Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038362 (stomatitis)
 8,852 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Treatment of movement disorders with trihexyphenidyl. 277 91

Cranial dystonia is normally considered as a pure movement disorder. Sensory symptoms have not received much attention, but we found ill-defined pain, discomfort, distortion of sensory modalities, 'phantom' kinetic or postural sensations in the orofacial areas subsequently involved by the dyskinesia in all of 11 consecutive patients, preceding by weeks or months the motor syndrome. Physicians were often mislead, initially making diagnoses such as trigeminal neuralgia, dental problems, sicca syndrome, chronic conjunctivitis, glossitis or stomatitis. The patients reported that the orofacial movements were at first willingly performed in order to decrease the discomfort which was felt in these facial areas before the movements finally escaped voluntary control and became socially disturbing. We suspect that the sensory symptoms, for which no objective substrate could be found, and which were always reported before and in the exact location of the subsequent dyskinesia, could be the earliest manifestation of an evolving process in cranial and perhaps other focal dystonias.
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PMID:Sensory symptoms in cranial dystonia: a potential role in the etiology? 833 60