Akathisia and Metoclopramide

Jungmann, E.; Schöffling, Κ.

doi:10.1016/s0140-6736(82)91077-7

Cited by 21 publications

(15 citation statements)

References 3 publications

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“…The visual analogue scales represent an attempt to elucidate the impressions of volunteers in previous studies who would report vaguely unpleasant experiences which were visible externally by their fidgety limbs and desire to get up. These symptoms have been reported previously (Bateman et al, 1978;Barnes et al, 1982;Jungmann & Schoffling, 1982) (Jungmann & Schoffling, 1982;Strum et al, 1983). The incidence of akathisia in the present study is similar to the six out of seven subjects who experienced akathisia in the study by Bateman et al (1978).…”

Section: Discussionsupporting

confidence: 85%

A comparison of the gastric and central nervous system effects of two substituted benzamides in normal volunteers.

McClelland¹,

Sutton²

1986

Brit J Clinical Pharma

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1 Eight healthy male volunteers participated in a single-blind, random allocation, crossover, comparison of intravenous metoclopramide (10 mg), the peripherally acting, gastrointestinal stimulant BRL 20627 (10 mg) and saline. 2 The central nervous system effects were assessed by quantitative electroencephalography (EEG) and by visual analogue scales. Gastric motility and emptying were assessed by epigastric impedance.3 Metoclopramide increased the EEG amplitude by 10.4% (a statistically significant, P < 0.05, effect) and increased frequencies above 22 Hz, whereas both BRL 20627 and placebo had only minor effect on the EEG frequencies and slightly decreased the EEG amplitude. Ratings on visual analogue scales showed that metoclopramide caused statistically significant (P < 0.01 difference from placebo) restlessness and slight but significantly less (P < 0.05 difference from placebo) feeling of happiness. 4 Epigastic impedance changes indicated that both metoclopramide and BRL 20627 increased gastric contractile activity, but the rate of gastric emptying was not significantly altered by either drug although it tended to be shortened following metoclopramide but not BRL 20627 treatment. 5 It is concluded that since the published animal data show that BRL 20627 has only weak dopamine antagonistic properties this study further implicates dopamine receptor blockade in the akathisia but not in the gastric effect of metoclopramide.

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Section: Discussionsupporting

confidence: 85%

A comparison of the gastric and central nervous system effects of two substituted benzamides in normal volunteers.

McClelland¹,

Sutton²

1986

Brit J Clinical Pharma

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“…The incidence of akathisia caused by metoclopramide varies in the literature 4 13–15 17 18 35 36. In a study of the effect of metoclopramide on prolactin and aldosterone, the incidence of akathisia was 25% after receiving 10 mg of metoclopramide intravenously 13.…”

Section: Discussionmentioning

confidence: 99%

“…In a study of the effect of metoclopramide on prolactin and aldosterone, the incidence of akathisia was 25% after receiving 10 mg of metoclopramide intravenously 13. For intravenous 10 mg bolus doses of metoclopramide, the incidence of restlessness seems to range from 20–25% 13 14. The speed of administration seems to be an important factor in determining the incidence of akathisia induced by metoclopramide 14 37.…”

Section: Discussionmentioning

confidence: 99%

“…It includes a subjective component that consists of intense feelings of internal discomfort and tension with a compulsive urge to move, as well as an objective component characterised by motor agitation, particularly affecting the legs, resulting in the observable inability to remain still either while sitting or standing 11 12. The reported incidence of akathisia is 20–25% after the intravenous administration of 10 mg metoclopramide to unpremedicated patients 13 – 15…”

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confidence: 99%

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Intravenous administration of metoclopramide by 2 min bolus vs 15 min infusion: does it affect the improvement of headache while reducing the side effects?

Parlak

Erdur

Parlak

et al. 2007

Postgraduate Medical Journal

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Objective: To determine the therapeutic effect (alleviation of vascular type headache) and side effects of a slow intravenous metoclopramide infusion over 15 min compared with those effects of a bolus intravenous metoclopramide infusion over 2 min in the treatment of patients with recent onset vascular type headache. Material and methods: All adults treated with metoclopramide for vascular type headache were eligible for entry into this clinical randomised double blinded trial. This study compared the effects of two different rates of intravenous infusion of metoclopramide over a period of 13 months at a university hospital emergency department. During the trial, side effects and headache scores were recorded at baseline (0 min), and then at 5, 15, 30 and 60 min. Repeated measures analysis of variance was used to compare the medication's efficacy and side effects. Results: A total of 120 patients presenting to the emergency department met the inclusion criteria. Of these, 62 patients (51.7%) were given 10 mg metoclopramide as a slow intravenous infusion over 15 min (SIG group) and 58 patients (48.3%) were given 10 mg metoclopramide intravenous bolus infusion over 2 min (BIG group). 17 of the 58 patients in the BIG group (29.3%) and 4 of the 62 patients (6.5%) in the SIG group had akathisia (p = 0.001). There were no significant differences between the BIG and SIG groups in terms of mean headache scores (p = 0.34) and no adverse reactions in the study period. Metoclopramide successfully relieved the headache symptom(s) of patients in both the BIG and SIG groups. Conclusion: Slowing the infusion rate of metoclopramide is an effective strategy for the improvement of headache and reducing the incidence of akathisia in patients with vascular type headache.

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“…Incidence ranges from 10 to 25% depending on the mode of metoclopramide administration [66,67]. Oral and intramuscular formulations have a lower rate of akithisia compared with intravenous administration.…”

Section: Extrapyramidal Reactionsmentioning

confidence: 99%

Metoclopramide in the treatment of diabetic gastroparesis

Lee¹,

Kuo²

2010

Expert Review of Endocrinology & Metabolism

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Gastroparesis is a chronic disorder that affects a significant subset of the population. Diabetes mellitus is a risk factor for the development of gastroparesis. Currently, metoclopramide is the only US FDA-approved medication for the treatment of gastroparesis. However, the FDA recently placed a black-box warning on metoclopramide because of the risk of related side effects, including tardive dyskinesia, the incidence of which has been cited to be as high as 15% in the literature. This review will investigate the mechanisms by which metoclopramide improves the symptoms of gastroparesis and will focus on the evidence of clinical efficacy supporting metoclopramide use in gastroparesis. Finally, we seek to document the true complication risk from metoclopramide, especially tardive dyskinesia, by reviewing the available evidence in the literature. Potential strategies to mitigate the risk of complications from metoclopramide will also be discussed. Keywords diabetes mellitus; gastroparesis; metoclopramide; tardive dyskinesiaGastroparesis is a chronic disorder characterized by impaired gastric emptying and altered motility in the upper GI tract in the absence of mechanical obstruction. It is estimated to affect approximately 5 million individuals in the USA and is most often seen in young individuals with a mean age of onset of 34 years. There is a large female-to-male predominance (4:1 ratio), and gastroparesis is frequently seen in diabetics [1]. It generally presents with nonspecific symptoms including early satiation, nausea, emesis, bloating, abdominal pain, heartburn, anorexia and weight loss. Gastroparesis is likely a heterogeneous condition with the most common etiologies having been identified as idiopathic (36%) and diabetes mellitus (30%) [2]. Numerous physiological factors may contribute to symptoms such as abnormalities in liquid and solid meal emptying, emptying of indigestible objects (e.g., fiber), and gastric and proximal small bowel contractility.The pathophysiology behind gastroparesis is varied and depends upon the etiology of disease. Vagal and/or autonomic neuropathy [3,4] play an important role in the development of diabetic gastroparesis and it is estimated to occur in up to 20-40% of patients with

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Akathisia and Metoclopramide

Cited by 21 publications

References 3 publications

A comparison of the gastric and central nervous system effects of two substituted benzamides in normal volunteers.

A comparison of the gastric and central nervous system effects of two substituted benzamides in normal volunteers.

Intravenous administration of metoclopramide by 2 min bolus vs 15 min infusion: does it affect the improvement of headache while reducing the side effects?

Metoclopramide in the treatment of diabetic gastroparesis

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