This movement disorder is characterized by unilateral, involuntary, episodic tonic and clonic contraction of muscles innervated by CN VII. It usually begins as twitches around the eye and progresses to involve the remaining
ipsilateral facial muscles, even during sleep. The spasms are painless, can be provoked by voluntary facial motion and emotional stress, and occur most often in middle-aged women. The exact etiology is unknown, but many believe that compression of the motor nerve root at the brain stem by a vascular loop causes focal demyelination and focal ectopic excitation. Impulses resulting from the chronic stimulation conduct centrifugally to the facial nerve nucleus, which causes hyperactivity of the nucleus with resultant bursts of hemifacial spasm. y The condition also has been seen after recovery from Bell's palsy. Hemifacial spasm must be differentiated from blepharospasm, which is an involuntary spasm involving both orbicularis oculi muscles.
This is a progressive, irregular fibrillation of individual facial muscle fibers. Usually, it begins in the frontalis and extends to involve all the ipsilateral facial muscles. Electromyographic findings include spontaneous activity of motor units at a rate of 30 to 70 per second. Common causes include pontine gliomas and multiple sclerosis.
Re-innervation Syndromes POSTPARALYTIC MOVEMENTS AND SYNKINESIS
Synkinesis is unintentional motion of a group of muscles when another group is voluntarily contracted. It results from postparalytic re-innervation of different muscles by axons from the same motor neuron. An example is eyelid closure when the patient smiles.
Also called Bogorad's syndrome, it is characterized by unilateral lacrimation during meals in patients with a history of facial palsy. After paralysis with neural degeneration, regenerating axons from the superior salivatory nucleus intended for the chorda tympani instead enter the greater superficial petrosal nerve. Rather than synapsing in the submandibular ganglion to regulate the sublingual and submandibular glands, these preganglionic parasympathetic fibers end up in the pterygopalatine ganglion. Therefore, during meals, the stimulus for increased salivation results in stimulation of the lacrimal gland, with a resultant increase in tearing.
Also known as Frey's syndrome, this results from anomalous re-innervation of sweat glands by axons intended for the parotid gland. Normally, sweat glands are innervated by postganglionic sympathetic fibers which are unique in that they use acetylcholine as the transmitter (rather than norepinephrine). The parotid gland is innervated by postganglionic parasympathetic fibers also using acetylcholine as their transmitter to regulate salivary flow. After parotidectomy, the cholinergic fibers originally intended for the parotid gland end up innervating the sweat glands. While eating, stimuli that should cause an increase in salivation instead lead to facial sweating. Parotidectomy is the most common cause.
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