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At least 19 recordsLinked to original sources
PubMed2004

Chronic myokymia limited to the eyelid is a benign condition.

BACKGROUND: Eyelid myokymia, unlike myokymia of the other facial muscles, is assumed to be a benign, self-limited disorder. However, no systematic follow-up study has been performed on patients with chronic, isolated eyelid myokymia to verify its benign nature. METHODS: Retrospective single-institution chart review of 15 patients examined between 1983 and 2002 with a diagnosis of isolated eyelid myokymia who have had at least 12 months of follow-up. RESULTS: In all patients, symptoms began as unilateral, weekly or biweekly, intermittent eyelid spasms, and progressed to daily spasms over several months. The mean duration of symptoms at first examination was 91 months (range 2.5 months to 20 years). In no patient was the myokymia the first manifestation of a neurologic disease, although one patient progressed to ipsilateral hemifacial spasm. Thirteen patients (86.7%) underwent neuroimaging that gave negative results. The myokymia resolved spontaneously in four patients. Of the remaining 11 patients, eight were treated with botulinum toxin injection at regular intervals, with most reporting an improvement in symptoms. CONCLUSION: Chronic isolated eyelid myokymia is a benign condition. It tends not to progress to other facial movement disorders or to be associated with other neurologic disease. It responds well to treatment with botulinum toxin.

Adolescent↗
PubMed1985

[Nuclear magnetic resonance imaging in a case of facial myokymia with multiple sclerosis].

A 59-year-old female of facial myokymia with multiple sclerosis was reported. In this case, facial myokymia appeared at the same time as the first attack of multiple sclerosis, in association with paroxysmal pain and desesthesia of the neck, painful tonic seizures of the right upper and lower extremities and cervical transverse myelopathy. The facial myokymia consisted of grossly visible, continuous, fine and worm-like movement, which often began in the area of the left orbicularis oculi and spread to the other facial muscles on one side. Electromyographic studies revealed grouping of motor units and continuous spontaneous rhythmic discharges in the left orbicularis oris suggesting facial myokymia, but there were no abnormalities on voluntary contraction. Sometimes doublet or multiplet patterns occurred while at other times the bursts were of single motor potential. The respective frequencies were 3-4/sec and 40-50/sec. There was no evidence of fibrillation. The facial myokymia disappeared after 4-8 weeks of administration of prednisolone and did not recur. In the remission stage after disappearance of the facial myokymia, nuclear magnetic resonance (NMR) imaging by the inversion recovery method demonstrated low intensity demyelinated plaque in the left lateral tegmentum of the inferior pons, which was responsible for the facial myokymia, but X-ray computed tomography revealed no pathological findings. The demyelinated plaque demonstrated by NMR imaging seemed to be located in the infranuclear area of the facial nerve nucleus and to involve the intramedurally root.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1993

[Myokymia].

Myokymia is one of the involuntary movements, which is characterized by undulatory muscle spasm, similar to the worm's crawl. Sometimes muscle pain, itchy sensation, dysautonomia and other symptoms are associated with it. Cases showing normal neurological findings are rare. Myokymia is caused by various diseases, such as, multiple sclerosis, hypothyroidism, Guillan-Barre syndrome and so on. Generally myokymia is classified into two types, i.e. limb myokymia and facial myokymia according to the site. On the other hand, myokymia with hyperhidrosis is known as Issacs syndrome. There are many opinions about the pathogenesis and mechanism in the myoneural junction, peripheral nerve or spinal cord, however these are not established. Further investigation of myokymia is expected.

Adult↗
PubMed1987

Electrophysiological study on limb myokymia in three women.

Physiological studies on three women with limb myokymia were carried out. The patients had diabetic neuropathy, neuromyotonia, and autonomic polyneuropathy, respectively. The EMG discharge pattern, coincident with myokymia, in a patient with myokymia and neuromyotonia differed from those with myokymia without neuromyotonia. In only the first patient did the electrical stimulation of nerves evoke "late repetitive response" (LRR), which resembled the wave forms of the myokymic discharge. Epidural and peripheral nerve blocks abolished myokymia in the first and second cases, but peripheral nerve block was without effect in the third patient. These findings indicate that myokymia originates in multiple sites of alpha motor neurons and that the pathophysiology may vary.

Adult↗
PubMed1995

[A case of myokymia with abnormal F responses].

We reported a case of myokymia with abnormal F response. A 60-year-old male with chronic alcoholism was admitted to our hospital with complaint of muscle cramp in both legs just after drinking. Neurological examination revealed muscle pain and weakness of the legs, absence of bilateral Achilles tendon reflexes and prominent myokymia in his right quadriceps femoris and left calf muscles. The electrophysiological examination showed reduced conduction velocity, high amplitude, increased number of phases and long duration of F responses suggesting increased excitability of motoneuron pool. The epidural nerve block brought about a disappearance of the myokymia and an improvement of the abnormal features of F response. The myokymia gradually tended to be milder in the clinical course. The relationship between the myokymia and the abnormal F responses indicated that the increased excitability of spinal motoneurons might play an important role on the generation of myokymia of this patient.

Electromyography↗
PubMed2000

Continuous facial myokymia in multiple sclerosis: treatment with botulinum toxin.

Continuous facial myokymia (CFM) is an involuntary undulating, vermicular movement that spreads across facial muscles and is associated with a characteristic electromyographic pattern. It is an infrequent clinical sign that almost always occurs in intrinsic brainstem lesions, particularly in multiple sclerosis (MS). It is usually present for only a few weeks, but it may persist for long periods of time being very troublesome for patients. We report 2 cases with MS and continuous hemifacial myokymia persisting for up to 1 month which disappeared after injection of botulinum toxin. Botulinum toxin A (BTX-A) has been used successfully to treat a variety of focal dystonias and occasionally in orbicularis myokymia, but its use has not been reported in continuous hemifacial myokymia. BTX-A appears to be effective and safe for treating persistent facial myokymia in MS patients.

Adult↗
PubMed1997

Experimental facial myokymia in cat.

INTRODUCTION: The objective of this study was to describe facial myokymia in experimental animals accompanying kainic acid affects on facial motor neurons. MATERIAL & METHODS: Anesthetized cats were injected with kainic acid into the pons adjacent to the facial nucleus. Facial movements appeared shortly after the injections and facial electromyographic potentials were recorded. Cats were killed up to 4 weeks later, the brainstems were processed histologically, and the number of neurons in the facial nucleus counted. RESULTS: Cats receiving injection of kainic acid adjacent to facial nucleus all developed spontaneous writhing movements of the face ipsilateral to the injection site, clinically resembling facial myokymia in humans. Transient facial paresis, lasting several weeks, appeared in some of the cats. Facial myokymia occurred independent of histological evidence of neuronal loss in facial nucleus, whereas facial paresis occurred in all but one of the animals with significant neuronal loss in the facial nucleus. Placing a needle into the superior olive without injecting kainic acid or injections of kainic acid into cochlear nucleus was not accompanied by facial myokymia or subsequent facial paresis. CONCLUSION: Facial movements in cats similar to myokymia in humans accompanies kainic acid injections adjacent to the nucleus of the facial nerve.

Animals↗
PubMed2002

Superior oblique myokymia: magnetic resonance imaging support for the neurovascular compression hypothesis.

Superior oblique myokymia is a rare movement disorder thought to be caused by vascular compression of the trochlear nerve. Direct display of such neurovascular compression by magnetic resonance imaging has been lacking. The goal of this study was to assess the presence of neurovascular contacts in patients with superior oblique myokymia, using a specific magnetic resonance imaging protocol. A total of 6 patients suffering from right superior oblique myokymia underwent detailed neuro-ophthalmological examination, which showed tonic or phasic eye movement. All patients underwent magnetic resonance imaging, using a magnetic resonance imaging Fourier transform constructive interference in steady-state sequence in combination with magnetic resonance imaging time of flight magnetic resonance arteriography both before and after the administration of Gd-DTPA. With this protocol, the trochlear nerve could be visualized on 11 of 12 sides (92%). Arterial contact was detected at the root exit zone of the symptomatic right trochlear nerve in all 6 patients (100%). No arterial contact was identified at the root exit zone of the asymptomatic left trochlear nerve in any of the 5 left nerves visualized. In conclusion, superior oblique myokymia can result from neurovascular contact at the root exit zone of trochlear nerve, and therefore should be considered among the neurovascular compression syndromes.

Adult↗
PubMed2001

Functional changes and adverse reactions after successful treatment of hereditary myokymia: a case report.

Myokymia is a vermiform motion of muscle that can be found in conditions in which there is pathology to the peripheral nerve to that muscle. There are inherited syndromes that can present with muscle cramping and myokymia that have been described, but little information exists on long-term follow-up. In this case study, a 12-year-old girl had an inherited form of myokymia, as determined by clinical examination, electromyographic findings, and family history. The mode of inheritance appeared to be autosomal dominant with reduced penetrance. Carbamazepine was used successfully to treat this disorder. Measurements were made of strength and endurance before and after treatment; significant improvement was seen in endurance with little effect on strength. The patient was able to discontinue carbamazepine without return of symptoms and subsequently was not limited in her activities. Return of symptoms was seen with prednisone treatment for exacerbated asthma. The symptoms resolved with restarting the carbamazepine and weaning of the prednisone. Discussion is presented on the possible mechanism by which anticonvulsant and steroid therapy exert their effects on myokymia.

Anti-Inflammatory Agents↗
PubMed1994

Idiopathic generalized myokymia.

Idiopathic generalized myokymia (IGM) is a rare, heterogeneous, and poorly understood syndrome. We present analysis of 75 reported cases in the world literature. IGM affects men and women equally, with a mean age of onset 29 +/- 19 years. Patients' common presenting complaints are stiffness (60%), cramps (12%), weakness (12%), and muscle twitching (4%). Family history is positive in 30%. In addition to generalized clinical myokymia (92%), abnormal neurologic findings include: hyporeflexia (70%), weakness (45%), grip myotonia (39%), and calf hypertrophy (16%). Electrical activity consisting of spontaneous continuous motor unit activity and/or electrical myokymia was documented in all patients. When electrical myokymia was observed (66%), the grouped discharges where irregular and had an interburst frequency of 2-300 Hz. Both phenytoin and carbamazepine are effective treatments. We conclude that IGM has a wide spectrum of symptoms and severity and should be considered in all patients that present with stiffness, cramps, or muscle twitching. EMG greatly aids in diagnosis.

Adult↗
PubMed1981

Facial myokymia in the course of a pontine tumor.

A patient with facial myokymia, suffering from an infiltrating grade II astrocytoma originating within the pons with vegetations invading the cerebellopontine angle, was studied clinically and electromyographically from 1973 to 1979. The myokymias started in the muscles of the right side of the face and later spread to the left side. The latter point is worth noting because the myokymias of the left side were detectable by EMG but not by inspection. They preceded clinical and instrumental evidence of a contralateral spread of tumoral damage to the brainstem. From the physiopathogenetic angle they point up the importance of a mechanism of hyperexcitability and release of the facial motoneuronal pool. The results of the EMG study suggest that the persistence of myokymia, its association with an ingravescent neurogenic impairment of the facial musculature and its polymorphism in the course of pontine tumors are more reliable features than their discontinuity and rhythmicity.

Adult↗
PubMed1975

Hereditary myokymia and periodic ataxia.

A kindred in which at least 11 individuals in 3 consecutive generations have continuous muscle movement, i.e., myokymia, and periodic ataxia, has been studied. Three patients, a 24-year-old woman, her 4-year-old son and her 27-year-old sister, have been studied in detail. The disorder is inherited as an autosomal-dominant trait and presents in early childhood with attacks of ataxia of 1-2 min in duration, with associated jerking movements of the head, arms and legs. Attacks are provoked by abrupt postural change, emotional stimulus, and caloric-vestibular stimulation. At the age of 12 years approximately, facial and extremity myokymia appears. Physical findings include large calves, normal muscle strength and widespread myokymia of face, hands, arms and legs with a hand posture resembling carpopedal spasm. EMG studies at rest showed continuous spontaneous activity of otherwise normal motor units. Nerve conduction velocities were normal. Gastrocnemius biopsy in 2 patients showed fiber type grouping and small angular fibers, and was consistent with denervation. Histographic analysis of the biopsies demonstrated enlargement of both fiber types, particularly of Type I fibers. These findings are consistent with chronic denervation and an abnormality of motor neuron population or firing. The myokymia described here is of interest not only because of its genetic association with a movement disorder, but also because the muscle findings support a peripheral basis for the muscle movements.

Adolescent↗
PubMed1988

Myokymia in the course of Bell's palsy. An electromyographic study.

Facial myokymia has been described in association with many morbid conditions, most frequently multiple sclerosis (MS) and brainstem tumors (BST). Very few reports deal with myokymia in the course of Bell's palsy, despite high frequency of the disease. A series of 88 consecutive patients with Bell's palsy is presented, in which serial EMG controls were performed in the initial phases of facial palsy. Twenty three showed myokymic activity detected by EMG, while clinically evident myokymia could be observed only in 8. EMG features did not reveal any peculiarity as compared with myokymic discharges reported in other pathological situations. Considering the high incidence of myokymic activity reported in the course of Bell's palsy, it is the authors' opinion that an occasional finding of myokymia, both clinically evident or detected by EMG, should not necessarily lead one to suspect serious aetiologies.

Electromyography↗
PubMed1994

Facial myokymia due to acoustic neurinoma.

The case of a 62-year-old female patient who presented with facial myokymia is reported. The patient had a 13-year history of progressive left-sided hearing loss. In further course, involuntary, wormlike, rippling movements of the left facial muscles developed. Computed tomography revealed a tumor located in the left cerebellopontine angle. Electrophysiologic examinations confirmed the diagnosis of facial myokymia. The tumor, which evolved from the eighth cranial nerve, was totally removed microsurgically. The tumor was histologically verified to be an acoustic neurinoma. Postoperatively, the patient had a facial nerve paralysis, and the facial myokymia was no longer present. The present case provides further evidence that facial myokymia may be triggered by alterations at one of various sites along the course of the motor axons of the facial nerve.

Facial Muscles↗
PubMed2002

Gabapentin attenuates superior oblique myokymia.

PURPOSE: To investigate therapeutic effects of oral gabapentin therapy on superior oblique myokymia. DESIGN: Observational case series with measurement of visual acuity and eye movements before, during, and after therapy. METHODS: Two adult patients with superior oblique myokymia, refractory to other therapies, were treated with gabapentin orally after informed consent was obtained. Eye movements were measured using the magnetic search coil technique. RESULTS: Superior oblique myokymia completely resolved after starting gabapentin. CONCLUSION: Gabapentin may be an effective treatment for superior oblique myokymia; a double-blind study seems justified.

Acetates↗
PubMed1991

Exercise-induced myokymia with congenital spinal stenosis.

Myokymia and myokymic discharges are observed in a variety of neurologic conditions. An unusual case of myokymia induced by exercise and febrile illness presented in an 11-yr-old male with congenital spinal stenosis. Myokymia was not generalized, but occurred below the level of his umbilicus. We hypothesize that local spinal cord ischemia was the underlying mechanism for this rare phenomenon. The pathophysiology, clinical features and electrodiagnostic findings of myokymia are reviewed.

Child↗
PubMed1976

Facial myokymia and brain stem tumor.

An autoptic case of facial myokymia in glioma of the pons is described. The facial myokymia was the only symptom for many years. The authors emphasize the importance of the facial myokymia as a precocious sign of pons tumor and stress the meaning of the EMG in the differential diagnosis between facial myokymia in brain stem tumor and facial hyperkinesa in other diseases.

Adult↗
PubMed1986

Calcium and myokymia of brainstem origin.

In five patients with Guillain-Barré syndrome, clinical myokymia increased and myokymic burst amplification occurred when ionized Ca++ was lowered by hyperventilation. Myokymia decreased when ionized Ca++ was increased after IV infusion of CaCl2. These responses were absent or diminished in the four patients with myokymia due to brainstem lesions, suggesting that the blood-brain barrier impedes the effects of altered serum ionized Ca++ on axonal excitability. Altering serum Ca++ can distinguish peripheral and central myokymia.

Action Potentials↗