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At least 19 recordsLinked to original sources
PubMed1995

Development and application of a specific and sensitive radioimmunoassay for trihexyphenidyl to a pharmacokinetic study in humans.

A radioimmunoassay (RIA) for trihexyphenidyl was developed through the use of a bovine thyroglobulin conjugate of trihexyphenidyl hemisuccinate. Immunization of New Zealand white rabbits with this drug-protein conjugate yielded antisera, for which the antibody titer and specificity were evaluated. An antiserum that had the highest titer and minimal cross-reactivities to major metabolites of trihexyphenidyl, such as trihexyphenidyl N-oxide (2%), hydroxytrihexyphenidyl (1%), and the antipsychotic drugs fluphenazine (< 1%), flupenthixol (< 1%), chlorpromazine (< 1%), and haloperidol (< 1%), was selected for development of a RIA. The described RIA enables the quantitation of 7.8 pg of trihexyphenidyl in 200 microL of human plasma with a mean coefficient of variation of < 6% across the range of the standard curve. Assay specificity was further demonstrated by comparison of results obtained directly and after selective extraction of trihexyphenidyl from replicate samples. This RIA procedure was applied to the analysis of steady state plasma samples obtained from patients undergoing treatment with trihexyphenidyl (2-8 mg) and plasma samples obtained from eight healthy male volunteers after administration of a single 4 mg oral dose of the drug. The results of the latter single dose studies demonstrated that the mean +/- SD for the peak concentration (Cmax), the time to Cmax (Tmax), the rate of absorption (Ka), and the area under the curve from 0 to 72 h (AUC0-72) were found to be 7.15 +/- 2.58 ng/mL, 1.32 +/- 0.58 h, 2.07 +/- 0.93 1/h, and 201 +/- 71 ng h/mL, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Binding and functional profiles of the selective M1 muscarinic receptor antagonists trihexyphenidyl and dicyclomine.

The selectivity profiles of the muscarinic receptor antagonists dicyclomine and trihexyphenidyl have been examined in binding and functional studies and compared with those of pirenzepine and atropine. 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. Their affinity values lay in a narrow range (3.7-14 nM) approaching that of atropine (1.6 nM). Competition experiments against [3H]-N-methylscopolamine in cardiac and glandular (salivary) membranes revealed differences between the drugs examined. Dicyclomine, trihexyphenidyl and pirenzepine displayed low affinity for the cardiac and intermediate affinity for the glandular receptors. Thus, the drugs appeared to discriminate between the M1 (cortical) and the peripheral muscarinic subtypes (cardiac and glandular). However, atropine displayed similar affinities for either subtype with IC50s varying only slightly (1.6-4.6 nM). The rank order of selectivity was: pirenzepine greater than dicyclomine greater than trihexyphenidyl greater than atropine. Mirroring the binding data, pirenzepine, dicyclomine and trihexyphenidyl showed a tenfold greater ability at inhibiting M1-receptor mediated ganglionic responses (McN A-343 pressor effect in pithed rats and nictitating membrane contraction in cats) than at inhibiting peripheral muscarinic responses in the heart and cardiovascular smooth muscle (vagal bradycardia in rats and cats and vagally-induced vasodilatation in cats). The muscarinic antagonists so far examined can be categorized into two groups. Trihexyphenidyl, dicyclomine and pirenzepine, included in one group, are characterized by a higher affinity for the neuronal (M1) muscarinic receptor, hence they antagonize functional responses mediated by the M1 subtype. Atropine, a member of the other group, shows essentially no selectivity. 6 Differentiation of M1 and peripheral muscarinic receptor subtypes appears to be a property not confined to tricyclics such as pirenzepine but shared by diverse chemical structures. Both trihexyphenidyl and dicyclomine appear to be useful pharmacological tools in the classification of muscarinic receptor subtypes.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed1995

Chronic blockade of muscarinic cholinergic receptors by systemic trihexyphenidyl (Artane) administration modulates but does not mediate the dopaminergic regulation of striatal prepropeptide messenger RNA expression.

A striatal dopaminergic denervation leads to changes in the expression of messenger RNA encoding prepropeptides contained in striatal efferent neurons. Such a dopaminergic lesion also abolishes a functional equilibrium between dopaminergic and cholinergic transmissions, generally believed to operate within the neostriatum, which constitutes the theoretical basis for the clinical use of antimuscarinic drugs in extrapyramidal diseases. It is possible, therefore, that changes in prepropeptide messenger RNA expression are mediated by an alteration in cholinergic transmission. 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. Two weeks after the lesion, trihexyphenidyl was continuously administered through an osmotic minipump (5 mg/day for 15 days) to half of the lesioned and sham-operated rats, the other half receiving the vehicle. Using quantitative in situ hybridization histochemistry, messenger RNAs were analysed at two rostrocaudal levels (anterior and central) of the neostriatum. In parallel, M1 muscarinic receptors were measured by autoradiography of [3H]pirenzepine binding sites. In sham-operated rats, trihexyphenidyl administration produced a significant increase (17-27%) in M1 binding sites. In addition, preproenkephalin messenger RNA levels were decreased (-38%) in the central part, while preprodynorphin messenger RNA levels were significantly increased (+22%) at both striatal levels. In 6-hydroxydopamine-lesioned rats, the expected changes in messenger RNAs were observed when ipsi- versus contralateral side values were compared, but changes were not always detected when comparison was established between values from the dopamine-denervated neostriatum and those from sham-operated rats. The trihexyphenidyl administration in 6-hydroxydopamine-lesioned animals was unable to reproduce the up-regulation of M1 receptors, even in the intact neostriatum. This antimuscarinic treatment further increased preproenkephalin messenger RNA levels in the denervated anterior neostriatum, amplifying the ipsi- versus contralateral difference. It also potentiated the imbalance in preprotachykinin messenger RNA expression, mainly as a result of an increase of preprotachykinin messenger RNA levels in the intact neostriatum. In contrast, trihexyphenidyl treatment by increasing preprodynorphin messenger RNA in both neostriata abolished the ipsi- versus contralateral difference observed in lesioned rats. 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. These results question the neostriatum as the site of action of antimuscarinic drugs in producing their therapeutic effect in extrapyramidal syndromes.

Animals↗
PubMed1998

Effects of trihexyphenidyl on MMSE and CAMCOG scores of medicated elderly patients with schizophrenia.

The purpose of this study was to assess the effects of an anticholinergic (trihexyphenidyl) antiparkinsonian medication on the Mini-Mental State Examination (MMSE) and the Cambridge Cognitive Examination (CAMCOG) scores in long-term institutionalized elderly patients with schizophrenia. Seventeen schizophrenic (DSM-III-R) inpatients on long-term medication who had received trihexyphenidyl for at least 6 consecutive months were compared for MMSE scores, CAMCOG scores, and other demographic and clinical variables with 14 patients not receiving any anticholinergic agent for the same time period. Results showed that age, years of education, illness duration, length of current hospital stay, the Manchester Scale scores, and chlorpromazine daily equivalent dose in mg were not different in the two groups compared. Extrapyramidal signs such as tremor, rigidity, and bradykinesia were more frequent in trihexyphenidyl receivers. The scores of MMSE (p < .007) and CAMCOG (p < .005) and CAMCOG subscales of orientation (p < .03), language (p < .01), and memory (p < .002) were significantly lower among trihexyphenidyl receivers, as was the Social and Occupational Functioning Assessment Scale score (p < .05). In addition, the MMSE and CAMCOG scores were significantly lower for patients receiving 10 mg of trihexyphenidyl a day compared with those receiving 5 mg/day and nonusers. It is suggested that trihexyphenidyl in usual clinical doses may impair total MMSE and CAMCOG scores as well as some of the CAMCOG subscales in this patient population. However, only a prospective study, preferably double-blind and controlled, with measures of change will validate this conclusion.

Aged↗
PubMed1997

No effect of the anticholinergic drugs trihexyphenidyl and biperiden on the plasma concentrations of bromperidol and its reduced metabolite.

Effects of the anticholinergic drugs trihexyphenidyl and biperiden on plasma concentrations of bromperidol and its reduced metabolite were studied. Subjects comprised 20 schizophrenic inpatients taking bromperidol, 6-18 mg/ day for 1-9 weeks. Patients were randomly allocated to one of two treatment sequences: trihexyphenidyl-biperiden (n = 12) or biperiden-trihexyphenidyl (n = 8). Each sequence consisted of two 2-week phases, with no washout period between the two phases. The daily dose of trihexyphenidyl was 8 mg and that of biperiden 6 mg. Plasma concentrations of bromperidol and reduced bromperidol were measured using high-performance liquid chromatography (HPLC). There was no significant difference in plasma bromperidol or reduced bromperidol concentrations among baseline, trihexyphenidyl and biperiden phases: 7.3 +/- 3.7 versus 7.2 +/- 4.1 versus 7.0 +/- 4.3 ng/ml and 2.0 +/- 2.1 versus 2.2 +/- 2.1 versus 1.9 +/- 2.0 ng/ml, respectively. The present study thus suggests that neither trihexyphenidyl nor biperiden affects plasma concentrations of bromperidol and its reduced metabolite.

Adult↗
PubMed1998

Effect of trihexyphenidyl, a non-selective antimuscarinic drug, on decarboxylation of L-dopa in hemi-Parkinson rats.

In vivo microdialysis was used to study the effect of the non-selective muscarinic antagonist, trihexyphenidyl, on the decarboxylation of levodopa (L-dopa) in the striatum of hemi-Parkinson rats. In normal rats, continuous perfusion of trihexyphenidyl (1 mM) via the microdialysis probe induced a significant increase in striatal dopamine release, followed by a decrease to below baseline values. A similar effect was observed, though less pronounced, in denervated striatum of rats with a unilateral 6-hydroxydopamine lesion of the nigrostriatal pathway. In these hemi-Parkinson rats, continuous striatal perfusion of trihexyphenidyl had no effect on the biotransformation of locally applied L-dopa (2 microM for 20 min) to dopamine in either intact or denervated striatum. However, systemic administration of trihexyphenidyl (1.5 mg/kg i.p.) produced an attenuation of the L- dopa-induced dopamine release in the intact striatum (contralateral to the lesion) of hemi-Parkinson rats. This effect was absent in the denervated striatum of these animals. We confirmed that L-dopa induces an increase in striatal dopamine output which is influenced by the severity of the dopaminergic denervation. The absence of an effect of trihexyphenidyl locally applied in the striatum, on biotransformation of L-dopa suggests that the site of action of antimuscarinic drugs may not be in the striatum and, therefore, remains unclear. The mechanism of action of these drugs is not well understood but appears more complicated than previously thought.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1994

Antagonism by (R)- and (S)-trihexyphenidyl of muscarinic stimulation of adenylyl cyclase in rat olfactory bulb and inhibition in striatum and heart.

1. Activation of muscarinic receptors in rat olfactory bulb stimulates adenylyl cyclase activity. This response was competitively antagonized by the (R)- and (S)-enantiomers of trihexyphenidyl with pA2 values of 8.84 and 6.09, respectively. 2. Similarly, in rat striatal homogenates, muscarinic inhibition of adenylyl cyclase activity was antagonized by the (R)- and (S)-enantiomers with pA2 values of 8.75 and 6.12, respectively. 3. In contrast, in rat myocardium the muscarinic inhibition of the adenosine 3':5'-cyclic monophosphate (cyclic AMP) formation was more weakly antagonized by trihexyphenidyl, with a particularly marked loss (15 fold) in activity of the (R)-enantiomer. The (R)- and (S)-enantiomers had pA2 values of 7.64 and 5.72, respectively. 4. Each muscarinic response was completely antagonized by increasing concentrations of (R)-trihexyphenidyl with a Hill coefficient not significantly different from unity. 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. The affinities of these receptors for the antagonists are similar to those shown by the striatal receptors. This finding supports the hypothesis that both the muscarinic stimulation of adenylyl cyclase in the olfactory bulb and the muscarinic inhibition of the enzyme in striatum are mediated by activation of a receptor subtype pharmacologically equivalent to the m4 gene product. On the other hand, the weaker affinities and the lower stereoselectivity for the trihexyphenidyl enantiomers exhibited by the muscarinic inhibition of adenylyl cyclase in the heart are consistent with the involvement of M2 receptors in this response.

Acetylcholine↗
PubMed1998

Trihexyphenidyl interactions with the dopamine D1-selective receptor agonist SKF-82958 and the D2-selective receptor agonist N-0923 in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced hemiparkinsonian monkeys.

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. Trihexyphenidyl was then studied in combination with the selective dopamine receptor D1 agonist SKF-82958 [(+/-)-6-chloro-7-8-dihydroxy-3-allyl-1-phenyl-2,3,4,5-tetrahydro- 1H-benzazepine hydrobromide] and the selective D2 agonist N-0923 [(-)2-(N-propyl-N-2-thienylethyl)amino-5-hydroxytetralin HCl] on rotational behavior in five 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned hemiparkinsonian monkeys. Given alone, trihexyphenidyl had no effect on ipsiversive and slightly enhanced contraversive circling. Contraversive circling produced by 74.8 and 234 micrograms/kg SKF-82958 i.m. was potentiated by increasing doses of trihexyphenidyl. On the other hand, contraversive circling produced by 10 and 32 micrograms/kg N-0923 i.m. was progressively reduced with increasing doses of trihexyphenidyl. The results obtained indicate differential actions on circling behavior between a selective M1 muscarinic cholinergic receptor antagonist and selective D1 and D2 receptor agonists in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine monkey model of hemiparkinsonism.

Animals↗
PubMedDate not supplied

Crossover clinical trial of benapryzine and trihexyphenidyl in Parkinsonian patients.

A crossover clinical trial of benapryzine and trihexyphenidyl in ten parkinsonian patients during a four-month study is described. The improvement from initial disability ranged from 29.5 to 64.4 per cent for benapryzine and from 27.2 to 64.9 per cent for trihexyphenidyl. The effect of benapryzine and trihexyphenidyl on most parkinsonian symptoms did not differ significantly. Patients taking benapryzine had significantly fewer of the common side effects of trihexyphenidyl but more sialorrhea. It is uncertain whether benapryzine is superior to trihexylphenidyl in the treatment of Parkinson's disease.

Aged↗
PubMed1987

Effectiveness of trihexyphenidyl against pendular nystagmus and palatal myoclonus: evidence of cholinergic dysfunction.

Palatal myoclonus and acquired pendular nystagmus result from lesions in dentatorubroolivary pathways. We have investigated the effect of high doses of the anticholinergic drug trihexyphenidyl in four patients with palatal myoclonus and in four patients with acquired pendular nystagmus. The movements of each patient were videotaped three times: before administration of trihexyphenidyl, at the time of maximum or effective dosage, and after withdrawal from trihexyphenidyl. In five patients the movements were also electrographically recorded. A neurologist not familiar with the patients reviewed the tapes and rated the changes. In seven of eight patients, administration of trihexyphenidyl resulted in marked improvement of both movements and complaints by patients. This observation indicates that disturbance of cholinergic mechanisms plays an important role in the pathophysiology of these two movement disorders.

Adolescent↗
PubMed1989

Treatment of movement disorders with trihexyphenidyl.

The clinical efficacy of the trihexyphenidyl was investigated in 100 patients with movement disorders. The study group consisted of 54 women and 46 men. Their ages ranged from 18 to 70 years, and their duration of illness varied from a few months to 36 years. Each patient had a videotape of the movements and a neurological examination, before administration of the drug, at the time of maximum or effective dosage, and one week after withdrawal from trihexyphenidyl. The drug was administered at an initial total daily dose of 2 mg and gradually increased to a total daily dose of 60 mg over a period of 4-6 weeks. Improvements were rated both clinically and from the videotapes. Three groups of movement disorders demonstrated a significant response to trihexyphenidyl: (1) dystonia 37%; tonic torticollis demonstrated a significantly better response than the clonic variant (80% vs. 22%). (2) rhythmic-oscillatory movements of brainstem-cerebellar origin (palatal myoclonus, pendular nystagmus, facial myokymia) 90%; (3) cerebellar tremor 75%. Among 32 responders, 17 (56%) continued taking trihexyphenidyl beyond 24 months. Side effects consisted of dryness of the mouth, jitteriness, stomatitis, blurred vision, and forgetfulness.

Adolescent↗
PubMed1988

Effects of 4 weeks treatment with chlorpromazine and/or trihexyphenidyl on the pituitary-gonadal axis in male paranoid schizophrenics.

Serum prolactin (PRL), luteinizing hormone (LH) and testosterone (T) levels were estimated in a group of 30 male paranoid schizophrenics before and after 4 weeks treatment with chlorpromazine and/or trihexyphenidyl, and in a group of 14 healthy male individuals. After treatment with chlorpromazine (100 mg t.i.d., p.o.), 10 patients presented a significant increase in serum PRL values and a significant decrease in serum T values. A significant increase in serum PRL values was also found in 10 patients who were treated with chlorpromazine (100 mg t.i.d., p.o.) plus trihexyphenidyl (5 mg t.i.d., p.o.). No significant difference in any of the investigated endocrine parameters was detected in 10 patients after 4 weeks administration of trihexyphenidyl (5 mg t.i.d., p.o.). Following chlorpromazine treatment with or without concomitant administration of trihexyphenidyl, 20 patients showed a significant increase in serum PRL levels and a significant decrease in serum LH and T levels.

Adult↗
PubMed1992

Antiparkinsonian drugs memantine and trihexyphenidyl potentiate the anticonvulsant activity of valproate against maximal electroshock-induced seizures.

Memantine increased the threshold for electroconvulsions, when administered at 1.0-6.0 mg/kg (i.p.) and given in subthreshold doses of 0.0156, 0.0625, 0.125 and 0.5 mg/kg (i.p.) potentiated the protective efficacy of valproate, against maximal electroshock (50 mA)-induced seizures in mice, lowering the ED50 from 235 to 197, 172, 164 and 130 mg/kg, respectively. Trihexyphenidyl, applied in doses of 30 and 50 mg/kg (i.p.), did not influence the electroconvulsive threshold per se but when combined with valproate, strongly enhanced its anticonvulsant activity against maximal electroshock-induced seizures lowering the ED50 from 206 to 103 and 46 mg/kg, respectively. The chimney test and retention testing in mice revealed that administration of memantine at 0.5 mg/kg (i.p.) or trihexyphenidyl at 30 mg/kg (i.p.) together with valproate in doses of 130 or 103 mg/kg (i.p.), respectively, resulted in motor impairment and caused impairment of long-term memory, similar to the effects of valproate alone, when applied at its ED50 against maximal electroshock. Neither memantine nor trihexyphenidyl altered the total level of valproate in plasma. It may be concluded that the potentiation of the anticonvulsant activity of valproate, by memantine and trihexyphenidyl, is not associated with a pharmacokinetic interaction.

Animals↗
PubMed1984

Trihexyphenidyl dependence.

Trihexyphenidyl, a synthetic anticholinergic, is frequently used concurrently with neuroleptics to control extrapyramidal side effects. We present two case reports of trihexyphenidyl abuse which concur with the increasing concern expressed regarding the abuse potential of trihexyphenidyl. In one of the cases a double-blind, placebo-controlled withdrawal was conducted and monitored on a number of physiological parameters and the Hamilton Anxiety Rating Scale. A recognizable withdrawal syndrome followed discontinuation of the drug. In addition to the abuse potential it is suggested that dependence liability be considered in maintenance therapy with trihexyphenidyl and other antiparkinsonians.

Adult↗
PubMed1985

Withdrawal of trihexyphenidyl.

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. In a group of 22 psychiatric patients receiving long-term antipsychotic medication concurrently with trihexyphenidyl the effects of trihexyphenidyl withdrawal were studied double-blind and placebo controlled. Anxiety, psychotic symptoms, extrapyramidal symptoms and salivary flow were monitored. Blood pressure, pulse, sleep duration, weight and body temperature were recorded daily. The result was a recognizable withdrawal syndrome indicated by an increase in anxiety with various physical complaints, as well as evidence of orthostatic hypotension and tachycardia. A temporary deterioration was noted in psychotic symptomatology and extrapyramidal symptoms. The majority of the parameters regained baseline values, indicating the symptoms were related to the discontinuation of trihexyphenidyl and supporting the existence of a withdrawal syndrome.

Adult↗
PubMed1996

Botulinum toxin versus trihexyphenidyl in cervical dystonia: a prospective, randomized, double-blind controlled trial.

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. METHODS: This trial compares the effectiveness of BTA with that of trihexyphenidyl in a prospective, randomized, double-blind design. Sixty-six consecutive patients with ICD were randomized to treatment with trihexyphenidyl tablets plus placebo injection or placebo tablets plus BTA injections. Tablets were administered daily according to a fixed schedule. Dysport or saline was injected under EMG guidance at study entry and again after 8 weeks. Patients were assessed for efficacy at baseline and after 12 weeks by different clinical rating scales. RESULTS: Sixty-four patients completed the study, 32 in each group. Mean dose of BTA was 292 mouse units (first session) and 262 mouse units (second session). Mean dose of trihexyphenidyl was 16.25 mg. The changes on the Disability section of the Toronto Western Spasmodic Torticollis Rating Scale (TWSTRS-Disability) (primary outcome), Tsui Scale, and the General Health Perception Subscale were significantly in favor of BTA. More patients treated with BTA had an improvement of at least three points on the TWSTRS-Disability (14 versus 6) and on the Tsui Scale (23 versus 12). Adverse effects were significantly less frequent in the BTA group. CONCLUSION: BTA is significantly more effective in the treatment of ICD, with less adverse effects.

Adult↗
PubMed1996

Trihexyphenidyl abuse in schizophrenic patient: a case report.

Trihexyphenidyl is a synthetic anticholinergic used in psychiatric patient for the relief of neuroleptic-induced extrapyramidal symptoms. It has been reported to have mood elevating, euphorigenic and socially-stimulating effects. The case presented is of anti-cholinergic abuse by a chronic schizophrenic who abused trihexyphenidyl, up to 200 mg per day, to achieve an euphoric effect. The drug was partly prescribed in psychiatric clinics, but mostly bought in the drugstore. The discontinuance of trihexyphenidyl produced anxiety, which was relieved by anxiolytics. The patient also feigned extrapyramidal symptoms to get anticholinergic injections during drug abstinence. A high dose of trihexyphenidyl may precipitate anticholinergic toxic psychosis and interfere with the therapeutic effects of antipsychotics by impeding their absorption. Given a large number of patients receiving this medication, clinicians should be alert when prescribing this drug, especially for patients who have abuse potential. As this agent has never been under public surveillance and is available in local pharmacies, the health authorities should be concerned with its abuse potential.

Adult↗
PubMed1993

Orobuccal dyskinesia associated with trihexyphenidyl therapy in a patient with Parkinson's disease.

Dyskinesia is a common adverse effect complicating chronic dopaminergic therapy for Parkinson's disease. Movements are frequently choreic in nature and have been ascribed to overstimulation of "supersensitive" striatal postsynaptic dopamine receptors. Anticholinergic medications, despite some clinical efficacy in Parkinson's disease, have rarely been reported to cause dyskinesia. We report a patient with Parkinson's disease who developed orobuccal dyskinesia while being treated with trihexyphenidyl (Artane). Dyskinesia was observed following the introduction of trihexyphenidyl, resolved with its discontinuation, and reappeared with its reinstitution. Carbidopa-levodopa (Sinemet) alone did not cause dyskinesia but augmented dyskinesia associated with trihexyphenidyl.

Dyskinesia, Drug-Induced↗