Duloxetine-related panic attacks

Side-effects arising on the grounds of antidepressant administration pose as a substantial obstacle hindering successful depressive disorder treatment. Side-effects, especially those severe or those manifested through dramatic clinical presentations such as panic attacks, make the treatment far more difficult and shake patients' trust in both the treatment and the treating physician. This case report deals with a patient experiencing a moderately severe depressive episode, who responded to duloxetine treatment administered in the initial dose of 30 mg per day with as many as three panic attacks in two days. Upon duloxetine withdrawal, these panic attacks ceased as well. The patient continued tianeptine and alprazolam treatment during which no significant side-effects had been seen, so that she gradually recovered. Some of the available literature sources have suggested the possibility of duloxetine administration to the end of generalised anxiety disorder and panic attack treatment. However, they are outnumbered by the contributions reporting about duloxetine-related anxiety, aggressiveness and panic attacks. In line with the foregoing, further monitoring of each and every duloxetine-administered patient group needs to be pursued so as to be able to evaluate treatment benefits and weigh them against risks of anxiety or panic attack onset.     

Nocturnal panic attacks

The panic-respiration connection has been presented with increasing evidences in the literature. We report three panic disorder patients with nocturnal panic attacks with prominent respiratory symptoms, the overlapping of the symptoms with the sleep apnea syndrome and a change of the diurnal panic attacks, from spontaneous to situational pattern. The implication of these findings and awareness to the distinct core of the nocturnal panic attacks symptoms may help to differentiate them from sleep disorders and the search for specific treatment.     

Modeling panic attacks

The isomorphism of dorsal periaqueductal gray-evoked defensive behaviors and panic attacks was appraised in the present study. Thresholds of electrically induced immobility, trotting, galloping, jumping, exophthalmus, micturition and defecation were recorded before and after acute injections of anxiolytic, anxiogenic and antidepressant drugs. Antidepressant effects were further assessed 24 h after injections of 7–14- and 21-day treatments. Chronic administration of clomipramine (CLM, 5–10 mg/kg) a clinically effective antipanic drug increased the thresholds of immobility (24%), trotting (138%) galloping (75%), jumping (45%) and micturition (85%). The 21-day treatment with fluoxetine (FLX, 1 mg/kg) virtually abolished galloping without changing the remaining responses. Galloping thresholds were also increased by 5 mg/kg acute injections of CLM (19%) and FLX (25%). In contrast, chronically administered maprotiline (10 mg/kg), a noradrenaline (NE) selective reuptake inhibitor, selectively increased the thresholds of immobility (118%). Diazepam (1.8 mg/kg) and midazolam (MDZ, 2.5 mg/kg) failed in attenuating the somatic defensive responses. Yet, the sedative dose of MDZ (5 mg/kg) attenuated immobility. The panicogenic drug, pentylenetetrazole (50 mg/kg), markedly decreased the thresholds of galloping (−51%) and micturition (−66%). These results suggest that whereas immobility is a NE-mediated attentional response, galloping is the panic-like behavior best candidate.     

Hyperventilation and panic attacks

The role of hyperventilation in the aetiology of panic attacks is still unclear. This paper briefly reviews the role of hyperventilation and abnormal respiration to panic attacks and examines the experimental evidence. Evidence has been found that physiological variables such as paCO2 and pH are involved in the aetiology of panic attacks and panic disorder but the extent and the nature of the involvement of cognitive variables is undetermined. Based on current evidence, there is a need to integrate cognitive variables with the physiological framework proposed by the hyperventilation theory. Until clear experimental evidence is produced about the relationships between cognitive and physiological factors, the applicability of hyperventilation in the aetiology and treatment of panic attacks remains in question.     

Hypoglycemia and panic attacks

Many patients with panic disorder believe hypoglycemia causes their symptoms. Of 10 patients with panic disorder given sodium lactate to induce panic, none had evidence of low blood sugar levels when they began to experience anxiety symptoms.     

Hyperventilation and panic attacks

The symptoms of hyperventilation syndrome and panic disorder are very similar. A questionnaire was used to assess the incidence of panic disorder in 274 patients; 35% of the patients with hyperventilation and only 5% of the non-hyperventilating patients showed panic disorder. The authors conclude that hyperventilation plays an important role in panic disorder and in generalized anxiety disorder.     

Psychopathological description of hyperventilation-induced panic attacks: a comparison with spontaneous panic attacks

Our aim was to describe the clinical features of hyperventilation-induced panic attacks (HPA) in panic disorder patients - DSM-IV - and to compare them with their spontaneous panic attacks and with spontaneous panic attacks in panic disorder (PD) patients not sensible to the hyperventilation challenge test. We reexamined 88 previously studied PD patients when they were submitted to a hyperventilation challenge test. They were induced to hyperventilate (30 breaths/min) for 4 min and anxiety scales were applied before and after the test. A total of 51.1% (n = 45) PD patients had a panic attack after hyperventilating - HPA (chi(2) = 13.11, d.f. = 1, p = 0.017). The clinical symptoms of the most severe panic attack were recorded by the HPA patient and by the PD patients not sensible to this test (non-HPA; n = 43, 48.9%) in a diary during a 1-week period and then compared. The HPA group had more respiratory symptoms (chi(2) = 15.26, d.f. = 1, p < 0.001), fulfilling the criteria for the respiratory PD subtype (75.6%), the disorder started later (Mann-Whitney, p < 0.001), had a higher familial prevalence of PD (chi(2) = 19.45, d.f. = 1, p = 0.036), and had more previous depressive episodes (chi(2) = 18.74, d.f. = 1, p < 0.001). The HPA group had similar symptomatology in spontaneous attacks and HPA. The HPA group may be regarded as a subgroup of the respiratory panic disorder subtype with diagnostic and therapeutic implications.     

Hyperventilation-induced panic attacks in panic disorder with agoraphobia

Eight minutes of hyperventilation to an end-tidal PCO2 of less than 20 mmHg led to a panic attack in 7 of 12 patients with panic disorder with agoraphobia and only 1 of 12 normal controls. Patients experienced greater increases in panic symptoms than controls during hyperventilation. Patients who reported more distress from somatic symptoms of hyperventilation during the preceding week were more likely to panic during hyperventilation. Patients who panicked during hyperventilation exhibited a delayed recovery of normocapnia following hyperventilation. Hyperventilation by this protocol is an effective means of inducing panic attacks in the laboratory. A hyperventilation challenge may identify a subgroup of patients for whom hyperventilation symptoms are frequently associated with panic.     

Insulin-induced hypoglycemia and panic attacks

To investigate whether hypoglycemia might trigger panic attacks, the authors administered intravenous insulin to 10 patients with panic disorder. All subjects developed hypoglycemia but no panic anxiety. They reported symptoms of adrenergic hyperactivity but differentiated them from spontaneous panic attacks.     

Sleep apnea and panic attacks

A survey of 301 sleep apnea patients demonstrated that obstructive sleep apnea may cause nocturnal panic attack symptoms. Sleep apnea should be considered in the differential diagnosis of nocturnal panic disorder.     

Sleep disorders and panic attacks

The aim of this work is to describe the clinical and polisomnographical characteristics of patients suffering prevailing night panic attacks. The most usual therapeutics are also briefly mentioned. The Polisomnography and especially the EGG are mentioned as the methods which allow the most accurate diagnosis since the night panic attack produces patognomonical disturbances.     

Salivary cortisol in panic attacks

OBJECTIVE: Documentation of hypothalamic-pituitary-adrenal (HPA) axis disturbance in panic disorder has been inconsistent. Increased cortisol levels have been associated with altered HPA function due to stress. The authors examined salivary cortisol levels in spontaneously occurring, unprovoked panic attacks. METHOD: Patients with panic disorder (N=25) collected saliva samples when panic attacks occurred. Levels of cortisol in the saliva samples were determined and were compared with levels in comparison samples of saliva obtained 24 hours after the panic attack occurred. RESULTS: During spontaneous panic attacks there was a subtle but significant elevation of cortisol levels, compared with levels obtained 24 hours later. No significant correlations were found between the cortisol elevations during panic attacks and the severity of the attack as measured by using the Acute Panic Inventory or the severity of illness as measured by using the Panic and Agoraphobia Scale. CONCLUSIONS: Saliva sampling may be a useful method for investigating neuroendocrine parameters during spontaneously occurring panic attacks.     

Infrequent and limited-symptom panic attacks

Due to their prevalence and relationship to agoraphobia, panic attacks are receiving considerable attention. The DSM-III requires that they include at least four associated symptoms and occur at least weekly for a diagnosis of panic disorder. This study of panic symptoms and frequency in 68 panic sufferers addresses the validity of these DSM-III requirements in terms of symptom patterns and phobic avoidance. Using chi-square, Fisher, and t-test analyses, this study found no clinical distinction between frequent (occurring at least weekly) and infrequent panic attacks. When comparing limited-symptom attacks (associated with less than four symptoms) with full-blown panic attacks, as expected, symptom frequencies were greater (p less than .05) in full-blown attacks, with the exceptions of feelings of unreality and fear of dying, going crazy, or losing control. Phobic avoidance did not differ between limited-symptom and full-blown attacks. This study not only demonstrates the arbitrary nature of the DSM-III requirements for a diagnosis of panic disorder but recognizes the importance of limited-symptom attacks to the development of agoraphobia.