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Biomedical subjects

D F Klein

Publications and source records attributed to D F Klein.

At least 109 records · Page 6Linked to original sources
PubMed1993

Clinical psychopharmacologic practice. The need for developing a research base.

The advent of psychotropic drugs has enormously improved psychiatric care. Nonetheless, our practice is not optimum. Current knowledge is not regularly applied. It has been repeatedly shown that the majority of patients with psychiatric illness go undiagnosed, and even if diagnosed, they are inappropriately or ineffectively treated, both by clinical psychiatrists and by primary care practitioners. Improved care depends on practitioner education, often referred to as "technology transfer."

Clinical Competence↗
PubMed1993

Computed tomography and neurological soft signs in obsessive-compulsive disorder.

Computed tomography was used to compare the following three groups: obsessive-compulsive disorder (OCD) patients with high scores on a soft neurological sign examination, OCD patients with low soft neurological sign scores, and control subjects. Neuranatomical structures were measured using quantitative volumetric analysis. OCD patients with high soft sign scores had significantly increased ventricular volumes compared with OCD patients with low soft sign scores and control subjects. Caudate and lenticular nucleus volumes did not differ between groups.

Adult↗
PubMed1993

Reanalysis of the National Institute of Mental Health Treatment of Depression Collaborative Research Program General Effectiveness Report.

The National Institute of Mental Health (NIMH) Treatment of Depression Collaborative Research Program General Effectiveness Report statistical analyses are criticized. Their analyses, which fostered the belief that criticized. Their analyses, which fostered the belief that the active treatments were indistinguishable, were compromised by an inappropriately stringent level of significance with regard to both heterogeneity of slope and pairwise group differences. Once slope heterogeneity is detected, the Johnson-Neyman technique is more appropriate than arbitrary sample subdivision. All of these tactics lowered power substantially. Our reanalysis indicates a reasonable ordering for the treatments with medication superior to the psychotherapies and the psychotherapies somewhat superior to placebo. These effects are particularly marked among the more symptomatic and impaired patients. The lack of dosage by severity analyses renders the severity findings ambiguous. Scientific and public health implications are discussed.

Analysis of Variance↗
PubMed1993

Should the government assure scientific integrity?

The author argues that the somewhat Orwellian Office of Research Integrity needs careful scrutiny as to whether it should exist at all or whether its purported social benefits could be better achieved by other mechanisms. First, social issues specifically related to scientific misconduct need to be clarified so as to consider alternative regulatory measures. Constructive social policy requires balanced judgments that keep all goals in view and strives to promote science and to deal effectively with what may go awry (for example, falsification and fabrication, and plagiarism). Second, the regulation of scientific misconduct raises important questions, such as whether universities are able to police themselves. But is government regulation the best answer? The author suggests that a freestanding, nonprofit investigative foundation be formed and staffed by experts in investigations of scientific fraud as well as legal experts aware of investigative and due-process issues. Such a structure would remove the government from regulation (a boon) and relieve the university of the conflicts inherent in a duty to investigate and judge allegations. By the same token, the scientific community, including professional societies, would be at the center of the policing efforts of the foundation.

Academic Medical Centers↗
PubMed1993

A double-blind crossover trial of imipramine and phenelzine for outpatients with treatment-refractory depression.

OBJECTIVE: Data from controlled studies concerning the response rates of patients to a second antidepressant medication after they have been unresponsive to a systematic trial of another antidepressant are extremely useful to clinicians for rational prescription of pharmacotherapy. Such information allows making an accurate prognosis, sustaining realistic hope in the patient, and achieving the best possible therapeutic outcome. This study was designed to add to the scanty literature available on this subject. METHOD: Eighty-nine mood-reactive, nonmelancholic, mainly chronically depressed outpatients at a university research clinic who were unresponsive to vigorous double-blind trials of imipramine or phenelzine were crossed over to treatment with the other drug under double-blind conditions. RESULTS: Of 46 patients previously unresponsive to imipramine who completed phenelzine treatment, 31 (67%) responded to phenelzine. Of 22 patients previously unresponsive to phenelzine who completed imipramine treatment, nine (41%) responded to imipramine. The difference in response rates was statistically significant. Even after they had shown no response to 7 weeks of placebo and 6 weeks of imipramine treatment, 10 (83%) of 12 patients who then completed treatment with phenelzine responded. CONCLUSIONS: These data suggest that among chronically ill, mood-reactive depressed patients with many symptoms of atypical depression, phenelzine is strikingly effective in those who have been nonresponders to imipramine and should be tried in such patients.

Adult↗
PubMed1993

The effect of acetazolamide on ventilation in panic disorder patients.

OBJECTIVE: Patients with panic disorder are behaviorally hypersensitive to CO2 inhalation and may also be biologically hypersensitive. A report by Mathew et al. showed, however, that administration of the carbonic anhydrase inhibitor acetazolamide, which is believed to increase brain CO2 level, did not cause panic in panic disorder patients. The authors of the present study noted that respiratory frequency did not increase in the earlier experiment and wondered whether respiratory stimulation occurred during acetazolamide administration, as would be expected if CO2 level increases significantly. METHOD: Ten patients with panic disorder and six normal control subjects received injections of acetazolamide, 1 g i.v., as per the Mathew et al. protocol, during breath by breath measurement of both tidal volume and frequency of respiration. RESULTS: Three patients had panic attacks, one before receiving acetazolamide, one during the injection, and one 2 minutes after injection. Only the last of these attacks appeared possibly attributable to acetazolamide. None of the control subjects panicked. Neither patients nor control subjects exhibited meaningful change in tidal volume, respiratory frequency, or minute ventilation, and both groups experienced a trend toward significant decrease in overall levels of anxiety and dyspnea after acetazolamide injection. CONCLUSIONS: The authors replicated the earlier finding that acetazolamide is not panicogenic in patients with panic disorder but also showed that at the dose given, there is no meaningful effect on ventilation. If acetazolamide does affect CO2 levels it does so in a way that does not stimulate ventilation. Therefore, the acetazolamide injection results of Mathew et al. and of the present study do not challenge hypotheses linking panic attacks to hypersensitive respiratory control mechanisms.

Acetazolamide↗
PubMed1993

Diagnostic and substance specificity of carbon-dioxide-induced panic.

OBJECTIVE: The authors assessed the substance and diagnostic specificity of carbon-dioxide-induced panic since, in addition to the specific biochemical effects of inhaled carbon dioxide (CO2), simple physiologic distress is also frequently implicated as a panicogenic factor during respiratory challenge studies with CO2 in patients with anxiety disorders. METHOD: Eighteen patients with panic disorder, 20 with social phobia, and 23 psychiatrically normal subjects inhaled a mixture of 35% CO2 and 65% O2 for 30 seconds through a face mask. They also breathed for 30 seconds through a valve reducing the diameter of the airway. A double-blind, counterbalanced, randomized design was used. RESULTS: In spite of important similarities between the two interventions, including the induction of equal amounts of subjective respiratory distress, carbon dioxide inhalation was significantly more potent than increased airway resistance in provoking panic in the anxiety disorder patients. The patients with panic disorder were significantly more sensitive to CO2 than were the patients with social phobia or the normal subjects. CONCLUSIONS: Carbon dioxide inhalation appears to have a specific panicogenic effect in panic patients that goes beyond simple breathlessness.

Administration, Inhalation↗
PubMed1993

Loss of drug effects during continuation therapy.

OBJECTIVE: This study sought to determine what proportion of relapses during continuation therapy with antidepressants can be attributed to loss of nonspecific placebo effects while the patients are taking the drugs. METHOD: Depressed patients were studied over a 12-week period. One hundred sixty-four patients were randomly assigned to placebo, 174 to imipramine, and 169 to phenelzine. At 6 weeks 35 were judged to be responders to placebo, 70 to imipramine, and 96 to phenelzine. These patients continued their double-blind treatment for weeks 7-12. RESULTS: Thirty-one percent of the patients who were taking placebo, approximately 12% who were taking imipramine, and approximately 9% who were taking phenelzine relapsed in the 7- to 12-week phase. Two different methods of estimating relapses suggested that during the first 3 months of treatment, a large percentage of the relapses of patients taking drugs was attributable to the loss of nonspecific placebo effects rather than true drug effects. CONCLUSIONS: A considerable proportion of relapses in the first 3 months of treatment with antidepressants appears to be due to loss of placebo effects. These clinically relevant data may be used to encourage patients who relapse during this period, and who erroneously conclude that anti-depressant effects are temporary, to try another medication.

Antidepressive Agents↗
PubMed1993

Further evidence that a placebo response to antidepressants can be identified.

OBJECTIVE: The authors' goal was to analyze the acute phase of antidepressant drug treatment to identify placebo responses. METHOD: Patients rated as improved after 6 weeks of double-blind treatment with imipramine or phenelzine were followed for an additional 6 weeks of double-blind treatment. Initial responses were classified according to the speed of improvement (abrupt or gradual), the persistence or nonpersistence of improvement, and the timing of improvement (early or late onset). RESULTS: It was predicted that patients with nonpersistent, abrupt responses to the drugs were actually experiencing a placebo response and would have the worst prognosis. In fact, this group accounted for a disproportionate number of the relapses. Nonpersistent responders to a drug had a 23.7% relapse rate, but persistent responders had only a 9.0% relapse rate, a significant difference. CONCLUSIONS: The authors conclude that a significant proportion of relapses within the first 6 weeks of treatment with an active drug are not related to loss of a true drug effect. Rather, some are related to loss of nonspecific placebo effects, and abrupt nonpersistent responses during drug treatment are most likely the result of placebo effects.

Antidepressive Agents↗
PubMed1993

A comparison of treated and untreated simple phobia.

The authors compared 25 treated and 58 untreated subjects with simple phobia uncomplicated by other lifetime anxiety disorders. The treated individuals reported more phobias involving dogs and cats, elevators, and transportation; most had multiple phobias; and many experienced panic attacks in the context of their phobias. The untreated individuals typically reported only one phobia, which was often related to blood-injury and was seldom complicated by panic symptoms.

Anxiety Disorders↗
PubMed1993

Carbon dioxide hypersensitivity, hyperventilation, and panic disorder.

OBJECTIVE: The purpose of this article is to offer a comprehensive, data-based explanation of the relationship between hyperventilation and panic disorder linking CO2 hypersensitivity, cognitive/behavioral factors, and the respiratory effects of antipanic pharmacologic and psychological treatments. METHOD: The authors conducted a computerized search of MEDLINE for relevant articles. RESULTS: Some panic patients have a chronic, subtle respiratory disturbance. Acute hyperventilation is neither necessary nor sufficient for panic to occur. Respiratory abnormalities in panic patients may adaptively aim at coping with a hypersensitive CO2 chemoreceptor system. Pharmacologic panicogens also stimulate the respiratory system, causing hyperventilation. Triggering this hypersensitive respiratory control mechanism may incite panic. Antipanic medications may reset the receptor threshold. Misattribution and catastrophic interpretation of somatic symptoms or the sense of loss of control may contribute to panic symptoms. Behavioral interventions such as desensitization or breathing retraining may block the full-blown attack. Cognitive strategies through cognitive control of respiration may supplement and accentuate these interventions. CONCLUSIONS: Panic disorder may be due to an inherently unstable autonomic nervous system, coupled with cognitive distress.

Alkalosis, Respiratory↗
PubMed1993

Fluoxetine for hypochondriacal patients without major depression.

Hypochondriasis without concomitant depression is often considered to be unresponsive to pharmacotherapy. Given marked similarities between hypochondriasis and obsessive-compulsive disorder, we decided to conduct an open trial of high-dose fluoxetine for patients with DSM-III-R hypochondriasis who did not meet criteria for major depression. Ten of 16 patients were much improved at the end of 12 weeks. A comparison of baseline and week 12 scores by the use of a paired-samples t-test revealed a statistically significant reduction in hypochondriacal concerns, as measured by the Heightened Illness Concern Clinical Global Impression Severity scale, the Whiteley Index of Hypochondriasis, and the Heightened Illness Concern Questionnaire. These results suggest that fluoxetine may be a useful therapy for hypochondriacal patients without marked depressive features--a group previously considered to be treatment refractory.

Adult↗
PubMed1993

Columbia atypical depression. A subgroup of depressives with better response to MAOI than to tricyclic antidepressants or placebo.

We summarise a series of studies using a MAOI to help establish the validity of a subgroup of depressives referred to as atypical depressives. Patients with reactive mood meeting DSM-III criteria for depressive illness who had associated atypical features (which include hyperphagia, hypersomnolence, leaden paralysis, and rejection sensitivity) were randomised to imipramine, phenelzine and placebo. Non-responders were crossed over, and in all there were over 400 patient trials. Phenelzine consistently was found to be superior to imipramine. Only in trials which included patients lacking atypical, vegetative symptoms was imipramine found to equal phenelzine. We conclude that the researcher and the clinician should consider the relevance of the atypical depressive syndrome.

Antidepressive Agents, Tricyclic↗
PubMed1993

Mixed anxiety depression. For and against.

The subject of mixed anxiety depression has been the topic of a somewhat confused discussion. At one point, it was held that anxiety and depression were both manifestations of an underlying affective disorder, but systematic work by Martin Roth and others clearly demonstrated that anxiety disorders could be separated from depressive disorders via a multivariate scale. Interestingly, spontaneous panic attacks were among the highest loading items on this scale. Nonetheless, it was plain that many patients were simultaneously anxious and depressed. Interest then grew in understanding the evolution of these syndromes over time. In general, anxiety syndromes antecede depressive syndromes, although there are many exceptions. For instance, some people only develop panic attacks when in the midst of a depressive episode. To attempt to understand these complexities, detailed family studies have been attempted with often contradictory results. We shall present family study data indicating that patients with comorbid panic disorder and depression have different familial patterns from those with panic disorder alone. In addition, a practical question is whether there exist patients, primarily in private settings, who present with symptoms of anxiety and depression but do not meet full criteria for any of the currently defined syndromes. Such patients are often referred to as subsyndromal or subthreshold patients. Epidemiological data indicates that such patients exist and that their symptomatology is associated with social and functional impairment. Recently the DSM IV field trial has specifically addressed this issue by clinical investigations of primary care and psychiatric facilities. These results will be reported.

Anxiety Disorders↗
PubMed1993

Psychiatric manifestations of Lyme borreliosis.

BACKGROUND: Lyme borreliosis (Lyme disease), a tick-borne spirochetal illness, has later manifestations that may include arthritic, neurologic, ophthalmologic, and cardiac symptoms. Recent reports suggest psychiatric symptoms may also be part of the clinical picture. METHOD: Using a structured interview (SCID), we interviewed three patients who had developed a psychiatric disorder for the first time after infection with Borrelia burgdorferi. RESULTS: During Lyme borreliosis, one patient had major depression and panic disorder, one patient had an organic mood syndrome with both depression and mania, and the third patient had panic disorder. These disorders remitted after adequate antibiotic treatment. CONCLUSION: While depression has been previously linked to neuroborreliosis, this is the first report to link panic disorder and mania with borrelial infection. Because of the rapid rise of Lyme borreliosis nationwide and the need for antibiotic treatment to prevent severe neurologic damage, mental health professionals need to be aware of its possible psychiatric presentations.

Adult↗
PubMed1992

Exercise tolerance in panic disorder patients.

Sixteen panic patients and fifteen normal controls performed submaximal exercise testing on a bicycle ergometer. Only one patient subject panicked. Biochemical, physiological, and psychological data showed similar exercise tolerance in both patients and controls. Exercise-induced distress and lactate increment do not appear to cause panic attacks.

Adult↗