A comparison of panic disorder and agoraphobia with panic attacks.
Explore the source record for details and available documents.
Adult↗
Biomedical subjects
O G Cameron
Publications and source records attributed to O G Cameron.
The daily distribution of panic attacks.
Explore the source record for details and available documents.
Adolescent↗
The effect of elevated systemic cortisol levels on plasma catecholamines in Cushing's syndrome patients with and without depressed mood.
This study explored the effect of elevated systemic cortisol levels on plasma epinephrine and norepinephrine, and hemodynamic variables, in patients with active Cushing's syndrome; ratings of depressed mood were also obtained. Norepinephrine levels were significantly negatively correlated with 24 h urinary free cortisol levels. Cushing's patients without depressed mood showed more robust negative correlations than those with depressed mood. The inverse relationship between norepinephrine and cortisol is consistent with data obtained previously in acute studies of normal subjects. Mechanisms which might explain these relationships include changes in control of catecholamine production, release, and or metabolic clearance in Cushing's patients. The decrease in the strength of association in depressed Cushing's patients is consistent with prior studies that suggest abnormal relationships between hypothalamic-pituitary-adrenocortical activity and noradrenergic function in major depressive disorder.
Adult↗
Hypothalamic-pituitary-adrenal axis activity in panic disorder: effects of alprazolam on 24 h secretion of adrenocorticotropin and cortisol.
Pre-clinical and some clinical evidence suggests that central overdrive within the hypothalamic-pituitary-adrenal (HPA) axis may play a role in panic disorder, and that the anti-panic efficacy of alprazolam may involve its ability to inhibit this drive. Detailed examination of 24 h secretion of adrenocorticotropin (ACTH) and cortisol in 20 panic patients had revealed subtle HPA axis abnormalities prior to treatment. In order to determine whether these abnormalities resolve with alprazolam therapy, these patients were re-studied over a full circadian cycle after 12 weeks on alprazolam. Alprazolam produced substantial improvement in clinical status which was accompanied by nearly full resolution of pre-treatment hypercortisolemia. The impact of treatment on ACTH was more complex and influenced by symptom severity. The results are consistent with the hypotheses that HPA axis regulation is subtly disturbed in panic disorder and that impact on the HPA axis may play a role in alprazolam's mechanism of efficacy.
Adrenocorticotropic Hormone↗
Circadian symptom fluctuations in people with anxiety disorders.
Circadian rhythm abnormalities have been demonstrated in people with depression, including a tendency toward maximal symptom severity in the morning. Although a few studies have suggested that symptoms in people with anxiety are worse later in the day, no detailed study of this observation has been reported. In 86 patients with anxiety disorders (63 with panic disorder or agoraphobia with panic attacks), anxiety symptoms tended to be more severe in the afternoon or evening than in the morning, with no abnormalities of heart rate or oral temperature. This is the first systematic demonstration of a circadian fluctuation of mood in any disorder other than depression.
Adult↗
Menstrual fluctuation in the symptoms of panic anxiety.
Ten women with DSM-III-defined panic attacks (five with and five without agoraphobia) had symptom severity rated daily, weekly, and retrospectively through one full menstrual cycle. Substantial fluctuations in retrospective ratings of severity were observed, with the premenstrual week being rated as most severe. Daily and weekly ratings showed much smaller fluctuations in the predicted direction. Possible reasons for this outcome are considered.
Adult↗
Medial frontal cortex involvement in PTSD symptoms: a SPECT study.
The regional cerebral blood flow (rCBF) responses to a combat stress-related auditory stimulus was examined in Vietnam veterans diagnosed with posttraumatic stress disorder (PTSD). Based on prior data in healthy subjects, we hypothesized that the medial prefrontal cortex may be involved in the processing of stress responses. Twelve male veterans diagnosed with PTSD, 11 age-matched, combat-exposed subjects without PTSD, and 12 healthy control subjects were studied with single-photon emission tomography and the blood flow tracer [99mTc]-HMPAO. Subjects were studied twice, while listening to combat sounds or white noise. Significant increases in the blood flow to the medial prefrontal cortex were observed in PTSD patients, but not in the control groups, which correlated at trend levels with psychophysical measures of stress response. These data support the involvement of the medial prefrontal cortex in the pathophysiology of PTSD, possibly mediating some of its symptoms.
Acoustic Stimulation↗
Beta-adrenergic blockade does not prevent hypoglycemia awareness in non-diabetic humans.
This study's purpose was to test whether beta-adrenergic blockade reduces awareness of hypoglycemia. Six non-diabetic human adults received six experimental sessions each, one with each combination of intravenous propranolol (0.0, 0.05, and 0.15 mg/kg) followed by intravenous regular insulin (2 and 4 units). Physiological, biochemical, and symptom variables, and choice (was an active or an inactive substance administered?) were measured at 15, 30, and 45 min after insulin. Insulin dose and time after insulin administration significantly influenced choice, but propranolol did not significantly influence choice. Adrenergic symptoms were not prominent. These results may or may not apply to individuals with disorders of adrenergic function such as diabetic autonomic neuropathy.
Adult↗
Peripheral catecholamine levels and the symptoms of anxiety: studies in patients with and without pheochromocytoma.
We studied the correlation of plasma and urinary epinephrine (E) and norepinephrine (NE) levels with anxiety symptoms in three patient groups: 1) pheochromocytoma (PH+) (n = 17); 2) hypertensives with elevated catecholamine levels shown not to have a PH (PH-) (n = 25); and 3) patients with panic disorder (PD) (n = 23). Structured interviews and four self-rated anxiety scales were used: the SCL-90R Anxiety and Phobic Anxiety scales, and the Spielberger State/Trait Anxiety Inventories. The SCL-90R Somatization scale (which measures 12 somatic symptoms) was also utilized. None of the PH+ patients met DSM-III criteria for PD. Two met criteria for generalized anxiety disorder (GAD). Of the PH- patients, two had PD, two had GAD, and three had both. Urinary and plasma E did not show significant positive correlations with any of the four anxiety scales in any of the three patient groups. In both the PH+ and PH- groups, E was significantly correlated with the SCL-90R Somatization scale. NE was not significantly correlated with any of the four anxiety scales in the PH+ group. In contrast, in the PH- group, plasma NE was significantly correlated with anxiety on all anxiety scales (r = +0.55 to +0.77, p less than 0.05). Furthermore, in the PH- group, plasma NE was significantly correlated with those items of the SCL-90R Anxiety scale measuring the cognitive rather than the noncognitive symptoms of anxiety. In the PD group as well, plasma NE showed a significant correlation with the SCL-90R Anxiety Scale (r = +0.67, p less than 0.05). Taken together, our observations suggest that: 1) the effects of catecholamines in the periphery derived from a source independent of nervous system control (such as a PH) are not sufficient to elicit an anxiety disorder meeting DSM-III criteria; and 2) in patients without an autonomous source of peripheral catecholamines, NE in the periphery results from sympathetic nervous system activation and probably reflects, rather than causes, anxiety.
Adrenal Gland Neoplasms↗
Venous plasma epinephrine levels and the symptoms of stress.
It is widely believed that increases in circulating epinephrine (adrenaline) levels contribute substantially to the physical sensations (symptoms) associated with stress. Using a drug discrimination choice procedure, it was demonstrated that the plasma epinephrine levels at which healthy human subjects reliably discriminate between infusions of epinephrine and saline are higher than the levels typically observed in situations of mental stress. Choice of epinephrine versus saline was strongly associated with a subjective perception of a change in the action of the heart, but only moderately associated with the venous plasma epinephrine levels attained and only weakly associated with actual changes in heart rate and peripheral blood pressure. These results imply that epinephrine release from the adrenal gland plays at most a small role in the production of the somatic symptoms of mental stress.
Adult↗
Platelet alpha 2-adrenoreceptors, catecholamines, hemodynamic variables, and anxiety in panic patients and their asymptomatic relatives.
The objectives of this study were to a) replicate our prior finding of a decreased number (Bmax) of platelet alpha 2-adrenoreceptors in panic disorder, b) determine if binding is also decreased in asymptomatic first-degree relatives of panic patients (known to be at increased risk for developing panic), and c) evaluate the effect of treatment on the presumptive decrease in binding (i.e., is the decrease a state or a trait marker for panic?). Panic patients had clonidine and yohimbine platelet-binding assays, symptom ratings, and measurement of lying and standing plasma epinephrine, norepinephrine, systolic and diastolic blood pressure, and heart rate before treatment, after approximately 2 months of medication (fluoxetine, tricyclics, or alprazolam) and/or cognitive behavioral treatment, and after symptom remission while drug free; normal subjects had determinations of the same measures at approximately the same time intervals. Relatives of both groups had one determination only of all measures. Tritiated clonidine binding was decreased and lying heart rate was increased in patients before treatment. Magnitude of binding decrease was correlated with symptom severity and standing norepinephrine. No binding abnormality was seen in first-degree relatives of patients. Treatment increased clonidine binding in patients. Both patients and relatives of patients showed significantly increased standing plasma norepinephrine in comparison to controls. There is a state-related decrease in binding, associated with symptom severity and norepinephrine, in panic disorder. Abnormal reactivity of norepinephrine to standing might be a marker for increased likelihood of panic development in individuals at risk.
Adult↗
Effects of yohimbine on cerebral blood flow, symptoms, and physiological functions in humans.
OBJECTIVE: Increases in adrenergic activity are associated with stress, anxiety, and other psychiatric, neurological, and medical disorders. To improve understanding of normal CNS adrenergic function, CBF responses to adrenergic stimulation were determined. METHODS: Using PET, the CBF changes after intravenous yohimbine, an alpha2-adrenoreceptor antagonist that produces adrenergic activation, were compared with placebo in nine healthy humans. Heart rate, blood pressure, Paco2, plasma catecholamines, and symptom responses were also determined. RESULTS: Among nonscan variables, yohimbine produced significant symptom increases (including a panic attack in one subject), a decrease in Paco2 due to hyperventilation, increases in systolic and diastolic blood pressure, and a trend toward a significant norepinephrine increase. Among scan results, yohimbine produced a significant decrease in whole-brain absolute CBF; regional decreases were greatest in cortical areas. Medial frontal cortex, thalamus, insular cortex, and cerebellum showed significant increases after normalization to whole brain. Medial frontal CBF change was correlated with increases in anxiety. A panic attack produced an increase instead of a decrease in whole-brain CBF. Factors potentially contributing to the observed CBF changes were critically reviewed. Specific regional increases were most likely due in large part to activation produced by adrenergically induced anxiety and visceral symptoms. CONCLUSIONS: This study supports the relationship of anxiety and interoceptive processes with medial frontal, insular, and thalamic activation and provides a baseline for comparison of normal yohimbine-induced CNS adrenergic activation, adrenergically-based symptoms, and other markers of adrenergic function to stress, emotion, and the adrenergic pathophysiologies of various CNS-related disorders.
Adrenergic alpha-Antagonists↗
Interoception: the inside story--a model for psychosomatic processes.
OBJECTIVE: To comprehend psychosomatic processes, it will be necessary to understand the brain's influences on bodily functions and also the body's afferent sensory input to the central nervous system, including the effects of this input on behavior and cognitive functions, especially emotion. The objective of this Presidential Address is to review what is known circa the year 2000 of the processes and mechanisms of visceral sensory psychobiology, often called interoception. METHODS: Over 1000 publications that have appeared since the 19th century were reviewed to prepare this review, including a group that are specifically cited here. RESULTS: Factors and data were reviewed that were identified as germane to understanding interoception. These included definitional issues, historical roots, the neural basis, studies and results in the cardiovascular-respiratory and alimentary-gastrointestinal systems, studies of emotion, and studies in people with mental disorders. Drug and hormone effects, pain, proprioception, and phantom limb or organ factors, and the role of awareness were briefly described. Methodological issues, methods of study including functional imaging, and possible future directions for study were identified. CONCLUSIONS: Understanding the physical basis of psychosomatic processes, including the so-called mind-body problem, will require a detailed understanding the psychobiology of interoception.
Brain↗
Effects of ACTH and prednisone on mood: incidence and time of onset.
Prior studies of mood and cognitive changes produced by ACTH and glucocorticoids have not characterized accurately the incidence or time of onset of these changes. In this study mood and cognitive reactions of fifteen medical patients treated with ACTH or prednisone were studied prospectively. ACTH produced a lessening of dysphoria by the third treatment day, and mild euphoric reactions occurred in three of seven of the patients treated. Prednisone produced a reduction of dysphoria by the seventh day, but no euphoric reactions in the eight patients treated with it. Neither medical symptom improvement nor elevation of plasma cortisol levels in the patients given ACTH appeared to account for the results. The mechanism of the observed mood change remains to be elucidated.
Adrenocorticotropic Hormone↗
Anxiety, type A behavior, and cardiovascular disease.
Males with anxiety disorders appear to have increased mortality due to circulatory system disease, and Type A behavior is a risk factor for coronary heart disease (CHD). Thus, we determined Type A behavior in anxious patients. Fifty-seven DSM-III defined anxiety disorder patients completed the Jenkins Activity Survey (JAS) and Symptom Checklist-90-Revised (SCL-90-R). Significantly more male (92%) than female (52%) anxious patients had Type A behavior. Correlations between the JAS scales and SCL-90-R subscales were also different between male and female patients; in males, significant correlations were observed for SCL-90-R anxiety with both JAS Type A and JAS Hard-Driving and Competitive, and for SCL-90-R hostility with JAS Hard-Driving and Competitive. However, there were no consistent correlations between the JAS and the SCL-90-R subscales in females. A trend for fathers of anxious patients to have an increased prevalence of CHD was also observed. The increased incidence of Type A behavior in male, but not in female, anxious patients suggest a mechanism for increased mortality due to circulatory disease in male anxiety patients.
Adult↗
Hypercortisolism in diabetes mellitus.
Explore the source record for details and available documents.
Adrenocortical Hyperfunction↗