Thyrotrophin-Releasing Hormone (TRH) Stimulation Test in Manic-Depressive Illness

Kirkegaard, C.; Bjørum, N.; Cohn, D.; Lauridsen, Ulrik Birk

doi:10.1001/archpsyc.1978.01770320111011

Cited by 106 publications

(19 citation statements)

References 14 publications

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“…Similar data have been reported by previous authors [8][9][10][11][12][13]. Also, our patients tended to have higher posttreatment TSH values at 14.00 and 24.00 h, in comparison to their pretreatment values; however, this difference reaches statistical signif icance for only TSH values at 24.00 h. These findings are not at variance with Kirkegaard et al's [14] demonstra tion that the acute administration of neuroleptics to 10 normal subjects resulted in a significant increase in the TSH response to TRH, compared to the control experi ment which was performed to them 1 week before the second TRH test. The above findings might be consid ered as suggesting that the sensitivity of the pituitary thyrotrophs to stimulation with TRH at 14.00 and 24.00 h of the same day, particularly at 24.00 h, in our schizophrenic patients was increased during the 6 weeks' neuroleptic treatment.…”

Section: Discussionsupporting

confidence: 92%

Effects of Six Weeks’ Neuroleptic Treatment on the Pituitary-Thyroid Axis in Schizophrenic Patients

et al. 1986

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In order to investigate (a) the effects of 6 weeks’ neuroleptic treatment on the pituitary-thyroid axis in 25 male schizophrenic patients, and (b) the diurnal variation in the thyrotropin (TSH) and prolactin (PRL) responses to thyrotropin-releasing hormone (TRH) in these patients, the TRH stimulation test was performed in each of them at 14.00 and 24.00 h of the same day, both before and after 6 weeks’ treatment with neuroleptics (chlorpromazine or fluspirilene). Also, serum thyroxine (T₄), in vitro radioactive triiodothyronine uptake (RT3 U) and free-thyroxine index (FTI) values were estimated from the pre-TRH blood sample. We found no evidence of diurnal variation in the TSH response to TRH in the schizophrenic patients, before or after 6 weeks’ neuroleptic treatment. Only drug-free schizophrenic patients had significantly higher PRL responses to TRH at 14.00 h than those at 24.00 h. After 6 weeks’ neuroleptic treatment, schizophrenic patients tended to have lower FTI values; also, they had significantly higher basal TSH and PRL values, as well as significantly augmented TSH and PRL responses to TRH, in comparison to their pretreatment values. These findings render possible the diagnosis of subclinical hypothyroidism in neuroleptic-treated schizophrenic patients.

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Section: Discussionsupporting

confidence: 92%

Effects of Six Weeks’ Neuroleptic Treatment on the Pituitary-Thyroid Axis in Schizophrenic Patients

et al. 1986

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“…The second approach involves the synthesis of positron-labeled ligands or drugs of interest in the study of patients with affective disorders and other psychiatric diseases. With such agents local brain pharmacokinetics can be measured in vivo {l, 21. In addition, positronlabeled ligands for various receptor classes can be studied in a homogeneous psychiatric population.…”

Section: Pet Methods and Data Analysismentioning

confidence: 99%

Positron emission tomographic study of affective disorders: Problems and strategies

et al. 1984

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Because anatomical studies of psychiatric disorders in humans have been largely unsuccessful, and because pharmacological interventions in patients with mental illness can be analyzed by means of biochemical assay techniques, positron emission tomography (PET) provides an exciting new means to study mental illness. Using fluorine-18-labeled fluorodeoxyglucose and PET to measure local cerebral glucose utilization, the investigators examined patients with affective disorders and normal age-matched controls. Patients with unipolar depression were studied in a drug-free baseline state following short-term administration of methylphenidate and in a euthymic state in long-term follow-up. Patients with bipolar disorders were studied in either the manic or depressed phases of illness and again in a euthymic state in long-term follow-up. Age-matched controls were studied both with and without methylphenidate administration. The results demonstrate that metabolic subgrouping of patients may be possible. Mood changes produced by pharmacological agents resulted in changes in the patterns of metabolism when compared with the baseline state. Problems associated with the use of PET to study mental illness fall into the categories of patient classification (diagnosis, state, trait, ambient conditions, and mental processes) and data analysis (anatomical and statistical). These problems, the limitations of the present techniques, and strategies for their improvement are discussed. Despite these difficulties, PET should prove to be a fruitful means of exploring the human biochemical abnormalities associated with mental illness.

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“…However, in a study of a mixture of patients with unipolar depression, bipolar depression, mania, and mixed manicdepressive disorder, the TSH response to the infusion of 200 μg of thyrotropin-releasing hormone was decreased in all these disorders compared with the response of patients with reactive depression, paranoid psychosis, or neurotic depression [27]. Bottlender and colleagues [28] reported that the switch rate to mania was significantly higher in a group of patients with a lower basal TSH level than in a group of patients with a higher basal TSH among those who were admitted due to bipolar depression.…”

Section: Hypothalamic-pituitary-thyroid Axis/thyroid Hormonesmentioning

confidence: 94%

Switching to Hypomania and Mania: Differential Neurochemical, Neuropsychological, and Pharmacologic Triggers and Their Mechanisms

Fang

Kemp

Calabrese

et al. 2010

Curr Psychiatry Rep

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Current data suggest that monoamines, acetylcholine, amino acids, cortisol, thyroid hormones, and melatonin may be involved in the pathophysiology of bipolar disorder (BPD). Any neuropsychological or pharmacologic factor causing a disturbance in these neurochemicals may trigger manic/hypomanic switching. Antidepressants, stimulants, anticholinergics, steroids, and thyroid hormone have been reported to cause treatment-emergent mania (TEM) in BPD, but only recently have the traditional antidepressants been systematically studied. Paroxetine, 20 mg/d, monotherapy in treatment of acute, relatively "pure" bipolar I and II depression, and fluoxetine monotherapy in bipolar II depression conferred a similar risk as placebo for TEM. Paroxetine or bupropion adjunctive therapy to mood stabilizer(s) had a similar risk as placebo for treatment of TEM in real world patients with bipolar depression during continuation treatment. Venlafaxine was shown to have an increased risk of TEM compared with bupropion and sertraline. The evolving literature continues to support the role of mood stabilizers in preventing future mood episodes of BPD.

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Thyrotrophin-Releasing Hormone (TRH) Stimulation Test in Manic-Depressive Illness

Cited by 106 publications

References 14 publications

Effects of Six Weeks’ Neuroleptic Treatment on the Pituitary-Thyroid Axis in Schizophrenic Patients

Effects of Six Weeks’ Neuroleptic Treatment on the Pituitary-Thyroid Axis in Schizophrenic Patients

Positron emission tomographic study of affective disorders: Problems and strategies

Switching to Hypomania and Mania: Differential Neurochemical, Neuropsychological, and Pharmacologic Triggers and Their Mechanisms

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