Relationship between substance abuse and panic attacks

This study was done to determine the strength of association between substance abuse and panic states, including subsyndromal panic, its temporal relationship, and self-medication for panic using abusable substances. A community-based sample was screened for panic using DSM-III-R criteria. Panic and matched control groups participated in a structured interview concerning the presence of substance abuse, use of substances to treat panic symptoms, and the age-of-onset of panic and substance abuse. Of 97 individuals with panic, 39% had abused at least one substance. None of the panic disorder-subsyndromal panic differences reached significance. Only 10% of subjects reported using alcohol and 6% reported ever using illicit drugs to treat their panic. The majority (63%) of those abusing alcohol reported that alcohol use began prior to onset of panic, and the majority (59%) of those abusing illicit drugs reported that drug use began first. This study documents the panic-substance abuse relationship even in those with subsyndromal panic. Substance abuse began prior to onset of panic and substances were used to self-medicate for panic attacks by only a few subjects.     

The clinical spectrum of panic attacks

Current psychiatric nosologies associate recurrent panic attacks mainly with panic disorder, and agoraphobia with panic attacks, circumscribing their clinical relevance to the anxiety group of diagnosis. Through selected clinical presentations and a literature review the authors propose the existence of a cross-syndromal panic-anxiety represented by the recurrent panic attack that crosses the borders of any single group of diagnosis. This concept is of relevance for clinical psychiatry and may also constitute an important source of variance in psychiatric research.     

Nortriptyline in the treatment of panic disorder and agoraphobia with panic attacks

Thirty-four consecutive patients with panic disorder or agoraphobia with panic attacks were treated with nortriptyline at the LAC-USC Medical Center's Anxiety Disorders Clinic. Fourteen (67%) of the 21 completers totally lost their panic attacks, five (24%) showed partial improvement, and two (10%) showed no improvement. The relationship of treatment outcome to pretreatment and posttreatment measures of depression is discussed, in addition to the potential role of nortriptyline in treating panic attacks in clinical practice.     

Pentagastrin induced panic attacks: enhanced sensitivity in panic disorder patients

The effects of pentagastrin, a synthetic analogue of the cholecystokinin tetrapeptide (CCK₄), were studied in 15 patients with panic disorder and 15 healthy controls. Three different intravenous dosages of pentagastrin (0.1, 0.3 and 0.6 µg/kg) and saline were investigated. Subjects were randomly allocated to two of the four treatment groups and tested on two separate occasions, 1 week apart, using an unbalanced double-blind incomplete block design. The mean panic rate with pentagastrin was 55% (12/22) for patients and 5% (1/22) for controls. None of the subjects panicked with saline. The frequency of panic attacks between the three pentagastrin doses in patients was not different. One control subject had a panic-like attack at the highest dose of pentagastrin. These findings concur with previous studies on the panicogenic effect of CCK₄ and pentagastrin and suggest a greater sensitivity for CCK receptor agonists in patients suffering from panic disorder than in healthy controls.     

Alprazolam, propranolol, and placebo in the treatment of panic disorder and agoraphobia with panic attacks

Fifty-five patients completed a 5-week double-blind study comparing alprazolam, propranolol, and placebo in the treatment of panic disorder and agoraphobia with panic attacks. There was no concomitant behavioral treatment. Patient and therapist rating scales included Sheehan's Panic and Anxiety Attack Scales, the Marks-Sheehan Phobia Scale, the Hamilton Anxiety Scale, the Hamilton Depression Scale, and the Side Effects Checklist. The results generally support the efficacy of alprazolam, but not propranolol, in the treatment of panic disorder and agoraphobia with panic attacks. The significance of the results are discussed, as well as a number of the unique aspects of our procedures and patient population.     

The influence of panic attacks on response to phenelzine and amitriptyline in depressed outpatients

A total of 169 depressed outpatients completed a 6-week double-blind study designed to compare the relative efficacy of a tricyclic antidepressant (amitriptyline) with a monoamine oxidase inhibitor (phenelzine). Various "target" symptoms reported to predict preferential response to monoamine oxidase inhibitors were assessed. The major finding within the whole patient sample, based on results from serial self-report and interviewer-rated scales, was that phenelzine-treated patients showed greater improvements in anxiety symptoms than did patients treated with amitriptyline. Because of the heterogeneity of the sample, patients were classified into homogeneous subgroups of clinical interest. Data analyses of these subgroups detected important drug treatment differences not discernible by analysis of data from the overall sample. Panic attacks and corresponding anxiety symptoms were reported by about one third of the patients, more often by patients with major depression than with minor depression. Patients who reported "spells of terror or panic" responded preferentially to phenelzine on several measures, particularly on items measuring anxiety. Results suggest that phenelzine may be a preferred drug for treating depressed patients with panic attacks.     

Delayed increase in LDL cholesterol following pentagastrin-induced panic attacks

Objective Panic disorder (PD) has been associated with an increased risk for cardiovascular (CV) morbidity and mortality. There are inconsistent reports of increased low-density lipoprotein cholesterol (LDL-C) in patients with PD. Studies have reported a correlation between cholesterol levels and the intensity and frequency of panic attacks (PAs), suggesting that an elevation in cholesterol could be due to physiological and neurochemical changes that occur during and after a PA. The objective of our study was to show that the occurrence of a PA is associated with an increase in LDL-C. Materials and methods We used a double-blind, placebo-controlled crossover design with randomized injections of placebo and pentagastrin in 18 patients with PD (11 men, 7 women) and 33 healthy-control subjects (24 men, 9 women). Results Pentagastrin-induced PAs were associated with a statistically significant 10.4% delayed (24 h) increase in LDL-C levels in male subjects. Such an effect was not observed in female subjects. Conclusion LDL-C levels are directly affected by the occurrence of a PA in males. These findings, in association with previous reports of increased cholesterol levels in PD patients, suggest that a chronic increase in LDL-C as a result of frequent PAs may be one of the mechanisms that contributes, at least in male patients, to previously reported increased CV risk in patients with PD. The gender difference and the temporal association between PAs and increased LDL-C may explain the inconsistency in the findings of previous investigations of cholesterol levels in PD patients.     

Increased ACTH concentrations associated with cholecystokinin tetrapeptide-induced panic attacks in patients with panic disorder.

Preclinical findings on the role of corticotropin releasing hormone (CRH) in stress and anxiety, on the interaction of CRH and cholecystokinin (CCK) in modulating anxiety, as well as the blunted corticotropin (ACTH) response to CRH in panic disorder suggest that CRH may play a role in panic disorder. To further characterize the role of the hypothalamic-pituitary-adrenocortical (HPA) system in panic disorder, we compared patients with and without CCK tetrapeptide (CCK-4) induced panic attacks. Twenty-four patients with panic disorder were given injections of CCK-4 (25 micrograms). Panic attacks, psychopathological changes, as well as ACTH and cortisol secretion were recorded. Fifteen of the 24 patients experienced a panic attack after CCK-4. ACTH secretion was significantly higher in the patients with CCK-4-induced panic attacks than in those without such attacks. The patients without CCK-4-induced attacks had a brief but less pronounced increase in ACTH concentrations. Cortisol concentrations were not significantly increased after CCK-4 administration. The increased ACTH concentrations suggest that the activation of the HPA system in CCK-4-induced panic attacks plays a physiological role. CRH may be involved in experimentally-occurring and perhaps in naturally-occurring panic attacks as well.     

Substance use and non-clinical panic attacks in a young adult sample

This study examines panic attacks and substance use in a non-clinical, young adult sample. Two hundred seventy-nine college students completed questionnaires that assessed non-clinical panic attacks, alcohol and drug use behavior, and anxiety and depression symptoms. Non-clinical panickers (n = 25) were significantly more likely than non-panickers (N = 222) to report using sedatives, but not alcohol, cocaine, stimulants, or other drugs. Among non-clinical panickers, sedative use was not associated with distress about panic attacks, panic attack frequency, the occurrence of unexpected attacks, or general anxiety or depression symptoms. Coping-motivated alcohol use, though not associated with non-clinical panic, was significantly associated with anxiety and depression symptoms. These results are discussed in terms of theories of the co-morbidity between substance use and panic disorder.     

The relationship between the chemical structure and neurotoxicity of alkyl organophosphorus compounds

Thirty-six alkyl organophosphorus compounds have been tested for neurotoxicity in the chicken. The individual compounds were chosen to enable the importance of each portion of the molecule to be assessed in relation to the property of neurotoxicity. Seventeen substances were found to be neurotoxic, fifteen for the first time. All of these contained fluorine. On the basis of the results reported, certain predictions have been made about the chemical structure of compounds which would be expected to be neurotoxic. The importance of fluorine suggests that it plays a direct role in the development of the biochemical lesion, and this may occur as the result of its being carried by the molecule as a whole to specific areas in the nervous system. By the action of cholinesterase, the P-F bond may be ruptured and ionic fluorine liberated where it blocks some metabolic cycle.