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Biomedical subjects

D F Klein

Publications and source records attributed to D F Klein.

At least 73 records · Page 4Linked to original sources
PubMed1997

Divalproex treatment of disruptive adolescents: a report of 10 cases.

BACKGROUND: To report an open trial of divalproex sodium in 10 adolescents with chronic temper outbursts and mood lability. METHOD: Ten adolescents meeting screening criteria for chronic temper outbursts and mood lability were followed for 5 consecutive weeks on open divalproex sodium treatment. Temper outburst frequency and mood swings severity at pretreatment and posttreatment were compared by using paired t tests. Subjects continued to be followed to judge persistence of response. RESULTS: All subjects showed clear improvement at 5 weeks and maintained it during follow-up while taking medication. Rapid relapse and recovery occurred in 5 of 6 patients who discontinued and then resumed medication. CONCLUSION: Divalproex sodium may be helpful in teenagers who have explosive tempers and severe mood swings, and benefits may generalize to school and family life.

Adolescent↗
PubMed1997

Clomipramine treatment of panic disorder: pros and cons.

BACKGROUND: Controlled trials suggest that clomipramine may be a highly effective antipanic drug. Lowering the starting dose may alleviate troublesome initial side effects and increase acceptability and compliance. METHOD: Fifty-eight patients with DSM-III-R panic disorder with or without agoraphobia underwent 13 weeks of clomipramine treatment. Starting at 10 mg/day, the dose was gradually increased to a mean dose of 97 mg/day. RESULTS: While completers showed highly significant improvement, the benefits were severely limited by a high dropout rate due to adverse reactions occurring mostly during the first 2 weeks of treatment. CONCLUSION: Given the alternatives, clomipramine should not be used as a first-line antipanic medication.

Adult↗
PubMed1996

Chronological milestones to guide drug change. When should clinicians switch antidepressants?

BACKGROUND: We attempt to identify the time when patients whose conditions are unimproved while receiving antidepressants are unlikely to respond and should have their treatment changed. METHODS: A total of 593 patients were studied. The course of treatment for patients was examined to determine the weeks at which patients who received drug therapy had a better chance of being rated as responders at the study end (week 6) vs patients who received placebo. RESULTS: At the end of week 3, 19 (32%) of the 59 patients who received drug therapy and 6 (10%) of the 57 patients who received placebo and who never minimally improved were rated as responders at week 6. For those who showed no improvement by week 4, the effects of drug therapy and the placebo were equal. Patients who received drug therapy and whose conditions were unimproved but who had been minimally improved at some point had a superior prognosis with drug therapy vs placebo until week 4. Of those unimproved at week 4 but minimally improved at some point previously, 20 (39%) of the 51 patients who received drug therapy vs 3 (8%) of the 36 patients who received placebo were rated as responders at week 6. Of the 75 patients who minimally improved while receiving drug therapy at the end of week 5, 33 (44%) had a chance of being rated a responder at the end of week 6 vs 9 (26%) of the 35 patients receiving placebo. CONCLUSIONS: Patients tolerant of an adequate dose, whose conditions have never been at least minimally improved by the end of week 4, should have their treatment regimen altered. These patients represented a minority of drug-treated patients in the sample studied (ie, 39/392 [10%]). Patients whose conditions minimally improve at some prior week but not after week 5 should have their treatment changed. Patients whose conditions minimally improve in week 5 should continue treatment until week 6.

Adolescent↗
PubMed1996

Panic disorder and social phobia: effects of comorbidity on familial transmission.

The aim of this study was to examine effects of comorbidity of panic disorder and social phobia on familial transmission of each of these disorders. Rates of panic disorder and social phobia were compared in directly interviewed relatives of four proband groups: (1) panic disorder, (2) social phobia, (3) panic disorder and social phobia, and (4) never ill controls. Anxiety disorder probands had no additional lifetime anxiety disorder comorbidity. The familial pattern of the comorbid (panic disorder and social phobia) probands resembled that of the panic disorder group: an increased rate of panic disorder but not social phobia as compared to relatives of controls. Relatives of social phobia probands had an increased rate of social phobia but not panic disorder. These data indicate that social phobia in individuals who subsequently develop panic disorder: (1) differs with respect to familial transmission from social phobia which occurs without lifetime anxiety comorbidity; and (2) may be nonfamilial and/or causally related to panic disorder. Additional studies in larger epidemiologic samples are required to assess generalizability of these findings.

Adult↗
PubMed1996

Symptoms essential to the experience of sodium lactate-induced panic.

We report on subjective ratings and symptoms experienced before and during sodium lactate infusion by patients with panic disorder or agoraphobics with panic attack (DMS-III-R criteria). Symptoms were assessed using the Acute Panic Inventory (API). During the lactate infusion 59% of the patients were rated by an attending psychiatrist as having experienced lactate-induced panic attacks. Patients experiencing lactate-induced panic attacks overwhelmingly rated this experience as very similar to their typical naturally occurring attacks. Among the individual API symptoms items at baseline (prelactate) only Afraid in general (r = 0.26) was significantly, but not strongly, correlated with the panic response. Controlling for baseline symptom levels, the most robust partial correlations of symptomatic increment with panic were Desire to flee (0.70), Fear of losing control (0.57), Afraid in general (0.49), and Dyspnea (0.48). Using a dichotomized symptom increment greater than 1, 13 of 29 API items indicated a panic response to lactate infusion; the best were Dyspnea, Feeling confused, Afraid in general, Difficulty speaking, Difficulty concentrating, Desire to flee, and Fear of losing control. A logistic regression analysis showed that among baseline measures, Afraid in general and Feeling confused significantly predicted panic. For dichotomized change scores, Afraid in general, Dyspnea, and Dizziness/lightheadedness significantly indicated panic. In these analyses three symptom items stand out as the most predictive and revealing of panic to lactate infusion: Afraid in general, Dyspnea, and Desire to flee. These results are discussed in the context of Klein's (1993) suffocation false alarm theory of panic.

Dose-Response Relationship, Drug↗
PubMed1996

Can the effects of antidepressants be observed in the first two weeks of treatment?

Recently the claim that there is a lag in the time of onset of antidepressant effects has been questioned. This issue rests on contrasting the time course of ultimate responders versus nonresponders on imipramine and amitriptyline. It is concluded that in 1 week on antidepressants "clinicians were capable of detecting changes in general states between the groups and the specific effects of depressed mood and anxiety and the physical expression of distress" (Katz et al. 1987). To examine this issue, we first used the design in which ultimate responders and ultimate nonresponders to antidepressants were compared at 1 and 2 weeks. Clearly there were statistically significant differences between ultimate responders and nonresponders on drug. However, the same was true on placebo. When the ultimate responders on placebo were contrasted to the ultimate responders on drug at 1 and 2 weeks using the Clinical global Impression (CGI) scale and the Hamilton Depression Rating Scale (HDRS), there was no difference between drug and placebo. This was also true for a subgroup of patients who met the criteria for melancholia. We conclude that, if the effects of nonspecific improvement are partialed out, there is no evidence of a medication effect at 1 and 2 weeks.

Analysis of Variance↗
PubMed1996

Preventing hung juries about therapy studies.

A series of arguments are presented that emphasize the importance of comparatively evaluating psychotherapies with appropriate pharmacotherapy and pill placebo. The lack of a pill-placebo arm has rendered moot those studies that compared pharmacotherapy directly with psychotherapy because of the lack of an internal sample defining calibration with regard to medication responsivity. The National Institute of Mental Health (NIMH) Treatment of Depression Collaborative Research Program is critically discussed because this program incorporated the recommended design features but still led to substantial controversy. The inclusion of a pill-placebo arm in future therapeutic studies is most desirable. NIMH should initiate a funded program specifically for multisite, pill-placebo-controlled studies of psychotherapy, pharmacotherapy, and their combination, jointly sponsored and supervised by skilled psychopharmacologists and psychotherapists.

Bias↗
PubMed1996

Panic disorder and agoraphobia: hypothesis hothouse.

Panic disorder and agoraphobia have been postulated to occur when (1) fear is elicited by some automatic mechanism that requires catastrophic cognition, (2) there is a flaw in the physiology of fear, with special reference to the noradrenergic system, or (3) a putative suffocation alarm mechanism sends out false alarms. The presence of a suffocation alarm system has been supported by studies of children who lack this protective mechanism because they suffer from congenital central hypoventilation syndrome. Antidepressants with serotonin activity seem to control panic disorder by down-regulating the suffocation alarm system. Serotonin selective reuptake inhibitors (SSRIs) are among the most effective drugs for panic disorder, emphasizing the role of serotonin in respiratory regulation. Dyspnea and hyperventilation are the cardinal signs of a panic attack. Because carbon monoxide (CO) does not cause panic, it may sabotage the suffocation alarm system by acting as an inhibitory neurotransmitter within the carotid body.

Agoraphobia↗
PubMed1996

Ambulatory monitoring of respiration in anxiety.

An ambulatory monitor, body suit, and calibration procedure were developed to compare the respiration of seven patients with panic disorder and twelve normal volunteers. Subjects wore a body suit with Respitrace bands, connected to a portable respiratory monitor for a period of 24 hours. Breath by breath values for respiratory rate and tidal volume were computed every two minutes. There was a significant difference between patients and controls in their patterns of minute ventilation during sleep. Tidal volume, rather that respiratory rate increases characterized the periods of anxiety and limited symptom attacks.

Adult↗
PubMed1995

Instructional set does not alter outcome of respiratory challenges in panic disorder.

In an attempt to reproduce the findings of Rapee et al (1986) that instructional set could alter the anxiogenic effects of carbon dioxide inhalation, 45 patients with panic disorder received two sets of instructions and then underwent a series of respiratory challenges (room air hyperventilation, 5% and 7% CO2 inhalation). The instructions failed to alter the anxiogenic response to any of the interventions.

Administration, Inhalation↗
PubMed1995

Effects of intravenous diazepam pretreatment on lactate-induced panic.

The psychological and physiological effects of acute low-potency benzodiazepine administration on lactate-induced panic were examined in 10 patients with panic disorder (PD). The patients, who had panicked during a standard sodium-lactate infusion, underwent a repeat infusion modified by pretreatment with intravenous diazepam (5 mg). Acute Panic Inventory (API) scores preceding the second lactate infusion, which were associated with diazepam pretreatment, were significantly reduced in compared with those measured before the first lactate infusion. However, the second visit "fear of doom" item of the API was significantly reduced relative to the same time point of the first visit 35 min before lactate infusion, when diazepam had not yet been administered. Thus, the reduction of prelactate anxiety preceding the second infusion appeared to reflect both pharmacological and nonpharmacological contributions. The diazepam pretreatment condition was associated with a significantly increased infusion duration and a significant attenuation of rate of API symptom increase in response to lactate. Despite significant attenuation of lactate infusion effects associated with the diazepam pretreatment condition, 7 of 10 patients experienced a second panic attack. This pilot study suggests that diazepam pretreatment is associated with a marked reduction of symptomatic response during a second lactate infusion, although the magnitude of attenuation observed was insufficient to block lactate-induced panic in a majority of lactate-vulnerable PD patients.

Adult↗
PubMed1995

Rebreathing tests in panic disorder.

In order to compare the ventilatory response of panic patients and normal controls, 21 panic disorder patients with agoraphobia and 21 normal controls underwent the Read rebreathing test. Panic patients panicked significantly more during the test, responded with more respiratory rate and less tidal volume, but showed no hypersensitivity to inhaled carbon dioxide compared to normal controls.

Adult↗
PubMed1995

Generalized social phobia. Reliability and validity.

OBJECTIVE: To investigate the reliability and validity of DSM-III-R "generalized" social phobia by examining interrater agreement and comparing patients with generalized and "nongeneralized" social phobia on demographic characteristics, clinical variables, and familial social phobia. DESIGN: Two senior clinicians classified 129 patients attending an anxiety clinic as having DSM-III-R social phobia that is generalized (fears most social situations) or nongeneralized (less than most) based on independent narrative review. RESULTS: Good reliability was achieved (kappa = 0.69). Patients with generalized social phobia were more often single, had earlier onsets of social phobia, had more interactional fears, and had higher rates of atypical depression and alcoholism. Familial social phobia was more common among patients with generalized social phobia than patients with nongeneralized social phobia and controls, with no difference between the latter two groups. CONCLUSIONS: Generalized social phobia (1) can be distinguished reliably from nongeneralized social phobia, (2) is a valid subtype, and (3) may characterize a familial form of the disorder.

Adult↗
PubMed1995

Specificity in familial aggregation of phobic disorders.

BACKGROUND: To investigate whether each of three DSM-III-R phobic disorders (simple phobia, social phobia, and agoraphobia with panic attacks) is familial and "breeds true." DESIGN: Rates of each phobic disorder were contrasted in first-degree relatives of four proband groups: simple phobia, social phobia, agoraphobia with panic attacks, and not ill controls. Phobia probands were patients who had one of the phobia diagnoses but no other lifetime anxiety comorbidity. RESULTS: We found moderate (two- to fourfold increased risk) but specific familial aggregation of each of the three DSM-III-R phobic disorders. CONCLUSIONS: These results support a specific familial contribution to each of the three phobia types. However, conclusions are limited to cases occurring without lifetime anxiety comorbidity and do not imply homogeneity within categories.

Adult↗
PubMed1995

Imipramine treatment of cocaine abuse: possible boundaries of efficacy.

A 12-week placebo-controlled, randomized clinical trial was undertaken to evaluate imipramine as a treatment for cocaine abuse, and to examine whether its effect may be limited to subgroups defined by route of use or by diagnosis of depression. One-hundred thirteen patients were randomized, stratified by route of use and depression. All patients received weekly individual counseling. Compared to placebo the imipramine group showed greater reductions in cocaine craving, cocaine euphoria, and depression, but the effect of imipramine on cocaine use was less clear. A favorable response, defined as at least 3 consecutive, urine-confirmed, cocaine-free weeks was achieved by 19% (11/59) of patients on imipramine compared to 7% (4/54) on placebo (P < 0.09). The imipramine effect was greater among nasal users--33% (9/27) response on imipramine vs. 5% (1/22) on placebo (P < 0.02). Response was also more frequent, but not significantly so, among depressed users on imipramine (26%, 10/38) than on placebo (13%, 4/31) (P < 0.19). Response rates were low in intravenous and freebase users and those without depression. Considered together with the literature on desipramine, these data suggest tricyclic antidepressants are not promising as a mainstay of treatment for unselected cocaine abusers. However, tricyclics may be useful for selected cocaine abusers with comorbid depression or intranasal use, or in conjunction with a more potent psychosocial intervention.

Adolescent↗