Biperiden effects and plasma levels in volunteers

Hollmann, Markus W.; Brode, E; Greger, G.; Müller-Peltzer, Herbert; N, Wetzelsberger

doi:10.1007/bf00556903

Cited by 34 publications

(17 citation statements)

References 3 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Peak plasma concentrations of 4 to 5 ~g/L occur within 1 to 1.5 hours in healthy volunteers following an oral dose of biperiden 4mg (Hollman et al 1984;Ottoila & Taskinen 1981), with a lag time of 0.5 hours to the appearance of detectable concentrations in the plasma. Oral bioavailability was 29%.…”

Section: Absorption and Distributionmentioning

confidence: 98%

Clinical Pharmacokinetics of Anti-Parkinsonian Drugs

Cedarbaum

1987

Clinical Pharmacokinetics

172

View full text Add to dashboard Cite

Of the neurological disorders, none can claim a battery of therapeutic agents based upon as rational a pharmacology as can Parkinson's disease. In this review, the clinical pharmacokinetics of the major classes of anti-Parkinsonian drugs is discussed. Although they are the oldest drugs in the anti-Parkinsonian armamentarium, little pharmacokinetic data are available regarding the anticholinergic and antihistaminic agents. Based on elimination half-lives of 10 to 18 hours, most could probably be effectively given on a twice-daily schedule. Amantadine is unique among anti-Parkinsonian agents both in lacking a clearly defined mechanism of action and in being eliminated from the body exclusively by renal excretion of unchanged drug. Thus the normal decline of renal function in the elderly Parkinsonian population becomes an important factor in avoiding potential drug toxicity. The pharmacokinetics and pharmacodynamics of levodopa are complex. Since it is an amino acid, it follows metabolic pathways and must compete for absorption and brain uptake with a number of large neutral amino acids. It has a short elimination half-life and, as Parkinson's disease progresses, the brain loses its capacity to store the drug and becomes dependent in a moment-to-moment fashion on plasma levodopa concentrations, creating therapeutic response fluctuations in over 50% of patients. Pharmacokinetic considerations in the management of these response fluctuations are discussed. The newest class of anti-Parkinsonian agents are the direct acting dopamine receptor agonists. These drugs, all derivatives of ergot, have more prolonged durations of anti-Parkinsonian action than levodopa. However, other than bromocriptine, clinical experience with members of this class of drugs is still limited.

show abstract

Section: Absorption and Distributionmentioning

confidence: 98%

Clinical Pharmacokinetics of Anti-Parkinsonian Drugs

Cedarbaum

1987

Clinical Pharmacokinetics

172

View full text Add to dashboard Cite

show abstract

“…In addition, cholinergic activation is associated with EEG desynchronization and arousal from sleep, and no oral cholinergic agent with an adequate half-life was available. We selected biperiden as the anticholinergic agent for the following reasons: (1) it is selective for M 1 receptors, causes fewer peripheral anticholinergic side effects, and is better tolerated by subjects (Syvalahti et al 1987;Eltze and Figala 1988;Avissar and Schreiber 1989); (2) its blockade of catecholamine reuptake is less pronounced than that of other oral anticholinergics (Horn et al 1971;Modell et al 1989); and (3) its pharmacokinetics make it a good choice for studying cholinergic mechanisms in sleep (Hollmann et al 1984;Grimaldi et al 1986;Gillin et al 1991). There were no other reports on the effects of biperiden on sleep measures when we started our study, and the doses of 6 and 10 mg that were selected were somewhat higher than those used in two studies that were published subsequently (Gillin et al 1991;Salin-Pascual et al 1991).…”

Section: Effects Of Biperiden On Polysomnographic Measures In Schizopmentioning

confidence: 99%

The Cholinergic System in Schizophrenia Reconsidered: Anticholinergic Modulation of Sleep and Symptom Profiles

Tandon

Taylor

DeQuardo

et al. 1999

Neuropsychopharmacology

View full text Add to dashboard Cite

Receptors, Cholinergic; Receptors, muscarinic; Parasympathetic nervous system; Sleep, REM; Symptoms, positive; Symptoms, negative The dopamine (DA) hypothesis has dominated biochemical and pharmacological research on schizophrenia for about two decades. Although pharmacological data implicate increased DA activity in the pathogenesis of positive symptoms of schizophrenia, there is minimal association with negative symptoms (Crow 1980;Andreasen and Olsen 1982;Angrist et al. 1980). The poorly elucidated pathogenesis of negative symptoms and the unique properties of the atypical antipsychotic clozapine (Jibson and Tandon 1998) have encouraged a reappraisal of the role of the DA system in schizophrenia. Newer approaches to evaluating neurochemical abnormalities in schizophrenia include consideration of other neurotransmitter systems. Models of DA-serotonin (Meltzer 1989), DA-glutamate (Carlsson and Carlsson 1990), DA-acetylcholine (Tandon and Greden 1989), and DA-norepinephrine (van Kammen et al. 1990) interactions have been proposed. Although these models still accord DA a significant role in schizophrenia pathophysiology, they suggest that altered balance between DA and one (or more) of these other neurotransmitter systems may be the principal neurochemical abnormality related to the production of schizophrenic symptoms. Some of the earliest pharmacological treatments for schizophrenia included cholinergic agents (Cohen et al. 1944;Collard et al. 1946;Pfeiffer and Jenney 1957), and in the 1970s, several investigators suggested that cholinergic activity may be reduced in schizophrenia (Friedhoff and Alpert 1973;Janowsky et al. 1973;Davis et al. 1975;Singh and Kay 1979). There was no direct evidence of altered cholinergic functioning in schizophrenic patients, however, and pharmacological trials with cholinergic agents were generally ineffective (Rowntree et al. 1950;Gerlach et al. 1977;Davis and Berger 1978). With few exceptions (Johnstone et al. 1983;Singh et al. 1987), cholinergic mechanisms were increasingly considered irrelevant to the pathophysiology of schizophrenia and discussed predominantly with reference to the treatment of undesirable extrapyramidal side effects of neuroleptics (Richelson 1984). Indirect evidence from several lines of research, however, suggests that the cholinergic system may differentially influence positive and negative symptoms in schizophrenia (Tandon and Greden 1989).We and others have been conducting various studies to evaluate the role of the cholinergic system in schizophrenia, based on a primary hypothesis that DA-acetylcholine (ACh) interactions are of central importance in the production of positive and negative symptoms of schizophrenia (Tandon and Greden 1989;Tandon and Greden 1991). Based on available data and on observations of the course of positive and negative symptoms during the acute phase of the illness (Donlon and Blacker 1973;Docherty et al. 1978;Tandon et al. 1990a), we posited a role for disruption in DA-ACh balance in the expression of positive and negat...

show abstract

“…The Hodges Lehmann estimates and Tukey confidence intervals based on Wilcoxon's signed rank statistic were used to estimate the differences and evaluate the hypothesis that there is no difference in the pharmacokinetic and pharmacodynamic parameters between the three treatment sessions (Hollander 1973). Figure 1 shows the mean remoxipride plasma concentration vs time curves for the single 100 mg remoxipride dose when administered alone and when given 30 min after biperiden.…”

Section: Study Design and Dosagementioning

confidence: 99%

Interaction study between remoxipride and biperiden

Yisak¹,

Farde

Bahr³

et al. 1993

Psychopharmacology

View full text Add to dashboard Cite

Twelve healthy male volunteers took part in a double-blind randomised cross-over study composed of three treatment sessions: remoxipride 100 mg; remoxipride 100 mg plus biperiden 4 mg; and biperiden 4 mg. Plasma and urine concentrations of remoxipride and biperiden, plasma prolactin levels, salivary flow and adverse events were recorded to assess pharmacodynamic interactions. Remoxipride and biperiden had no effect on each other's plasma concentrations. Biperiden did not affect the urinary recovery or renal clearance of remoxipride. Prolactin levels were unaffected by biperiden but increased following remoxipride administration. Differences in prolactin Cmax and tmax following remoxipride versus concomitant (remoxipride + biperiden) treatment were not statistically significant. However, a slight but statistically significant (P = 0.04) increase in prolactin AUC was observed after concomitant treatment. No significant differences could be observed between the recorded salivary flow in all the treatment sessions. Single doses of remoxipride and biperiden showed no pharmacokinetic or pharmacodynamic interaction.

show abstract

Biperiden effects and plasma levels in volunteers

Cited by 34 publications

References 3 publications

Clinical Pharmacokinetics of Anti-Parkinsonian Drugs

Clinical Pharmacokinetics of Anti-Parkinsonian Drugs

The Cholinergic System in Schizophrenia Reconsidered: Anticholinergic Modulation of Sleep and Symptom Profiles

Interaction study between remoxipride and biperiden

Contact Info

Product

Resources

About