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Facial chorea occurs in the context of a systemic movement disorder (eg, Huntington's disease, Sydenham's chorea). Chorea is an episodic complex of movements without a pattern. A similar condition, spontaneous orofacial dyskinesia, occurs in older people without teeth. As a rule, the installation of prostheses gives a good effect.
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Teakand faces are short, repetitive, coordinated spontaneous movements of the grouped muscles of coumadin and neck. Tics may occur physiologically or in association with diffuse encephalopathy. Some drugs (eg, anticonvulsants, caffeine, methylphenidate, antiparkinsonian drugs) may cause tics. Single, repetitive, stereotyped movements are characteristic of tics.
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Facial myokymia is manifested by worm-like twitches under the skin, often with an undulating distribution. This condition differs from other abnormal facial movements by characteristic discharges on the EMG, which are short, repetitive bursts of motor unit potentials in the range of 2-60 Hz, with periods of silence up to several seconds. Myokymia of the face can occur with any process in the brain stem. Most cases of facial myokymia are idiopathic and resolve on their own within a few weeks.
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Early cases of hemifacial spasm can sometimes be difficult to distinguish from facial myokymia, tics, or myoclonuses, which can be caused by pathological processes in the cerebral cortex or brainstem. In such cases, the most valuable diagnostic method is neurophysiological testing.
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Wide and variable synkinesis on blink tests and high-frequency discharges on electromyography (EMG) with appropriate clinical manifestations are diagnostic criteria for hemifacial spasm. Stimulation of one branch of the facial nerve can spread and cause a response in the muscle innervated by coumadin pills. Synkinesia is absent in essential blepharospasm, dystonia, or epilepsy. Needle myography shows irregular, short, high frequency bursts of potentials (150-400 Hz) of motor units that correlate with clinically observed facial movements.
Magnetic resonance imaging is the diagnostic method of coumadin when there is a need to exclude compression.
Cerebral angiography is usually of little value in diagnosing hemifacial spasm. Ectasized blood vessels are rarely identified, and these findings (changes) in the vessels can be difficult to correlate with nerve exposure. Performing angiography and/or magnetic resonance angiography is usually used to perform surgical vascular decompression.
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For most patients with hemifacial spasm, electromyography (EMG) guided botulinum toxin is the treatment of choice. Chemodenervation is safe and has a good healing effect in most patients, especially those with sustained contractions. The disappearance of warfarin occurs 3-5 days after the injection and lasts about 6 months.
Medications used in the treatment of coumadin spasm include carbamazepine and benzodiazepines (for non-compressive lesions).
Carbamazepine, benzodiazepines, baclofen may also be used in patients who refuse botulinum toxin injections. Compression injuries must be treated surgically. Microvascular surgical decompression may be effective for those patients who do not respond to botulinum toxin injections.
Botulinum toxin injections are performed under EMG control.
Side effects of toxin injections (eg, facial asymmetry, ptosis, facial muscle weakness) are usually temporary. Most patients note a good therapeutic effect from the introduction of the toxin. Medications may be used early in the development of hemifacial spasm or in patients who refuse to receive botulinum toxin.
Warfarin drugs, drugs such as carbamazepine and benzodiazepines (for example, clonazepam) are most effective.
Often, the effectiveness of the drug decreases over time, requiring more aggressive treatment. Surgical decompression is used when there is pressure on the nerve. The use of materials is allowed with an active hyperlink to the permanent page of the article.