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Biomedical subjects

T W Uhde

Publications and source records attributed to T W Uhde.

At least 91 records · Page 5Linked to original sources
PubMed1988

Lack of efficacy of carbamazepine in the treatment of panic disorder.

The authors conducted a controlled study of carbamazepine in the treatment of 14 patients with panic disorder. Although there was a statistically significant reduction in symptoms of anxiety on several measures, only one of the patients was judged to have a marked and sustained clinical improvement while taking carbamazepine. Forty percent of the patients had a decrease in frequency of panic attacks during carbamazepine treatment, 50% had an increase, and 10% showed no change. The presence of either EEG abnormalities or prominent psychosensory symptoms did not predict response to carbamazepine. These findings are discussed within the context of an epileptiform model for panic disorder.

Adult↗
PubMed1988

Neuroendocrine effects of diazepam in normal subjects following brief painful stress.

The neuroendocrine effects of 5 and 10 mg of oral diazepam were assessed in 10 normal subjects under baseline (prestress) and laboratory-controlled stressful conditions. Although the 10-mg diazepam dose had no effect on cortisol at baseline, it significantly reduced the increase in cortisol produced by 15 minutes of exposure to a painful electrical stimulus. There were no significant effects on growth hormone, beta-endorphin or ACTH, either at baseline or after painful stimulation.

Adult↗
PubMed1988

Panic disorder and major depression. A tale of two syndromes.

Considerable research has been conducted to clarify relationships between panic disorder and major depression. From a number of perspectives, it now appears that panic disorder and major depression are not identical illnesses. While many patients with panic disorder are likely to experience an episode of major depression at some point during their lives, the timing of this occurrence is highly variable. While depression may be an expected and understandable result of having to live with chronic anxiety and phobic avoidance, the available evidence suggests that such a hypothesis is not particularly tenable. Depression can occur in individuals with or without severe agoraphobia and in individuals ill with panic for greater or lesser periods of time. Comorbidity in panic, particularly for social phobic or obsessive-compulsive symptomatology, does serve as a risk factor for the lifetime occurrence of depression and may denote a more severe illness. Biologic markers (Table 4), while of limited diagnostic utility in clinical practice, may reveal important pathophysiologic similarities and differences between panic disorder and major depression. Current evidence points to many areas of biologic overlap, with some important areas of independence (Fig. 7A). Although not extensively discussed in this chapter, several clinical parameters paint an analogous picture (Fig. 7B). There is a need for future studies of biologic markers in individuals over time, in various phases of illness. Furthermore, the study of multiple biologic markers in the same individuals would be a worthwhile pursuit, perhaps leading toward the delineation of underlying pathophysiologic mechanisms. In summary, then, we favor a conceptualization of panic disorder and major depression as nonidentical disorders with many shared characteristics. Future studies as suggested above, particularly when coupled with the power of genetic studies not described in this chapter, may eventually lead to a clearer demarcation of the boundaries between these two intriguing psychiatric syndromes.

Anxiety Disorders↗
PubMed1988

Exogenous factors in panic disorder: clinical and research implications.

Because panic disorder has an underlying biologic and probably genetic basis, the role of factors outside the organism in initiating and sustaining panic is often overlooked. The authors review certain exogenous factors that seem capable of triggering attacks and/or increasing their frequency and intensity: self-administered pharmacologic agents (caffeine, alcohol, nicotine, over-the-counter cold preparations, cannabis, cocaine); habits (sleep deprivation, diet, exercise, relaxation, hyperventilation); and aspects of the environment (fluorescent lighting, life stressors). There may be a specificity to the action of some of these factors, because certain factors previously thought to trigger panic attacks (e.g., pain, hypoglycemia) have been proved not to have this effect. Although the clinical significance of many of the exogenous factors discussed still awaits empirical confirmation, attention to such factors during the initial evaluation of a patient with panic disorder may be helpful in formulating a successful treatment plan.

Anxiety Disorders↗
PubMed1987

Effects of diazepam on cognitive processes in normal subjects.

The effects of 10 mg orally-administered diazepam on various aspects of cognition were examined in ten male subjects. Diazepam produced a subjective sense of cognitive impairment and impaired auditory vigilence, immediate recognition of twice presented words, and context-dependent free recall. There was a trend for a significant proportion of subjects to show impairment in delayed recognition of twice-presented words. There was no impairment of context-independent semantic memory, or of subjects' ability to judge how well they had performed on the free recall task. In fact, subjects' subjective sense of cognitive impairment was correlated with their performance on context-dependent memory tasks.

Adult↗
PubMed1987

Motor activity in depressed patients treated with carbamazepine.

Motor activity in 19 depressed patients treated with carbamazepine was assessed using self-contained monitors worn on the wrist. Those whose depression improved demonstrated significant increases in motor activity. Nonresponders as a group did not show decreased motor activity, suggesting that carbamazepine was not producing sedation or hypoactivity at clinically relevant doses. Activity counts were negatively correlated with ratings of global severity of depression on the Bunney-Hamburg Scale and with degree of motor retardation rated on the BPRS during treatment. The selective increases in motor activity in those who improved are consistent with psychomotor changes related to amelioration of depression.

Adult↗
PubMed1987

Platelet [3H]imipramine binding in patients with panic disorder.

[3H]imipramine binding to platelets was measured in 17 drug-free panic disorder patients and 14 healthy controls. No difference in Bmax or Kd values was found between the two groups. Patients with a past history of major melancholic depression or severe agoraphobia had similar binding parameters as panic disorder patients without a history of depression or severe agoraphobia.

Adult↗
PubMed1987

Glucose utilization in the temporal cortex of affectively ill patients: positron emission tomography.

As temporal lobe dysfunction has been postulated in the affective disorders, the authors investigated glucose utilization in the temporal lobes of 13 affectively ill patients in comparison with 18 normal volunteer controls and 17 previously reported schizophrenic patients, following injections of fluorine 18-2-deoxy-D-glucose (FDG) during somatosensory stimulation to the right forearm. Using a boundary-finding algorithm to outline each temporal lobe, maximum glucose use relative to maximums elsewhere in the same positron emission tomography (PET) slice were calculated. In a small group of moderately to severely depressed patients, this relative measure was significantly reduced in the right (with a similar trend in the left) temporal lobe compared to normal volunteers and the other comparison groups. The lack of a significant increase in glucose utilization, measured either as a maximum or in relation to other areas in the PET scan slice, suggests that a temporal lobe activation or a seizure-like process is not generally occurring during active depressive phases of the illness.

Affective Disorders, Psychotic↗
PubMed1987

Plasma adenosine levels: measurement in humans and relationship to the anxiogenic effects of caffeine.

The effects of caffeine on plasma adenosine were examined in eight healthy normal volunteers. Subjects were randomly administered on 4 separate days, in a double-blind fashion, either placebo or three different doses of caffeine (240, 480, and 720 mg). Adenosine concentrations, measured by high performance liquid chromatography, were in the micromolar range when samples were drawn into tubes containing dipyridamole to prevent adenosine reuptake by red blood cells. Plasma adenosine levels did not change after caffeine administration. The effects of caffeine on anxiety were related to changes in plasma caffeine but not plasma adenosine levels. The potential interest of caffeine as a chemical model of anxiety is discussed.

Adenosine↗
PubMed1987

Differential time course of antidepressant effects after sleep deprivation, ECT, and carbamazepine: clinical and theoretical implications.

The pattern and time course of antidepressant response to different treatment modalities provide important clinical information and hints about underlying neurobiological mechanisms. Depressed patients who responded to 1 night's sleep deprivation (11 of 33 patients) showed maximal improvement on day 1 and deterioration in mood thereafter. In contrast, slower onset and more sustained effects were observed following carbamazepine (12 of 37) or electroconvulsive therapy (ECT) (8 of 8). Nearly maximal improvement required about 2 weeks for ECT and 3 weeks for carbamazepine. Possible differential or common biological mechanisms with differential times of action are implied by these data, which are of importance to the neuroscientist attempting to uncover neural substrates of antidepressant response and the clinician attempting to find rapid onset, yet sustained antidepressant treatments.

Carbamazepine↗
PubMed1987

Correlates of antimanic response to carbamazepine.

Nineteen acutely manic patients were studied in a double-blind trial of carbamazepine in doses averaging 1240 mg/day, achieving blood levels of 10.4 +/- 2.2 micrograms/ml. Clinical improvement in mood and psychomotor components of the manic syndrome was rapid in onset, generally parallel to that observed in previous patients treated with neuroleptics, and was associated with increases in the total hours of nighttime sleep. Compared to the seven nonresponders, the 12 patients who improved were significantly more manic during the baseline placebo period, tended to be more dysphoric, and were significantly more rapid cyclers over their entire course of illness as assessed by episodes in the year before NIMH admission (7.0 +/- 5.6 vs. 2.7 +/- 2.4 in the nonresponders). While improvement was robust in responders, it was not always complete, and some of these patients remained mildly to moderately symptomatic. All seven patients with a negative family history of affective illness in first degree relatives were responders, while those with a positive family history were equally divided. These preliminary data suggest that several predictors of poor response to lithium carbonate (manic severity, anxiety and dysphoria, rapid cycling, and negative family history) may be associated with good antimanic response to carbamazepine.

Antipsychotic Agents↗
PubMed1987

Obsessive-compulsive symptoms in panic disorder.

Previous reports have noted an increased prevalence of obsessive-compulsive symptoms in patients with panic disorder. The authors found a prevalence of obsessive-compulsive symptoms in 19 (27%) of 70 patients with panic disorder. Compared to a subgroup of 25 patients with classic features of panic disorder and no obsessive-compulsive symptoms, the subgroup with obsessive-compulsive symptoms had an earlier onset of illness, were more likely to have personal and family histories of major depression and substance abuse, and showed a poorer outcome after treatment.

Adult↗
PubMed1987

[Acute anxiety attacks and phobia. Historical aspects and clinical manifestations of the agoraphobia syndrome].

This article describes the evolution of the concept of agoraphobia since its initial description in 1871 until its inclusion in the most recent american diagnostic classifications. In most cases, agoraphobia appears to be secondary to the occurrence of repeated panic attacks, that may also lead to the development of chronic generalized anxiety or hypochondriac syndromes. The main clinical, biological and therapeutic features of panic disorders, a clinical entity that is part of the previous syndromes, are reviewed and discussed according to the most recent studies. Panic disorders appear to be distinct from mood disorders but their relationship to other anxiety disorders is still a matter of controversy.

Acute Disease↗
PubMed1986

Dopaminergic effects of carbamazepine. Relationship to clinical response in affective illness.

Carbamazepine, a drug used widely to treat epilepsy and trigeminal neuralgia, has been shown to be effective in the acute and prophylactic treatment of manic-depressive illness. While the time course of its antimanic effects parallels that of classic neuroleptics, indirect clinical evidence, such as lack of parkinsonian side effects and tardive dyskinesia, suggests that carbamazepine does not act by blocking dopamine receptors. To assess the effects of carbamazepine on dopamine mechanisms, we measured the dopamine metabolite homovanillic acid (HVA) in the cerebrospinal fluid of affectively ill patients before and after treatment. Carbamazepine did not alter basal concentrations of HVA, but decreased probenecid-induced accumulations of HVA, paralleling results in animal studies. In 25 patients, lower baseline cerebrospinal fluid HVA levels were related to subsequent better acute antidepressive responses to carbamazepine. While the precise mechanism of carbamazepine's effects on dopaminergic systems remains to be determined, this study provides further evidence that carbamazepine does not have a biochemical profile typical of neuroleptics.

Adult↗
PubMed1986

Effects of one night's sleep deprivation on mood and behavior in panic disorder. Patients with panic disorder compared with depressed patients and normal controls.

The effects of one night's sleep deprivation on mood and behavior were evaluated in 12 patients with panic disorder, ten depressed patients, and ten controls. In contrast to the improvement in symptoms of anxiety and depression shown by the majority of depressed patients, the response of patients with panic disorder as a group did not differ from that of normal controls, although a subgroup did experience noticeable worsening in their symptoms of anxiety, with 40% experiencing panic attacks on the day following sleep deprivation. Electroencephalographic recordings with nasopharyngeal electrodes on the day following sleep deprivation were normal, further suggesting that patients with panic disorder do not have seizure activity characteristic of temporal lobe epilepsy.

Adult↗
PubMed1986

Effect of carbamazepine on mean urinary free cortisol excretion in patients with major affective illness.

Carbamazepine, a tricyclic anticonvulsant effective in the treatment of major affective disorder, has been observed to induce cortisol non-suppression following dexamethasone administration. The mechanism of this effect has not been clearly established. In this study, the authors report carbamazepine-induced elevations of mean urinary free cortisol in patients with affective illness. The theoretical and practical implications of these findings are discussed.

Carbamazepine↗