Pivotal role of tissue plasminogen activator in the mechanism of action of electroconvulsive therapy.

Electroconvulsive therapy is an important treatment option for major depressive disorders, acute mania, mood disorders with psychotic features, and catatonia. Several hypotheses have been proposed as electroconvulsive therapy's mechanism of action. Our hypothesis involves many converging pathways facilitated by increased synthesis and release of tissue-plasminogen activator. Human and animal experiments have shown that tissue-plasminogen activator participates in many mechanisms of action of electroconvulsive therapy or its animal variant, electroconvulsive stimulus, including improved N-methyl-D-aspartate receptor-mediated signaling, activation of both brain-derived neurotrophic factor and vascular endothelial growth factor, increased bioavailability of zinc, purinergic release, and increased mobility of dendritic spines. As a result, tissue-plasminogen activator helps promote neurogenesis in limbic structures, modulates synaptic transmission and plasticity, improves cognitive function, and mediates antidepressant effects. Notably, electroconvulsive therapy seems to influence tissue-plasminogen activator metabolism. For example, electroconvulsive stimulus increases the expression of glutamate decarboxylase 65 isoform in γ-aminobutyric acid-releasing neurons, which enhances the release of tissue-plasminogen activator, and the expression of p11, a protein involved in plasminogen and tissue-plasminogen activator assembling. This paper reviews how electroconvulsive therapy correlates with tissue-plasminogen activator. We suggest that interventions aiming at increasing tissue-plasminogen activator levels or its bioavailability - such as daily aerobic exercises together with a carbohydrate-restricted diet, or normalization of homocysteine levels - be evaluated in controlled studies assessing response and remission duration in patients who undergo electroconvulsive therapy.

A randomized, naturalistic, parallel-group study for the long-term treatment of panic disorder with clonazepam or paroxetine.

This long-term extension of an 8-week randomized, naturalistic study in patients with panic disorder with or without agoraphobia compared the efficacy and safety of clonazepam (n = 47) and paroxetine (n = 37) over a 3-year total treatment duration. Target doses for all patients were 2 mg/d clonazepam and 40 mg/d paroxetine (both taken at bedtime). This study reports data from the long-term period (34 months), following the initial 8-week treatment phase. Thus, total treatment duration was 36 months. Patients with a good primary outcome during acute treatment continued monotherapy with clonazepam or paroxetine, but patients with partial primary treatment success were switched to the combination therapy. At initiation of the long-term study, the mean doses of clonazepam and paroxetine were 1.9 (SD, 0.30) and 38.4 (SD, 3.74) mg/d, respectively. These doses were maintained until month 36 (clonazepam 1.9 [SD, 0.29] mg/d and paroxetine 38.2 [SD, 3.87] mg/d). Long-term treatment with clonazepam led to a small but significantly better Clinical Global Impression (CGI)-Improvement rating than treatment with paroxetine (mean difference: CGI-Severity scale -3.48 vs -3.24, respectively, P = 0.02; CGI-Improvement scale 1.06 vs 1.11, respectively, P = 0.04). Both treatments similarly reduced the number of panic attacks and severity of anxiety. Patients treated with clonazepam had significantly fewer adverse events than those treated with paroxetine (28.9% vs 70.6%, P < 0.001). The efficacy of clonazepam and paroxetine for the treatment of panic disorder was maintained over the long-term course. There was a significant advantage with clonazepam over paroxetine with respect to the frequency and nature of adverse events.

Tapering clonazepam in patients with panic disorder after at least 3 years of treatment.

High-potency benzodiazepines, such as clonazepam, are frequently used in the treatment of panic disorder (PD) because of their rapid onset of action and good tolerability. However, there is concern about their potential to cause withdrawal symptoms. We aimed to develop a protocol for safely tapering off clonazepam in patients with PD who had been receiving treatment for at least 3 years. A specific scale for judging withdrawal was also developed, the Composite Benzodiazepine Discontinuation Symptom Scale. We selected 73 patients with PD who had been asymptomatic for at least 1 year and who wished to discontinue the medication. The trial consisted of a 4-month period of tapering and an 8-month follow-up period. The dosage of clonazepam was decreased by 0.5 mg per 2-week period until 1 mg per day was reached, followed by a decrease of 0.25 mg per week. The mean dosage at the start of tapering was 2.7 +/- 1.2 mg/d. In total, 51 (68.9%) of the patients were free of the medication after the 4 months of tapering according to the protocol, and 19 (26.0%) of the patients needed another 3 months to be free of medication. Clonazepam discontinuation symptoms were mostly mild and included mainly: anxiety, shaking/trembling/tremor, nausea/vomiting, insomnia/nightmares, excessive sweating, tachycardia/palpitations, headache, weakness, and muscle aches. The improvement in PD and general well-being was maintained during both the taper and follow-up phases. Clonazepam can be successfully discontinued without any major withdrawal symptoms if the dose is reduced gradually. We recommend reducing the dosage of clonazepam after intermediate-term use by 0.25 mg/wk.

Double-blind comparison of 30 and 60 mg tranylcypromine daily in patients with panic disorder comorbid with social anxiety disorder.

Our objective was to explore the dose-response relationship in patients with panic disorder and social anxiety disorder comorbidity (DSM-IV). After 1 week of no-drug washout, 36 such patients were assigned to a double-blind controlled comparison of the effects of 30 mg and 60 mg of tranylcypromine, and were followed up for 12 weeks. The main instrument used to measure the number of panic attacks was the Sheehan Panic and Anticipatory Anxiety Scale. The primary outcome measure for social anxiety disorder symptoms was the mean change from baseline in the Liebowitz Social Anxiety Scale (LSAS). After 12 weeks of treatment, panic attacks were reduced 69.6% from baseline in the 30-mg group (n=19) compared with a 74.8% reduction in the 60-mg group (n=17). Twelve patients (70.6%) of the higher dose group and 14 patients (68.4%) of the lower dose were completely free of panic attacks. There was no difference in efficacy between the tranylcypromine groups in the panic disorder symptoms. The 60-mg dose was more efficacious as measured by the LSAS scores, showing a significant difference in relation to the lower group. Mean change from baseline in LSAS total score (mean+/-SD) for 30-mg group was 17.9+/-14.7 and for the 60-mg group was 35.0+/-14.8. The social anxiety symptom scale showed a two-fold greater change with the 60-mg dose, and the 30-mg dose group could be considered the equivalent of a placebo control group. Tranylcypromine--60 mg daily--was found effective in the treatment of panic disorder and social anxiety disorder comorbidity.

Demographic and clinical features of panic disorder comorbid with bipolar I disorder: a 3-year retrospective study.

BACKGROUND: Mood disorders are considered related to anxiety disorders and their association may determine clinical course and prognosis. We aimed to describe with retrospective methodology the demographic, clinical, and treatment features in a group of panic disorder comorbid with bipolar I disorder (PD-BI) patients who were been treated for at least 3 year-period and compare them with bipolar I (BI) patients who were treated during the same period. METHOD: We compared the demographic and clinical data of 26 PD-BI, 28 BI, and 25 panic disorder (PD) outpatients without history of comorbidity with mood disorder were diagnosed and treated for at least 3 years in the Federal University of Rio de Janeiro. RESULTS: PD group have a higher educational level, are more married, and are more economically active. In the PD-BI and BI patients the disorders started earlier. They also turn out to have an equivalent pattern in the presence of drug abuse episodes, moderate or severe depressive episodes, psychotic episodes, suicide attempts, maniac episodes, mixed episodes, use of fewer days of antidepressants and benzodiazepines, and use of more days of antipsychotics and mood stabilizers. The PD-BI and the BI groups had a higher frequency of depressive episodes and psychotic episodes. LIMITATIONS: It is a retrospective data description based on a naturalistic treatment. The sample has a small size and the some data could be different in a large sample. CONCLUSION: PD-BI patients have demographic, clinical and therapeutic features similar to BI and the data support its validation as a special severe bipolar I disorder subgroup.

Panic disorder respiratory subtype: a comparison between responses to hyperventilation and CO2 challenge tests.

In this study 117 panic disorder patients were divided into a respiratory subtype group and a non-respiratory subtype group. The respiratory subtype patients were observed to be more sensitive to the 35% CO(2) inhalation challenge test and the hyperventilation test than the non-respiratory subtype patients.

A caffeine challenge test in panic disorder patients, their healthy first-degree relatives, and healthy controls.

Our aim was to observe the induction of anxiety symptoms and panic attacks by a caffeine challenge test in panic disorder (PD) patients (DSM-IV) and their healthy first-degree relatives. We randomly selected 25 PD patients, 27 healthy first-degree relatives of probands with PD, and 22 healthy volunteers with no family history of PD. In a randomized double-blind experiment performed over two occasions 7 days apart, 480 mg caffeine and a caffeine-free solution were administered in a coffee form. Using specific panic attack criteria, 52.0% (n=13) PD patients, 40.7% (n=11) first-degree relatives (chi2=1.81, df=1, P=0.179), and none of the control subjects had a panic attack after the test (chi2=51.7, df=2, P<0.001). In this caffeine challenge test, PD patients and their first-degree relatives were more sensitive than healthy volunteers to the panic attack symptoms but less sensitive to headache, increase in blood pressure, and insomnia. Our data suggest that there is an association between panic attacks after the intake of 480 mg of caffeine in PD patients and their first-degree relatives. There is a clear differentiation of PD patients and their first-degree relatives by a caffeine test from the healthy group.

Clinical features of respiratory and nocturnal panic disorder subtypes.

Our aim is to compare the panic disorder (PD) respiratory subtype and the nocturnal panic subtype. A group of 193 PD patients (DSM-IV) was examined in the Laboratory of Panic and Respiration in the Institute of Psychiatry of the Federal University of Rio de Janeiro. The diagnoses were made using the SCID-I for DSM-IV. The subtypes were the respiratory (with 4 out of 5 prominent respiratory symptoms during the panic attacks [PA]) vs. non-respiratory, likewise PD with nocturnal (during sleep) PAs vs. PD with only diurnal PAs. The respiratory subtype accounted for 56.5% (n=109) of our sample; the non-respiratory subtype, 43.5% (n=84); the nocturnal subtype, 49.2% (n=95); and the non-nocturnal subtype, 50.8% (n=98). Despite a rich literature concerning correlations between the respiratory system and nocturnal panic attacks, our data do not support these findings, as the comparison of proportions in the respiratory and nocturnal groups did not differ. The non-nocturnal subtype was significantly associated with agoraphobia, and the respiratory subtype was not associated with these variables.

Caffeine and 35% carbon dioxide challenge tests in panic disorder.

Our aim was to compare the demographic and clinical features of panic disorder (PD) patients with agoraphobia-DSM-IV-who had a panic attack after both an oral caffeine and the 35% carbon dioxide (CO2) challenge tests (responsive group) and compare them with PD patients who did not have a panic attack after both tests (non-responsive group). We examined 83 PD patients submitted to a 35% CO2 test and to an oral caffeine (480 mg) intake within 1 week interval. A panic attack was induced in 51 (61.4%) patients during the CO2 test (chi2=31.67, df=1, p<0.001) and in 38 (45.8%) patients during the caffeine test (chi2=18.28, df=1, p=0.023). All patients who had a panic attack during the caffeine test also had a panic attack during the CO2 test (n=38)-responsive group. The responsive had more (chi2=24.55, df=1, p=0.008) respiratory PD subtype, disorder started earlier (Mann-Whitney, p<0.001) had a higher familial prevalence of PD (chi2=20.34, df=1, p=0.019), less previous alcohol abuse (chi2=23.42, df=1, p<0.001), and had more previous depressive episodes (chi2=27.35, df=1, p<0.001). Our data suggest that there is an association between respiratory PD subtype and hyperreactivity to challenge tests: CO2 and oral caffeine.

Caffeine challenge test in panic disorder and depression with panic attacks.

Our aim was to observe if patients with panic disorder (PD) and patients with major depression with panic attacks (MDP) (Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria) respond in a similar way to the induction of panic attacks by an oral caffeine challenge test. We randomly selected 29 patients with PD, 27 with MDP, 25 with major depression without panic attacks (MD), and 28 healthy volunteers. The patients had no psychotropic drug for at least a 4-week period. In a randomized double-blind experiment performed in 2 occasions 7 days apart, 480 mg caffeine and a caffeine-free (placebo) solution were administered in a coffee form and anxiety scales were applied before and after each test. A total of 58.6% (n = 17) of patients with PD, 44.4% (n = 12) of patients with MDP, 12.0% (n = 3) of patients with MD, and 7.1% (n= 2) of control subjects had a panic attack after the 480-mg caffeine challenge test (chi(2)(3) = 16.22, P = .001). The patients with PD and MDP were more sensitive to caffeine than were patients with MD and healthy volunteers. No panic attack was observed after the caffeine-free solution intake. The patients with MD had a lower heart rate response to the test than all the other groups (2-way analysis of variance, group by time interaction with Greenhouse-Geisser correction: F(3,762) = 2.85, P = .026). Our data suggest that there is an association between panic attacks, no matter if associated with PD or MDP, and hyperreactivity to an oral caffeine challenge test.

Personality traits spectrum in panic disorder and major depression.

OBJECTIVE: Our aim was to identify the personality traits in patients with panics disorder, major depression and with both disorders (comorbidity). METHOD: Diagnoses were made with the Structured Clinical Interview for DSM-IV before the treatment, and the personality evaluation with the Maudsley Personality Inventory was made during the follow-up. Four groups were analyzed: a control group (n = 30), a major depression without panic disorder group (n = 45); a panic disorder without major depression group (n = 56) and a comorbidity group (n = 21), with major depression and panic disorder, simultaneously. RESULTS: All disorder groups had significantly higher neuroticism means when compared to the control group. The highest mean was in the comorbidity group, followed by the major depression group and the panic disorder group. The difference of neuroticism means between the comorbidity group and the panic disorder group also reached statistical significance. The lowest extraversion mean was in the comorbidity group, followed by the major depression group, the panic disorder group, and the control group. Compared to normal controls, extraversion was significantly low in the comorbidity and major depression groups. CONCLUSION: In our sample, there was a continuum of personality traits between panic disorder and major depression and, the co-occurrence of these disorders was associated with accentuated personality traits.

Personality traits spectrum in panic disorder and major depression

OBJECTIVE: Our aim was to identify the personality traits in patients with panics disorder, major depression and with both disorders (comorbidity). METHOD: Diagnoses were made with the Structured Clinical Interview for DSM-IV before the treatment, and the personality evaluation with the Maudsley Personality Inventory was made during the follow-up. Four groups were analyzed: a control group (n = 30), a major depression without panic disorder group (n = 45); a panic disorder without major depression group (n = 56) and a comorbidity group (n = 21), with major depression and panic disorder, simultaneously. RESULTS: All disorder groups had significantly higher neuroticism means when compared to the control group. The highest mean was in the comorbidity group, followed by the major depression group and the panic disorder group. The difference of neuroticism means between the comorbidity group and the panic disorder group also reached statistical significance. The lowest extraversion mean was in the comorbidity group, followed by the major depression group, the panic disorder group, and the control group. Compared to normal controls, extraversion was significantly low in the comorbidity and major depression groups. CONCLUSION: In our sample, there was a continuum of personality traits between panic disorder and major depression and, the co-occurrence of these disorders was associated with accentuated personality traits.

OBJETIVO: Identificar os traços de personalidade presentes em pacientes com transtorno do pânico, depressão maior e comorbidade. MÉTODO: Os diagnósticos foram feitos com o Structured Clinical Interview para o DSM-IV antes do início do tratamento, e a avaliação dos traços de personalidade com o Maudsley Personality Inventory foi feita durante o acompanhamento desses pacientes. Quatro grupos foram comparados: um grupo controle (n = 30), um grupo de depressão maior sem transtorno do pânico (n = 45); um grupo de transtorno do pânico sem depressão maior (n = 56) e um grupo de comorbidade (n = 21), com transtorno do pânico e depressão maior, simultaneamente. RESULTADOS: Todos os grupos de pacientes tiveram médias de neuroticismo significativamente maiores quando comparados ao grupo controle. A maior média foi no grupo de comorbidade, seguida pelas dos grupos de depressão maior e transtorno do pânico. A diferença de neuroticismo entre o grupo de comorbidade e de transtorno do pânico também foi estatisticamente significativa. Entre os grupos de pacientes, a menor média de extroversão foi a do grupo de comorbidade, seguida pelas de depressão maior e transtorno do pânico. Quando comparados ao grupo controle, apenas os grupos de comorbidade e depressão maior tiveram extroversão significativamente mais baixa. CONCLUSÃO: Na nossa amostra, houve uma continuidade de traços de personalidade entre o transtorno do pânico e a depressão maior, e a sobreposição de sintomas de pânico-agorafobia e de depressão estava associada a traços de personalidade acentuados.

Comparison between hyperventilation and breath-holding in panic disorder: patients responsive and non-responsive to both tests.

Our aim was to compare the demographic and psychopathological features of panic disorder (PD) patients who underwent hyperventilation and breath-holding challenge tests, and to describe the features of patients who had a panic attack after both tests versus those patients who did not experience panic after either test. Eighty-five PD patients were induced to hyperventilate (30 breaths/min) for 4 min, and a week later to hold their breath for as long as possible four times with a 2-min interval in between. Anxiety scales were applied before and after the tests. Patients who responded with a panic attack to both tests (BPA, n = 25) were compared with patients who experienced spontaneous panic attacks but did not panic in response to the two tests (NPA, n = 16). The BPA group had a significantly higher presence of respiratory symptoms during a panic attack. The criteria for the respiratory PD subtype were fulfilled in 18 (72.0%) BPA patients and in 6 (37.5%) NPA patients. The BPA patients had a later onset of panic disorder and a higher familial prevalence of PD. Our data suggest that there is a distinction between PD patients who were sensitive to both hyperventilation and breath-holding tests and PD patients who were not affected by the challenge tests. The panic attack may be a final common pathway for different types of stimuli, and respiratory tests may characterize different PD subgroups.

Psychopathological profile of 35% CO2 challenge test-induced panic attacks: a comparison with spontaneous panic attacks.

Our aim was to describe the clinical features of 35% CO2-induced panic attacks in patients with panic disorder (PD) (Diagnostic and Statistical Manual and Mental Disorders, Fourth Edition) and compare them with the last spontaneous panic attack in patients with PD who had not had a panic attack after the 35% CO2 challenge test. We examined 91 patients with PD submitted to the CO2 challenge test. The test consisted of exhaling as fully as possible, took a fast vital capacity breath, held their breath for 8 seconds, exhaled, and then repeated the fast vital capacity breath, again holding for 8 seconds. The patients inhaled the 35% CO2/65% O2 mixture or atmospheric compressed air, randomly selected in a double-blind design. Scales were applied before and after the test. A total of 68.1% (n = 62) patients with PD had a panic attack (responders) after the CO2 test (chi2(1) = 25.87, P = .031). The last spontaneous panic attack and the symptom profile from the patients with PD who had not had a panic attack after the test (n = 29, 31.9%) were described to compare. The responders had more respiratory symptoms (chi2(1) = 19.21, P < .001), fulfilling the criteria for respiratory PD subtype (80.6%); the disorder started earlier (Mann-Whitney, P < .001), had a higher familial prevalence of PD (chi2(1) = 20.45, P = .028), and had more previous depressive episodes (chi2(1) = 27.98, P < .001). Our data suggest that there is an association between respiratory PD subtype and hyperreactivity to a CO2 respiratory challenge test. The responders may be a subgroup of respiratory PD subtype with future diagnostic and therapeutic implications.

35% Carbon dioxide and breath-holding challenge tests in panic disorder: a comparison with spontaneous panic attacks.

Respiration and its control mechanisms may represent an important system involved in abnormal anxiety. Our aim was to compare the demographic and clinical features of patients with panic disorder (PD) with agoraphobia (DSM-IV) who had a panic attack after both the 35% carbon dioxide (CO(2)) test and the breath-holding test (CPA group), and compare them with PD patients who did not have a panic attack after both tests (NPA group). We examined 76 patients with PD who were administered a 35% CO(2)test and a breath-holding test within a 1-week interval. Anxiety scales were applied before and after each test. A panic attack was induced in 50 (65.8%) patients during the CO(2)test (chi(2) = 28.44, df = 1, P<.001) and in 40 (52.6%) patients during the breath-holding test (chi(2) = 15.35, df = 1, P = .036). All patients who had a panic attack during the breath-holding test also had a panic attack during the CO(2)test (n = 40; CPA group). Twenty-six (34.2%) patients with PD did not have a panic attack after both respiratory tests (NPA group). The CPA group had more (chi(2) = 21.67, df = 1, P = .011) respiratory PD subtype. In the CPA group, the disorder started earlier (Mann-Whitney, P<.001), had a higher familial prevalence of PD (chi(2) = 18.34, df = 1, P = .028), and had more previous depressive episodes (chi(2) = 23.59, df = 1, P<.001). Our data suggest that there is an association between respiratory PD subtype and the response to respiratory challenge tests: CO(2)and breath-holding. The CPA may be confirmed as a subgroup of respiratory PD subtype.

A three-year follow-up study of patients with the respiratory subtype of panic disorder after treatment with clonazepam.

The demographic, clinical and therapeutic features of the respiratory subtype of panic disorder (PD) versus the non-respiratory subtype were studied in a prospective design. Sixty-seven PD outpatients (DSM-IV), who had previously been categorized into respiratory (n=35) and non-respiratory (n=32) subgroups, were openly treated with clonazepam for a 3-year period. The principal measure of efficacy was the number of panic attacks, obtained from the Sheehan Panic and Anticipatory Anxiety Scale. In the first 8 weeks of treatment (acute phase), the respiratory subtype group had a significantly faster response to clonazepam. During the follow-up (weeks 12-156), the two subgroups did not differ significantly in the number of panic attacks experienced from baseline to end point. Patients in the respiratory subtype were characterized by a later onset of disorder and a family history of PD. Patients in the non-respiratory subgroup had a significantly higher number of past depressive episodes than those in the respiratory subgroup. The respiratory subgroup had a faster response after 8 weeks of treatment and an equivalent response in the 3-year follow-up period. Clonazepam had a sustained therapeutic effect over the entire treatment period.

Diurnal panic attacks with and without nocturnal panic attacks: are there some phenomenological differences?

OBJECTIVE: To compare nocturnal and diurnal panic attacks in a cross-sectional study and in a longitudinal prospective short-term follow-up. METHODS: We selected 57 panic disorder (PD) subjects (DSM-IV) and rated them with the Panic Disorder Severity Scale (PDSS) at baseline and after 30 days of treatment with nortriptyline, and with the Eysenck Personality Inventory and the Brown Attention Deficit Disorder (ADD) Scale at baseline. RESULTS: The sample was divided into a nocturnal and diurnal panic attack (NDPA) group--57.9% (n = 33)--and a diurnal panic attack (DPA) group--42.1% (n = 24). The groups showed a similar mean age at onset of PD and a pattern of prominent respiratory symptoms. The PDSS did not differ between the groups following short-term treatment (p = 0.451). There were also neither significant differences in Neuroticism (p = 0.094) and Extroversion (p = 0.269) nor in the Brown ADD Scale (p = 0.527). CONCLUSION: In our study, patients with both nocturnal and diurnal panic attacks showed similar features in their phenomenology and short-term outcome when compared to pure diurnal panic attacks patients.

Demographic and clinical features of schizoaffective (schizobipolar) disorder--a 5-year retrospective study. Support for a bipolar spectrum disorder.

BACKGROUND: Schizobipolar disorder is considered related to both schizophrenia and bipolar disorder. We aimed to describe with retrospective methodology the demographic, clinical, and treatment features in a group of schizobipolar disorder patients who have been treated for at least a 5-year period and compare them with bipolar I and schizophrenic patients who were treated during the same period. METHOD: We compared the demographic and clinical data of 61 schizobipolar, 57 bipolar I, and 55 schizophrenic outpatients who were diagnosed and treated for at least 5 years in the outpatient clinic in the Federal University of Rio de Janeiro. RESULTS: The schizobipolar disorder patients had a profile similar to the bipolar I patients but are significantly different from schizophrenic patients in educational level, marital status, occupation, drug and alcohol abuse episodes, presence of depressive, mixed and maniac episodes, family history of bipolar I and mood disorders, and use of medications. Only the age of onset, suicide attempts, and family history of suicide are not significantly different among the groups. The schizophrenic patients used antipsychotics for more days and the schizobipolar and bipolar I used more antidepressants and mood stabilizers. 37 (60.6%) schizobipolar patients had their diagnosis changed to bipolar disorder by their physician in different periods during the period studied. LIMITATIONS: It is a retrospective data description based on a naturalistic treatment. The family history was collected from the patient and whenever possible from one first-degree relative. CONCLUSION: Schizobipolar disorder patients have demographic, clinical and therapeutic features similar to bipolar I patients and data support its definite inclusion in the bipolar spectrum group.

Diurnal panic attacks with and without nocturnal panic attacks: are there some phenomenological differences?

OBJETIVO: Comparar ataques de pânico noturnos e diurnos em um estudo de acompanhamento prospectivo de curto prazo. MÉTODOS: Selecionamos 57 indivíduos com transtorno do pânico (TP) segundo o DSM-IV e os classificamos com a Panic Disorder Severity Scale (PDSS) na linha de base e após 30 dias de tratamento com nortriptilina, e com o Eysenck Personality Inventory e a escala Brown Attention Deficit Disorder (ADD) na linha de base. RESULTADOS: A amostra foi dividida em um grupo com ataques de pânico noturnos e diurnos (NDPA) - 57,9% (n = 33) - e um grupo com ataques de pânico diurnos (DPA) - 42,1% (n = 24). Os grupos tiveram idades médias de início de transtorno do pânico e um padrão de sintomas respiratórios proeminentes similares. A Panic Disorder Severity Scale não apresentou diferencas entre os grupos após tratamento de curto prazo (p = 0,451). Tampouco houve diferencas significativas em Neuroticismo (p = 0,094) e Extroversão (p = 0,269) e na escala Brown Attention Deficit Disorder (p = 0,527). CONCLUSAO: Em nosso estudo, os pacientes com ataques de pânico noturnos e diurnos tiveram características similares quanto aos seus resultados fenomenológicos e resultados em curto prazo em comparacão com pacientes que tiveram somente ataques diurnos de pânico.

Do social anxiety disorder patients belong to a bipolar spectrum subgroup?

BACKGROUND: It has been proposed that all forms of bipolar disorder-perhaps all primary affective disorders-are best conceptualized as a spectrum of related illness, clinically overlapping but not necessarily genetically uniform illnesses. We aim to describe with retrospective methodology the demographic, clinical, and therapeutic response in a group of social anxiety disorder (SA) patients who improves while taking antidepressants and compare them with bipolar II (B-II) patients. METHODS: 57 SA outpatients (DSM-IV) were diagnosed and naturalistic efficacious treated with selective serotonin reuptake inhibitors (SSRI). Their demographic, clinical features and therapeutic response were compared with 41 DSM-IV bipolar II patients in their starting evaluations in our outpatient clinic in the Federal University of Rio de Janeiro, Brazil. RESULTS: There is a sub-group of SA patients who improves while taking antidepressants and presents a clear hypomanic phase. Their improvement is identical to a mild/moderate hypomanic state. Without the antidepressant, the symptoms of SA return. The SA and B-II patients have a similar number of previous depressive episodes, alcohol abuse, suicide attempts, and family history for mood disorder. LIMITATIONS: It is a retrospective data description based on a naturalist follow-up. CONCLUSION: Some SA patients have demographic, clinical and therapeutic features similar to B-II patients and they might just be a Bipolar-III sub-group with a higher level of complains to social situations and without spontaneous hypomania during lifetime.