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Interaction of estradiol, testosterone, and progesterone in the modulation of hormone-dependent aggression in the female rat.

Female rats that had become aggressive as a result of cohabiting with a sterile male were ovariectomized and implanted with Silastic tubes of estradiol, testosterone, and progesterone, estradiol and testosterone alone, or with empty tubes. The implants were designed to model serum concentrations present during the last week of pregnancy (estradiol, 0.06 ng/ml; testosterone, 2.6 ng/ml; progesterone, 70 ng/ml). Following a test of aggression 1 week postoperatively, estradiol and testosterone implants were replaced with ones designed to maintain the lower hormone levels present following parturition (0.02 ng/ml; 0.6 ng/ml, respectively). Progesterone was not replaced. At the first aggression test, females with estradiol and testosterone alone displayed significantly more aggression than females with these hormones plus progesterone. Both groups were more aggressive than females without hormone replacement. Following the exchange of large implants for small ones, females that previously had progesterone increased in aggression while females that previously had only estradiol and testosterone decreased in aggression. Both groups continued to be more aggressive than the group without hormone replacement. High serum progesterone present near the end of pregnancy appears to moderate the expression of aggression supported by estradiol and testosterone. Conversely, progesterone's decline at parturition appears to produce a rebound facilitation of aggression even though serum estradiol and testosterone simultaneously decline.

Aggression↗

Aggressive behaviour in immature captive Nile crocodiles, Crocodylus niloticus, in relation to feeding.

This study presents five aspects of aggressive behaviour in juvenile Nile crocodiles, Crocodylus niloticus, as observed in five cohorts of 6-18 month-old animals. During this period, the animals grew from a range of 35-55 cm, to a range of 65-115 cm. 1) Stock density related to aggression: decrease in density resulted in significant decrease in the frequency of agonistic events, with 0.64 events/100 crocodiles/min observed in a density of 6.7 crocodiles/m2, compared to 0.26 events/100 crocodiles/min observed in a density of 4.7 crocodiles/m2. 2) Aggression during feeding: in all five groups, there was a significantly higher level of aggression during feeding times. 3) Aggression related to body size: the largest crocodiles were the most aggressive group in agonistic events, mainly against the smallest ones. The largest group, the medium sized, was the least involved in agonistic events. 4) Aggression related to food preference: crocodile food preference was live fish > live chicks > dead fish > ground meat. Except for one food type (live chicks), a significant (p < 0.05) correlation was found between food preference and feeding related aggression in the prey diet groups. 5) Aggression related to an artificial selection for size: removal of the largest crocodiles (which formed 30% of the stock) from the population caused a dramatic decrease in all forms of aggressive behaviour.

Aggression↗

In quest for a possible association between heightened social aggression and excessive alcohol drinking in the rat.

Many clinical studies show that a sizeable proportion of male alcoholics are also inclined to act violently and aggressively. Given this association in humans, we asked whether a relationship exists between ethanol intake and aggressive behaviour in laboratory rats. In a first test of the hypothesis, we measured ethanol intake in male rats made aggressive by periodic contacts with sexually active females. Although the males became significantly more aggressive, there was no concomitant enhancement of alcohol consumption. In another experiment, observations of ethanol drinking in lactating rats exhibiting maternal aggression revealed no alteration in ethanol intake relative to nonlactating control females. However, because water intake was substantially elevated in the maternal rats, there was a net decrease in ethanol preference. The final experiment examined aggressiveness in chronically food-restricted male rats. In line with previous studies, this procedure increased ethanol drinking, but it did not enhance aggressive behaviour. It is concluded that, in our rats, there is no apparent association between the level of social aggression and the voluntary intake of ethanol in a two-bottle choice paradigm. The possibility remains, though, that alcohol drinking is better related to other forms of aggression, such as defensive or predatory aggression.

Aggression↗

Rodent models of aggressive behavior and serotonergic drugs.

Various models of rodent agonistic behaviour are described, which differentiate between offensive and defensive/flight models. Particular attention is given to one male and one female paradigm for offensive aggression, viz. resident-intruder or territorial (RI) and maternal aggression (MA). After an overview of the serotonin (5-HT) system in the CNS, a description is given of the ligands available. Subsequently the effects of various drugs affecting serotonergic transmission in the RI- and MA-paradigms are described. The 5-HT1A agonists buspirone, ipsapirone and 8-OH-DPAT decreased aggression in RI and MA, but simultaneously led to a marked decrease in social interest and activity, indicative of a non-specific anti-aggressive profile. Non-selective 5-HT1 agonists, such as RU 24969, eltoprazine (DU 28853), and TFMPP reduced aggression quite specific and did not decrease social interest or exploration, but sometimes even increased these behaviours. In RI and MA the behavioural effects of these drugs were roughly similar. In contrast, MA was more sensitive to the treatment with the 5-HT reuptake blocker fluvoxamine, which blocked RI aggression only non-specifically at the highest dose. DOI, a 5-HT2 and 5-HT1C agonist, decreased aggressive behaviour and increased inactivity, without affecting social interest and exploration in RI as well as MA. This was, however, accompanied by 'wet dog shaking', characteristic of 5-HT2-receptor stimulation. The non-specific 5-HT agonist (and 5-HT3 antagonist) quipazine also induced 'wet dog shaking' at doses which suppressed aggression, social interest and exploration but increased inactive behaviours (sitting and lying). The discussion attempts to delineate a role for 5-HT receptor subtype involvement in the modulation of aggression, with the restrictions we clearly face with regard to the lack of specific serotonergic agonists and antagonists for certain receptor subtypes. By and large, male and female rats react similarly to treatment with serotonergic drugs stressing the consistent role of 5-HT in different forms of aggression.

Aggression↗

Intermale aggression in corticotropin-releasing factor receptor 1 deficient mice.

The anxiogenic neuropeptide, corticotropin-releasing factor (CRF), has a complex effect on intermale aggression. CRF receptor 1 (CRFR1) is the primary receptor for CRF and in this study, we examined in detail isolation-induced intermale aggression in CRFR1 deficient mice. All mice contained a mixed 50:50 inbred/outbred background to improve aggressive performance. Mice were isolated for 4 weeks prior to 2 consecutive days of aggression testing using the resident-intruder paradigm. Mice were also tested for anxiety on the elevated plus maze. Relative to littermate wild-type (WT) controls, CRFR1-mutant mice exhibited normal levels of intermale aggression over the 2 test days in terms of percentage showing aggression, number of attacks, time aggressive, and latency to first attack. In terms of sites of attacks on intruders, CRFR1-deficient mice attacked the ventral portion of the mid-section (including belly) significantly less frequently than WT males on test day 1, but these differences did not reach significance on test day 2. No other differences in sites of attacks were observed. Tail rattling also did not differ between groups. Importantly, KO males showed decreased anxiety relative to WT mice (consistent with previous reports) as evidenced by spending significantly more time on the open arms and significantly less time on the closed arms of the elevated plus maze. Plus maze performance did not correlate with any measure of levels of aggression, suggesting a dissociation between altered levels of anxiety and aggressive performance. Taken together, the results suggest that the activation CRFR1 is not necessary for the normal production of isolation-induced intermale aggression.

Aggression↗

The activation of prefrontal cortical neurons in aggression--a double labeling study.

Violence is associated with prefrontal deficits in humans, suggesting that this brain area inhibits aggressiveness. Its role, however, remains controversial, as certain subdivisions of the prefrontal cortex become activated by fights in rodents. Disparate human findings also show that this area is acutely activated by aggression under certain conditions. We explored prefrontal neuronal activation patterns in resident rats exposed to psychosocial (sensory contact with the intruder) and aggressive encounters. Both psychosocial and aggressive encounters increased c-Fos activation in the prelimbic (PrL), anterior cingular (Cg1), agranular insular (AI), ventral (VO) and lateral orbital (LO) cortices. The infralimbic (IL) and medial orbital (MO) cortices were activated significantly by aggressive encounters only. No other prefrontal regions were activated by psychosocial or aggressive encounters. The overwhelming majority of activated cells were pyramidal (glutamatergic) cells in the Cg1, IL, PrL, MO, and VO, whereas interneuron and pyramidal cell activation was similar in AI and LO. When rats showed violent aggression, the activation of GABAergic inhibitory cells decreased in these two, and two other areas (IL and MO). Notably, the latter two areas appeared to be specifically involved in aggressive behavior. The change occurred in a recently developed model of violent aggression. In this model, pyramidal cell activation in the above mentioned four areas (IL, MO, AI, and LO) predicted over 95% of variation in attack counts in general and violent attacks in particular. Based on these data, we present a tentative hypothesis on the involvement of the prefrontal cortex in the control of aggression.

Adrenalectomy↗

Repeated cocaine exposure during adolescence alters glutamic acid decarboxylase-65 (GAD65) immunoreactivity in hamster brain: correlation with offensive aggression.

Male Syrian hamsters (Mesocricetus auratus) treated with low-dose (0.5 mg/kg/day) cocaine throughout adolescence (P27-P56) display highly escalated offensive aggression. The current study examined whether adolescent cocaine exposure influenced the immunohistochemical localization of glutamic acid decarboxylase-65 (GAD65), the rate-limiting enzyme in the synthesis of gamma-aminobutyric acid (GABA), a fast-acting neurotransmitter implicated in the modulation of aggression in various species and models of aggression. Hamsters were administered low doses of cocaine throughout adolescence, scored for offensive aggression using the resident-intruder paradigm, and then examined for changes in GAD65 immunoreactivity in areas of the brain implicated in aggression control. When compared with saline-treated control animals, aggressive cocaine-treated hamsters showed significant differences in the area covered by GAD65 puncta in several notable aggression regions, including the anterior hypothalamus, the medial and central amygdaloid nuclei, and the lateral septum. However, no differences in GAD65 puncta were found in other aggression areas, such as the bed nucleus of the stria terminalis, the ventrolateral hypothalamus, and the corticomedial amygdala. Together, these results suggest that altered GABA synthesis and function in specific aggression areas may be involved in adolescent cocaine-facilitated offensive aggression.

Age Factors↗

Glucocorticoid interaction with aggression in non-mammalian vertebrates: reciprocal action.

Socially aggressive interaction is stressful, and as such, glucocorticoids are typically secreted during aggressive interaction in a variety of vertebrates, which may both potentiate and inhibit aggression. The behavioral relationship between corticosterone and/or cortisol in non-mammalian (as well as mammalian) vertebrates is dependent on timing, magnitude, context, and coordination of physiological and behavioral responses. Chronically elevated plasma glucocorticoids reliably inhibit aggressive behavior, consistent with an evolutionarily adaptive behavioral strategy among subordinate and submissive individuals. Acute elevation of plasma glucocorticoids may either promote an actively aggressive response via action in specialized local regions of the brain such as the anterior hypothalamus, or is permissive to escalated aggression and/or activity. Although the permissive effect of glucocorticoids on aggression does not suggest an active role for the hormone, the corticosteroids may be necessary for full expression of aggressive behavior, as in the lizard Anolis carolinensis. These effects suggest that short-term stress may generally be best counteracted by an actively aggressive response, at least for socially dominant proactive individuals. An acute and active response may be evolutionarily maladaptive under chronic, uncontrollable and unpredictable circumstances. It appears that subordinate reactive individuals often produce compulsorily chronic responses that inhibit aggression and promote submissive behavior.

Aggression↗

Aggression and psychopathology in treatment-resistant inpatients with schizophrenia and schizoaffective disorder.

Positive psychotic symptoms, such as threat/"control-override" delusions or command hallucinations, have been related to aggression in patients with schizophrenia. However, retrospective data collection has hampered evaluation of the direct influence of psychopathology on aggressive behavior. In this study, we monitored aggressive behavior and psychopathology prospectively and in close temporal proximity in 157 treatment-resistant inpatients diagnosed with chronic schizophrenia or schizoaffective disorder participating in a 14-week double-blind clinical trial. Aggressive behavior was rated with the overt aggression scale (OAS). Psychopathology was assessed using the positive and negative syndrome scale (PANSS). At baseline, subjects who would be aggressive during the study had higher scores on only two PANSS items: hostility and poor impulse control. During the study PANSS positive subscale scores were significantly higher in aggressive subjects. Total PANSS scores were higher within 3 days of an aggressive incident, as were positive and general psychopathology subscale scores. However, in a smaller subsample for whom PANSS ratings were available within 3 days before aggressive incidents, only scores on the PANSS positive subscale were significantly higher. These findings in chronic, treatment resistant inpatients support the view that positive symptoms may lead to aggression.

Aggression↗

A neural network underlying individual differences in emotion and aggression in male golden hamsters.

In rodents, aggressive behavior can be altered by experimental manipulations of emotional responsiveness. The goal of this study was to identify characteristics of emotional reactivity associated with individual differences in aggressive behavior and their integration within a common neural network. Male golden hamsters were first screened for offensive aggression. Then, the animals were trained through immediate reinforcement and tested for their adaptation to a delayed reward. Similar protocols have been used to test behaviors associated with frustration. At first, all hamsters showed increased frequency of bar pressing per reward during delayed reinforcement. However, Low-Aggression animals were able to adapt to the delay and showed a decreased rate of bar pressing per reward within 5 days. In contrast, High-Aggression animals maintained a high rate of bar pressing per reward. In addition, brains were collected after immediate reward training or delayed reward testing, and labeled for pCREB-immunoreactivity as a marker of trans-synaptic activity. In High-Aggression individuals, elevated density of cyclic AMP response element binding protein, phosphorylated (pCREB) immunostaining was found within the anterior hypothalamus, an area critical to the control of aggression. Delayed reinforcement was associated with enhanced pCREB immunostaining within the central amygdala, medial amygdala and preoptic area/hypothalamus continuum. Further analysis of the data also showed a positive correlation in labeling density between the lateral septum and the anterior hypothalamus, specifically in Low-Aggression animals exposed to delayed reward. Therefore, as High-Aggression individuals lack control of their emotional reactivity, they are also characterized by a de-synchronization between the inhibitory output of the septum and the aggression areas of the hypothalamus. Finally, our data also show that frustration is associated with an extensive activation of the preoptic area/hypothalamus continuum and amygdala.

Aggression↗

Association of aggressive behavior in Korean male schizophrenic patients with polymorphisms in the serotonin transporter promoter and catecholamine-O-methyltransferase genes.

The incidence of aggressive behavior in patients with schizophrenia is higher than in the general population. Among particular gene polymorphisms posited to be involved in psychiatric disorders, the catecholamine-O-methyltransferase (COMT) and serotonin transporter (5-HTTPR) genes have been the focus of recent research on aggression. In this study, we hypothesized that both the COMT and the 5-HTTPR genotypes may be dependent on and related to aggression in Korean patients with schizophrenia. The subjects were 168 unrelated male schizophrenic patients diagnosed according to DSM-IV. Among two psychiatric hospital staff and medical university students, 158 unrelated male subjects with no lifetime history of psychiatric disorders were recruited to establish the COMT and 5-HTTPR genotype distribution in the general population. All episodes of aggression from the last discharge to readmission were rated. The Total Overt Aggression Scale (OAS) score (sum of the scores of all episodes of aggression), highest OAS score (highest individual episode score, 0-16), OAS category, and OAS category score (mean score within each category) were recorded. There were statistically significant effects of COMT genotype on the mean OAS 4 (physical aggression against other people) score and the highest OAS score. The most predictive was the OAS 4 score. There was a statistically significant effect of 5-HTTPR genotype on mean total score. Thus, the COMT gene is associated with the severity of aggression and with physical aggression against other people, whereas the 5-HTTPR gene is associated with the summary score of all episodes of aggression.

Adult↗

CSF testosterone and 5-HIAA correlate with different types of aggressive behaviors.

We studied the potential roles of testosterone and serotonin in various forms of aggressive and violent behaviors by measuring each biochemical and behaviour in free-ranging adolescent male nonhuman primates. Our results showed that (1) CSF free testosterone concentrations were positively correlated with overall aggressiveness, but not with measures of impulsivity. (2) CSF 5-HIAA concentrations were negatively correlated with impulsive behavior, and severe, unrestrained aggression, but not with overall rates of aggression. High rates of impulsive behavior were positively correlated with severe, unrestrained aggression, but not overall rates of aggression. (3) Dimensional analyses showed that while subjects with low CSF 5-HIAA exhibited high rates of aggression, high CSF testosterone further augmented rates and intensity of aggression in subjects with low CSF 5-HIAA. We conclude that high CSF free testosterone concentrations are associated with competitive aggression, while low CSF 5-HIAA concentrations are associated with severe aggression which results from impaired impulse control, and perseverance.

Aggression↗

Effects of alcohol consumption on lateralized aggression in Anolis carolinensis.

Previous work has suggested that the lizard Anolis carolinensis, like many other reptiles, has a functionally split brain. Specifically, the left eye of this species projects primarily to the right hemisphere (and vice versa), there is no corpus callosum, and the physical placement of the eyes restricts their field(s) of vision to one region of hemispace. The current experiment used this preparation to examine the effect of alcohol administration and withdrawal on lateralized brain functioning during territorial aggression. Thirteen adult males were divided into control (CON) or alcohol (ETOH) groups. Baseline territorial aggression was assessed, following which ETOH subjects were then given twice daily solutions of 19% alcohol. After 19 days of ETOH consumption, territorial aggression was again assessed. Eye use during aggressive encounters was measured either following short periods (24 h) of alcohol withdrawal, or 90 m following alcohol consumption. Control subjects were found to have a predominance of left eye/right hemisphere-mediated aggressive responses, as has previously been reported. Alcohol withdrawn subjects were found to have a suppression of left eye/right hemisphere-mediated aggression. This reached statistical significance on several measures of aggression, including the number of dewlaps and headbob (P < 0.001) and the total number of aggressive responses (P = 0.001). Consumption of ETOH reversed this pattern and reinstated the normal pattern of left eye/right hemisphere dominance during aggression. Conversely, right eye/left hemisphere mediation of aggression was found to be increased, or not affected, during alcohol withdrawal, and to show no differences from CON following ETOH administration. Extrapolating from other recent findings in this species, these results suggest that the stress caused by ETOH withdrawal on the CNS may differentially effect the right hemisphere of the brain while having little effect on the left.

Aggression↗

Cerebrospinal fluid monoamine and metabolite concentrations and aggression in rats.

In humans and other primates low cerebrospinal fluid (CSF) levels of the major serotonin (5-HT) metabolite 5-hydroxyindoleacetic acid (5-HIAA) have been correlated to high aggressiveness. This finding forms the basis of the 5-HT deficiency hypothesis of aggression. Surprisingly, this correlation has not been confirmed in rodents so far, while manipulation studies aimed to investigate the link between 5-HT and aggressive behaviour are mostly carried out in rodents. In this study the relation between aggression and CSF monoamine and metabolite concentrations was investigated in male Wildtype Groningen rats. In sharp contrast to the hypothesis and our expectation, a clear positive correlation was found between the individual level of trait-like aggressiveness and CSF concentrations of 5-HT, 5-HIAA, norepinephrine (NE), dopamine (DA), and 3,4-dihydroxyphenylacetic acid (DOPAC). Shortly after the acute display of aggressive behaviour (as a state-like phenomenon), decreased 5-HT levels and an increase in 5-HIAA/5-HT ratio and NE concentrations were found. Surprisingly, pharmacological challenges known to influence 5-HT transmission and aggressive behaviour did not affect CSF 5-HT and 5-HIAA concentrations, only the NE level was increased. Lesioning 5-HT terminals by 5,7-dihydroxytryptamine (5,7-DHT) administration caused a decrease in CSF 5-HT and 5-HIAA, but without affecting aggressive behaviour. The observed positive correlation between CSF 5-HIAA and trait aggressiveness makes it questionable whether a direct extrapolation of neurobiological mechanisms of aggression between species is justified. Interpretation of CSF metabolite levels in terms of activity of neural substrates requires a far more detailed knowledge of the dynamics and kinetics of a neurotransmitter after its release.

3,4-Dihydroxyphenylacetic Acid↗

Association between experience of aggression and anxiety in male mice.

The sensory contact technique increases aggressiveness in male mice and allows an aggressive type of behavior to be formed as a result of repeated experience of social victories in daily agonistic confrontations. In the low aggressive and high emotional mice of CBA/Lac strain, repeated positive fighting experience leads to increased plus maze anxiety in the winners after 10 days of experience of victories and much more after 20 days. Behavioral reactivity to other conspecifics was significantly increased as revealed by the parameters of partition test, which measures aggressive motivation in the winners. Thus, anxiety as a consequence of repeated experience of aggression is associated with the increase of aggressive motivation in CBA/Lac mice. It is concluded, that: (1) Repeated experience of aggression provokes the development of anxiety in male mice. (2) The level of anxiety as well as its behavioral realization depends on the duration of aggressive experience and genetic strain. Genetically defined features of innate anxiety (trait or state) in individuals may determine the kind of association between aggressive experience, aggressive motivation and anxiety.

Aggression↗

Effect of 5-HTP and ketanserine on the aggressive reaction induced by food competition in dominant and submissive pigeons (Columba livia).

There is abundant literature about the effects of manipulation of 5-hydroxytryptamine (5-HT) systems on some killer behaviors as well as on social isolation and shock-induced aggression in rodents. In this work we have analyzed the effect of 5-HT manipulation on the aggressive behavior induced by food competition in undernourished pigeons. Adult males (n = 12) were caged individually and their body weight kept at 80-85% by a restricted diet. These were divided in pairs which were exposed daily to an aggressive interaction test (20 min) in a 1.5 x 1.5 x 2.0 m chamber bearing a central feeding device. Once consolidation of dominance was obtained in each pair, the dominant and the submissive members were injected subcutaneously, on alternating days, with 5-hydroxytryptophan (5-HTP) (7.5, 15 and 30 mg/kg), ketanserine (20 and 30 mg/kg) and a combination of ketanserine (20 mg/kg) and 5-HTP (7.5 mg/kg). Aggression was evaluated by scoring the frequency and time spent biting, wing beating, aggressive following and vocalizations, threatening and pushing the opponent in 20-min tests. The time spent running away was also scored. Intratest feeding was ascertained by weighing the subjects immediately before and after testing. The scores were compared with those obtained after saline injection on the preceding day (C-scores). 5-HTP (7.5 mg/kg) attenuated aggression without affecting feeding in dominant members, and decreased the time spent running away by submissives. Higher doses of 5-HTP decreased feeding but did not potentiate the anti-aggressive effects. The 5-HT2 antagonist, ketanserine did not affect aggression but decreased feeding at the dose of 30 mg/kg. Ketanserine injection clearly prevented the anti-aggressive effects of 5-HTP but caused a decrease of feeding. Results show that 5-HT stimulation in pigeons can preferentially block aggression in this particular experimental situation. It is suggested, in addition, that 5-HT2 receptors might be involved in such an effect.

5-Hydroxytryptophan↗

Genomic and non-genomic effects of glucocorticoids on aggressive behavior in male rats.

An increasing body of evidence suggests that glucocorticoids--besides their well-known genomic effects--can affect neuronal function via mechanisms that do not involve the genome. Data obtained mainly in amphibians and birds suggest that such mechanisms play a role in the control of behavior. Acute glucocorticoid treatments increase aggressive behavior in rats, but the mechanism of action has not been investigated to date. To clarify the issue, we have assessed the aggressiveness of male rats after treating them with the corticosterone synthesis inhibitor metyrapone, corticosterone, and the protein synthesis inhibitor cycloheximide. Metyrapone applied intraperitoneally (i.p.) decreased the aggressiveness of residents faced with smaller opponents. Corticosterone administered i.p. 20 or 2 min before a 5-min encounter abolished these changes irrespective of the delay of behavioral testing. Thus, the effects of glucocorticoids on aggressive behavior occurred in less than 7 min (the delay and duration of testing taken together), and lasted more than 25 min. Corticosterone applied centrally (infused into the right lateral ventricle) also stimulated aggressive behavior rapidly, which shows that the effect was centrally mediated. The protein synthesis inhibitor cycloheximide did not affect the aggression-promoting effects of corticosterone when the hormone was injected 2 min before the aggressive encounter. Surprisingly, however, the effects were completely abolished when the hormone was injected 20 min before the encounter. These data suggest that glucocorticoids rapidly increase aggressive behavior via non-genomic mechanisms. In later phases of the aggressive encounter, aggressive behavior appears to be stimulated by genomic mechanisms.

Aggression↗

[Analysis and recording of aggressions in the ICU].

The objectives of this study are to determine if aggressions occur by the family or patient against the nursing staff of the Intensive Care Units (ICU), identify if the aggressions received are recorded; specify if the nurses know about the existence of resources available by the hospital site and verify if the nurses understand aggression to be the same thing. We have conducted a descriptive study using a questionnaire done between November and December 2004 regarding aggressions suffered at work. The study sample includes 150 nurses who work in the ICU and Coronary Unit of the Hospital Universitario de Bellvitge (HUB). Inclusion criteria is the nursing staff of the ICU of HUB. The results of the surveys show that there are aggressions in the ICU (62% of those surveyed have been physically assaulted and 68% verbally). Most of these aggressions were only reported verbally (73% in verbal aggressions, 75% in physical aggressions), these hardly being recorded in written form (2.5% of those assaulted verbally and 40% of those assaulted physically). The conclusions of this study are that a high percentage of the ICU nurses have suffered aggressions in their work, with repercussions in their personal and work life. They normally comment the aggressions with colleagues or bosses, although they do not put it in writing.

Adult↗