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Biomedical subjects

L H Price

Publications and source records attributed to L H Price.

At least 163 records · Page 9Linked to original sources
PubMed1989

Fluvoxamine as an antiobsessional agent.

The studies reviewed here suggest that the potent and selective serotonin reuptake inhibitor fluvoxamine is an effective treatment for OCD. Response to the antiobsessional effects of fluvoxamine is independent of baseline levels of depression. Additional studies are currently underway to determine if fluvoxamine is actually more effective in OCD than less potent blockers of serotonin reuptake (e.g., desipramine) (Goodman et al. unpublished data). However, since the clinical response to potent serotonin reuptake blockers is often incomplete or, in as many as one-third of patients, absent, the precise relevance of the monoamine reuptake blocking properties of these medications to the pathogenesis of OCD remains unclear.

Antidepressive Agents↗
PubMed1988

Serotonin function in obsessive-compulsive disorder. A comparison of the effects of tryptophan and m-chlorophenylpiperazine in patients and healthy subjects.

To evaluate the role of serotonin (5-HT) function in obsessive-compulsive disorder (OCD), behavioral and biochemical responses to the 5-HT receptor agonist m-chlorophenylpiperazine (MCPP) and the 5-HT precursor tryptophan were examined in healthy subjects and patients with OCD. Baseline prolactin levels and the prolactin rise following MCPP were significantly reduced in female patients compared with female healthy subjects. In contrast, the increase in prolactin level following tryptophan administration was not significantly different between male or female patients with OCD and the respective sex-matched healthy subjects. The prolactin responses to MCPP and tryptophan were both significantly higher in female patients and healthy subjects than in their male counterparts. The cortisol and growth hormone responses to MCPP and tryptophan were similar in the patients and healthy subjects and were not related to gender. The behavioral responses to MCPP or tryptophan were not consistently different between patients and healthy subjects, and neither MCPP nor tryptophan had effects on obsessive or compulsive symptoms. These results lend only partial support to the hypothesis that 5-HT dysfunction may be linked to the pathophysiology of OCD and point to the need for the evaluation of other neurotransmitter systems in future investigations of OCD.

Adult↗
PubMed1988

alpha 2-Adrenergic receptor sensitivity in depression. The plasma MHPG, behavioral, and cardiovascular responses to yohimbine.

alpha 2-Adrenergic receptors play a major role in the regulation of the noradrenergic system. To assess the function of these receptors relative to possible abnormalities in noradrenergic function in depression, responses to the alpha 2-antagonist yohimbine hydrochloride were investigated in 45 depressed patients and 20 healthy control subjects. Plasma 3-methoxy-4-hydroxyphenylglycol (MHPG), blood pressure (BP), pulse, subjective mood, and somatic symptoms were measured before and during yohimbine and placebo administration. The 25% increase in plasma MHPG levels produced by yohimbine did not differ between patients and controls. Mood responses also tended to be similar between groups, with patients reporting only minor improvement in depression following yohimbine. However, yohimbine caused significantly greater increases in somatic symptoms and tended to produce a greater increase in BP in patients than in controls. Evaluation of patient subgroups divided by the presence or absence of melancholia, psychosis, prominent anxiety, or personality disorder did not demonstrate consistent differences. In contrast, comparison of these findings with a prior study showed that patients with panic disorder and agoraphobia who received yohimbine manifested significantly greater increases in MHPG levels and ratings of anxiety, nervousness, and depression than depressed patients. These findings suggest that patients with major depression do not demonstrate marked abnormalities in alpha 2-adrenergic autoreceptor function.

Adult↗
PubMed1988

Effects of trazodone treatment on serotonergic function in depressed patients.

Changes in serotonergic (5HT) neurotransmission may mediate the therapeutic actions of some antidepressant drugs. In the present study, the 5HT precursor L-tryptophan (L-TRP) was administered intravenously to nine depressed patients before and during treatment with the triazolopyridine antidepressant trazodone (TRZ). Neuroendocrine, subjective mood, and cardiovascular responses to L-TRP were assessed. Unlike tricyclic antidepressants and monoamine oxidase inhibitors, TRZ did not enhance the prolactin response to L-TRP and had little effect on other measures. Since other studies indicate that the TRP-induced increase of prolactin in humans may reflect 5HT function, the present study suggests that TRZ treatment does not enhance net 5HT function in depressed patients.

Adult↗
PubMed1988

Noradrenergic and serotonergic receptor system function in panic disorder and depression.

Recent studies which have utilized the administration of neurotransmitter agonists and antagonists to study presynaptic and postsynaptic receptor system function in panic disorder and major depression are reviewed. In panic disorder, patients have been found to be overly sensitive to the alpha-2 adrenergic agonist clonidine, and the alpha-2-adrenergic antagonist yohimbine, but they have relatively normal responses to tryptophan, the precursor of serotonin, and MCPP, a directly acting serotonin agonist. In depression, patients appear to have relatively normal responses to clonidine and yohimbine except for some supersensitivity to yohimbine effects on blood pressure and subjective symptoms. In contrast to the panic disorder patients, depressed patients demonstrate a neuroendocrine subsensitivity to tryptophan. Taken together, these studies suggest a relative abnormality in the alpha-2-adrenergic regulation of the noradrenergic system in panic disorder and a subsensitivity of the serotonergic system in depression. The pharmacologic treatment response in panic disorder and depression is similar in that both conditions respond to tricyclic antidepressants and monoamine oxidase inhibitors, but different in that panic disorder does not respond to atypical antidepressants such as trazodone and bupropion, but does respond to benzodiazepines, in contrast to depression. The possible mechanisms involved in producing these findings and the methods to more fully study possible receptor system abnormalities in these illnesses are discussed.

Anxiety Disorders↗
PubMed1988

Sequence of drug administration in lithium augmentation: a case study.

A 25-year-old man was hospitalized twice for melancholia. During the first hospitalization he had no response to a trial of desipramine but improved after the addition of lithium; during the second hospitalization he had no response to lithium but improved after the addition of desipramine. Concurrent administration of lithium and a tricyclic may be effective in some patients who respond to neither drug alone, but the sequence of drug administration may not be a critical factor.

Adult↗
PubMed1988

Multiple sclerosis presenting as major depression: a diagnosis suggested by MRI scan but not CT scan.

A 43-year-old woman had melancholic major depression and mild incoordination. A magnetic resonance imaging (MRI) scan showed extensive lesions of the cerebral white matter that were not detected on a computed tomography (CT) scan. Since multiple sclerosis may initially present as depression, the differential sensitivities of MRI and CT scanning should be considered in deciding which neurodiagnostic studies should be conducted in depressed patients.

Adult↗
PubMed1987

Reserpine augmentation of desipramine in refractory depression: clinical and neurobiological effects.

Early studies showed dramatic improvement in some depressed patients when a brief course of parenteral reserpine was added to ineffective tricyclic antidepressant (TCA) treatment. We treated eight patients with DSM-III melancholic major depression with desipramine (DMI) greater than or equal to 2.5 mg/kg/day (plasma levels greater than 125 ng/ml) for at least 4 weeks. All patients failed to respond and received reserpine 5 mg IM b.i.d. over 2 days, in seven cases as a placebo-controlled, double-blind trial. One patient had dramatic resolution of depressive and psychotic symptoms within 48 h, but relapsed within 2 weeks; two other patients had transient hypomanic symptoms. Depression ratings did not significantly change for the sample as a whole, but plasma and cerebrospinal fluid (CSF) levels of 3-methoxy-4-hydroxyphenylethyleneglycol (MHPG) decreased and CSF levels of homovanillic acid (HVA) and 5-hydroxy-indoleacetic acid (5-HIAA) increased. Despite robust effects on central monoamine metabolism, reserpine augmentation appears insufficiently effective for routine use in managing refractory depression.

Adult↗
PubMed1987

Treatment of severe obsessive-compulsive disorder with fluvoxamine.

Ten obsessive-compulsive patients received single-blind treatment with fluvoxamine, a selective serotonin reuptake inhibitor, for several weeks following at least 2 weeks of placebo. The group showed significant improvement, as measured by several clinical scales and self-ratings; six patients were judged responders. Fluvoxamine appears effective in treating severe obsessive-compulsive disorder.

Adult↗
PubMed1986

Reliability and validity of the symptoms of major depressive illness.

In two consecutive studies, we examined the interrater reliability and then the concurrent validity of interview ratings for individual symptoms of major depressive illness. The concurrent validity of symptoms was determined by assessing the degree to which symptoms observed or reported during an interview were observed in daily behavior. Results indicated that most signs and symptoms of major depression and melancholia can be reliably rated by clinicians during a semistructured interview. Ratings of observable symptoms (signs) assessed during the interview were valid indicators of dysfunction observed in daily behavior. Several but not all ratings based on patient report of symptoms were at variance with observation. These discordant patient-reported symptoms may have value as subjective reports but were not accurate descriptions of observed dysfunction.

Adolescent↗
PubMed1986

Alpha 2-adrenergic receptor function in depression. The cortisol response to yohimbine.

There is evidence that the abnormalities in hypothalamic-pituitary-adrenal (HPA) axis function observed in patients with depression may be related to changes in central neurotransmitter receptor function. To evaluate this possibility further, the alpha 2-adrenergic receptor antagonist yohimbine hydrochloride, which increases brain norepinephrine turnover, was administered to 40 patients with DSM-III major depression (18 melancholic, 22 nonmelancholic) and 16 healthy controls. Plasma free 3-methoxy-4-hydroxyphenylglycol (MHPG) level was measured as an index of noradrenergic function, and plasma cortisol level was used to assess the HPA response. Baseline cortisol levels were elevated in melancholic depressed patients, but not in nonmelancholic patients, when compared with healthy controls. The cortisol response to yohimbine was significantly greater in depressed patients than in controls, despite similar MHPG responses between groups. Since there is evidence that stimulation of postsynaptic alpha 2-adrenergic receptors inhibits HPA axis function, the abnormally increased cortisol response to the alpha 2-antagonist yohimbine suggests a relative subsensitivity of postsynaptic alpha 2-adrenergic receptors in depression.

Adult↗
PubMed1986

Desipramine-yohimbine combination treatment of refractory depression. Implications for the beta-adrenergic receptor hypothesis of antidepressant action.

Preclinical investigations have shown that combined administration of the alpha 2-adrenergic receptor antagonist yohimbine hydrochloride and the tricyclic antidepressant desipramine hydrochloride produces a reduction in brain beta-adrenergic receptor function within four days. Since the ability of antidepressant treatments to reduce beta-adrenergic receptor function has been hypothesized to mediate antidepressant efficacy, it was predicted that combined desipramine-yohimbine treatment would be a more rapid-acting and potent antidepressant regimen than desipramine alone. In the present investigation, the effects of desipramine (N = 11) and desipramine-yohimbine (N = 10) treatment on depressive symptoms, norepinephrine turnover, and blood pressure were determined in patients with major depression who had a history of nonresponse to standard antidepressant treatments. Neither desipramine nor desipramine-yohimbine proved to be an effective treatment, although concomitant yohimbine administration did attenuate the ability of desipramine to decrease plasma free and 24-hour urinary 3-methoxy-4-hydroxyphenyl-ethyleneglycol levels and blood pressure. Fifteen of the 21 patients eventually had a good response to pharmacologic treatments, particularly a desipramine-lithium carbonate or lithium carbonate-tranylcypromine sulfate combination treatment (11 of 14 responded). This study provides evidence against the beta-adrenergic receptor hypothesis of antidepressant action.

Adult↗