedure simultaneously were associated with an increased odds of sedation failure at the initial dose. However, outpatients, patients undergoing hearing screening, and patients with sleep deprivation were favored regarding chloral hydrate sedative success. CONCLUSION: An alternative drug or drug combination is necessary in patients with heavier weight, those with a sedation history or sedation failure history, and those undergoing an MRI or more than one procedure simultaneously, whereas chloral hydrate is an appropriate sedation option for outpatients, patients undergoing hearing screening, and those with sleep deprivation.

Lactobacillus fermentum PS150 promotes non-rapid eye movement sleep in the first night effect of mice.

The first night effect (FNE) is a type of sleep disturbance caused by an unfamiliar environment, which leads to difficulty falling asleep and reduced sleep duration. Previously, we reported that Lactobacillus fermentum PS150 (PS150) improves sleep conditions in a pentobarbital-induced sleep mouse model. In this study, we aimed to evaluate the effect of PS150 on the FNE in mice. Briefly, mice were implanted with electrodes and orally administered PS150 for four weeks, and then the FNE was induced by cage changing. Analysis of polysomnographic signals revealed that intervention with PS150 restored non-rapid eye movement (NREM) sleep length under the FNE. Compared to diphenhydramine, a commonly used sleep aid, PS150 had no unwanted side effects, such as rapid eye movement (REM) sleep deprivation and fragmented sleep. Moreover, temporal analysis revealed that PS150 efficiently reduced both sleep latency and time spent restoring normal levels of REM sleep. Taken together, these results suggest that PS150 efficiently ameliorates sleep disturbance caused by the FNE. Additionally, V3-V4 16S rRNA sequencing revealed significant increases in Erysipelotrichia, Actinobacteria, and Coriobacteriia in fecal specimens of the PS150-treated group, indicating that PS150 induces gut microbiota remodeling.

The effects of caffeinated products on sleep and functioning in the military population: A focused review.

Military personnel rely on caffeinated products such as coffee or energy drinks (ED) to maintain a maximal level of vigilance and performance under sleep-deprived and combat situations. While chronic caffeine intake is associated with decreased sleep duration and non-restful sleep in the general population, these relationships are relatively unclear in the military personnel. We conducted a focused review of the effects of caffeinated products on sleep and the functioning of military personnel. We used a pre-specified search algorithm and identified 28 peer-reviewed articles published between January 1967 and July 2019 involving military personnel. We classified the findings from these studies into three categories. These categories included descriptive studies of caffeine use, studies evaluating the association between caffeinated products and sleep or functioning measures, and clinical trials assessing the effects of caffeinated products on functioning in sleep-deprived conditions. Most of the studies showed that military personnel used at least one caffeine-containing product per day during active duty and coffee was their primary source of caffeine. Their mean caffeine consumption varied from 212 to 285 mg/day, depending on the type of personnel and their deployment status. Those who were younger than 30 years of age preferred ED use. Caffeine use in increasing amounts was associated with decreased sleep duration and increased psychiatric symptoms. The consumption of caffeinated products during sleep deprivation improved their cognitive and behavioral outcomes and physical performance. Caffeine and energy drink consumption may maintain some aspects of performance stemming from insufficient sleep in deployed personnel, but excessive use may have adverse consequences.

Sleep Deprivation Interferes with JAK/STAT Signaling Pathway and Myogenesis in the Masseter Muscle of Rats.

OBJECTIVES: The aim of the study was to study the Janus kinase/tyrosine kinase-activated transduction factor (JAK/STAT) signaling pathway and myogenesis on the masseter muscle after sleep deprivation and to investigate the role of stress in this scenario. SUBJECTS AND METHODS: A total of 18 male Wistar rats were divided into the following groups: control (n = 6): animals were not submitted to any procedures, and paradoxical sleep deprivation and vehicle (PSD + V; n = 6): animals were subjected to PSD for 96 h and (PSD + MET; n = 6): animals were subjected to PSD for 96 h with administration of metyrapone. Paradoxical sleep deprivation was performed by the modified multiple platforms method. Histopathological analysis, histomorphometry, and immunohistochemistry were performed. RESULTS: The results showed the presence of inflammatory infiltrate in the PSD + V and PSD + MET groups and atrophy. Histomorphometry showed that the cellular profile area decreased, while cellular density increased in both experimental groups. Expression of p-STAT 3, MyoD, and MyoG increased in the PSD + V group, while the PSD + MET group showed increased expression of IL-6 and p-STAT 3. CONCLUSION: Our results suggest that sleep deprivation induces an inflammatory response and atrophy in the masseter muscle of rats.

High cortical delta power correlates with aggravated allodynia by activating anterior cingulate cortex GABAergic neurons in neuropathic pain mice.

Patients with chronic pain often report being sensitive to pain at night before falling asleep, a time when the synchronization of cortical activity is initiated. However, how cortical activity relates to pain sensitivity is still unclear. Because sleep is characterized by enhanced cortical delta power, we hypothesized that enhanced cortical delta power may be an indicator of intensified pain. To test this hypothesis, we used pain thresholds tests, EEG/electromyogram recordings, c-Fos staining, and chemogenetic and pharmacological techniques in mice. We found that sleep deprivation or pharmacologic enhancement of EEG delta power by reserpine and scopolamine dramatically decreased mechanical pain thresholds, but not thermal withdrawal latency, in a partial sciatic nerve ligation model of neuropathic pain mice. On the contrary, suppression of EEG delta power using a wake-promoting agent modafinil significantly attenuated mechanical allodynia. Moreover, when EEG delta power was enhanced, c-Fos expression decreased in most regions of the cortex, except the anterior cingulate cortex (ACC), where c-Fos was increased in the somatostatin- and parvalbumin-positive GABAergic neurons. Chemogenetic activation of GABAergic neurons in ACC enhanced EEG delta power and lowered mechanical pain thresholds simultaneously in naive mice. However, chemogenetic inhibition of ACC GABAergic neurons could not block mechanical allodynia. These results provided compelling evidence that elevated EEG delta power is accompanied with aggravated neuropathic pain, whereas decreased delta power attenuated it, suggesting that enhanced delta power can be a specific marker of rising chronic neuropathic pain and that wake-promoting compounds could be used as analgesics in the clinic.

Cumulative Childhood Lead Levels in Relation to Sleep During Adolescence.

STUDY OBJECTIVES: Lead exposure has been linked to adverse cognitive outcomes among children, and sleep disturbances could potentially mediate these relationships. As a first step, whether childhood lead levels are linked to sleep disturbances must be ascertained. Prior studies of lead and sleep are scarce and rely on parent-reported sleep data. METHODS: The study population included 395 participants from the Early Life Exposure in Mexico to Environmental Toxicants project, a group of sequentially enrolled birth cohorts from Mexico City. Blood lead levels measured from ages 1 to 4 years were used to calculate a cumulative measure of early childhood lead levels. Average sleep duration, sleep fragmentation, and movement index were assessed once between the ages of 9 and 18 years with wrist actigraphs worn for a continuous 7-day interval. Linear regression models were fit with average sleep duration, fragmentation, or movement as the outcome and cumulative lead levels divided into quartiles as the exposure, adjusted for age, sex, and maternal education. RESULTS: Mean (standard deviation) age at follow-up was 13.8 (1.9) years, and 48% of participants were boys. Median (interquartile range) cumulative childhood lead level was 13.7 (10.8, 18.0) µg/dL. Patients in the highest quartile of the cumulative childhood lead group had on average 23 minutes less sleep than those in the first quartile in adolescence (95% confidence interval [7, 39]; P, trend = .02). Higher cumulative lead level was associated with higher sleep fragmentation in younger adolescents (younger than 14 years) only (P, interaction = .02). CONCLUSIONS: Shorter sleep duration may represent an as-yet unrecognized adverse consequence of lead exposure in youth.

Pharmacological Modulation of Sleep Homeostasis in Rat: Novel Effects of an mGluR2/3 Antagonist.

Increasing vigilance without incurring the negative consequences of extended wakefulness such as daytime sleepiness and cognitive impairment is a major challenge in treating many sleep disorders. The present work compares two closely related mGluR2/3 antagonists LY3020371 and LY341495 with two well-known wake-promoting compounds caffeine and d-amphetamine. Sleep homeostasis properties were explored in male Wistar rats by manipulating levels of wakefulness via (1) physiological sleep restriction (SR), (2) pharmacological action, or (3) a combination of these. A two-phase nonlinear mixed-effects model combining a quadratic and exponential function at an empirically estimated join point allowed the quantification of wake-promoting properties and any subsequent sleep rebound. A simple response latency task (SRLT) following SR assessed functional capacity of sleep-restricted animals treated with our test compounds. Caffeine and d-amphetamine increased wakefulness with a subsequent full recovery of non-rapid eye movement (NREM) and rapid eye movement (REM) sleep and were unable to fully reverse SR-induced impairments in SRLT. In contrast, LY3020371 increased wakefulness with no subsequent elevation of NREM sleep, delta power, delta energy, or sleep bout length and count, yet REM sleep recovered above baseline levels. Prior sleep pressure obtained using an SR protocol had no impact on the wake-promoting effect of LY3020371 and NREM sleep rebound remained blocked. Furthermore, LY341495 increased functional capacity across SRLT measures following SR. These results establish the critical role of glutamate in sleep homeostasis and support the existence of independent mechanisms for NREM and REM sleep homeostasis.

Chronic high-caloric diet accentuates age-induced sleep alterations in mice.

Obesity and sleep disturbances comprise major health problems which are likely interrelated. Diet-induced obesity in young mice has been demonstrated to lead towards an altered sleep homeostasis. In the current study, we investigated the effect of chronic (12 weeks) high-caloric diet (HCD, 45% fat) consumption on sleep and the sleep electroencephalogram (EEG) in young and older mice (6-month-old, n = 9; 18-month-old, n = 8 and 24-month-old, n = 4) and compared with age-matched controls on normal chow (n = 11, n = 9 and n = 9 respectively). Half of the 24-month-old mice did not cope well with HCD, therefore this group has a lower n and limited statistical power. We recorded EEG and the electromyogram for continuous 48-h and performed a 6-h sleep deprivation during the second day. In aged HCD fed mice (18 months old) compared to young, an aging effect was still evident, characterized by decreased waking and increased NREM sleep in the dark period, decreased REM sleep during the light period, as well as increased slow-wave-activity (SWA, EEG power in NREM sleep in 0.5-4.0 Hz). Additionally, aged HCD treated mice showed increased NREM sleep and decreased waking, compared to age-matched controls, denoting an enhanced aging phenotype in the sleep architecture. Notably, an overall increase was found in the slow component of SWA (0.5-2.5 Hz) in aged HCD fed mice compared to age-matched controls. Our data suggest that the effect of aging is the dominant variable irrespective of diet. However, a synergistic effect of aging and diet is noted indicating that chronic HCD consumption exacerbates age-associated sleep alterations.

Juvenile myoclonic epilepsy and sleep.

Juvenile myoclonic epilepsy (JME) is a sleep-related epilepsy syndrome, and only a few studies have addressed the relationship between JME and sleep disorders. In this review, the sleep characteristics of patients with JME were summarized based on the features of circadian rhythm, the possible cause of the early morning seizures, the common subjective and objective sleep disorders, the alterations in sleep architecture, and the effect of sleep deprivation and sodium valproate (VPA). The aims of this study were to summarize the interaction between JME and sleep, to reveal JME sleep characteristics, to encourage clinicians to focus on JME and sleep, to heighten the positive diagnosis rate, to guide the treatment, to improve the prognosis, and to enhance the daily life quality of patients with JME. At the same time, this study aimed to present existing controversies, in order to necessitate further studies.

Dreamless: the silent epidemic of REM sleep loss.

We are at least as dream deprived as we are sleep deprived. Many of the health concerns attributed to sleep loss result from a silent epidemic of REM sleep deprivation. REM/dream loss is an unrecognized public health hazard that silently wreaks havoc with our lives, contributing to illness, depression, and an erosion of consciousness. This paper compiles data about the causes and extent of REM/dream loss associated with commonly used medications, endemic substance use disorders, rampant sleep disorders, and behavioral and lifestyle factors. It examines the consequences of REM/dream loss and concludes with recommendations for restoring healthy REM/dreaming.

Chronic sleep restriction promotes brain inflammation and synapse loss, and potentiates memory impairment induced by amyloid-ß oligomers in mice.

It is increasingly recognized that sleep disturbances and Alzheimer's disease (AD) share a bidirectional relationship. AD patients exhibit sleep problems and alterations in the regulation of circadian rhythms; conversely, poor quality of sleep increases the risk of development of AD. The aim of the current study was to determine whether chronic sleep restriction potentiates the brain impact of amyloid-ß oligomers (AßOs), toxins that build up in AD brains and are thought to underlie synapse damage and memory impairment. We further investigated whether alterations in levels of pro-inflammatory mediators could play a role in memory impairment in sleep-restricted mice. We found that a single intracerebroventricular (i.c.v.) infusion of AßOs disturbed sleep pattern in mice. Conversely, chronically sleep-restricted mice exhibited higher brain expression of pro-inflammatory mediators, reductions in levels of pre- and post-synaptic marker proteins, and exhibited increased susceptibility to the impact of i.c.v. infusion of a sub-toxic dose of AßOs (1pmol) on performance in the novel object recognition memory task. Sleep-restricted mice further exhibited an increase in brain TNF-α levels in response to AßOs. Interestingly, memory impairment in sleep-restricted AßO-infused mice was prevented by treatment with the TNF-α neutralizing monoclonal antibody, infliximab. Results substantiate the notion of a dual relationship between sleep and AD, whereby AßOs disrupt sleep/wake patterns and chronic sleep restriction increases brain vulnerability to AßOs, and point to a key role of brain inflammation in increased susceptibility to AßOs in sleep-restricted mice.

A Unified Model of Performance for Predicting the Effects of Sleep and Caffeine.

STUDY OBJECTIVES: Existing mathematical models of neurobehavioral performance cannot predict the beneficial effects of caffeine across the spectrum of sleep loss conditions, limiting their practical utility. Here, we closed this research gap by integrating a model of caffeine effects with the recently validated unified model of performance (UMP) into a single, unified modeling framework. We then assessed the accuracy of this new UMP in predicting performance across multiple studies. METHODS: We hypothesized that the pharmacodynamics of caffeine vary similarly during both wakefulness and sleep, and that caffeine has a multiplicative effect on performance. Accordingly, to represent the effects of caffeine in the UMP, we multiplied a dose-dependent caffeine factor (which accounts for the pharmacokinetics and pharmacodynamics of caffeine) to the performance estimated in the absence of caffeine. We assessed the UMP predictions in 14 distinct laboratory- and field-study conditions, including 7 different sleep-loss schedules (from 5 h of sleep per night to continuous sleep loss for 85 h) and 6 different caffeine doses (from placebo to repeated 200 mg doses to a single dose of 600 mg). RESULTS: The UMP accurately predicted group-average psychomotor vigilance task performance data across the different sleep loss and caffeine conditions (6% < error < 27%), yielding greater accuracy for mild and moderate sleep loss conditions than for more severe cases. Overall, accounting for the effects of caffeine resulted in improved predictions (after caffeine consumption) by up to 70%. CONCLUSIONS: The UMP provides the first comprehensive tool for accurate selection of combinations of sleep schedules and caffeine countermeasure strategies to optimize neurobehavioral performance.

Sleep disturbance as detected by actigraphy in pre-pubertal juvenile monkeys receiving therapeutic doses of fluoxetine.

Sleep disturbance is a reported side effect of antidepressant drugs in children. Using a nonhuman primate model of childhood selective serotonin reuptake inhibitor (SSRI) therapy, sleep was studied quantitatively with actigraphy. Two 48-h sessions were recorded in the home cage environment of juvenile male rhesus monkeys at two and three years of age, after one and two years of treatment with a therapeutic dose of the SSRI fluoxetine, and compared to vehicle treated controls. A third session was conducted one year after discontinuation of treatment at four years of age. During treatment, the fluoxetine group demonstrated sleep fragmentation as indexed by a greater number of rest-activity transitions compared to controls. In addition fluoxetine led to more inactivity during the day as indexed by longer duration of rest periods and the reduced activity during these periods. The fluoxetine effect on sleep fragmentation, but not on daytime rest, was modified by the monkey's genotype for polymorphisms of monoamine oxidase A (MAOA), an enzyme that metabolizes serotonin. After treatment, the fluoxetine effect on nighttime rest-activity transitions persisted, but daytime activity was not affected. The demonstration in this nonhuman primate model of sleep disturbance in connection with fluoxetine treatment and specific genetic polymorphisms, and in the absence of diagnosed psychopathology, can help inform use of this drug in children.

Sleep loss and recovery after administration of drugs related to different arousal systems in rats.

Sleep is homeostatically regulated suggesting a restorative function. Sleep deprivation is compensated by an increase in length and intensity of sleep. In this study, suppression of sleep was induced pharmacologically by drugs related to different arousal systems. All drugs caused non-rapid eye movement (NREM) sleep loss followed by different compensatory processes. Apomorphine caused a strong suppression of sleep followed by an intense recovery. In the case of fluoxetine and eserine, recovery of NREM sleep was completed by the end of the light phase due to the biphasic pattern demonstrated for these drugs first in the present experiments. Yohimbine caused a long-lasting suppression of NREM sleep, indicating that either the noradrenergic system has the utmost strength among the examined systems, or that restorative functions occurring normally during NREM sleep were not blocked. Arousal systems are involved in the regulation of various wakefulness-related functions, such as locomotion and food intake. Therefore, it can be hypothesized that activation of the different systems results in qualitatively different waking states which might affect subsequent sleep differently. These differences might give some insight into the homeostatic function of sleep in which the dopaminergic and noradrenergic systems may play a more important role than previously suggested.

Daily episodes of confusion · altered behavior · chronic sleep deprivation · Dx?

His neurologic exam was normal. Family history was positive for a cousin with narcolepsy but negative for seizures and obstructive sleep apnea. Polysomnography revealed moderate OSA with minimal oxygen desaturation. Inpatient video EEG monitoring captured several of the events that the patient and his wife had described; the patient seemed "uninhibited" in his behavior. His EEG, cardiac telemetry, oxygen saturation, blood pressure, and serum glucose level remained normal.

Efectos adversos de antipsicóticos atípicos, diferencias según sexo / Gender differences in the adverse effects of atypical antipsychotic drugs

Los efectos adversos de los antipsicóticos atípicos varían en función del sexo de los pacientes. Las mujeres tienen un peso medio inferior al de los hombres, y además, a nivel farmacocinético tienen un menor aclaramiento de algunos antipsicóticos como la clozapina y olanzapina. Entre los efectos secundarios más frecuentes en mujeres, cabe destacar el incremento del intervalo QT corregido. También el riesgo metabólico es mayor en mujeres: estas tienen más probabilidades de aumentar el peso tras tratamientos prolongados, sobre todo con clozapina y olanzapina. La prolactina se incrementa más en las mujeres que en los varones tras tratamiento antipsicótico. Este efecto secundario es más frecuente con amisulpride, risperidona y paliperidona. Entre los efectos secundarios extrapiramidales, la acatisia es también más frecuente en mujeres. En el futuro es necesario tener en cuenta la variable género al hacer el cálculo de la dosis y valoración de efectos secundarios tras el tratamiento antipsicótico (AU)

The adverse effects of atypical antipsychotic drugs vary depending on the sex of the patients. Females have a lower mean body weight than males, thus, at pharmacokinetic level, they have a lower clearance of some antipsychotics such as, clozapine and olanzapine. Among the most common adverse effects is highlighted the increase in corrected QT interval. Metabolic risks are also greater in females, with these being more likely to increase the weight after prolonged treatments, particularly with clozapine and olanzapine. Prolactin is increased more in females than in males after antipsychotic treatment. This adverse effect is more common with amisulpride, risperidone and paliperidone. Among the extrapyramidal secondary effects, akathisia is also more common in females. Gender variability should be taken into account in the future when calculating the dose, as well as when evaluating the adverse effects after antipsychotic treatment (AU)