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Biomedical subjects

G C Curtis

Publications and source records attributed to G C Curtis.

At least 37 records · Page 2Linked to original sources
PubMed1993

Maintenance drug therapy of panic disorder.

The efficacy of tricyclics and benzodiazepines in the short term (approximately 2-4 months) treatment of panic disorder is well demonstrated, but efficacy over the longer term is not considered established. The present study provided systematic data from a double blind comparison of maintenance therapy (up to 8 months) of panic disorder with or without agoraphobia with alprazolam, imipramine, or placebo in 181 patients who had responded to the same regimen in a randomized 8-week treatment trial. All three groups had improved during the first 2 months (active treatments more than placebo and about equal to each other), and all maintained or extended their improvement over the next 6 months without any significant change in dose. More than twice as many alprazolam and imipramine than placebo patients (15%) remained in treatment for the full 8 months and did slightly better on symptom measures than the remaining placebo patients. Both medications were well tolerated during the maintenance period. The data suggest sustained efficacy and safety of imipramine and alprazolam over an extended period. More specifically, they suggest that tolerance does not develop to the therapeutic effects of either drug.

Agoraphobia↗
PubMed1992

Endocrine, cardiovascular, and behavioral responses to clonidine in patients with panic disorder.

We examined adrenergic regulation in patients with panic disorder by challenging 10 patients and 14 age-matched and sex-matched controls with intravenous infusions of clonidine hydrochloride (2 micrograms/kg), an alpha 2-adrenoreceptor agonist. Growth hormone, 3-methoxy-4-hydroxyphenylglycol (MHPG), blood pressure, heart rate, and behavioral (anxiety, sedation) responses were monitored. The data replicated the previously reported finding of blunted growth hormone (GH) responses to clonidine in patients with panic disorder. Reported abnormalities in MHPG, cardiovascular, and behavioral responses of panic patients to clonidine infusion were not replicated. The robustly blunted GH response to clonidine in panic patients supports the adrenergic dysregulation hypothesis of panic disorder, but alternative interpretations of this finding are available and further study is needed.

Adrenergic Fibers↗
PubMed1991

Blunted growth hormone response to clonidine in patients with generalized anxiety disorder.

Patients with panic disorder or depression have abnormal responses to the alpha 2-adrenergic receptor partial agonist clonidine. Evidence linking anxiety to noradrenergic dysfunction and the presence of anxiety symptoms in both depression and panic suggest that abnormal responses to clonidine in these disorders could be due to the anxiety symptoms. To explore a possible link between "nonspecific" anxiety symptoms and abnormal responses to clonidine, patients with DSM-III-defined generalized anxiety disorder were given intravenous infusions of clonidine hydrochloride. Responses of plasma growth hormone, 3-methoxy-4-hydroxyphenylglycol, heart rate, blood pressure, and psychological states were determined in 11 patients with generalized anxiety disorder and 14 healthy subjects. Clonidine produced significantly smaller growth hormone responses in patients than in healthy controls. The two groups did not differ in 3-methoxy-4-hydroxyphenylglycol, heart rate, blood pressure, or psychological responses to clonidine. These results are compared with data from similar studies on patients with panic disorder and depression. The blunting of the growth hormone response to clonidine in all three disorders could be due to the presence of generalized anxiety symptoms. Subsensitivity of postsynaptic alpha 2-adrenoreceptors may be present in all three disorders; however, there are alternative interpretations of growth hormone blunting in response to clonidine. Blunting was observed in DSM-III-defined generalized anxiety disorder, whether or not the DSM-III-R criterion of excessive worry was also present.

Adult↗
PubMed1991

Mode of onset of simple phobia subtypes: further evidence of heterogeneity.

Previous research has demonstrated heterogeneity of the simple phobia diagnostic category. As a further test of the notion of heterogeneity of the DSM-III-R simple phobia diagnostic category, mode of onset was examined in a sample of simple phobic outpatients. Patients were separated into one of four subtypes: animal or insect, blood and injury, situational, and choking-vomit phobias. Careful study yielded five distinct mode-of-onset categories. Two researchers independently determined the mode of onset for the patients studied: direct trauma, spontaneous, vicarious learning, gradual, and lifelong. Significant mode of onset differences were observed across groups. Situational phobics reported a preponderance of spontaneous onsets as compared to the other groups studied. These results offer further evidence of the heterogeneity of the simple phobia diagnostic category and also support the contention that situational simple phobias are closely related to agoraphobia.

Adolescent↗
PubMed1990

Adrenergic status in anxiety disorders: platelet alpha 2-adrenergic receptor binding, blood pressure, pulse, and plasma catecholamines in panic and generalized anxiety disorder patients and in normal subjects.

In order to evaluate adrenergic function in anxiety disorders, platelet alpha 2-adrenergic binding parameters and supine and standing blood pressure, pulse, and venous plasma epinephrine and norepinephrine were determined in patients with panic attacks or generalized anxiety disorder and in normal subjects. The maximum number of binding sites (Bmax) for the partial agonist tritiated clonidine was significantly lower for both patient groups than for normal subjects, and the Bmax for the antagonist tritiated yohimbine was significantly lower for panic patients. There were no other substantive differences across groups. Prior exposure to psychotropic drugs might account for the results for clonidine binding, but not for yohimbine. The Bmax for clonidine was correlated with norepinephrine increases upon standing and, for panic patients, with the severity of full unexpected panic attacks. These data provide further evidence of adrenergic receptor abnormalities in people with anxiety disorders.

Adult↗
PubMed1990

Alpha 2-adrenoreceptor status in obsessive-compulsive disorder.

Ten patients with obsessive-compulsive disorder (OCD) and 13 normal control subjects received intravenous infusions of 2 X 10(-6) g/kg of clonidine and normal saline on separate days. Responses to the drug relating to plasma growth hormone (GH), 3-methoxy-4-hydroxyphenylglycol (MHPG), heart rate, blood pressure, and several symptoms were determined. Additionally, platelet alpha 2-adrenoreceptor binding was measured in most of the subjects. GH, MHPG, blood pressure, and heart rate responses to clonidine did not differ between groups. As expected, patients reported more symptoms than normal subjects, and clonidine was sedating for both groups. Patients did not differ from normal subjects in the symptom response to clonidine. The maximum number of binding sites (Bmax) for tritiated clonidine was significantly greater in OCD patients than in normals. This pattern of alpha 2-adrenoreceptor status is different than the patterns in major depression and panic anxiety.

Adult↗
PubMed1989

Positron emission tomographic evaluation of cerebral blood flow during state anxiety in simple phobia.

The present study was undertaken to clarify some of the conflicting findings of previous reports on the effect of state anxiety on cerebral blood flow (CBF). Seven subjects with simple phobia of small animals were studied to permit the generation of wide ranges of anxiety. Each subject received five positron emission tomography (PET) scans in a rest-fear-rest-fear-rest, repeated-measures paradigm. A population of eight normal controls was employed. The phobic stimuli produced significant increases in state anxiety during fear and significant differences in physiologic measurements between the fear and rest scans. Absolute global and regional CBF was significantly lower during fear scans than during rest scans; however, when hypocapnia resulting from anxiety-induced hyperventilation was taken into account, the pattern vanished, and all global and regional CBF differences among scans became not significant. Resting global and regional CBF values in the phobic subjects did not significantly differ from those of the normal controls. That a relationship between anxiety and CBF was not found in 35 scans among seven subjects strongly suggests that CBF changes induced by state anxiety are either not presently measurable by PET techniques or that such a relationship may not exist. These findings should also reduce concerns that subject anxiety may confound CBF measurements during routine PET scanning.

Anxiety Disorders↗
PubMed1989

Cardiac and neuroendocrine responses to exposure therapy in height phobics: desynchrony within the 'physiological response system'.

Subjective, behavioral, cardiovascular and neuroendocrine responses were intensively monitored in two height phobics over a full course of exposure therapy and at follow-up. Both subjects showed rising cortisol responses and stable, non-extinguishing norepinephrine responses to height exposure over the course of treatment, while improvement occurred in subjective and behavioral response systems. They had differing heart rate responses. Despite desynchrony amongst anxiety response systems and within the physiological 'system' at treatment conclusion, both subjects had successful outcomes which were preserved at follow-up. Implications for the measurement of the 'physiological response system' in behavioral research are discussed.

Adult↗
PubMed1989

Simple phobia: evidence for heterogeneity.

Although simple phobia is a residual category in DSM-III, clinical experience suggests at least four subtypes of this group. To test the validity of the subtypes, the authors compared patients with one of four simple phobias subtypes (n: animal-insect = 25, blood-injury = 9, situational = 46, choking-vomit = 8). Significant sex differences were observed; all animal and insect phobics and seven of eight choking-vomit phobics were female, while the other two groups showed approximately equal numbers of males and females. Mean age of onset was significantly older for situational phobics than animal-insect or blood-injury phobics; choking-vomit probands were intermediate. Frequency of situational phobias differed significantly among relatives of the four proband groups, with highest frequency being found among situational probands. Thus, these clinical and epidemiological variables support the separation of simple phobia into at least these four diagnostic groups.

Adult↗
PubMed1989

Neurophysiologic dysfunction in basal ganglia/limbic striatal and thalamocortical circuits as a pathogenetic mechanism of obsessive-compulsive disorder.

This article is intended to elucidate some of the neuropathogenetic mechanisms possibly operative in obsessive-compulsive disorder (OCD). Relevant literature is reviewed, with attention to psychologic, and pathologic considerations. Anatomy, neurochemistry, and known functional associations with neuropathological and behavioral abnormalities of implicated brain regions are discussed. The authors propose that dysfunction of neuronal circuits interconnecting the orbitofrontal cortex, basal ganglia/limbic striatum, and thalamus serves a critical role in the pathogenesis of OCD and that obsessive-compulsive symptoms occur when an aberrant positive feedback loop develops in the reciprocally excitatory frontothalamic neuronal interchange, which is inadequately integrated or inhibited by the ventromedial (limbic) portions of the striatum; the ventromedial striatum may serve to modulate activity in the frontothalamic circuit through a negative feedback loop.

Antidepressive Agents, Tricyclic↗
PubMed1989

Free 3-methoxy-4-hydroxyphenylglycol determined in plasma by liquid chromatography with coulometric detection.

We describe a simple "high-performance" liquid-chromatographic method for determining free 3-methoxy-4-hydroxyphenylglycol (MHPG) in plasma, with coulometric detection and with 4-methoxy-3-hydroxyphenylglycol (iso-MHPG) as the internal standard. MHPG and iso-MHPG are extracted from plasma into ethyl acetate and the extract is washed with a sodium bicarbonate solution, evaporated, reconstituted, and injected into a 25 x 0.4 cm column packed with 3-micron particles of C18 material. We used a mobile phase of acetate buffer (100 mmol/L, pH 5.0) and methanol (92:8 by vol) and an oxidation voltage of 0.5 V. The detection limit of the assay is 0.1 micrograms/L. The interassay CV for a sample with a mean MHPG concentration of 3.84 micrograms/L was 5.2%. The average absolute recovery for the method was 37%.

Adult↗
PubMed1988

Neuroendocrine findings in anxiety disorders.

Anxiety disorders are newly defined syndromes in which inappropriate state anxiety is the sole or primary symptom. Hormonal manifestations of acute stress are usually minimal or absent in these disorders. A number of findings suggest receptor downregulation or enzyme induction of sorts that would be expected to mute or dampen these responses.

Adrenocorticotropic Hormone↗
PubMed1988

Neuroendocrine findings in anxiety disorders.

Anxiety disorders are newly defined syndromes in which inappropriate state anxiety is the sole or primary symptom. Hormonal manifestations of acute stress are usually minimal or absent in these disorders. A number of findings suggest receptor down-regulation or enzyme induction of sorts that would be expected to mute or dampen these responses.

Agoraphobia↗
PubMed1987

Circadian fluctuation of plasma epinephrine in supine humans.

Previous studies have demonstrated circadian fluctuations of systemic catecholamines in man. However, methodological differences and conflicting results with epinephrine are apparent. In the present study, plasma and urinary epinephrine and norepinephrine and plasma cortisol were studied in healthy young adult males over 24 hr with 20 min plasma sampling and EEG monitoring of sleep. Plasma epinephrine did not have a circadian variation in supine subjects. Urinary epinephrine levels and small urinary circadian variations were increased by normal posture and activity. Sleep and sleep stage were not associated with different plasma epinephrine levels, and no ultradian fluctuation was observed. Levels of norepinephrine and cortisol were normal. Based on all studies to date, it appears that basal plasma epinephrine has either a very small amplitude or no circadian rhythm, but that changes in posture and activity or the rest/activity cycle may modify this pattern.

Activity Cycles↗
PubMed1987

Endocrine and physiological changes during "spontaneous" panic attacks.

Eight patients with DSM-III-defined panic attacks were compared to four normal subjects on hormonal and physiological variables measured at six predetermined times through 24 hr and also during nine "spontaneous" attacks. Levels at predetermined times were not different, other than a reduction of urinary unconjugated epinephrine in patients. Plasma prolactin was elevated at the peak of most of the attacks and correlated with attack severity. Plasma cortisol and growth hormone, and heart rate, were elevated during some attacks, and plasma norepinephrine showed small increases. Significant plasma epinephrine and MHPG changes were not observed.

Adult↗
PubMed1987

Ethanol retards desensitisation of simple phobias in non-alcoholics.

Twenty non-alcoholic patients with DSM-III defined simple phobias for small animals received behavioural approach tests and exposure therapy while under the influence of a moderately intoxicating dose of ethanol or after placebo administration. Ethanol did not demonstrate any acute anti-anxiety effect, but retarded the rate of behavioural in vivo desensitisation, without changing the final treatment outcome. State-dependent effects of ethanol on anxiety were not demonstrated. This study supports prior research indicating no anti-anxiety or 'tension-reducing' effects of ethanol for simple phobias.

Adult↗