Disease relevance of biperiden

• After biperiden treatment, however, hypercapnia elicited a response profile similar to that elicited by air, whereby subjective anxiety remained similar to preinhalation levels [1].
• The extent of sinus arrhythmia suppression was inversely correlated with the degree of M1 selectivity of the drugs used, advocating the use of M1-selective antiparkinsonian anticholinergics like biperiden in the treatment of extrapyramidal side effects [2].
• Consequently, the cardiac autonomic function was not affected by biperiden or the change in parkinsonism [3].
• We compared the effect of biperiden (M1 selective anticholinergic) and amantadine (dopaminergic) on neuroleptic-induced parkinsonian extrapyramidal symptoms (EPS) and tardive dyskinesia (TD)-type involuntary movements [4].
• In a schizophrenic patient, hypothermia was caused by combined treatment with zotepine, biperiden, and fluphenazine, although combined treatment with zotepine and biperiden had caused no side effects [5].

Psychiatry related information on biperiden

• Dose dependent inhibition of REM sleep in normal volunteers by biperiden, a muscarinic antagonist [6].
• The effects of biperiden on nap sleep after sleep deprivation in depressed patients [7].
• In three cases akathisia occurred; biperiden administration was necessary three times [8].
• We report the case of a 29-year-old patient with chronic non-active hepatitis C, a previous psychiatric history of polydrug abuse (cannabis, heroin and illegal use of the psychotropic drug biperiden) and anxiety disorder [9].
• Trihexyphenidyl increased wakefulness and decreased REM sleep while biperiden decreased REM sleep selectively [10].

High impact information on biperiden

• Twenty-three patients developed dystonia, two of them despite being treated with biperiden [11].
• The muscarinic antagonist biperiden produces a dose-dependent inhibition of (REM) sleep on acute administration [12].
• Development of tolerance after repeated administration of a selective muscarinic M1 antagonist biperiden in healthy human volunteers [12].
• Comparison of central and peripheral pharmacologic effects of biperiden and trihexyphenidyl in human volunteers [13].
• Biperiden treatment was associated with significantly lower scores on Benton Visual Retention Test (P < 0.003) and the visual subscale of Wechsler Memory Scale (WMS) (P < or = 0.02), with a trend to poorer scores on WMS total (P = 0.086) and the digit span (P = 0.07) and logical memory (P = 0.06) subscales [14].

Chemical compound and disease context of biperiden

• Carteolol, as well as propranolol and biperiden, inhibited the haloperidol-induced catalepsy [15].
• The effect of pilocarpine and biperiden on salivary secretion during and after radiotherapy in head and neck cancer patients [16].
• We examined this effect induced by trihexyphenidyl and biperiden, clinically used in the parkinsonism and schizophrenic patients, by using passive avoidance tasks [17].
• We investigated the effect of an anticholinergic (biperiden) and a dopamine agonist (apomorphine) on tremor, rigidity, and akinesia in patients with idiopathic Parkinson's disease [18].
• The rabbits, which were pretreated with indomethacin and a muscarinic antagonist (biperiden), responded with miosis to both CGRP fragments [19].

Biological context of biperiden

• In contrast, only biperiden prolonged the latencies of the evoked potentials (N1 peak, distal oesophagus: BIP 191 ms, TC 102 ms, saline 101 ms; P < 0.01; P1 peak: BIP 322 ms, TC 161 ms, saline 144 ms; P < 0.01) [20].
• Synaptosomal high-affinity uptake of [3H]DA was only weakly affected by budipine and biperiden (IC50 values, 11 and 9 microM, respectively) [21].
• METHODS: Nine healthy volunteers were randomized to receive 1.2 mg trospium chloride (TC), 5 mg biperiden (BIP) or saline i.v. Primary peristalsis was elicited by swallowing a 5 mL water bolus and secondary peristalsis by insufflation of 20 mL air, 10 times each [20].
• The effects of fasting on the pharmacokinetics of biperiden in rats were examined [22].
• Effect of fat tissue volume on the distribution kinetics of biperiden as a function of age in rats [23].

Anatomical context of biperiden

• The evoked overflow of [3H] in caudate nucleus slices preincubated with [3H]GABA was reduced by both budipine and biperiden [21].
• CONCLUSIONS: Both anticholinergic drugs depress oesophageal motility, but only the centrally-acting anticholinergic drug biperiden modifies the oesophageal evoked potentials, suggesting a central cholinergic transmission of the oesophageal afferent pathways [20].
• PURPOSE: We examined the subcellular distribution of the basic drugs, chlorpromazine (CPZ), imipramine (IMP) and biperiden (BP), in rat liver, and evaluated the contribution of lysosome (Lys) to their intracellular distribution in comparison with that of mitochondria (Mit) [24].
• These results suggest that the observed decrease of Vdss/BW in fasted rats reflects reduced capacity to trap biperiden in the body, especially in adipose tissue [22].
• METHODS: In an in vivo distribution, the concentrations of CPZ, IMP and BP in the liver subcellular fractions were determined [24].

Associations of biperiden with other chemical compounds

• 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 [25].
• The binding was markedly reduced in all brain regions after pretreatment with the non-selective muscarinic antagonist dexetimide and also the M1 antagonist biperiden [26].
• This result suggests that coadministration of haloperidol and biperiden specifically affects the ubiquitin-related system [27].
• The oral administration of levodopa significantly improved both the responses, whereas biperiden was ineffective [28].
• It is concluded that budipine and biperiden are use-dependent (uncompetitive) antagonists at the NMDA receptor, binding to the receptor-linked ion channel, but probably not to the MK-801 binding site [29].

Gene context of biperiden

• In the presented case fluvoxamine-induced akathisia in an OCD patient was partially resistant to the anticholinergic agent biperiden, and was successfully treated with the 5-HT2A/5-HT2C antagonist mianserin [30].
• Sabcomeline was not a selective ligand to M1 receptors as compared with biperiden in vivo [31].
• A similar effect has been reported with scopolamine, a nonselective muscarinic antagonist, but the main difference is that biperiden withdrawal was not followed by an REM sleep rebound [12].
• Biperiden treatment did not influence the effect of PE on the PRL levels [32].
• In comparison to biperiden, which has also antimuscarinic and NMDA receptor antagonistic properties, the anti-NMDA action of budipine is more prominent [33].

Analytical, diagnostic and therapeutic context of biperiden

• Twenty-six chronically medicated schizophrenic (DSM-III-R) in-patients received amantadine (200 mg/day) or biperiden (4 mg/day) for two weeks in a double-blind cross-over design [14].
• All the volunteers were studied under sleep laboratory conditions as follows: one acclimatization night, one baseline night, four nights with auditory stimulation either with placebo or biperiden, and two follow-up nights [34].
• One year after completed therapy, the quantity of secreted saliva could only be measured in the patients receiving biperiden during radiotherapy: it amounted to 16% of the average quantity of saliva secreted before the beginning of irradiation [16].
• In the first experiment a dose-response analysis was performed with intraventricular injection (IV ventricle) of biperiden [35].
• Aims and methods: In order to elucidate the neural mechanisms of delirium, we administered the anticholinergic drug, biperiden (40 mg/kg i.p.), to 10 adult male Wistar rats and examined the resulting polygraphic recordings, including electroencephalography (EEG), electrooculography (EOG), and electromyography (EMG), for 60 min following injection [36].

References