Movement disorders secondary to adulterated medication.
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Biomedical subjects
Publications and source records attributed to M C Scorticati.
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The development of dyskinesias is a common side effect during chronic levodopa therapy in parkinsonian patients. Recent reports suggest that amantadine, a drug with well known antiparkinsonian activity, is effective in the treatment of this complication. In order to evaluate its usefulness we conducted an open label, prospective and longitudinal study in 26 patients with Parkinson's disease (PD) on chronic levodopa therapy who presented peaks of dose dyskinesias. After 3 weeks' treatment dyskinesia severity was reduced by 70% (p < 0.0001) on the I SAPD scale and by 68.8% (p < 0.0002) on the UPDRS IV subscale. Patients were later evaluated every 45 days showing persistent drug benefit during follow-up ranging from 2 to 11 months (mean 6.5 months). One third of our series presented unwanted effects which were only severe enough in 2 cases to discontinue treatment. In the others, side effects were transient or readily abated with amantadine dose reduction. Our findings support amantadine as a safe and useful drug to treat levodopa-induced dyskinesias which on occasion prove as disabling as PD itself. Treatment with amantadine should routinely be considered before indicating pallidotomy for levodopa-induced dyskinesias.
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The objective of this paper was to evaluate the efficacy of diphenhydramine hydrochloride (DPH) in dystonic patients. In 1995, Truong et al reported encouraging results in five patients with idiopathic torsion dystonia (ITD) treated with DPH, an H1 antagonist with sedative and anticholinergic properties. Five patients with generalized ITD, one with secondary generalized dystonia and one with idiopathic segmental dystonia were included in the prospective study. Initially the response to intravenous administration of DPH versus placebo in two sessions a week apart was evaluated. Two weeks later all patients started oral DPH in increasing doses (range 100-300 mg, mean 164 mg). The degree of dystonia was determined by a modified University of Columbia Scale evaluating the baseline score, after placebo and DPH I.V. administration then at one and six months after starting oral treatment. The results were analyzed by Friedman's test for repeated measurements. On comparing scores for baseline severity, I.V. placebo and I.V. DPH presented a highly significant correlation (12.09; p = 0.00) as well as comparing baseline score with oral DPH at one and 6 months, treatment (12.78; p = 0.00). Functional score results were 9.5 p = 0.01 and 8.4 p = 0.02 at one and 6 months respectively. The most common side effects were somnolence and dizziness. It can be concluded that DPH proved effective in our patients with mild to moderate adverse effects not requiring drug withdrawal in any case. However, I.V. challenge was unable to predict the long-term response to oral medication perhaps due to the limited number of cases.
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Two brothers developed hemifacial spasm at 63 and 70 years of age. Spasms occurred on the left and right sides of the face, respectively. Computed tomography scan and magnetic resonance imaging failed to show any abnormality. In addition, a third sibling reported a history of a peripheral facial palsy, which remitted spontaneously without sequelae. This is the fourth description of familial hemifacial spasms. This family is unique in that hemifacial spasm presented on different sides in the two brothers, and involvement was limited to one generation. Age at onset was later than for other familial cases and similar to sporadic cases.
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We present the case of a 72-year-old woman with a history of a bipolar mood disorder chronically treated with lithium. Upon having the dose increased, she developed an acute confusional state accompanied by blepharospasm (BS) and apraxia of eyelid opening. Gait instability with frequent falls, pyramid tract signs, and postural tremor in both hands were also evident. On withdrawing lithium, symptoms remitted within 2 weeks. This patient illustrates that BS and apraxia of eyelid opening may be triggered by lithium overdose. Our case warrants the inclusion of lithium in the list of drugs liable to induce such movement disorders.
Hemifacial spasm features myoclonic-like, paroxysmal, unilateral muscle twitching, attributable to vascular compression at the facial pontine root entry zone. We present the case of an 85-year-old man who presented with idiopathic hemifacial spasm with onset 23 years before. For the last 5 years, he was successfully treated with botulinum toxin injections. However, occasional nitrate intake for precordial pain promptly triggered muscle twitching. Vasodilation may exacerbate not only cases of hemifacial spasm, but even of trigeminal neuralgia, both recognized as neurovascular compressive syndromes.