PubMed Health⌕ Search

Biomedical subjects

T W Uhde

Publications and source records attributed to T W Uhde.

At least 163 records · Page 9Linked to original sources
PubMed1983

Clinical studies of monoamine receptors in the affective disorders and receptor changes with antidepressant treatment.

Pre-clinical and clinical studies suggest that the responsiveness of monoamine and cholinergic receptors may be altered in the affective disorders and that antidepressants may modify the sensitivity of these receptors. The growth hormone response to clonidine is reduced in depressed patients compared to controls according to several independent studies, suggesting that post-synaptic alpha 2-adrenergic receptors may be less responsive in depressed patients. The cortisol response to clonidine is enhanced in depressed patients compared to controls in our study raising the possibility that cortisol hypersecretion in depressed patients may be related to noradrenergic dysfunction. The hypotensive response to clonidine is blunted in patients on chronic antidepressant treatment with either clorgyline or desipramine suggesting that pre-synaptic alpha 2-adrenergic receptors may subsensitize with chronic antidepressant treatment. The prolactin increase in response to fenfluramine is less in depressed patients compared to controls suggesting decreased functional activity of the serotonergic system in depression. Platelet alpha 2-adrenergic receptor number as measured by tritiated dihydroergocriptine (3H-DHE) binding is increased in depressed patients compared to controls, while cyclic 3'-5' adenosine monophosphate (cAMP) production in response to prostaglandin E1 (PGE1) and norepinephrine (NE) inhibition of PGE1-stimulated cAMP production are reduced in the platelets of depressed patients. Thus, it is not clear that increased 3H-DHE binding reflects increased functional responsiveness and might in fact be compensatory to decreases in functional responses of alpha 2-adrenergic receptors.

Clonidine↗
PubMed1983

Biochemical effects of carbamazepine: relationship to its mechanisms of action in affective illness.

Carbamazepine has a unique spectrum of clinical efficacy in paroxysmal pain syndromes and epilepsy, as well as in affective illness. Evidence of its therapeutic effects in lithium-resistant manic-depressive illness and schizoaffective illness is reviewed. The biochemical effects of carbamazepine as they might be related to either its anticonvulsant or psychotropic properties are presented and discussed. Carbamazepine alters classical neurotransmitter and second messenger systems, as well as a variety of neuropeptides which could relate to mechanisms of action or side effects. Comparison and contrast of the biological effects of carbamazepine with classical treatment agents, such as lithium carbonate, tricyclic antidepressants, and neuroleptics may help elucidate mechanisms underlying the pathophysiology of the mood disorders.

Bipolar Disorder↗
PubMed1983

Prophylactic efficacy of carbamazepine in manic-depressive illness.

Seven patients with rapidly cycling, lithium-resistant affective illness were followed for an average of 1.7 years during prophylactic treatment with carbamazepine administered on either a blind or an open basis. The number of manic and depressive episodes per year decreased significantly--from 16.4 before treatment to 5.6 during carbamazepine treatment; severity and duration of episodes were also reduced. Six of seven patients relapsed after carbamazepine dose reduction or discontinuation. These preliminary data add further support to the growing evidence that carbamazepine may be useful in the acute and prophylactic treatment of some lithium-resistant patients.

Antipsychotic Agents↗
PubMed1983

Growth hormone response to clonidine in obsessive-compulsive patients.

We have observed a lesser growth hormone response to intravenous clonidine administration in nine obsessive-compulsive disorder patients meeting research diagnostic criteria than in nine matched controls. The obsessive-compulsive disorder patients had higher plasma free 3-methoxy-4-hydroxyphenylglycol and plasma norepinephrine levels before clonidine than the controls. As blunted growth hormone responses to clonidine are also characteristic of affective disorder patients, these results support other observations of a psychobiologic affinity between these two groups and are also compatible with an association between increased presynaptic noradrenergic activity and decreased post-synaptic receptor responsiveness.

Adolescent↗
PubMed1983

[Treatment of panic attacks].

Acute anxiety is a common symptom in psychiatric and medical illnesses. Panic attacks i.e. discrete episodes of severe acute anxiety with clear "onset" and "offset" are frequently associated with agoraphobia and respond to tricyclic and MAO-inhibitor antidepressants. These agents appear to have specific antipanic efficacy independent of their antidepressant properties. Despite the frequent association between panic disorder and major depressive illness the nature and the extent of this relationship remain unclear.

Agoraphobia↗
PubMed1982

[Biochemical aspects of anxiety].

Alterations in biological systems may influence or accompany the symptoms of anxiety in human beings. Several biological systems such as the hypothalamic-pituitary-adrenal axis and the catecholaminergic systems may play important roles in the modulation of anxiety. The noradrenergic nucleus locus coeruleus may provide a useful model for the study and treatment of human feelings of fear, vigilance, alarm and anxiety. Substances that act selectively on this system, such as clonidine, may have anxiolytic properties. Furthermore, recent advances in the understanding of other neurotransmitter systems may have important implications. For example, the discovery of specific brain receptors for benzodiazepines (BDZ) and their endogenous ligands may result in more selective treatment of some conditions of pathological anxiety. The possible involvement of adenosine in the mode of action of both BDZ and methylxanthines such as caffeine may explain the antagonistic effects of these compounds.

Adenosine↗
PubMed1982

Growth hormone response to clonidine as a probe of noradrenergic receptor responsiveness in affective disorder patients and controls.

The growth hormone (GH) response to the alpha-adrenergic agonist clinidine was blunted in 19 depressed patients compared to 20 controls. The difference remained significant when age- and sex-matches pairs of patients and controls were compared from this sample, either including or excluding subjects with elevated GH baseline levels. Plasma levels of free 3-methoxy-4-hydroxyphenyl-glycol (MHPG) were assayed in blood samples drawn just before the clonidine infusion. A modest negative correlation was found between the plasma MHPG values and the magnitude of the GH responses to clonidine, although baseline plasma MHPG levels were not significantly different between patients and controls. The diminished GH response to clonidine observed suggests that many depressed patients may have decreased alpha-adrenoreceptor responsiveness. Decreased responsiveness may in some cases be associated with relatively increased indices of presynaptic noradrenergic availability. Such a model might have implications for understanding the functional status of the noradrenergic neurotransmitter system in depressed patients and the possible subtyping of affective disorder patients.

Clonidine↗
PubMed1982

Possible subsensitization of alpha 2-adrenergic receptors by chronic monoamine oxidase inhibitor treatment in psychiatric patients.

Clonidine was administered to nine psychiatric patients before and after chronic treatment (3 to 4 weeks) with clorgyline, a selective monoamine oxidase type A inhibitor with antidepressant efficacy. The hypotensive response to clonidine, believed to be mediated by brain alpha 2-adrenergic receptors, was significantly attenuated by chronic but not acute (2 to 3 days) clorgyline treatment, with a time course similar to the onset of its clinical efficacy. This study supports the hypothesis that subsensitization of alpha 2-adrenergic receptors plays an important role in clorgyline's antidepressant effects and may constitute a key contribution to the mode of action of other antidepressant treatments as well.

Adult↗
PubMed1982

Growth hormone response to clonidine unchanged by chronic clorgyline treatment.

The growth hormone (GH) response to the alpha 2-adrenergic agonist, clonidine, was determined before and after chronic clorgyline treatment in 10 psychiatric patients. No significant differences emerged in the magnitude of the GH response to clonidine before as compared to after clorgyline. These results do not support the hypothesis that postsynaptic alpha 2-adrenergic responsiveness is enhanced following chronic antidepressant treatment.

Adult↗
PubMed1982

Kindling and carbamazepine in affective illness.

Kindling represents a process in which increasing behavioral and convulsive responses occur to repetition of the same stimulus over time. Increased behavioral response can also occur to repetition of the same dose of psychomotor stimulant or dopamine agonist, i.e., behavioral sensitization. These two models, which may have important implications for the progressive development of psychopathology in a variety of neuropsychiatric syndromes, are reviewed. Carbamazepine, a drug of choice in treatment of temporal lobe and limbic seizures and effective in inhibiting kindling, has been used as a treatment of primary and secondary affective illness. The efficacy of carbamazepine in affective illness and its clinical and theoretical implications are discussed.

Affective Disorders, Psychotic↗
PubMed1982

Biological relationships between mania and melancholia.

Although opposite mood and psychomotor disturbances usually occur in mania and melancholia, clinical features may also be shared in common or may be present at the same time in both phases of manic-depressive psychosis. In a parallel fashion, most pharmacological agents are selectively effective in one mood phase (tricyclics and monoamine oxidase inhibitors for depression, and neuroleptics for mania) and frequently precipitate or exacerbate the opposite phase. These agents, therefore, may be affecting biological substrates mediating the opposing phase of affective illness. With the exception of electroconvulsive therapy and lithium chemotherapy, few treatments are effective in both mania and melancholia. It is noteworthy, therefore, that carbamazepine may be useful in the acute and prophylactic treatment of mania and melancholia, including some lithium non-responders and patients vulnerable to tricyclic-induced "mood switches". The clinical and biological effects of carbamazepine will be discussed with special emphasis on its biochemical action and the possible mechanisms by which it might influence biological substrates mediating both phases of manic-depressive illness. In addition, the theoretical implications of the presence of both shared and opposing clinical, pharmacological, and biochemical characteristics of the illness will be discussed.

Affective Disorders, Psychotic↗