Biomedical subjects
O G Cameron
Publications and source records attributed to O G Cameron.
The differential diagnosis of anxiety. Psychiatric and medical disorders.
This article has reviewed clinical and demographic features of the primary anxiety disorders and other psychiatric and medical disorders that often are associated with anxiety symptoms, highlighting differential diagnosis. In summary, phobic disorders (exogenous anxiety) are characterized by anxiety reliably elicited by specific environmental stimuli; the stimuli involved determine which type of phobia is diagnosed. In contrast, panic attacks and generalized anxiety (endogenous anxiety) involve symptoms of anxiety not associated only with specific eliciting stimuli. Panic disorder is differentiated from generalized anxiety disorder by the presence of discrete attacks; both disorders usually have some level of persistent anxiety. Obsessive-compulsive disorder is characterized by recurrent unwanted but irresistible thoughts and the ritualized repetitive acts resulting from these obsessions, in the absence of preexisting psychosis or depression. Finally, posttraumatic stress disorder involves various anxiety (and other) symptoms as a direct result of an obvious stressor. Depressive symptoms are frequently associated with anxiety. It is sometimes impossible to determine which is the primary disorder. Overlap of syndromes probably also occurs with other primary psychiatric disorders, especially somatoform disorders, adjustment disorder with anxious mood, and several personality disorders. Finally, primary anxiety can be confused with several medical syndromes, especially when the medical disorder has not been recognized. Nevertheless, research with patients with pheochromocytoma suggests that medical causes of anxiety may be qualitatively different from primary anxiety disorders, especially the psychic anxiety component. Attention to the clinical and demographic features listed in Table 4, as well as the use of newly-developed structured diagnostic interviews should usually lead to a correct diagnosis, as illustrated by the following examples. The onset of a fear of public speaking in mid-adolescence suggests an uncomplicated social phobia, whereas the onset in the mid-twenties of several social and other situational anxieties in a person with a previous history of panic attacks would be strongly suggestive of the panic-agoraphobia syndrome. The new onset of generalized anxiety symptoms and depression in a 45-year-old patient who has had a previous significant depression would suggest that this person's anxiety is part of, and secondary to, the affective disorder and not a primary anxiety disorder.(ABSTRACT TRUNCATED AT 400 WORDS)
Anxiety in patients with pheochromocytomas.
Anxiety has been considered an important clinical feature of patients with pheochromocytomas. We studied 17 patients with active pheochromocytoma to determine whether they experienced anxiety that met criteria of the Diagnostic and Statistical Manual of Mental Disorders, third edition, for either panic disorder or generalized anxiety disorder. Fifty-two patients with primary anxiety disorders were used as a comparison group. Six patients with pheochromocytomas had norepinephrine-secreting tumors and 11 had mixed-secretion tumors, with elevated levels of both epinephrine and norepinephrine. None of the 17 patients described the severe apprehension or fear characteristic of panic attacks and none described agoraphobia. One patient received a diagnosis of possible panic disorder, two met criteria for generalized anxiety disorder, and two met criteria for major depressive episode. Thus, the elevated levels of catecholamines secreted by pheochromocytomas are not sufficient to elicit an anxiety disorder.
Treatment of pavor nocturnus with alprazolam.
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Hypothalamic-pituitary-adrenocortical activity in patients with diabetes mellitus.
Several clinical and physiologic associations between depression and diabetes mellitus have been reported. In this study, a potential neuroendocrine association was studied by measuring hypothalamic-pituitary-adrenocortical (HPA) axis activity in patients with diabetes mellitus. Plasma cortisol levels and response to dexamethasone administration were determined in 54 diabetics. Twenty-three (55%) of forty-two 1-mg dexamethasone suppression tests (DSTs) performed in 34 subjects, with eight repeated tests, and two (10%) of twenty 2-mg DSTs demonstrated a blunting of normal suppression. None of a variety of potential demographic, physiologic, or mood factors predicted nonsuppression. This study replicates prior findings that HPA dysfunction occurs in association with diabetes, and invalidates the use of the 1-mg DST as a diagnostic marker for melancholia in patients with diabetes.
Adrenergic function in patients with panic anxiety.
Increased beta-adrenergic receptor sensitivity could account for many aspects of panic disorder. We tested this hypothesis by comparing 14 patients with six normal control subjects. The controls and eight patients had 14 blood samples taken, and heart rate and BP measured, during a four-hour protocol that included supine rest, a posture and isometric exercise stimulus, and a series of up to seven logarithmically increasing bolus intravenous doses of isoproterenol hydrochloride. The other six patients were studied only at rest. Patients had markedly elevated resting heart rate, substantially elevated levels of plasma epinephrine, cortisol, and growth hormone, mildly elevated plasma norepinephrine levels, and decreased heart rate responses to isoproterenol. These results suggest that beta-adrenergic receptor response is not increased, and may be decreased, in patients with panic disorder. Receptor down-regulation could result from the increased adrenergic function that these patients demonstrate, even in the absence of panic attacks.
Platelet alpha 2-adrenergic receptor binding and plasma catecholamines. Before and during imipramine treatment in patients with panic anxiety.
Specific binding of tritiated clonidine, an alpha 2-adrenergic receptor agonist, and tritiated yohimbine, an alpha 2-adrenergic receptor antagonist, to platelet membranes was measured in persons with panic attacks or major depression and in normal subjects. Plasma catecholamine levels were measured in patients with panic attacks and in normal subjects. The number of binding sites in patients with panic attacks, as measured with tritiated clonidine, was lower than in depressed persons and was the same as in normal subjects. The number in patients with panic attacks, as measured with tritiated yohimbine, was lower than in either depressives or normal subjects. Catecholamine levels were somewhat higher in patients with panic attacks than in normal subjects. Treatment with imipramine hydrochloride decreased the number of sites, as measured with either ligand, in both patient groups and increased catecholamine levels in patients with panic attacks.
The dexamethasone suppression test in panic disorder and agoraphobia.
Reports that imipramine and phenelzine prevent panic attacks in agoraphobia suggest the possibility that agoraphobia and/or panic disorder might be a clinical manifestation of underlying depression. To test this hypothesis, dexamethasone suppression tests (DSTs) were performed in 10 patients meeting DSM-III criteria for agoraphobia with panic attacks, 6 for panic disorder, and 4 whose diagnosis could have been either panic disorder or agoraphobia except that another axis I disorder precluded such a diagnosis. Abnormal DSTs were observed in only 3 patients and appeared to be attributable to causes other than panic attacks or agoraphobia. The results suggest that panic attacks and endogenous depression are separate disorders and that the antipanic properties of imipramine and phenelzine are separate from their antidepressant actions.
Clinical response to clonidine and imipramine, and platelet alpha 2-adrenoreceptors in a case of agoraphobia with panic attacks.
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Lithium carbonate treatment of mania associated with Klinefelter's syndrome.
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Comparison of acute and chronic lithium treatment on 3H-norepinephrine uptake by rat brain slices.
The effects of lithium chloride, given IP in high (2.5-15 mEq/kg) and low (1.25 mEq/kg) doses twice daily, upon 3H-norepinephrine uptake and retention were examined with slices from four regions of the rat brain, namely brain stem, hypothalamus, parietal cortex, and caudate nucleus. Control uptake was significantly higher in slices from the caudate nucleus and lower in brain stem slices than in slices from hypothalamus or parietal cortex. With the higher doses, uptake increased significantly in all regions after 2 days of treatment and returned to normal by 7 days. With the lowest dose, uptake was increased after 7 days but normal at 14 days. Only in caudate slices was there a second elevation of 3H-norepinephrine uptake after 21 days of treatment, which returned to normal by 42 days. No other effects were observed during 70 days of treatment with lithium. The correlation between changes in 3H-norepinephrine uptake and plasma lithium levels was studied.
An anticholinergic toxicity reaction to chlorpromazine activated by psychological stress.
A 42-year-old woman with a long-standing diagnosis of schizophrenia experienced two toxic reactions to 1200 mg of chlorpromazine while awaiting surgery for a locally metastatic carcinoma of the cervix. These reactions, which involved fever, increased pulse and respirations, and acute onset of obtundation, and which cleared after several hours, were produced by a medication and dose which had been well tolerated prior to the preoperative period. These reactions, typical of an acute anticholinergic syndrome, were precipitated by an interaction of the drug and a stress-induced change in her psychological state, due to anxiety about her cancer and impending surgery. This type of reaction has not been reported previously in a clinical setting.
Safe use of haloperidol in a patient with cardiac dysrhythmia.
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Drug-induced conditioned suppression: specificity due to drug employed as UCS.
The classical conditioning potential of several drugs was tested in rats by pairing a light CS with the drug UCSs; these stimuli were superimposed in a variable-interval 30 sec schedule for water reinforcement. Conditioning (suppression of bar-pressing in the presence of the CS) was definitely demonstrated with psilocybin (2.0 mg/kg), was suggested but not clearly shown with LSD (0.13 MG/kg), and was not evident with methyl atropine nitrate (50 mg/kg) or pentobarbital (25 mg/kg). These results indicate that previously demonstrated drug-induced conditioned suppression is not a nonspecific effect of unconditioned suppression but depends on the type of drug employed.
Letter: Children's behavior under stimulant drugs.
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A behavioral and pharmacological analysis of some discriminable properties of d-LSD in rats.
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Conditioned suppression of bar-pressing behavior by stimuli associated with drugs.
Ten naive male albino rats were trained to press a bar under a variable-interval 30-sec schedule with water as the reinforcer in two experiments. This behavior was disrupted by chlorpromazine in Experiment I (two rats) and by lysergic acid diethylamide (LSD) in both Experiment I (two rats) and Experiment II (six rats). The administration of the drug was paired with an originally neutral white light. After several pairings with either drug, the light also depressed behavior. When the light was no longer paired with drug, the depression effect extinguished much faster than is usually observed in conditioned suppression studies.
Ages of onset of DSM-III anxiety disorders.
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