Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003635 (apraxia)
 2,817 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Botulinum-A toxin (botAtox) was used in the treatment of blepharospasm (BS), idiopathic hemifacial spasm (HFS), idiopathic spasmodic torticollis (ST) and apraxia of eyelid opening (AEO). The injection of 7.5-30 U botAtox per eye spread over 3 or 4 sites in the palpebral part of orbicularis palpebrae (OP) reduced palpebral spasm in 12/13 cases of BS and in 7/8 cases of HFS. The effect lasted for 14.5 weeks on average (range 4-30 weeks). Palpebral ptosis (lasting 1-3 weeks) was the most frequent side effect (16/107 eyes treated) but was not related to dose of botAtox or number of inoculation sites. Injection of 60-160 U botAtox into the sternocleidomastoid, trapezius and splenius capitis muscles reduced ST objectively in 1/4 patients for about 4 weeks. In the other patients the reduction or abolition of the hypertrophy of the previous hyperactive muscles was accompanied by persistence or rearrangement of the dystonia pattern, suggesting a change in the pattern of activity of the neck muscles after botAtox. 5 U botAtox per eye spread over 4 sites in the OP significantly reduced the frequency of the episodes of involuntary eyelid closure in 2 patients with AEO but not BS. The therapeutic effect lasted for 7 months after the first treatment and for 8 months after the second in a 46 year old woman with a 6 month history while the second patient (72 year old parkinsonian) has now completed her 3rd month of treatment.
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PMID:Botulinum A toxin treatment for eyelid spasm, spasmodic torticollis and apraxia of eyelid opening. 238 98

We report a 74-year-old man with a lung cancer, who developed right leg weakness, neurogenic bladder, and multiple cranial nerve palsies. The patient was well until December of 1992, when he was 74-year-old, when he noted transient double vision; in February of 1993, he noted numb sensation and weakness in his right leg. Later in the same month, he developed overflow incontinence of urine and weakness in his right face. He also noted deafness in his left ear (he had a marked loss of hearing in his right ear since childhood because of otitis media). His weakness in his right leg had progressed, and he was admitted to our service on March 19, 1993. On admission, he was afebrile and BP was 130/50 mmHg. General physical examination was unremarkable. On neurologic examination, he was alert and oriented to all spheres; no dementia was noted nor were detected aphasia, apraxia, and agnosia. His optic fundi were unremarkable; ocular movement appeared normal, however, he complained of diplopia in far vision. Sensation of the face was intact. He had right facial palsy of peripheral type; he was unable to close his right eye, and Bell's phenomenon was observed on attempted eye closure. On the left side, he had facial spasm. He had marked bilateral deafness. He had no dysarthria or dysphagia. The remaining of the cranial nerves were intact. Motor wise, he was unable to stand or walk alone; weakness did not appear to account for his difficulty in gait; manual muscle testing revealed 4/5 weakness in his tibialis anterior muscle, 1/5 in the peroneus longus, 0/5 in his extensor hallucis longus and extensor digitorum longus, all on the right side. Brachioradial and quadriceps femoris reflexes were increased to 3/4; plantar response was equivocal on the right side, and flexor on the left. Sensory examination revealed loss of touch and pain sensation in the L5 and S1 distributions in his right leg: vibration and position sensations were also diminished in his right foot. He had overflow urinary incontinence with loss of bladder sensation. Marked nuchal stiffness was noted, however, no Kernig's sign or eye ball tenderness was present. Pertinent laboratory findings were as allows; WBC 8,100/microliters, Ht 42.5%, platelet 326,000/microliters, TP 6.8 g/dl, BUN 16 mg/dl, creatinine 0.54 mg/dl, glucose 95 mg/dl, Na 136 mEq/l, K 4.4 mEq/l, Cl 100 mEq/l; liver profile was normal; CEA 436.6 ng/ml, CA19-93 U/ml; urinalysis was normal.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 74-year-old man with urinary incontinence, right leg weakness and multiple cranial nerve palsies]. 766 22

An overview is given of the indications, results and complications with the use of botulinum A toxin injection therapy specifically in the treatment of facial dystonias. A total of 79 patients have been treated over a 5-year period. The patients were divided in four groups: essential blepharospasm, hemifacial spasm, apraxia of the opening of the eyes and spastic entropion. On average, the therapeutical effect started the third day after injection. The average duration of the beneficial effect was dependent of the underlying pathology. Local side effects were mild and systemic side effects were not seen. Botulinum A toxin therapy proved to have a reliable and reproducible effect in appropriate dosages, in 90% of the patients.
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PMID:Botulinum A toxin therapy in ophthalmology: a report of patients with facial dystonias. 804 37

This review deals with a variety of disorders of facial movement. Recent publications on blepharospasm, facial spasm, facial myokymia, apraxia of lid opening and facial paralysis are referenced and discussed. In blepharospasm, carefully performed electromyographic studies reveal a variety of abnormal patterns of contraction of the oribicularis oculi and the levator palpebrae muscles confirming the clinical impression that blepharospasm is not a homogeneous disease. Similar studies are furthering the understanding of apraxia of lid opening, which may involve sustained contraction of the orbicularis oculi with or without failure of levator palpebrae inhibition. In both conditions botulinum toxin A injected pretarsally appears to be the preferred treatment. Of interest with respect to apraxia of lid opening is that it may be the result of a failure to sustain eye opening as well as an inability to open the eyes voluntarily. Although the fact that bilateral facial spasm was found in only five of 702 patients with spasm suggests that it is infrequent, it is also possible that bilateral facial spasm may be underdiagnosed because of lack of awareness of its existence. Despite the continued enthusiasm of neurosurgeons for microvascular decompression, the preferred treatment for facial spasm continues to be botulinum toxin A injections. It appears that a lesion of the dorsolateral pontine postgenu portion of the facial nerve is responsible for the facial myokymia of patients with multiple sclerosis. Interest in the study of lid function has increased as a result of the advent of the search coil technique for recording lid movements. Recordings with this technique have proven useful in facial nerve palsy for monitoring the degree and course of recovery and as a means of judging the effectiveness of therapy.
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PMID:Disorders of facial motor function. 1016 53

The main objective in the treatment of blepharospasm is to decrease or cease the unwanted, repeated forced closure of the eyelids. This is best achieved by the use of botulinum toxin. In a minority of patients, botulinum toxin is either ineffective or poorly tolerated. In this group of patients, a trial with oral medication in the following order is warranted: trihexyphenidyl, baclofen, clonazepam, and tetrabenazine. Before going to the next medication, each of these drugs should be administered at the highest tolerated dosage for a period of 1 or 2 months. If, as often happens, all pharmacologic treatment attempts fail, and the patient is too disabled to remain untreated, he or she can be referred to an experienced plastic surgeon for a myectomy of the eyelid protractors. For treatment of apraxia of eyelid opening, botulinum toxin should be administered as the first treatment. If this fails, and vision is significantly impaired, the patient may be referred to a plastic surgeon for a frontalis suspension of the eyelid. Treatments of hemifacial spasm are aimed at decreasing or ending the annoying twitches of one side of the face. In this disorder, interference with vision is not a problem unless the contralateral eye is amblyopic. Despite isolated reports of spasm relief by drugs such as carbamazepine, oral medication is unlikely to be helpful. Botulinum toxin is the preferred treatment in hemifacial spasm patients. In some patients, relief from spasms can only be obtained at the cost of an ipsilateral upper lip droop of varying severity. Patients who are dissatisfied with the results of treatment with botulinum toxin, and are not willing to tolerate their condition, can be referred to an experienced neurosurgeon for microvascular decompression of the facial nerve. Pending success of ongoing attempts to reduce adverse effects, we believe that doxorubicin chemomyectomy, a recent treatment that has been used for both facial spasm and blepharospasm, is best administered in a research setting.
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PMID:Blepharospasm and Hemifacial Spasm. 1109 64

We review the existing literature on the involuntary facial movement disorders-benign essential blepharospasm, apraxia of eyelid opening, hemifacial spasm, and aberrant facial nerve regeneration. The etiology of idiopathic blepharospasm, a disorder of the central nervous system, and hemifacial spasm, a condition involving the facial nerve of the peripheral nervous system, is markedly different. We discuss established methods of managing patients and highlight new approaches.
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PMID:Review and update of involuntary facial movement disorders presenting in the ophthalmological setting. 2150 41