Disease relevance of trihexyphenidyl

• Although trihexyphenidyl has been used effectively for many years in the treatment of Parkinson's disease, little is known about its pharmacokinetics [1].
• Palatal myoclonus responding to trihexyphenidyl [2].
• The author describes the case of a patient who received neuroleptics and antiparkinsonian medications for more than 7 years and whose tardive dyskinesia symptoms disappeared after trihexyphenidyl was discontinued [3].
• Amantadine versus trihexyphenidyl in the treatment of neuroleptic-induced parkinsonism [4].
• In a patient with the syndrome of crural paresis and homolateral ataxia, administration of trihexyphenidyl resulted in improvement of disabling unilateral ataxia and gross intention tremor [5].

Psychiatry related information on trihexyphenidyl

• Effects of chronic treatment with trihexyphenidyl and carbamazepine alone or in combination with haloperidol on substance P content in rat brain: a possible implication of substance P in affective disorders [6].
• Trihexyphenidyl as a possible therapeutic option in clozapine-induced nocturnal enuresis [7].
• The amnestic state produced by biperiden and trihexyphenidyl was comparable to that observed after the administration of scopolamine [8].
• We report a case of severe withdrawal akathisia associated with suicidal and autoaggressive behaviour during a gradual transition from perphenazine/trihexyphenidyl to clozapine [9].
• In this study the anticholinergic drug, trihexyphenidyl, at low doses when administered chronically for one month to Parkinson disease patients caused a decrease in performance on recent but not immediate memory tests [10].

High impact information on trihexyphenidyl

• Using a sensitive radioreceptor assay for anticholinergic drugs, we assayed trihexyphenidyl in human serum and studied its pharmacokinetics following short-term and long-term administration to patients with dystonia [1].
• Pharmacokinetics of trihexyphenidyl after short-term and long-term administration to dystonic patients [1].
• METHODS: In a double-blind, randomized study we recorded the EMG activities of 420 neck muscles in 42 patients with CD before and after treatment with BTA or trihexyphenidyl [11].
• BACKGROUND: Botulinum toxin type A (BTA) is replacing trihexyphenidyl as the treatment of choice for idiopathic cervical dystonia (ICD), but there has never been a direct comparative study [12].
• Botulinum toxin versus trihexyphenidyl in cervical dystonia: a prospective, randomized, double-blind controlled trial [12].

Chemical compound and disease context of trihexyphenidyl

• Simultaneous Abnormal Involuntary Movement Scale ratings revealed no change in the dyskinetic movements between the conditions; there was a significant subjective improvement reported by the patients following the trihexyphenidyl HCl administration [13].
• The NT-induced catalepsy was inhibited by pretreatment with atropine, trihexyphenidyl or biperiden (each drug, 0.8-5.0 mg/kg, IP), anticholinergic drugs, and L-DOPA (100, 200 mg/kg, IP) [14].
• The dose of tetrabenazine was aimed at 75 mg daily; pimozide was increased (6 to 25 mg/day) until the dystonia was relieved or Parkinsonism and other side-effects prevented further increments; if necessary benzhexol (6 to 30 mg/day) then was added to control side-effects and to provide additional benefit [15].
• An electromyographic method was used to study the effect of combination therapy with L-dopa and trihexyphenidyl on tremor in thirty patients suffering from extrapyramidal motor system disease [16].
• Blepharospasm: a case study comparison of trihexyphenidyl (Artane) versus EMG biofeedback [17].

Biological context of trihexyphenidyl

• In this double-blind, randomized study, indices of central (memory, sedation) and peripheral (salivation, ratio of R-R interval on electrocardiogram) muscarinic function were evaluated in 14 healthy volunteers who received trihexyphenidyl, biperiden, and placebo [18].
• In the second experiment, trihexyphenidyl was administered in several doses (from 0.2 to 1.6 mg/kg), before the administration of oxotremorine, a muscarinic agonist, at a dose that readily facilitates masculine sexual behavior [19].
• In sham-operated rats, trihexyphenidyl administration produced a significant increase (17-27%) in M1 binding sites [20].
• The trihexyphenidyl administration in 6-hydroxydopamine-lesioned animals was unable to reproduce the up-regulation of M1 receptors, even in the intact neostriatum [20].
• 1 The absorption and tissue distribution of orally administered [14C]-chlorpromazine (CPZ) were compared in trihexyphenidyl (THP; Artane)-treated and control rats [21].

Anatomical context of trihexyphenidyl

• Scopolamine and trihexyphenidyl inhibited ex vivo binding of [3H] pirenzepine to M1 receptors in cerebral cortex, indicating ready penetration into the brain [22].
• Actions of trihexyphenidyl and benztropine on squid axon membranes [23].
• To test this hypothesis, we have examined in rats whether trihexyphenidyl, an antimuscarinic drug of wide clinical use, can counteract the changes in preproenkephalin, preprotachykinin and preprodynorphin messenger RNA expression produced by a unilateral 6-hydroxydopamine lesion of substantia nigra dopaminergic neurons [20].
• High stereoselectivity was observed for the enantiomers of trihexyphenidyl and trihexyphenidyl methiodide at muscarinic M1-receptors in field-stimulated rabbit vas deferens and at M2 alpha- and M2 beta-receptors in guinea-pig atrium and ileum, respectively [24].
• A strong correlation was found between the ratio of decrease in K(p,sf) after NH4Cl treatment and the specific activity of acid phosphatases, a marker of lysosomes, in each fraction (biperiden, r = 0.948; trihexyphenidyl, r = 0.945) [25].

Associations of trihexyphenidyl with other chemical compounds

• Effect of anticholinergic agents upon acquired nystagmus: a double-blind study of trihexyphenidyl and tridihexethyl chloride [26].
• Dicyclomine, trihexyphenidyl and pirenzepine demonstrated the highest affinity for the M1 muscarinic receptor subtype as revealed in competition experiments against [3H]-pirenzepine labelling of cortical membranes [27].
• Twelve adults with severe axial dystonia, and two children with life-threatening generalised dystonia were treated with a combination of a low constant dose of tetrabenazine to which were added pimozide and benzhexol as necessary [15].
• The effects of a combination of trihexyphenidyl and L-DOPA methyl ester given i.m. were studied 3-5 years after MPTP induced hemiparkinsonism in five female adult Macaca nemistrina monkeys [28].
• The effects of co-administration of benzhexol on the peripheral pharmacokinetics of oral levodopa in young volunteers [29].

Gene context of trihexyphenidyl

• Using a radioreceptor technique, we assayed serum trihexyphenidyl levels in patients with dystonia being treated chronically with high dosage [30].
• In conclusion, with the exception of preprodynorphin messenger RNA, trihexyphenidyl treatment was unable to counteract the imbalance in prepropeptide messenger RNA expression produced by a unilateral striatal dopaminergic denervation and even amplified this effect [20].
• The effects of the antiparkinsonian agent trihexyphenidyl, a selective M1 muscarinic cholinergic receptor antagonist, were studied in doses of 100, 320 and 1000 micrograms/kg i.m. alone [31].
• 5. The present study shows that the muscarinic receptors coupled to stimulation of adenylyl cyclase in the olfactory bulb display high stereoselectivity for the enantiomers of trihexyphenidyl [32].
• The purpose of this work was to characterize a novel ethosomal carrier containing trihexyphenidyl HCl (THP) and to investigate the delivery of THP from ethosomes versus classic liposomes [33].

Analytical, diagnostic and therapeutic context of trihexyphenidyl

• Electromyography in cervical dystonia: changes after botulinum and trihexyphenidyl [11].
• Development and application of a specific and sensitive radioimmunoassay for trihexyphenidyl to a pharmacokinetic study in humans [34].
• Capillary gas chromatography of trihexyphenidyl, procyclidine and cycrimine in biological fluids [35].
• Following their s.c. injection, trihexyphenidyl, atropine, dicyclomine, secoverine and methylatropine but not pirenzepine, inhibited both yawning and analgesia; there were clear differences in their potencies on the two responses [36].
• Trihexyphenidyl, a synthetic anticholinergic, used to control extrapyramidal symptoms arising from neuroleptic drug therapy has been a subject of controversy regarding the need for continuous antiparkinsonian therapy [37].

References