Parkifen

Dosage should be individualized. The initial dose should be low and then increased gradually, especially in patients over 60 years of age. Whether Trihexyphenidyl may best be given before or after meals should be determined by the way the patient reacts.

Idiopathic Parkinsonism: 1 mg of Trihexyphenidyl may be administered the first day. The dose may then be increased by 2mg increments at intervals of three to five days.

Drug-Induced Parkinsonism: Commence therapy with a single 1 mg dose increase the total daily dosage to 5-15 mg range if the extrapyramidal manifestations are not controlled.

Concomitant Use with Levodopa: When Trihexyphenidyl is used concomitantly with levodopa, the usual dose is 3-6 mg daily.

Minor side effects such as dryness of the mouth, blurring of vision, dizziness, mild nausea or nervousness. Patients with arteriosclerosis or with a history of idiosyncrasy to other drugs may exhibit reactions of mental confusion, agitation, disturbed behavior, or nausea and vomiting. Potential side effects are constipation, drowsiness, urinary hesitancy or retention, pupil dilation, increased intraocular tension, vomiting and headache.

Overdosage with Trihexyphenidyl produces typical central symptoms of atropine intoxication (the central anticholinergic syndrome). Signs & symptoms are: dilated and sluggish pupils, warm, dry skin, facial flushing, decreased secretions of mouth, pharynx, nose and bronchi, foul smelling breath, tachycardia etc. Neuropsychiatric signs such as delirium, disorientation, anxiety, hallucinations etc. The condition can progress to stupor, coma, paralysis, cardiac, respiratory arrest and death.

Trihexyphenidyl Hydrochloride is indicated as an adjunct treatment of all forms of parkinsonism (postencephalitic, arteriosclerotic & idiopathic). Additionally, it is indicated for the control of extrapyramidal disorders caused by central nervous system drugs such as dibenzoxazepines, phenothiazines, thioxanthenes & butyrophenones.

Trihexyphenidyl is a non-selective muscarinic acetylcholine receptor antagonist but binds with higher affinity to the M1 subtype. In vivo studies have shown that trihexyphenidyl demonstrates higher affinity for central muscarinic receptors located in the cerebral cortex and lower affinity for those located peripherally. Other studies suggest that trihexyphenidyl may modify nicotinic acetylcholine receptor neurotransmission, leading indirectly to enhanced dopamine release in the striatum. Although the anticholinergic has proven to be useful in the treatment of symptoms associated with Parkinson’s disease or other movement disorders, its mechanism of action has yet to be fully elucidated.

Patients with cardiac, liver, or kidney disorders, or with hypertensioon, should closely be monitored. Since Trihexyphenidyl HCI has parasympatholytic activity, it should be used with caution in patients with glaucoma, obstructive disease of the gastrointestinal or genitourinary tracts, and in elderly males with possible prostatic hypertrophy. Trihexyphenidyl is not recommended for use in patients with tardive dyskinesia unless they have concomitant Parkinson’s disease. Abrupt withdrawal of treatment for parkinsonism may result in acute exacerbation of parkinsonism symptoms; therefore, abrupt withdrawal should be avoided.

Antiparkinson drugs