Abnormal Muscle Response Research Articles

Abnormal muscle responses in hemifacial spasm: F waves or trigeminal reflexes?

Objective: In patients with hemifacial spasm (HFS), abnormal muscle responses (AMR) are frequently present. The objective of this study was to investigate whether the afferent input of AMR is mediated...

Abnormal muscle response monitoring during microvascular decompression for hemifacial spasm

Several studies have investigated the relation between intraoperative abnormal muscle response (AMR) findings and postoperative results in patients undergoing microvascular decompression (MVD) for hemifacial spasm (HFS). However, there is some debate over the reliability of AMR as an indicator of postoperative outcome. We investigated whether AMR findings obtained during MVD reflect postoperative outcome in patients with HFS. Subjects were 60 HFS patients who underwent AMR monitoring during MVD. AMR recordings were obtained from the mentalis muscle by electrical stimulation of the temporal branch of the facial nerve and from the orbicularis oculi muscles by stimulation of the marginal mandibular branch. Surgical outcome was compared with AMR findings at the completion of MVD. Mean follow-up was 61 months. HFS resolved completely in 50 patients in whom AMR disappeared intraoperatively and in 5 patients in whom the AMR amplitude was decreased at the end of MVD. Four patients showed HFS at the final follow-up examination despite cessation or decrease of AMR during surgery. In 1 patient, preoperative AMR waveforms persisted throughout MVD, but the postoperative outcome was excellent. Our findings suggest that intraoperative cessation or decreased amplitude of AMR at the end of surgery indicates a high likelihood of postoperative relief of HFS. We believe that intraoperative AMR monitoring is useful in MVD surgery for HFS.

Repetitive nerve stimulation in myasthenia gravis—relative sensitivity of different muscles

Objective: To correlate repetitive nerve stimulation (RNS) decrement in different muscles with the predominant clinical presentation in myasthenia gravis (MG), and to study single fibre EMG (SFEMG) sensitivity in ocular MG. Methods: Sixty-nine, untreated, consecutive patients suspected for MG were observed prospectively for a minimum of 6 months. Those who improved on medical treatment were diagnosed as MG. The others, in whom the neurophysiological studies were normal and that did not improve on medical treatment served as a control group, from which normative data for RNS and SFEMG was obtained. The MG patients were further classified in 3 subgroups according to the predominant clinical presentation: group I (ocular); group b (bulbar); and group a (axial). We performed RNS in nasalis, trapezius, anconeus, and abductor digiti minimi. All patients with ocular MG underwent jitter determination of the orbicularis oculi muscle. Results: Thirty-seven patients were diagnosed as MG (group I, 15; group b, 13; group a, 9). In group I, RNS was abnormal in 33% of the patients. RNS studies disclosed at least one abnormal muscle response in every patient in groups a and b. Trapezius was significantly more sensitive in group a, and anconeus and nasalis in group b ( P<0.01). Jitter was abnormal in all patients in group I, and the most sensitive parameter was an increased number of unstable pairs, 100%. Conclusions: Based on these observations, we recommend that a shoulder muscle, as the trapezius, should be studied first in the limb-axial presentation of MG, and the anconeus–nasalis muscles in predominant bulbar MG. In ocular MG, RNS is not sensitive and jitter should be performed in facial muscles. Significance: This paper shows the unequal sensitivity of several muscles to RNS in different forms of MG.

Trigeminal afferent input alters the excitability of facial motoneurons in hemifacial spasm.

To investigate whether skin or muscle afferent input via the trigeminal nerve alters the excitability of facial motoneurons in hemifacial spasm (HFS). Botulinum toxin type A (BTX) was injected only to the orbicularis oculi (O. oculi) muscle of 21 patients with idiopathic HFS, and the excitability of the orbicularis oris (O. oris) motoneurons was monitored. The synkinetic response (SR) of the blink reflex and abnormal muscle response (AMR) were recorded from the O. oris before and after treatment. BTX injections produced marked to moderate improvement in the O. oculi of all 21 patients and in the O. oris of 17 (81%). The rectified areas of SR1 and SR2 were smaller after treatment. In particular, the AMR area showed a reduction (p = 0.02). The significant lessening of spasms in the O. oris after BTX injection to the O. oculi and the concomitant reduction in excitability of O. oris neurons are consistent with the hypothesis that in HFS, skin or muscle afferent volleys via the trigeminal nerve enhance the excitability of facial nerve motoneurons.

Hemifacial spasm: intraoperative electromyographic monitoring as a guide for microvascular decompression.

Microvascular decompression is the logical and well-accepted treatment of choice for hemifacial spasm (HFS). In experienced hands, good to excellent results can be obtained. However, sometimes the exact site of the vascular compression is unclear. The aim of this study was to analyze whether intraoperative monitoring by stimulated electromyography of the facial nerve may help to improve the results of vascular decompression for HFS. In a series of 74 patients operated for HFS, the impact of intraoperative facial nerve monitoring on the surgical procedure was analyzed by use of the clinical and operative patient records. The role of this type of monitoring, with assessment of the so-called abnormal muscle response, was broken down into four categories: a guiding, a confirming, an indirect confirming, or an inconclusive role. The relationship between abnormal muscle response monitoring results and final surgical outcome was analyzed. The overall cure rate was 87.8%, including patients who had previously undergone unsuccessful operations. Complications were minor, and hearing impairment was found in 2.7% of patients. A guiding role of intraoperative monitoring was apparent in 33.8% of patients, and a confirming role was demonstrated in 52.7% of patients, which resulted in a positive contribution of approximately 87% for intraoperative facial monitoring in microvascular decompression for HFS. In patients defined as guiding cases, the cure rate was 92%. This study demonstrates the applicability and usefulness of intraoperative facial nerve monitoring in microvascular decompression operations for HFS.

Reduced sarco/endoplasmic reticulum Ca(2+) uptake activity can account for the reduced response to NO, but not sodium nitroprusside, in hypercholesterolemic rabbit aorta.

Hypercholesterolemia (HC) impairs acetylcholine-induced relaxation but has little effect on that caused by the NO donor sodium nitroprusside (SNP), suggesting that acetylcholine releases less NO from the endothelium in HC. The relaxation to authentic NO gas, however, is also impaired in HC aortic smooth muscle, indicating an abnormal smooth muscle response. NO relaxes arteries by both cGMP-dependent and -independent mechanisms, and the response involves calcium (Ca(2+)) store refilling via the sarco/endoplasmic reticulum calcium ATPase (SERCA). We studied the involvement of cGMP and SERCA in the smooth muscle response to NO and SNP in HC rabbit aorta. A selective guanylyl cyclase inhibitor, 1H-[1,2,4]-oxadiazole-[4,3-a]quinoxalin-1-one, eliminated SNP-induced relaxation but only partially blocked NO-induced relaxation in both normal and HC aorta. The residual relaxation to NO was still less in HC and, in both normal and HC aorta, was abolished by concomitant administration of the SERCA inhibitor cyclopiazonic acid (CPA). In contrast, CPA did not affect SNP-induced relaxation in either normal or HC aorta. SERCA activity measured by (45)Ca(2+) uptake was markedly decreased in HC, although SERCA2 protein expression did not change significantly. These data suggest that NO-induced relaxation but not that to SNP is partially mediated by cGMP-independent Ca(2+) uptake into sarco/endoplasmic reticulum and that reduced sarco/endoplasmic reticulum Ca(2+) pump function can account for the impaired response to NO in HC.

Electrophysiological determination of the site involved in generating abnormal muscle responses in hemifacial spasm.

In patients with hemifacial spasm (HFS), abnormal muscle responses due to abnormal cross-transmission are observed in facial muscles. However, the site in the facial nerve responsible for the cross-transmission remains a matter of controversy. We have developed a model in which by considering the electrophysiological parameters involved in producing the abnormal muscle response, we can determine the site of the abnormal cross-transmission within the facial nerve. This model was applied to HFS patients with three different etiologies: idiopathic, post-Bell's palsy, and post-XII-VII anastomosis. Our data show that: in idiopathic HFS, the cross-transmission may occur in the facial nerve at the level of the pontocerebellar angle; in post-Bell's palsy, it is inside the petrous bone; and in XII-VII anastomosis, it must be in the extracranial part of the facial nerve. The possible mechanisms for this cross talk are discussed in terms of ephaptic transmission or of a central hyperexcitability in the facial motor nucleus.

Electrophysiological Investigation of Hemifacial Spasm after Microvascular Decompression

In patients with hemifacial spasm, it has been said that the spasm is due to cross compression of the facial nerve by a blood vessel and that microvascular decompression (MVD) of the facial nerve is an effective treatment. The F waves, which result from backfiring of antidromically activated motor neurons of the facial motor nucleus, are indices of the excitability of the facial motor nucleus and are enhanced in patients with hemifacial spasm. Measuring blink reflexes and abnormal muscle responses (lateral spread), a characteristic sign of hemifacial spasm, has been used to investigate the mechanism of hemifacial spasm pathophysiologically. Thus the authors measured F waves of the facial muscle, blink reflexes, and abnormal muscle responses before and after MVD in patients suffering from hemifacial spasm to investigate the excitability of the facial motor nucleus and the course of the cure of hemifacial spasm after MVD. The authors obtained facial nerve-evoked electromyograms in 20 patients with hemifacial spasm before and after the MVD procedure. On the spasm side, the F waves and blink reflexes were enhanced preoperatively compared to those on the normal side and abnormal muscle responses were recorded in all patients. In 12 patients whose hemifacial spasm had not disappeared completely for 5.1 +/- 1.7 (mean +/- standard error) months following the MVD procedure, F waves were still enhanced significantly and abnormal muscle responses were still recordable, albeit at lower amplitude. Within 1 month after the hemifacial spasm had disappeared completely. F waves were still significantly enhanced in 17 patients and abnormal muscle responses were recorded in seven of 15 patients. Subsequently, the enhanced F waves and abnormal muscle responses disappeared completely. The authors' study supports the hypothesis that the cause of hemifacial spasm is hyperexcitability of the facial motor nucleus and suggests that additional surgery should not be performed for at least 2 years after MVD, because that period is necessary for the disappearance of the hyperexcitability of the facial motor nucleus.

Electrophysiological investigation of hemifacial spasm after microvascular decompression: F waves of the facial muscles, blink reflexes, and abnormal muscle responses.

In patients with hemifacial spasm, it has been said that the spasm is due to cross compression of the facial nerve by a blood vessel and that microvascular decompression (MVD) of the facial nerve is an effective treatment. The F waves, which result from backfiring of antidromically activated motor neurons of the facial motor nucleus, are indices of the excitability of the facial motor nucleus and are enhanced in patients with hemifacial spasm. Measuring blink reflexes and abnormal muscle responses (lateral spread), a characteristic sign of hemifacial spasm, has been used to investigate the mechanism of hemifacial spasm pathophysiologically. Thus the authors measured F waves of the facial muscle, blink reflexes, and abnormal muscle responses before and after MVD in patients suffering from hemifacial spasm to investigate the excitability of the facial motor nucleus and the course of the cure of hemifacial spasm after MVD. The authors obtained facial nerve-evoked electromyograms in 20 patients with hemifacial spasm before and after the MVD procedure. On the spasm side, the F waves and blink reflexes were enhanced preoperatively compared to those on the normal side and abnormal muscle responses were recorded in all patients. In 12 patients whose hemifacial spasm had not disappeared completely for 5.1 +/- 1.7 (mean +/- standard error) months following the MVD procedure, F waves were still enhanced significantly and abnormal muscle responses were still recordable, albeit at lower amplitude. Within 1 month after the hemifacial spasm had disappeared completely. F waves were still significantly enhanced in 17 patients and abnormal muscle responses were recorded in seven of 15 patients. Subsequently, the enhanced F waves and abnormal muscle responses disappeared completely. The authors' study supports the hypothesis that the cause of hemifacial spasm is hyperexcitability of the facial motor nucleus and suggests that additional surgery should not be performed for at least 2 years after MVD, because that period is necessary for the disappearance of the hyperexcitability of the facial motor nucleus.

Prospective study of microvascular decompression in hemifacial spasm.

Although, in most cases, the symptoms of hemifacial spasm (HFS) disappear immediately after microvascular decompression (MVD), in some cases, they disappear more gradually. The objectives of this study were to observe the time course and the rate of the delayed resolution and to attempt to explain the phenomenon through long-term follow-up of HFS after MVD. Two hundred and sixty-one patients with HFS who underwent MVD were followed up to observe clinical changes. Two hundred and twenty-six of the 261 patients were followed up for a duration of 6 months to 2 years, from 1985 to 1995. After the 1st week of the surgery, 61.1% of the patients were rated as having achieved excellent results. When the patients were followed up for more than 6 months, however, the rate improved to 82.7%. The clinical results of HFS after MVD improved significantly with time (P < 0.05). Delayed resolution of HFS was observed in 37.4% of the patients who experienced complete resolution; it was the most important factor for clinical improvement during the follow-up period. Abnormal muscle response immediately after MVD in the operating room was also positively correlated with resolution during the follow-up period (correlation coefficient = 0.3099, P < 0.05). In conclusion, the clinical picture of HFS after MVD improves with time, and abnormal muscle response can be used as a prognostic indicator for the resolution of HFS during the follow-up period.

Abnormal muscle response (lateral spread) and F-wave in patients with hemifacial spasm

In patients with hemifacial spasm (HFS) the spasm is due to cross compression of the facial nerve by a blood vessel and microvascular decompression (MVD) has proved to be a successful treatment. Abnormal muscle response (AMR), which can be elicited by one facial nerve branch stimulation in muscles innervated by other branches of the facial nerve, is specific for patients with HFS, and the AMR consists of a constant response occurring about 10 ms after stimulus and an afterdischarge with long duration (variable response, autoexcitation). The F-wave in facial muscles is a small recurrent discharge that antidromically propagates to the facial motonucleus and returns orthodromically down the same axon. We measured the AMRs and F-waves of facial muscles in HFS patients in order to investigate the relationship of both potentials and the origin of the AMRs. We obtained facial nerve evoked electromyograms from 10 HFS patients. The afterdischarges of the AMRs and the enhanced F-waves were always elicited at the same time by marginal mandibular branch stimulation of the facial nerve. There was a linear correlation between the duration of these two potentials in each case. Between the duration of the afterdischarge of the AMRs elicited in the mentalis muscles by the zygomatic branch stimulation of the facial nerve and that of the F-waves in the mentalis muscles, there was also a linear correlation in 10 cases. These results suggest that the F-wave and the afterdischarge have the same origin and that the AMR is an exaggerated F-wave.

F-wave in patients with hemifacial spasm: Observations during microvascular decompression operations

In patients with hemifacial spasm (HFS), the spasm is due to cross compression of the facial nerve by a blood vessel. There are currently two hypotheses how the cross compression can cause HFS: 1. the spasm is caused by ephaptic transmission and hyperexcitability at the site of compression; and 2. the spasm is caused by hyperexcitability in the facial motonucleus. In peripheral nerves, F-waves, which result from the backfiring of antidromically activated anterior horn cells, have been proposed as indices of anterior horn cell excitability. Enhancement of the F-waves in facial muscles also indicates increased excitability of the facial motonucleus. On the other hand, abnormal muscle response (AMR), which can be elicited by stimulating one branch of the facial nerve and recording electromyographically from muscles innervated by other branches of the facial nerve, is specific for patients with HFS. We have therefore measured the AMRs and the F-waves in the facial muscle of HFS patients under anesthesia in order to investigate the excitability of the facial motonucleus. We obtained facial nerve evoked electromyograms from 14 HFS patients during microvascular decompression (MVD) operation. The F-waves, obtained with surface electrodes from the mentalis muscle, were defined as the second response after the M-wave. The F-waves in facial muscles cannot usually be elicited during surgical anesthesia using inhalation anesthetics. However, the F-waves were elicited on the spasm side in 10 out of 14 patients with HFS and the F-waves disappeared after MVD under anesthesia, as the early responses (R1) of the blink reflex were elicited on the spasm side before MVD under anesthesia. The F-waves elicited during anesthesia were suppressed significantly, compared with those before MVD. These results suggest that excitability in facial motonucleus increased on the spasm side.

Electrophysiological investigation of hemifacial spasm: F-waves of the facial muscles.

In patients with hemifacial spasm (HFS), the spasm is due to cross-compression of the facial nerve by a blood vessel. There are currently two hypotheses for the mechanism of HFS: 1) the spasm is caused by ephaptic transmission and an increase in excitability at the site of compression; and 2) the spasm is caused by hyperexcitability in the facial nerve nucleus. In peripheral nerves, F-waves, which result from the backfiring of antidromically activated anterior horn cells, have been proposed as indices of proximal motoneuron conduction and anterior horn cell excitability. Enhancement of the F-waves indicates increased anterior horn cell excitability. We have therefore measured F-waves in the facial muscle of HFS patients in order to investigate the excitability of the facial nerve nucleus. The authors obtained facial nerve evoked responses from 20 HFS patients before microvascular decompression (MVD), 10 HFS patients after MVD and 10 healthy controls. The F-waves, obtained with surface electrodes from the mentalis muscle, were the second response after the M-wave. On the patient's spasm side, the F-wave duration, F/M amplitude ratio and frequency of F-wave appearance significantly increased compared with those of the normal side or healthy controls; minimum latency and chronodispersion did not significantly differ between these groups. In patients whose spasm disappeared completely following MVD, the abnormal muscle response (lateral spread), which is a characteristic sign of HFS, and the enhancement of the F-wave eventually also disappeared. Because of the correlation between HFS and F-waves, the authors' study supports the hypothesis that the cause of HFS is hyperexcitability of the facial motonucleus.

Intraoperative monitoring of microvascular decompression in hemifacial spasm.

The significance of intraoperative electrophysiologic monitoring during microvascular decompression was evaluated prospectively in 261 patients with the hemifacial spasm from 1985 to 1995. The patients were divided into a monitored group and a non-monitored group. Identification of the offending vessels was facilitated by the monitoring during the surgical procedure and the complication rate of the monitored group was significantly lower than that of the non-monitored group (p < 0.05). In addition, the abnormal muscle response continued to improve during the follow-up period, thus the electrophysiological status of the hemifacial spasm after the microvascular decompression improved significantly with time (p < 0.05). In conclusion, intraoperative monitoring is useful for identifying the exact offender among multiple vessels, and lowering the complication rate of the microvascular decompression for the hemifacial spasm.

PS-50-3 Improved decremental responses in hemiplegic limbs of two patients with myasthenia gravis and cerebral infarction

Objective: To correlate repetitive nerve stimulation (RNS) decrement in different muscles with the predominant clinical presentation in myasthenia gravis (MG), and to study single fibre EMG (SFEMG) sensitivity in ocular MG.Methods: Sixty-nine, untreated, consecutive patients suspected for MG were observed prospectively for a minimum of 6 months. Those who improved on medical treatment were diagnosed as MG. The others, in whom the neurophysiological studies were normal and that did not improve on medical treatment served as a control group, from which normative data for RNS and SFEMG was obtained. The MG patients were further classified in 3 subgroups according to the predominant clinical presentation: group I (ocular); group b (bulbar); and group a (axial). We performed RNS in nasalis, trapezius, anconeus, and abductor digiti minimi. All patients with ocular MG underwent jitter determination of the orbicularis oculi muscle.Results: Thirty-seven patients were diagnosed as MG (group I, 15; group b, 13; group a, 9). In group I, RNS was abnormal in 33% of the patients. RNS studies disclosed at least one abnormal muscle response in every patient in groups a and b. Trapezius was significantly more sensitive in group a, and anconeus and nasalis in group b (P<0.01). Jitter was abnormal in all patients in group I, and the most sensitive parameter was an increased number of unstable pairs, 100%.Conclusions: Based on these observations, we recommend that a shoulder muscle, as the trapezius, should be studied first in the limb-axial presentation of MG, and the anconeus–nasalis muscles in predominant bulbar MG. In ocular MG, RNS is not sensitive and jitter should be performed in facial muscles.Significance: This paper shows the unequal sensitivity of several muscles to RNS in different forms of MG.

Pathophysiology of obstructive sleep apnoea.

The pathophysiology of obstructive sleep apnoea (OSA) is complex and incompletely understood. A narrowed upper airway is very common among OSA patients, and is usually in adults due to nonspecific factors such as fat deposition in the neck, or abnormal bony morphology of the upper airway. Functional impairment of the upper airway dilating muscles is particularly important in the development of OSA, and patients have a reduction both in tonic and phasic contraction of these muscles during sleep when compared to normals. A variety of defective respiratory control mechanisms are found in OSA, including impaired chemical drive, defective inspiratory load responses, and abnormal upper airway protective reflexes. These defects may play an important role in the abnormal upper airway muscle responses found among patients with OSA. Local upper airway reflexes mediated by surface receptors sensitive to intrapharyngeal pressure changes appear to be important in this respect. Arousal plays an important role in the termination of each apnoea, but may also contribute to the development of further apnoea, because of reduction in respiratory drive related to the hypocapnia which results from postapnoeic hyperventilation. A cyclical pattern of repetitive obstructive apnoeas may result. A better understanding of the integrated pathophysiology of OSA should help in the development of new therapeutic techniques.

Recordings from the facial motonucleus in rats with signs of hemifacial spasm

We recorded evoked potentials from the facial motonucleus of rats in response to electrical stimulation of the temporal branch of the facial nerve in which chronic irritation from a blood vessel had caused the development of an abnormal muscle response. The abnormal muscle response that can be recorded from face muscles that are innervated by one branch of the facial nerve in response to electrical stimulation of a different branch is regarded to be a sign of hemifacial spasm. In the recordings from the motonucleus in rats that showed such an abnormal muscle response (model rats) there was a late component at a latency of about 5 msec, in addition to the early component with a latency of 1.5-2.5 msec that is also observed in normal rats. The latency of the electromyographic potentials recorded from the mentalis-orbicularis oris muscles in response to stimulation of the facial motonucleus was about 2 msec. The latency of the abnormal muscle response obtained from the mentalis muscle in the model rats was about 7 msec. This value is close to the sum of the conduction time from the motonucleus to the mentalis muscle (2 msec) and the latency of the late response from the motonucleus (5 msec). Similar results were obtained in rats in which the facial nerve had been chronically stimulated electrically and which had developed an abnormal muscle response. The results of this study further support the hypothesis that the hyperactivity of the facial motonucleus is the pathophysiology of hemifacial spasm.

Facial nerve demyelination and vascular compression are both needed to induce facial hyperactivity: a study in rats.

It is generally assumed that hemifacial spasm (HFS) is caused by vascular compression of the facial nerve at the root exit zone (REZ), but the mechanism for the development of HFS is not known. Evidence has been previously presented that the signs of HFS are caused by hyperactivity of the facial motonucleus that is caused by the irritation to the facial nerve from the vascular contact. This assumption has been supported by the finding that daily electrical stimulation of the facial nerve in the rat facilitates the development of an abnormal muscle response that is a characteristic sign of HFS in man and is an indication of an abnormal cross-transmission that makes it possible to elicit a contraction of muscles innervated by one branch of the facial nerve by electrically stimulating another branch of the facial nerve. In the present study we show that close contact between a peripheral branch of the facial nerve and an artery also facilitates the development of an abnormal muscle response, but only if the facial nerve has previously been slightly injured (by a chromic suture) at the location of the arterial contact. We also show that blocking neural conduction in the facial nerve proximal to the artificial vascular compression abolishes the abnormal muscle contraction, which supports the assumption that the anatomical location of cross-transmission that is causing the abnormal muscle response is central to the vascular compression, most likely in the facial motonucleus. These findings may explain why the facial nerve is only susceptible to vascular compression near its REZ, where an injury to its myelin is more likely to occur than where the nerve is covered with schwann cell myelin.

Chronic electrical stimulation of the facial nerve causes signs of facial nucleus hyperactivity.

The proximal segment of the facial nerve in rats was stimulated electrically daily for a duration of 2-10 min. After 4-8 weeks of such stimulation, 12 of 18 rats developed abnormal muscle responses that could be demonstrated by recording the electromyographic response from lower face muscles (the mentalis muscle) while the temporal branch of the facial nerve was being stimulated electrically. This abnormal electromyographic response consists of activity that appears in the latency range 6.5-15 ms. In addition, these chronically stimulated rats developed signs of facial synkinesis on the side that had been chronically stimulated. This could be demonstrated by recording electromyographic activity when the blink reflex was being elicited by electrical stimulation of the ophthalmic nerve. Rats in which electrodes had been implanted but which had not been stimulated did not develop any abnormal electromyographic activity. The abnormal electromyographic activity that could be recorded in rats that had been stimulated chronically could not be recorded 4-8 weeks after the stimulation had been terminated. We interpret these results to indicate that chronic electrical stimulation of the facial nerve can render the facial motonucleus hyperactive, and that the signs of this hyperactivity (abnormal muscle response and synkinesis) are similar to those typically seen in patients with hemifacial spasm. We thus presume that these results support the hypothesis that it is the irritation of the facial nerve from a compressing blood vessel that causes the facial nucleus to become hyperactive in patients with hemifacial spasm.

Abnormal response from the sternocleidomastoid muscle in patients with spasmodic torticollis: observations during microvascular decompression operations.

Electromyographic (EMG) recordings from patients undergoing microvascular decompression (MVD) operations to relieve spasmodic torticollis were studied. When EMG potentials were recorded from the sternocleidomastoid muscle in response to electrical stimulation of the spinal accessory nerve (SAN) at the neck, an abnormal (delayed) response was seen in 9 of 12 patients who had unilateral symptoms. In 5 patients with bilateral symptoms, no such delayed response was seen. We assume that this abnormal muscle response depends on an abnormal cross-transmission. Neural conduction time measurements, using electrical stimulation of the intracranial portion of the SAN, indicated that the location of this cross-transmission was more central than the vascular compression of the SAN. We hypothesize that this location might be in the motonucleus of the SAN. Similarities between these abnormal EMG findings in patients with spasmodic torticollis and those reported earlier in patients with hemifacial spasm (HFS) are presented.