Kappa-opioid receptor blockade in the inferior colliculus of prey threatened by pit vipers decreases anxiety and panic-like behaviour.

The dorsal midbrain comprises dorsal columns of the periaqueductal grey matter and corpora quadrigemina. These structures are rich in beta-endorphinergic and leu-enkephalinergic neurons and receive GABAergic inputs from substantia nigra pars reticulata. Although the inferior colliculus (IC) is mainly involved in the acoustic pathways, the electrical and chemical stimulation of central and pericentral nuclei of the IC elicits a vigorous defensive behaviour. The defensive immobility and escape elicited by IC activation is commonly related to panic-like emotional states. To investigate the role of κ-opioid receptor of the IC in the antiaversive effects of endogenous opioid receptor blockade in a dangerous situation, male Wistar rats were pretreated in the IC with the κ-opioid receptor-selective antagonist nor-binaltorphimine at different concentrations and submitted to the non-enriched polygonal arena for a snake panic test in the presence of a rattlesnake and, after 24 h, prey were resubmitted to the experimental context. The snakes elicited in prey a set of antipredatory behaviours, such as the anxiety-like responses of defensive attention and risk assessment, and the panic-like reactions of defensive immobility and either escape or active avoidance during the elaboration of unconditioned and conditioned fear-related responses. Pretreatment of the IC with microinjections of nor-binaltorphimine at higher concentrations significantly decreased the frequency and duration of both anxiety- and panic-attack-like behaviours. These findings suggest that κ-opioid receptor blockade in the IC causes anxiolytic- and panicolytic-like responses in threatening conditions, and that kappa-opioid receptor-selective antagonists can be a putative coadjutant treatment for panic syndrome treatment.

Panicolytic-like effects of environment enrichment on male mice threatened by Bothrops jararaca lancehead pit vipers.

Environment enrichment (EE) is a well-known eustress model showing beneficial effects in different psychiatric diseases, but its positive properties in panic disorders are not yet established. The confrontation between prey and predator in complex arenas has been validated as a putative panic attack model. The principal aim of this work was to investigate the role of the EE on panic-like defensive responses elicited by mice threatened by venomous snakes. After 6 weeks of exposure either to an enriched or standard environments, 36 male mice were habituated in a complex polygonal arena for snakes containing an artificial burrow and elevated platforms for escape. The animals were confronted by Bothrops jararaca for 5 min, and the following antipredatory responses were recorded: defensive attention, stretched attend posture, flat back approach, prey versus predator interaction, oriented escape behavior, time spent in a safe place, and number of crossings. Mice threatened by snakes displayed several antipredatory reactions as compared to the exploratory behavior of those animals submitted to a nonthreatening situation (toy snake) in the same environment. Notably, EE causes anxiolytic- and panicolytic-like effects significantly decreasing the defensive attention and time spent in safe places and significantly increasing both prey versus predator interaction and exploratory behavior. In conclusion, our data demonstrate that EE can alter the processing of fear modulation regarding both anxiety- and panic-like responses in a dangerous condition, significantly modifying the decision-making defensive strategy.

Augmented anandamide signalling in the substantia nigra pars reticulata mediates panicolytic-like effects in mice confronted by Crotalus durissus terrificus pit vipers.

RATIONALE: The endocannabinoid modulation of fear and anxiety due to the on-demand synthesis and degradation is supported by a large body of research. Although it has been proposed that anandamide (AEA) in the substantia nigra pars reticulata (SNpr) seems to be important for the organisation of innate fear-related behaviours, a role for endogenous AEA has yet to be clarified. METHODS: Mice were treated with the fatty acid amide hydrolase (FAAH) selective inhibitor URB597 at different concentrations (0.01, 0.1, 1 nmol/0.1 µL) in the SNpr and confronted by rattlesnakes (Crotalus durissus terrificus). The most effective dose of URB597 (1 nmol) was also preceded by microinjections of the CB1 receptor antagonist AM251 (0.1 nmol) into the SNpr, and mice were then confronted by the venomous snake. RESULTS: URB597 (0.1 and 1 nmol) in the SNpr decreased the expression of defensive behaviours such as defensive attention, escape, and time spent inside the burrow of mice confronted by rattlesnakes. Moreover, pretreatment of SNpr with AM251 suppressed these antiaversive effects of URB597 in this midbrain structure. CONCLUSION: Overall, these data clearly indicate that the panicolytic consequences of endogenous AEA enhancement in the SNpr are mediated by CB1 receptor signalling.

Panic disorder respiratory subtype: psychopathology and challenge tests - an update

Panic disorder (PD) pathophysiology is very heterogeneous, and the discrimination of distinct subtypes could be very useful. A subtype based on respiratory symptoms is known to constitute a specific subgroup. However, evidence to support the respiratory subtype (RS) as a distinct subgroup of PD with a well-defined phenotype remains controversial. Studies have focused on characterization of the RS based on symptoms and response to CO2. In this line, we described clinical and biological aspects focused on symptomatology and CO2 challenge tests in PD RS. The main symptoms that characterize RS are dyspnea (shortness of breath) and a choking sensation. Moreover, patients with the RS tended to be more responsive to CO2 challenge tests, which triggered more panic attacks in this subgroup. Future studies should focus on discriminating respiratory-related clusters and exploring psychophysiological and neuroimaging outcomes in order to provide robust evidence to confirm RS as a distinct subtype of PD.

Panic Disorder and Chronic Caffeine Use: A Case-control Study.

BACKGROUND: Acute administration of caffeine produces panic attacks in most Panic Disorder (PD) patients, but little is known about chronic caffeine use in these patients. OBJECTIVE: To assess caffeine use in patients with PD and to ascertain if caffeine consumption is associated with sociodemographic or clinical features. METHODS: 65 adults with PD and 66 healthy controls were included in the current study. Their caffeine intake within the previous week was quantified with a questionnaire and compared. Harmful caffeine use was defined as consumption above 400 mg/day of caffeine. We tested for correlations between caffeine intake, demographic and clinical features. RESULTS: Patients consumed significantly more caffeine than controls (P < 0.001). 14% (N = 9) of the PD patients made harmful use of caffeine. The use of caffeine-containing medications was observed in 40% (N = 26) of the PD patients and 6% (N = 4) of controls. Consumption of energy drinks was observed in 11% (N = 7) of PD patients and in none of the healthy subjects. Patients reported sleeping significantly less than controls (P < 0.001). In PD patients, caffeine consumption was not correlated with the presence of panic attacks or comorbidity with depression. The use of benzodiazepines or sedative medications was not correlated with caffeine intake. CONCLUSION: High caffeine consumption in PD patients could be explained by the development of tolerance with regular use of this substance. Subtypes of sensitive and non-sensitive PD patients could also explain why some of these patients are able to tolerate high doses of caffeine.

Selective serotonin reuptake inhibitors and benzodiazepines in panic disorder: A meta-analysis of common side effects in acute treatment.

BACKGROUND: Benzodiazepines (BZs) and selective serotonin reuptake inhibitors (SSRIs) are effective in the pharmacologic treatment of panic disorder (PD). However, treatment guidelines favor SSRIs over BZs based on the belief that BZs are associated with more adverse effects than SSRIs. This belief, however, is currently supported only by opinion and anecdotes. AIM: The aim of this review and meta-analysis was to determine if there truly is evidence that BZs cause more adverse effects than SSRIs in acute PD treatment. METHODS: We systematically searched Web of Science, PubMed, Cochrane Central Register of Controlled Trials, and clinical trials register databases. Short randomized clinical trials of a minimum of four weeks and a maximum of 12 weeks that studied SSRIs or BZs compared to placebo in acute PD treatment were included in a meta-analysis. The primary outcome was all-cause adverse event rate in participants who received SSRIs, BZs, or placebo. RESULTS: Overall, the meta-analysis showed that SSRIs cause more adverse events than BZs in short-term PD treatment. Specifically, SSRI treatment was a risk factor for diaphoresis, fatigue, nausea, diarrhea, and insomnia, whereas BZ treatment was a risk factor for memory problems, constipation, and dry mouth. Both classes of drugs were associated with somnolence. SSRIs were associated with abnormal ejaculation, while BZs were associated with libido reduction. BZs were protective against tachycardia, diaphoresis, fatigue, and insomnia. CONCLUSION: Randomized, blinded studies comparing SSRIs and BZs for the short-term treatment of PD should be performed. Clinical guidelines based on incontrovertible evidence are needed.

Panicolytic-like effect of µ1-opioid receptor blockade in the inferior colliculus of prey threatened by Crotalus durissus terrificus pit vipers.

BACKGROUND: The endogenous opioid peptide system has been implicated in the neural modulation of fear and anxiety organised by the dorsal midbrain. Furthermore, previous results indicate a fundamental role played by inferior colliculus (IC) opioid mechanisms during the expression of defensive behaviours, but the involvement of the IC µ1-opioid receptor in the modulation of anxiety- and panic attack-related behaviours remains unclear. Using a prey-versus-snake confrontation paradigm, we sought to investigate the effects of µ1-opioid receptor blockade in the IC on the defensive behaviour displayed by rats in a dangerous situation. METHODS: Specific pathogen-free Wistar rats were treated with microinjection of the selective µ1-opioid receptor antagonist naloxonazine into the IC at different concentrations (1.0, 3.0 and 5.0 µg/0.2 µL) and then confronted with rattlesnakes ( Crotalus durissus terrificus). The defensive behavioural repertoire, such as defensive attention, flat back approach (FBA), startle, defensive immobility, escape or active avoidance, displayed by rats either during the confrontations with wild snakes or during re-exposure to the experimental context without the predator was analysed. RESULTS: The blockade of µ1-opioid receptors in the IC decreased the expression of both anxiety-related behaviours (defensive attention, FBA) and panic attack-related responses (startle, defensive immobility and escape) during the confrontation with rattlesnakes. A significant decrease in defensive attention was also recorded during re-exposure of the prey to the experimental apparatus context without the predator. CONCLUSION: Taken together, these results suggest that a decrease in µ1-opioid receptor signalling activity within the IC modulates anxiety- and panic attack-related behaviours in dangerous environments.

The endogenous opioid system modulates defensive behavior evoked by Crotalus durissus terrificus: Panicolytic-like effect of intracollicular non-selective opioid receptors blockade.

BACKGROUND: There is a controversy regarding the key role played by opioid peptide neurotransmission in the modulation of panic-attack-related responses. AIMS: Using a prey versus rattlesnakes paradigm, the present work investigated the involvement of the endogenous opioid peptide-mediated system of the inferior colliculus in the modulation of panic attack-related responses. METHODS: Wistar rats were pretreated with intracollicular administration of either physiological saline or naloxone at different concentrations and confronted with rattlesnakes ( Crotalus durissus terrificus). The prey versus rattlesnake confrontations were performed in a polygonal arena for snakes. The defensive behaviors displayed by prey (defensive attention, defensive immobility, escape response, flat back approach and startle) were recorded twice: firstly, over a period of 15 min the presence of the predator and a re-exposure was performed 24 h after the confrontation, when animals were exposed to the experimental enclosure without the rattlesnake. RESULTS: The intramesencephalic non-specific blockade of opioid receptors with microinjections of naloxone at higher doses decreased both anxiety- (defensive attention and flat back approach) and panic attack-like (defensive immobility and escape) behaviors, evoked in the presence of rattlesnakes and increased non-defensive responses. During the exposure to the experimental context, there was a decrease in duration of defensive attention. CONCLUSIONS: These findings suggest a panicolytic-like effect of endogenous opioid receptors antagonism in the inferior colliculus on innate (panic attack) and conditioned (anticipatory anxiety) fear in rats threatened by rattlesnakes.

Decrease in NMDA receptor-signalling activity in the anterior cingulate cortex diminishes defensive behaviour and unconditioned fear-induced antinociception elicited by GABAergic tonic inhibition impairment in the posterior hypothalamus.

Acute γ-aminobutyric acid (GABA) disinhibition in the posterior hypothalamus (PH) elicits defensive reactions that are considered anxiety- and panic attack-like behaviour, and these defensive reactions are followed by antinociception. Evidence indicates that the PH connects with the medial prefrontal cortex, particularly the anterior cingulate cortex (ACC), which seems to regulate these unconditioned fear-induced defensive responses. However, few studies have shown the participation of cortical regions in the control of behavioural and antinociceptive responses organised by diencephalic structures. It has been suggested that the glutamatergic system can mediate this cortical influence, as excitatory imbalance is believed to play a role in both defensive mechanisms. Thus, the aim of the present study was to investigate the involvement of ACC glutamatergic connections via blockade of local N-methyl-D-aspartate (NMDA) receptors to elaborate panic-like defensive behaviours and unconditioned fear-induced antinociception organised by PH neurons. Wistar rats were treated with microinjections of 0.9% NaCl or LY235959 (a selective NMDA receptor antagonist) in the ACC at different concentrations (2, 4 and 8 nmol/0.2µL), followed by GABAA receptor blockade in the PH. Defensive reactions were analysed for 20min, and the nociceptive threshold was then measured at 10-min intervals for 60min. Pretreatment of the ACC with LY235959 reduced both panic-like defensive behaviour and fear-induced antinociception evoked by PH GABAergic disinhibition. Our findings suggest that ACC NMDA receptor-signalled glutamatergic inputs play a relevant role in the organisation of anxiety- and panic attack-like behaviours and in fear-induced antinociception.

Critical neuropsychobiological analysis of panic attack- and anticipatory anxiety-like behaviors in rodents confronted with snakes in polygonal arenas and complex labyrinths: a comparison to the elevated plus- and T-maze behavioral tests

Objective: To compare prey and snake paradigms performed in complex environments to the elevated plus-maze (EPM) and T-maze (ETM) tests for the study of panic attack- and anticipatory anxiety-like behaviors in rodents. Methods: PubMed was reviewed in search of articles focusing on the plus maze test, EPM, and ETM, as well as on defensive behaviors displayed by threatened rodents. In addition, the authors’ research with polygonal arenas and complex labyrinth (designed by the first author for confrontation between snakes and small rodents) was examined. Results: The EPM and ETM tests evoke anxiety/fear-related defensive responses that are pharmacologically validated, whereas the confrontation between rodents and snakes in polygonal arenas with or without shelters or in the complex labyrinth offers ethological conditions for studying more complex defensive behaviors and the effects of anxiolytic and panicolytic drugs. Prey vs. predator paradigms also allow discrimination between non-oriented and oriented escape behavior. Conclusions: Both EPM and ETM simple labyrinths are excellent apparatuses for the study of anxiety- and instinctive fear-related responses, respectively. The confrontation between rodents and snakes in polygonal arenas, however, offers a more ethological environment for addressing both unconditioned and conditioned fear-induced behaviors and the effects of anxiolytic and panicolytic drugs.

Características básicas do transtorno do pânico / Basic features of panic disorder

O objetivo é caracterizar o Transtorno do Pânico (TP) com ênfase em seu diagnóstico e tratamento. O TP é um dos transtornos de ansiedade, caracterizado por ataques de pânico recorrentes acompanhados por uma persistente preocupação com ataques adicionais e alterações mal adaptativas do comportamento (Associação Americana de Psiquiatria - DSM-V). Sua etiologia ainda não é conhecida, mas deve envolver uma interação de fatores genéticos, de desenvolvimento e ambientais que resultam em altera- ções no funcionamento de algumas áreas cerebrais. O tratamento farmacológico de primeira escolha é com o uso de antidepressivos inibidores seletivos da recaptação de serotonina, os quais apresentam uma latência de 20 a 30 dias para o início do efeito. (AU)

The aim of this paper is to characterize the Panic Disorder (PD) with an emphasis on diagnosis and treatment. PD is one of the anxiety disorders, characterized by recurrent panic attacks accompanied by a persistent preoccupation with additional attacks and maladaptive behavioral changes (American Psychiatric Association ­ DSM-V). Its etiology is not known, but should involve an interaction of genetic, developmental and environmental factors that result in changes in the functioning of some brain areas. The pharmacological treatment of choice is with the use of selective serotonin reuptake inhibitors, which has a latency of 20 for 30 days for the beginning of the therapeutic effect. (AU)

Unravelling cortico-hypothalamic pathways regulating unconditioned fear-induced antinociception and defensive behaviours.

The medial prefrontal cortex can influence unconditioned fear-induced defensive mechanisms organised by diencephalic neurons that are under tonic GABAergic inhibition. The posterior hypothalamus (PH) is involved with anxiety- and panic attack-like responses. To understand this cortical mediation, our study characterised anterior cingulate cortex (ACC)-PH pathways and investigated the effect of ACC local inactivation with lidocaine. We also investigated the involvement of PH ionotropic glutamate receptors in the defensive behaviours and fear-induced antinociception by microinjecting NBQX (an AMPA/kainate receptor antagonist) and LY235959 (a NMDA receptor antagonist) into the PH. ACC pretreatment with lidocaine decreased the proaversive effect and antinociception evoked by GABAA receptor blockade in the PH, which suggests that there may be descending excitatory pathways from this cortical region to the PH. Microinjections of both NBQX and LY235959 into the PH also attenuated defensive and antinociceptive responses. This suggests that the blockade of AMPA/kainate and NMDA receptors reduces the activity of glutamatergic efferent pathways. Both inputs from the ACC to the PH and glutamatergic hypothalamic short links disinhibited by intra-hypothalamic GABAA receptors blockade are potentially implicated. Microinjection of a bidirectional neurotracer in the PH showed a Cg1-PH pathway and PH neuronal reciprocal connections with the periaqueductal grey matter. Microinjections of an antegrade neurotracer into the Cg1 showed axonal fibres and glutamatergic vesicle-immunoreactive terminal boutons surrounding both mediorostral-lateroposterior thalamic nucleus and PH neuronal perikarya. These data suggest a critical role played by ACC-PH glutamatergic pathways and AMPA/kainate and NMDA receptors in the panic attack-like reactions and antinociception organised by PH neurons.

Panic attack history and smoking topography.

BACKGROUND: Little is known about panic attacks and puffing topography, a behavioral index of the value of smoking reinforcement. This study examined smoking style during the course of smoking of a single cigarette among adult daily smokers with and without a history of panic attacks. METHOD: Participants (n=124, Mage=43.9, SD=9.7; 44.4% female) were non-treatment seeking daily smokers. Lifetime panic attack history was assessed via diagnostic assessment; 28.2% (n=35) of the sample had a panic attack history. Participants smoked one cigarette during an ad libitum smoking trial. Puff volume, duration, and inter-puff interval were measured using the Clinical Research Support System (CReSS) pocket device. RESULTS: Regression analyses revealed that panic attack status was not associated with significant differences in average puff volume, duration, or inter-puff interval. Multi-level modeling was used to examine puffing trajectories. Puff-level data revealed that there was a significant quadratic time x panic effect for puff volume and duration. Those with a panic attack history demonstrated relatively sustained levels of both puff volume and duration over time, whereas those without a history of panic attacks demonstrated an increase followed by a decrease in volume and duration over time. These effects were not accounted for by the presence of general psychopathology. DISCUSSION: Smokers with a panic attack history demonstrate more persistent efforts to self-regulate the delivery of nicotine, and thus may be at risk for continued smoking and dependence. Tailored treatment may be needed to address unique vulnerabilities among this group.

Cross-national epidemiology of panic disorder and panic attacks in the world mental health surveys.

CONTEXT: The scarcity of cross-national reports and the changes in Diagnostic and Statistical Manual version 5 (DSM-5) regarding panic disorder (PD) and panic attacks (PAs) call for new epidemiological data on PD and PAs and its subtypes in the general population. OBJECTIVE: To present representative data about the cross-national epidemiology of PD and PAs in accordance with DSM-5 definitions. DESIGN AND SETTING: Nationally representative cross-sectional surveys using the World Health Organization Composite International Diagnostic Interview version 3.0. PARTICIPANTS: Respondents (n = 142,949) from 25 high, middle, and lower-middle income countries across the world aged 18 years or older. MAIN OUTCOME MEASURES: PD and presence of single and recurrent PAs. RESULTS: Lifetime prevalence of PAs was 13.2% (SE 0.1%). Among persons that ever had a PA, the majority had recurrent PAs (66.5%; SE 0.5%), while only 12.8% fulfilled DSM-5 criteria for PD. Recurrent PAs were associated with a subsequent onset of a variety of mental disorders (OR 2.0; 95% CI 1.8-2.2) and their course (OR 1.3; 95% CI 1.2-2.4) whereas single PAs were not (OR 1.1; 95% CI 0.9-1.3 and OR 0.7; 95% CI 0.6-0.8). Cross-national lifetime prevalence estimates were 1.7% (SE 0.0%) for PD with a median age of onset of 32 (IQR 20-47). Some 80.4% of persons with lifetime PD had a lifetime comorbid mental disorder. CONCLUSIONS: We extended previous epidemiological data to a cross-national context. The presence of recurrent PAs in particular is associated with subsequent onset and course of mental disorders beyond agoraphobia and PD, and might serve as a generic risk marker for psychopathology.

Relevance of dorsomedial hypothalamus, dorsomedial division of the ventromedial hypothalamus and the dorsal periaqueductal gray matter in the organization of freezing or oriented and non-oriented escape emotional behaviors.

Electrical stimulation of the periaqueductal gray matter and ventromedial hypothalamus in humans showed the involvement of both these structures in panic attacks. The aim of this work was to make clear the role of dorsal periaqueductal gray (dPAG) matter, dorsomedial hypothalamus (DMH) and the dorsomedial part of the ventromedial hypothalamus (dmVMH) in panic attack-like behaviors. DMH, dmVMH and dPAG of Wistar rats were treated with N-methyl- d-aspartic acid (NMDA) at different doses. The rodents were then kept in a polygonal arena with a burrow to record panic attack-like responses and oriented defensive behaviors. In dmVMH, 6nmol of NMDA elicited alertness, freezing and oriented escape. The same set of behaviors was elicited by DMH neurons when stimulated by 9nmol of NMDA. Treatment of dmVMH with 9nmol of NMDA elicited typical explosive behaviors followed by freezing and oriented behaviors. The stimulation of the dPAG with NMDA at different doses provoked alertness and freezing (1nmol) or alertness, freezing, tail twitching, explosive behavior and oriented escape (3nmol), and explosive behavior followed by long-lasting freezing (6nmol). These data suggest that mainly dPAG plays a role in panic attack-like behaviors that resemble panic syndrome in humans. However, hypothalamic nuclei like dmVMH that mainly elicits oriented escape, can also produce explosive reaction when stimulated with 9nmol NMDA, whereas, DMH plays a role in coordinating defensive behaviors.

The carbon dioxide challenge test in panic disorder: a systematic review of preclinical and clinical research

This systematic review assesses the current state of clinical and preclinical research on panic disorder (PD) in which the carbon dioxide (CO2) challenge was used as a trigger for panic attacks (PAs). A total of 95 articles published from 1984 to 2012 were selected for inclusion. Some hypotheses for PD evolved greatly due to the reproducibility of PAs in a controlled environment using the safe and noninvasive CO2 test. The 35% CO2 protocol was the method chosen by the majority of studies. Results of the test report specific sensitivity to hypercapnia in PD patients of the respiratory PD subtype. The CO2 challenge helped assess the antipanic effects of medication and non-pharmaceutical approaches such as physical exercise and cognitive behavioral therapy. The test was also used in studies about the genetic component of PD, in which twins and relatives of PD patients were analyzed.

The role of 5-HT1A receptors in the anti-aversive effects of cannabidiol on panic attack-like behaviors evoked in the presence of the wild snake Epicrates cenchria crassus (Reptilia, Boidae).

The potential anxiolytic and antipanic properties of cannabidiol have been shown; however, its mechanism of action seems to recruit other receptors than those involved in the endocannabinoid-mediated system. It was recently shown that the model of panic-like behaviors elicited by the encounters between mice and snakes is a good tool to investigate innate fear-related responses, and cannabidiol causes a panicolytic-like effect in this model. The aim of the present study was to investigate the 5-hydroxytryptamine (5-HT) co-participation in the panicolytic-like effects of cannabidiol on the innate fear-related behaviors evoked by a prey versus predator interaction-based paradigm. Male Swiss mice were treated with intraperitoneal (i.p.) administrations of cannabidiol (3 mg/kg, i.p.) and its vehicle and the effects of the peripheral pre-treatment with increasing doses of the 5-HT1A receptor antagonist WAY-100635 (0.1, 0.3 and 0.9 mg/kg, i.p.) on instinctive fear-induced responses evoked by the presence of a wild snake were evaluated. The present results showed that the panicolytic-like effects of cannabidiol were blocked by the pre-treatment with WAY-100635 at different doses. These findings demonstrate that cannabidiol modulates the defensive behaviors evoked by the presence of threatening stimuli, and the effects of cannabidiol are at least partially dependent on the recruitment of 5-HT1A receptors.

Defense mechanisms in cardiovascular disease patients with and without panic disorder / Mecanismos de defensa en pacientes cardiópatas con y sin crisis de angustia

Introduction Throughout the investigation of psychosocial factors in cardiovascular diseases, type A personality, anger, hostility, anxiety, and depression have been proved to participate in this kind of sufferings. Cardiac patients exposed more frequently to life stressing events than patients who do not suffer a cardiac disease might lack adaptive coping defense mechanisms to protect them or use maladaptive defense mechanisms that facilitate the pathogenic effects of anxiety. Few studies have been done in Mexico related to psychological defense mechanisms; none of them was related to medically ill patients. In the present study, the use of defense mechanisms by cardiac patients with panic disorder (panic attack) was compared to the use of defense mechanisms by patients that present similar cardiovascular pathologies but without mental disorders. Material and method The present investigation was made as a comparative and explanatory study with a nonexperimental design. The sample was constituted by two groups: one of 33 cardiac patients diagnosed with panic attack and another group, used as control, of 30 cardiac outpatients without psychiatric disorder; all attended the Instituto Nacional de Cardiología Ignacio Chávez (Mexico City). The 63 cardiac patients were evaluated using the Structured Interview for the Diagnosis of Axis I, Hamilton's Anxiety Scale, Hopkins's 90 Symptom Checklist and the Defensive Styles Questionnaire, self-report instrument whose reliability and validity has been established for Mexican patients with panic disorder. The statistical analysis was made through chi-square test, Student's t test, Pearson correlation and a gradual multiple regression analysis. Results Within the group of cardiac patients with panic attack, 72.73% were female patients and 27.27% male, with an average age of 38.52 ± 14.18 years and 5.73 ± 2.75 years of schooling. The group of cardiac patients used as control was formed by 30 subjects also in its majority female (56.7%), with an age of 45.27 ± 14.51 years and an average of 5.67 ± 3.31 years of schooling. The patients of the group with panic disorder had higher levels of anxiety and used more maladaptive defense mechanisms, such as social isolation and inhibition, tended to use more somatization and less the adaptive defenses (suppression, work orientation, sublimation, affiliation and humor), in comparison to the group without mental disorder. The criteria for panic disorder (DSM-IV) correlated directly with somatization; the ones from major depression correlated directly with regression and inversely with humor and socioeconomical level; the score in Hamilton's Anxiety Scale with maladaptive defenses as social isolation, acting out and somatization; the SCL-90 with the maladaptive defenses acting out, projection and regression. The multiple regression analysis determined that regression and somatization contributed to the panic disorder symptomatology, and leads to major depressive disorder; projection, somatization and social isolation to anxiety's intensity and reaction formation, humor, regression, fantasy, inhibition, projective identification, passive aggression and omnipotence in general to the psychiatric symptoms. Discussion The greater use of maladaptive defenses by the cardiac patients group with panic disorder allows to conclude that low level defenses are related to the symptoms of this mental disorder. This group showed relation between levels of anxiety, psychological discomfort and the use of maladaptive defenses such as social isolation, inhibition and somatization, tending to isolate themselves and presenting in a corporal or <> form, through somatization, many physical symptoms. The observation of the use by cardiac patients without mental disorder of suppression, work orientation, sublimation, affiliation and humor, all of them adaptive defenses, reinforces this conclusion.

Introducción Gracias a la investigación de los factores psicosociales de las enfermedades cardiovasculares, se ha demostrado la participación de la conducta tipo A, enojo, hostilidad, aislamiento social, estrés, ansiedad y depresión en este tipo de padecimientos. La depresión asociada con frecuencia al infarto agudo del miocardio incrementa el riesgo de morir; los niveles altos de angustia se asocian al aumento en el riesgo de enfermedad coronaria y muerte súbita. Los pacientes cardiópatas expuestos a sucesos estresantes de la vida con más frecuencia que los pacientes que no padecen cardiopatía pueden carecer de mecanismos de defensa y afrontamiento adaptativos que los protejan o bien usan mecanismos de defensa desadaptativos que facilitan los efectos patogénicos de la ansiedad. En México se han realizado pocos estudios respecto a los mecanismos psicológicos de defensa y no hay estudios acerca del tema en pacientes médicamente enfermos. Conocer la forma en que el sujeto afronta su enfermedad permitiría una intervención psicoterapéutica oportuna en los pacientes médicos con el objetivo de mejorar su adaptación psicosocial y quizás su supervivencia. Por lo anterior, el objetivo del presente estudio es comparar el uso de los mecanismos de defensa de los pacientes cardiópatas con trastorno de angustia (crisis de angustia) con el de pacientes con patología cardiovascular similar pero sin trastornos mentales. Material y método Se realizó un estudio de tipo comparativo y explicativo con un diseño no experimental. La muestra estuvo constituida por dos grupos, uno de 33 pacientes cardiópatas diagnosticados con crisis de angustia y otro grupo, utilizado como control, de 30 sujetos cardiópatas sin trastorno psiquiátrico; todos acudían a Consulta Externa del Instituto Nacional de Cardiología Ignacio Chávez. Los 63 pacientes cardiópatas fueron evaluados utilizando la Entrevista Estructurada para el Diagnóstico del Eje I, la Escala de Ansiedad de Hamilton, la Lista de 90 Síntomas de Hopkins y el Cuestionario de Estilos Defensivos, instrumento autoaplicable que evalúa mecanismos de defensa adaptativos y desadaptativos del que se ha establecido su confiabilidad y validez en pacientes mexicanos con trastorno de angustia. El análisis estadístico se realizó a través de la chi cuadrada, t de Student, correlación de Pearson y un análisis de regresión múltiple gradual. Resultados Dentro del grupo de cardiopatías con crisis de angustia, 72.73% eran pacientes femeninos y 27.27% masculinos, con edad promedio de 38.52 ± 14.18 años y 5.73 ± 2.75 años de escolaridad. El grupo de pacientes cardiópatas, que se utilizó como control, estuvo constituido por 30 sujetos, también en su mayoría femeninos (56.7%), de 45.27 ± 14.51 años de edad con promedio de 5.67 ± 3.31 años de escolaridad. Los pacientes del grupo con trastorno de angustia tuvieron niveles más altos de ansiedad y utilizaron más mecanismos de defensa desadaptativos como aislamiento social e inhibición, tendieron a usar la somatización y utilizaron menos defensas adaptativas (supresión, orientación al trabajo, sublimación, afiliación y humor), en comparación con el grupo sin trastorno mental. Los criterios del trastorno de angustia (DSM-IV) se correlacionaron con la somatización; los de la depresión mayor, directamente con la regresión e inversamente con el humor y con el nivel socioeconómico; la puntuación de la Escala de Ansiedad de Hamilton, con defensas desadaptativas como aislamiento social, exoactuación y somatización; el SCL-90, con las defensas desadaptativas exoactuación, proyección y regresión. El análisis de regresión múltiple determinó que la regresión y la somatización contribuyeron a la sintomatología del trastorno de angustia, el consumo en el trastorno depresivo, la proyección, somatización y aislamiento social en la intensidad de la angustia y la formación reactiva, humor, regresión, fantasía, inhibición, identificación proyectiva, pasivo-agresividad y omnipotencia en la sintomatología psiquiátrica general. Discusión El mayor uso de defensas desadaptativas por parte del grupo de pacientes cardiópatas con trastorno de angustia permite concluir que las defensas de bajo nivel se relacionan con los síntomas de este trastorno mental. Este grupo mostró relación entre los niveles de ansiedad y malestar psicológico y la utilización de defensas desadaptativas como el aislamiento social, inhibición y somatización. Asimismo, tendió a aislarse y a manifestar en forma corporal o <>, a través de la somatización, muchos síntomas físicos. La observación de que los pacientes cardiópatas sin trastorno mental utilizaron la supresión, orientación al trabajo, sublimación, afiliación y humor, todas ellas defensas adaptativas, refuerza esta conclusión.

Some notes on a historical perspective of panic disorder

This article aims to describe important points in the history of panic disorder concept, as well as to highlight the importance of its diagnosis for clinical and research developments. Panic disorder has been described in several literary reports and folklore. One of the oldest examples lies in Greek mythology - the god Pan, responsable for the term panic. The first half of the 19th century witnessed the culmination of medical approach. During the second half of the 19th century came the psychological approach of anxiety. The 20th century associated panic disorder to hereditary, organic and psychological factors, dividing anxiety into simple and phobic anxious states. Therapeutic development was also observed in psychopharmacological and psychotherapeutic fields. Official classification began to include panic disorder as a category since the third edition of the American Classification Manual (1980). Some biological theories dealing with etiology were widely discussed during the last decades of the 20th century. They were based on laboratory studies of physiological, cognitive and biochemical tests, as the false suffocation alarm theory and the fear network. Such theories were important in creating new diagnostic paradigms to modern psychiatry. That suggests the need to consider a wide range of historical variables to understand how particular features for panic disorder diagnosis have been developed and how treatment has emerged.