Cases reported "Hyperkinesis"

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1/6. Intraputaminal infusion of nerve growth factor to support adrenal medullary autografts in Parkinson's disease. One-year follow-up of first clinical trial.

    Experimental studies in rodents show that beta-nerve growth factor can increase the survival, neurite outgrowth, and functional effect of grafts of adrenal chromaffin cells to the basal ganglia. We, therefore, have begun to investigate whether treatment with nerve growth factor might also increase the functional effect of autografts of adrenal medullary tissue in patients with Parkinson's disease. Previous studies have shown that stereotactic implantation of adrenal tissue pieces produces a transient functional improvement that lasts for a few months. This report describes a trial of grafting of adrenal chromaffin tissue into the putamen, supported by infusion of nerve growth factor. The patient is a 63-year-old woman with a 19-year history of Parkinson's disease, now complicated by on-off phenomena and drug-induced hyperkinesia, despite optimized medical management. The left adrenal gland was removed, and the medulla was dissected into 1- to 2-mm3 pieces in a solution containing nerve growth factor purified from mouse submandibular gland. Pieces were implanted in six tracts 3 to 4 mm from a previously placed cannula in the left putamen. Through the cannula, nerve growth factor was infused for 23 days for a total dose of 3.3 mg. Clinical assessment consisted of global ratings for rigidity and/or hypokinesia and for drug-induced hyperkinesia. Measures of gait and fine-motor control were also made. The motor readiness potential and auditory evoked potentials were recorded.(ABSTRACT TRUNCATED AT 250 WORDS)
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2/6. Hyperkinesias after hypoglossofacial nerve anastomosis--treatment with botulinum toxin.

    Hypoglossofacial nerve anastomosis is a successful method for restoration of facial nerve function. Facial hyperkinesis, however, are a common side effect of this therapy and have been a major therapeutical problem ever since. We are reporting a patient whose facial hyperkinesias responded favourably to botulinum toxin carefully injected into the most affected muscles. EMG studies are illustrating the effect of botulinum toxin on the facial hyperkinesias as well as on voluntary muscle activation.
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3/6. Botulinum toxin to suppress hyperkinesias after hypoglossal-facial nerve anastomosis.

    Facial hyperkinesias are a common side effect of hypoglossal-facial nerve anastomoses. We report a patient whose facial hyperkinesias were suppressed by botulinum toxin injections a treatment recently introduced in the therapy of craniocervical dystonias. EMG studies are used to document the effect of botulinum toxin on the facial hyperkinesias as well as on voluntary muscle activation.
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4/6. Bell's palsy: management of sequelae using EMG rehabilitation, botulinum toxin, and surgery.

    Fifteen percent of patients who have had an acute episode of Bell's palsy will be left with debilitating facial dysfunction. This chapter describes our approach to managing a variety of hypo- and hyperkinetic disorders caused by injury and faulty regeneration of the facial nerve, using electromyographic rehabilitation (EMGR) (13 patients), Oculinum toxin injection (14 patients), or surgical reanimation (72 patients). Improvement was noted after EMGR in 12 of 13 patients (92%), all 14 patients treated with Oculinum experienced temporary improvement, and improvement was noted in 66 of 72 patients who underwent surgery (92%). The indications, techniques, and results of these three rehabilitative methods are discussed.
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5/6. Huntington's disease: survival of large striatal neurons in the rigid variant.

    A morphometric method was employed to investigate the relationship of rigidity and hyperkinesia to the degree of striatal and nigral nerve cell loss in one patient with the rigid variant of Huntington's disease and four patients with hyperkinetic chorea. Both striatal neuron populations, small and medium-sized neurons and large neurons, were affected in the patients with hyperkinetic chorea, whereas the large neurons were preserved in the patient with the rigid variant. The substantia nigra was slightly involved in each patient. The findings suggest that the rigid variant of Huntington's disease may reflect the unbalanced activity of residual, mostly large, striatal neurons, inhibiting the substantia nigra.
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6/6. facial nerve disorders: anatomical, histological and clinical aspects.

    Three main problems of facial nerve pathology and surgery are considered in this paper. The intraneural anatomy of the facial nerve with its consequences for surgery, especially surgery for facial hyperkinesia, is studied and an original method of selective funicular neurolysis is proposed as a symptomatic operation. Quantitative and qualitative findings in the normal facial nerve are compared to findings in nerves after palsy. The results show that the introduction of neurometric methods for the quantitative assessment may yield further parameters in the judgement of past pathological processes within the nerve. Finally, prognosis of peripheral facial palsy, seen through electrophysiological testing methods, is discussed.
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