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Following a recent report that apomorphine hydrochloride alleviates the involuntary movements of Huntington chorea, we have investigated another dopamine receptor agonist, bromocriptine, in this disease. A double-blind crossover study in six patients showed that rather than improving chorea, bromocriptine induced an exacerbation. This finding supports the view that choreatic movements correlate with overactivity in dopaminergic systems.
Eight women with senile dementia and buccolinguofacial dyskinesias (BLFD) were given bromcriptine mesylate )from 2.5 to 20.0 mg daily). The frequency of their abnormal movements was quantiated by a method consisting of repeated counts (220 measurements per patient). In six patients, the mean frequency of BLFD was lower during bromocriptine mesylate therapy )even at daily doses of 10 mg or less) as compared with placebo; this result was statistically significant in four of the six. The second day after cessation of bromocriptine therapy, there seemed to be a rebound effect in six patients. These phenomena are discussed in light of the possible existence of presynaptic "autoreceptors" that would explain the paradoxical effects produced by a number of dopamine agonists.
Bromocriptine mesylate (2-bromo-alpha-ergocryptine) has proved to be useful in reducing the size of prolactin-secreting pituitary adenomas, but little evidence has accumulated about its effectiveness within the first two weeks of therapy. The patient described herein showed a rapid reduction in the size of the suprasellar extension of a prolactinoma and a dramatic improvement of the primary visual field abnormalities within two weeks of starting bromocriptine therapy. This experience exemplifies the potential use of the drug in acutely decompressing the anterior intracranial visual pathways.
Seven patients with vascular dementia completed an 8-month randomized double-blind crossover trial of bromocriptine in a dosage of up to 30 mg per day. Patients were assessed using a modified UCLA Parkinson Rating Scale of symptoms and signs, and neuropsychological testing including the Wechsler Adult Intelligence Scale-Revised, Wechsler Memory Scale, modified Thurstone Word Fluency Test, Wisconsin Card Sort, a test of visual vigilance, and a reaction time task. Subjects failed to perform significantly better on any measure while on bromocriptine, and on several measures their performance while on the drug was worse.
We administered bromocriptine (Parlodel) to arthritic mice immediately postpartum, and found that the drug suppressed the clinical exacerbation of joint involvement that was seen in untreated animals. Approximately 50% reduction in severity of disease was achieved with bromocriptine (P less than 0.001). The effect may be due to suppression of the prolactin release that normally occurs postpartum.
Myocardial infarction in puerperium is infrequently reported. Spasm, coronary dissection, or atheromatous etiology has been described. Bromocriptine has been implicated in several previous case reports of myocardial infarction in the puerperium. Our case (including an inadvertent rechallenge) suggests such a relationship. Although generally regarded as "safe," possible serious cardiac effects of bromocriptine should be acknowledged.
Bromocriptine is a dopamine agonist that induces postural hypotension and can be used as an antihypertensive. The drug inhibits release of norepinephrine (NE) from an isolated artery by stimulating presynaptic receptors. In normotensive subjects it lowers both plasma and cerebrospinal fluid (CSF) levels of NE by 50% and lowers blood pressure moderately in standing subjects and slightly in recumbent subjects. Through central and peripheral mechanisms, bromocriptine inhibits sympathetic nervous discharge of NE.
Twenty-four cocaine addicts who experienced withdrawal symptoms were studied for six weeks in a double-blind design. Half of the group received daily treatment with bromocriptine and the other half with placebo. Significant relief with bromocriptine was seen almost immediately and continued throughout the detoxification period. The authors speculate that the results are consistent with the "dopamine-depletion model" of cocaine withdrawal.
We studied 77 women with hyperprolactinemic infertility and possible ovulatory disturbances. Galactorrhea was present in 27. Ovulation was normal in 15, 21 were anovulatory and 41 had luteal phase deficiency. All patients received bromocriptine for three months, resulting in normal serum prolactin levels. After that time, if no pregnancy occurred, clomiphene (with or without human chorionic gonadotropin) or human menopausal gonadotropin and human chorionic gonadotropin were added to the treatment. The overall pregnancy rate was 65%. The incidence of hyperprolactinemia in infertile patients is higher than expected, and patients with luteal phase deficiency can benefit from treatment with bromocriptine and ovulatory agents.
In Parkinson's disease, effects of medications on the progression of the underlying disease can be assessed clinically by evaluating patients at baseline prior to treatment and at endpoint following medication washout. With this design, it is critical to employ a washout of sufficient duration to ensure elimination of all symptomatic effects. To assess the time course of resolution of symptomatic effects, we evaluated 31 patients with early Parkinson's disease for 2 weeks following discontinuation of levodopa-carbidopa and bromocriptine after 14 months of treatment. Patients had previously been randomly assigned to treatment with selegiline or placebo, and these had been discontinued 2 months earlier. Data from 20 patients with a clear washout of clinical benefit were used to investigate quantitative models describing the time course of total (Activities of Daily Living + motor) Unified Parkinson's Disease Rating Scale score change. The mean half-life of loss of clinical benefit was 7.9 days (95% confidence interval, 2.2-30.4 days). This indicates that a washout period of 32 days (4 half-lives) may be required to eliminate approximately 90% of the long-term symptomatic effects of levodopa-carbidopa and bromocriptine following their withdrawal from patients with early Parkinson's disease.
Anomia is a commonly found in aphasia and has been attributed to a loss of representations (storage deficit) or to a loss of access to these representations (retrieval deficit). Bromocriptine, a dopamine agonist, was tested on four patients, two men and two women, with nonfluent aphasia. The patients were tested in an open-label ABBA design using a stochastic model that measured the degree of storage and retrieval deficits. All patients showed significant improvements in word retrieval. Bromocriptine may be a useful adjunct in the treatment of selected patients with a nonfluent aphasia in which retrieval deficits play a major role.
The morphological effect of chronic synthetic and secretory inhibition of the intermediate lobe of the rat pituitary induced by bromocriptine treatment was studied using morphometric techniques in combination with electron microscopy. On the basis of granule diameters, a heterogeneous cell population was shown in the normal intermediate lobe. Bromocriptine treatment did not induce any change in the volume fraction, number or location of electron-dense secretory granules. Instead, there was a shift toward a more homogeneous cell population containing smaller granules, the mean granule volume being reduced by approximately 30%. The volume fraction of electron-lucent granules or vacuoles was markedly reduced, indicating a functional significance of these organelles. The volume of the Golgi apparatus was not significantly altered, but the number of condensing granules within the Golgi area was reduced. The volume of the intermediate lobe was decreased, apparently due to a decrease in the mean cell volume.
Effects of fibroblast growth factor (FGF) and of bromocriptine, a dopaminergic receptor agonist, on the mitotic index in the organ-cultured anterior pituitary gland of the rat were investigated, using the colchicine metaphase-arrest technique. It has been found that FGF increases the mitotic index in the anterior pituitary explants. By contrast bromocriptine inhibits the mitogenic effect of FGF.
The pharmacological effects of bromocriptine on human detrusor muscle were investigated by an in vitro isometric method. Both a direct stimulating effect and an anticholinergic effect were demonstrated. These effects, together with an alpha-adrenergic blocking effect reported in a previous paper, are correlated with the published clinical effects of bromocriptine in patients with primary and secondary unstable detrusors.
Porphyrin biosynthesis was examined in the Harderian gland of the male golden hamster by fluorometric assays of gland porphyrin content and by measuring the activity of a rate-limiting enzyme for haem biosynthesis, 5-aminolaevulinic acid synthase. Both porphyrin content and enzyme activity are low in normal male glands but were greatly raised in males castrated for 6 weeks. However, porphyrin synthesis remained at basal levels in castrates given the dopamine agonist bromocriptine; this suppression could be reversed by simultaneous prolactin administration, and castrated males receiving prolactin alone exhibited very high enzyme activity and porphyrin content. Bromocriptine also prevents the morphological feminisation of the Harderian gland which would normally occur after castration; again, the simultaneous administration of prolactin permits feminisation to occur. The results support the hypothesis that, while androgens have an inhibitory effect on porphyrin synthesis within this model, other factors, including prolactin, are permissive.
Porphyrin biosynthesis was examined in the Harderian gland of the female golden hamster by fluorometric assays of gland porphyrin content and by measuring the activity of a rate-limiting enzyme for haem biosynthesis, delta-aminolaevulinic acid synthase. Both porphyrin content and enzyme activity are high in normal female glands. Enzyme activity was lowered in females ovariectomised for 6 weeks, and both enzyme activity and porphyrin content were greatly lowered in ovariectomised females given the dopamine agonist bromocriptine; this suppression could be prevented by simultaneous prolactin administration. Bromocriptine (but not ovariectomy alone) also masculinised the morphology of the Harderian gland, resulting in the appearance of type II cells and polytubular complexes; again, the simultaneous administration of prolactin prevented masculinisation. The results support the hypothesis that while androgens have an inhibitory effect on porphyrin synthesis within this model, prolactin may have a major facilitatory role.
A patient is described with a large prolactinoma with expansion into the sphenoid sinus. During bromocriptine treatment an intrasellar area of gas developed, continuous with the air in the sinus. No operation was performed, bromocriptine was continued. During the regression of the tumor, the area of air disappeared.
Behavioral evidence for tolerance and supersensitivity during and after chronic (30 day) administration of bromocriptine (BRC) or bromocriptine + L-dopa in mice was assessed by measuring wheel running (WR) behavior during and after chronic drug administration, and apomorphine- and methylphenidate-(MP-)induced stereotyped gnawing after termination of chronic injections. In both BRC and BRC + L-dopa groups, tolerance developed fairly quickly to the depressing effect of BRC on WR seen on day 1 of drug administration. Mice receiving BRC showed significant increases in WR by week 2 of chronic drug administration, which persisted for at least two days after the termination of chronic injections. During the first week after termination of chronic injections, low doses of both apomorphine and MP induced significantly more stereotyped gnawing in BRC and BRC + L-dopa mice than in the control mice or the mice treated with L-dopa alone. This behavioral evidence for dopaminergic supersensitivity after chronic BRC administration may have relevance for the clinical use of BRC in combination with L-dopa or other dopamine agonists.