Observation of Effects of Different Surgical Treatments on Unilateral Masticatory Muscle Spasm.

BACKGROUND: Unilateral masticatory muscle spasm is a rare disease without a generally accepted and efficacious treatment plan. OBJECTIVE: We sought to compare the effects of different surgical treatments on unilateral masticatory muscle spasm. METHODS: A retrospective analysis of the surgical treatment and effects of 10 cases of unilateral masticatory muscle spasm occurred between February 2010 and September 2016. Three cases underwent complete amputation of the trigeminal motor branch, 3 cases underwent partial amputation of the trigeminal motor branch, and 4 cases received only vascular decompression. All patients were followed up by telephone interview after surgery. RESULTS: In the simple vascular decompression group, 3 cases were cured and 1 was cured after a delay. Of these 3 cases, 1 case became aggravated 2 years after the operation, 1 case became aggravated 5 years after the operation, and 1 case showed no change during the follow-up period. In the partial amputation group, 2 cases were cured and 1 case was alleviated. Of the 2 patients who were cured, 1 suffered recurrence 2 years later, while the other case showed no recurrence during the follow-up period. In the complete amputation group, 1 case was cured with a delay and 2 cases were cured immediately with no recurrence during the follow-up. Mild atrophy of the temporal muscle occurred gradually with no restriction of the mouth opening in 2 cases. CONCLUSIONS: Complete amputation of the trigeminal nerve did achieve better effects than pure microvascular decompression and partial amputation of the trigeminal motor branch, but it may lead to mild temporal muscle atrophy.

Hemimasticatory spasm: clinical and electrophysiologic observations.

Hemimasticatory spasm is a rare disorder of the trigeminal nerve that produces involuntary jaw closure due to paroxysmal unilateral contraction of jaw-closing muscles. We report three patients with this disorder. Electrophysiologic studies demonstrated normal blink and masseter reflexes. The masseter inhibitory reflex was absent during periods of spasm. Needle electromyography demonstrated irregular bursts of motor unit potentials that were identical to the pattern observed in hemifacial spasm. The electrophysiologic findings suggest ectopic excitation of the trigeminal motor root or its nucleus, an abnormality that is analogous to ectopic excitation of the facial nerve in hemifacial spasm. One patient improved temporarily with surgery, one improved while on treatment with carbamazepine, and another responded favorably to botulinum toxin injection.

Focal facial spasm.

An unusual case of focal facial spasm modified by factors affecting the peripheral facial nerve was investigated in a 32-year-old woman with involuntary contractions at the left mouth and nasal area. Voluntary facial movements were normal. The involuntary spasms ceased with digital pressure over the facial nerve in the left stylomastoid area. A difference between voluntary and these involuntary facial movements occurred both with local anesthetic blockade and with crushing of the facial nerve. Blink reflexes demonstrated unilateral left synkinesis, and facial EMG showed clonic discharges and individual motor units that discharged rapidly (200 Hz). Treatment with diphenylhydantoin, carbamazepine, and prednisone was ineffective. Neurolysis of the peripheral facial nerve resulted in temporary relief, whereas biofeedback controlled the spasms. Focal facial spasms may represent a disorder of the facial nucleus influenced by both peripheral and central mechanisms.

Pathophysiology of hemifacial spasm: I. Ephaptic transmission and ectopic excitation.

We studied 62 patients with hemifacial spasm to test the presence of ephaptic transmission and ectopic excitation. The zygomatic and mandibular branches of the facial nerve were stimulated separately, recording simultaneously from the orbicularis oculi and mental muscles. Antidromic impulses were transmitted bidirectionally between the two branches. Transmission took place in a fraction of slow conducting motor nerve fibers. After-activity and late-activity were recorded as single potentials or trains, suggesting autoexcitation of fibers. The interspike frequency was 250 to 350 Hz. Hyperventilation produced synchronous clonic-tonic activity, suggesting ectopic excitation caused by hypocalcemia. Ectopic excitation and ephaptic transmission are important pathophysiologic factors in hemifacial spasm.

Hemifacial spasm: results of electrophysiologic recording during microvascular decompression operations.

Electrophysiologic recordings were made from patients with hemifacial spasm (HFS) during microvascular decompression (MVD) operations to see if spasm and synkinesis are caused by ephaptic transmission at the site of lesion (root entry zone [REZ] of the facial nerve). The response from the orbicularis oculi muscle to electrical stimulation of the marginal mandibular nerve had a 2.2-msec longer latency (average of 16 patients) than the sum of the conduction times of the parts of the facial nerve that would be involved if the response was the result of ephaptic transmission at the REZ of the seventh cranial nerve. Similar results were obtained when the zygomatic branch of the facial nerve was stimulated. These results indicate that the facial motonucleus is involved in HFS.

Sleep bruxism is a disorder related to periodic arousals during sleep.

There is evidence that sleep bruxism is an arousal-related phenomenon. In non-REM sleep, transient arousals recur at 20- to 40-second intervals and are organized according to a cyclic alternating pattern. Polysomnographic recordings from six subjects (two females and four males) affected by sleep bruxism (patients) and six healthy age-and gender-matched volunteers without complaints about sleep (controls) were analyzed to: (1) compare the sleep structure of bruxers with that of non-complaining subjects; and (2) investigate the relations between bruxism episodes and transient arousals. Patients and controls showed no significant differences in conventional sleep variables, but bruxers showed a significantly higher number of the transient arousals characterized by EEG desynchronization. Bruxism episodes were equally distributed between non-REM and REM sleep, but were more frequent in stages 1 and 2 (p < 0.0001) than in slow-wave sleep. The great majority of bruxism episodes detected in non-REM sleep (88%) were associated with the cyclic alternating pattern and always occurred during a transient arousal. Heart rate during the bruxism episodes (69.3+/-18.2) was significantly higher (p < 0.0001) than that during the pre-bruxing period (58.1+/-15.9). Almost 80% of all bruxism episodes were associated with jerks at the anterior tibial muscles. The framework of the cyclic alternating pattern offers a unified interpretation for sleep bruxism and arousal-related phenomena.

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.

On the origin of synkinesis in hemifacial spasm: results of intracranial recordings.

Recordings were made from facial muscles and the facial nerve near its entrance into the brain stem in patients with hemifacial spasm (HFS). The purpose of this study was to determine if the synkinesis commonly seen in patients with HFS could be linked to ephaptic transmission at the presumed site of the lesion (at the root entry zone (REZ) of the facial nerve). When the mandibular branch of the facial nerve was electrically stimulated, a response could be recorded from the orbicularis oculi muscles during the operation. The latency of the earliest response was 11.03 +/- 0.66 msec (mean response of seven patients +/- standard deviation (SD]. With equivalent stimulation a response could also be recorded from the facial nerve near the REZ; the latency of this response was 3.87 +/- 0.36 msec. Stimulation of the facial nerve at the same location yielded a response from the orbicularis oculi muscle, with a latency of 4.65 +/- 0.25 msec. The latency of the earliest response from the orbicularis oculi muscle to stimulation of the marginal mandibular branch of the facial nerve (11.3 msec) is thus larger than the sum of the conduction times from the points of stimulation of the marginal mandibular branch to the REZ of the facial nerve and from the REZ of the facial nerve to the orbicularis oculi muscle (8.52 +/- 0.38 msec). It is therefore regarded as unlikely that the earliest response of the orbicularis oculi muscle to stimulation of the mandibular branch of the facial nerve is a result of "crosstalk" in the facial nerve at a location near the REZ, and it seems more likely that HFS caused by injury of the facial nerve is a result of reverberant activity in the facial motonucleus, possibly caused by mechanisms that are similar to kindling.

Factors influencing the therapeutic effect of muscle afferent block for oromandibular dystonia and dyskinesia: implications for their distinct pathophysiology.

Oromandibular dystonia (OMD) is a focal dystonia manifested by involuntary masticatory and/or lingual muscle contractions. Muscle afferent block (MAB) by injecting anaesthetic and alcohol intramuscularly is recently used for the treatment of OMD. To study the factors affecting the efficacy of MAB, 44 patients with OMD were treated by local injection of lidocaine and ethanol. They were divided into four groups (spastic, rhythmic, dyskinetic, and task-specific) according to the pattern of incisal movement and involuntary contraction. We used a clinical scaling protocol in terms of four parameters (mastication, speech, pain, and discomfort) to evaluate the change of symptoms objectively. The relationship of improvement in clinical scores with various parameters was assessed statistically. The overall objective improvement was 60.2 +/- 29.5%. The scores decreased significantly (P<0.0001, paired t-test) after MAB. The maximal incisal velocity significantly correlated inversely with the clinical improvement, and MAB was particularly effective for spastic contraction. Dyskinetic and rhythmic groups showed variable and significantly less improvements than the spastic group. MAB is highly effective for OMD, but not for the patients with dyskinetic symptoms. The jaw movement pattern is an important factor for predicting the outcome. The difference in the response to MAB in OMD and oral and/or orofacial dyskinesia suggests the distinct pathophysiology between the two.

Skeletal muscle: anatomy, physiology, and pathophysiology.

Many questions remain to be answered. The intention here is to attempt to place in perspective a portion of what is known and understood scientifically, to make working sense of the pathophysiologic process so that we as clinicians can "in our mind's eye" understand what it is that we are trying to treat with what now seems to be a multitude of therapies. When a patient presents to your office with acute or chronic, or both, myofascial pain dysfunction syndrome, some basic questions must be addressed. Is the disease process genetic (intrinsic) or acquired (extrinsic), or both? It is the purpose of diagnosis to unearth the underlying predispositions that patients may exhibit. Often the predispositions are quite obvious (gross postural discrepancies and skeletal and dental malrelationships( or they may be consummately subtle (endocrinopathies and behavioral patterns). It seems that the main job to be completed is diagnosis followed by the utilization of well-known physical medicine (conservative) techniques that treat the source of the disorder: the myofascial trigger zone.

Diaphragmatic cramp as a possible cause of noncardiac chest pain and referred mandibular pain.

The initial assumption that sudden acute chest pain may be of cardiac origin is justifiable, but when this proves not to be the case the patient is left with little explanation of the cause. It is suggested here that diaphragmatic cramp may be a cause of some undiagnosed noncardiac chest pains associated with mandibular referred pain. The phrenic nerve provides both motor and sensory innervation to the diaphragm, while the trigeminal nerve carries sensation from the mandibular teeth. Both nerves originate in separate nuclei close together in the lower medulla. Interconnections between these nuclei and others higher up in the brain may provide one explanation for this problem.

Multiple sclerosis and oral care.

Multiple sclerosis is a complex neurological condition affecting sensory and motor nerve transmission. Its progression and symptoms are unpredictable and vary from person to person as well as over time. Common early symptoms include visual disturbances, facial pain or trigeminal neuralgia and paraesthesia or numbness of feet, legs, hands and arms. These, plus symptoms of spasticity, spasms, tremor, fatigue, depression and progressive disability, impact on the individual's ability to maintain oral health, cope with dental treatment and access dental services. Also, many of the medications used in the symptomatic management of the condition have the potential to cause dry mouth and associated oral disease. There is no cure for multiple sclerosis, and treatment focuses on prevention of disability and maintenance of quality of life. Increasingly a multi-disciplinary team approach is used where the individual, if appropriate his/her carer, and the specialist nurse are key figures. The dental team plays an essential role in ensuring that oral health impacts positively on general health.

[Neurophysiological study of hemifacial spasm--F wave of the facial muscles].

We studied the F wave of the facial muscles on both the normal side and the spastic side in 14 patients with hemifacial spasm. The purpose of this study was to determine if the mechanism of hemifacials spasm originates in ephaptic transmission in the facial nerve at the site of vascular compression or in a hyperexcited facial motor nucleus. Larger amplitude, longer duration and shorter latency F waves in the peripheral nerves than in normals indicate anterior horn cell hyperexcitability. We found abnormal potentials exhibiting synkinesis (lateral spread), a typical electrophysiological finding in hemifacial spasm, in the facial nerve evoked electromyograms of the 14 patients, none of whom had experienced facial palsy or facial nerve block. Electrical stimulation was delivered transcutaneously to the most distal portion of the marginal mandibular branch of the facial nerve. Using surface electrodes the F waves were obtained over the mentalis muscle as the second response after the M wave. While the F waves were normal on the patients' normal side, on the spastic side, their duration was longer (mean duration about 1.9 times that of the normal side), their onset latency was slightly shorter, and their F/M amplitude latency was greater than on the normal side. After microvascular decompression, the facial spasm and abnormal F-wave findings resolved. Onset latency was not increased, and on the spastic side some patients displayed facial spasm clinically and electrophysiologically for one year after MVD. In other words, there was hardly any focal demyelination of the facial nerve, so it is possible that ephaptic transmission and ectopic excitation are the mechanism of HFS.(ABSTRACT TRUNCATED AT 250 WORDS)

[Abnormal evoked EMG and blink reflex responses in patients with hemifacial spasm (HFS)].

Abnormal evoked EMG and blink reflex responses have been observed on the affected side in patients with HFS. These characteristic responses were used as methods of preoperative differential diagnosis, and the disappearance of these abnormal responses during intraoperative monitoring was assessed as confirmation of nerve decompression. The subjects were 30 patients with a diagnosis of HFS. Three responses were evaluated: 1) the orbicularis oris muscle (OR) response to stimulation of the orbicularis oculi muscle branch (OB), OB-->OR; 2) the orbicularis oculi muscle (OC) response to stimulation of the marginal mandibular branch (MB), MB-->OC; and 3) the (OR) response to stimulation of the supraorbital nerve (SO), SO-->OR. The facial nerve in the root exit zone was compressed by a vessel in all 21 patients diagnosed as typical HFS who had abnormal responses, and OB-->OR was always detected. The MB-->OC and SO-->OR detection rates were low (50% and 25%, respectively) when the interval since the onset of HFS was less than 3 years, but increased to 78% and 67%, respectively, when it was 3 to 5 years, and all three abnormal responses were always detected when the interval was more than 5 years. In 17 of the patients these responses began to change and eventually disappeared before decompression of the facial nerve, and in 2 patients they persisted even after decompression. Abnormal responses disappeared at the time of decompression in only 2 patients, and their HFS was completely cured postoperatively. These findings confirmed that disappearance of abnormal responses is not a very useful guide for facial nerve decompression.(ABSTRACT TRUNCATED AT 250 WORDS)

[Neurophysiological study on hemifacial spasm--the abnormality and origin of the electromyographic response to stimulation of the facial nerve].

Electromyographic responses (MD-OC) of the orbicularis oculi muscle to stimulation of ipsilateral marginal mandibular branch of the facial nerve were recorded in 20 patients with hemifacial spasm, pre-, post-operatively and during operations to relieve it by microvascular decompression, and the abnormal features and origin of the MD-OC were investigated. On the affected side, the MD-OC were recorded in pre- and during operative state, and disappeared with disappearance of hemifacial spasm after microvascular decompression, while no response was recorded in pre-, during and post-operative state on the healthy side. In 17 patients, the MD-OC was recorded continuously during operation. In all cases except for one case in whom the MD-OC was recorded even the end of operation, the MD-OC disappeared on several stage of procedure from dural opening through vascular mobilization. The compound nerve action potential (MD-VII) to stimulation of the marginal mandibular branch was recorded from the facial nerve near its root entry zone after exposure of the intracranial portion. There were two patterns in the records, i.e., one group consisting of early component and the other consisting of early and late component. The MD-VII was only consisted of the early component in 12 cases in whom the MD-OC have already disappeared, and was consisted of the early and late component in 5 cases in whom the MD-OC still recorded. And in 2 cases of the later, the late component disappeared simultaneously with disappearance of the MD-OC during vascular mobilization.(ABSTRACT TRUNCATED AT 250 WORDS)

Tetanus: pathophysiology, treatment, and the possibility of using botulinum toxin against tetanus-induced rigidity and spasms.

Tetanus toxin, the product of Clostridium tetani, is the cause of tetanus symptoms. Tetanus toxin is taken up into terminals of lower motor neurons and transported axonally to the spinal cord and/or brainstem. Here the toxin moves trans-synaptically into inhibitory nerve terminals, where vesicular release of inhibitory neurotransmitters becomes blocked, leading to disinhibition of lower motor neurons. Muscle rigidity and spasms ensue, often manifesting as trismus/lockjaw, dysphagia, opistotonus, or rigidity and spasms of respiratory, laryngeal, and abdominal muscles, which may cause respiratory failure. Botulinum toxin, in contrast, largely remains in lower motor neuron terminals, inhibiting acetylcholine release and muscle activity. Therefore, botulinum toxin may reduce tetanus symptoms. Trismus may be treated with botulinum toxin injections into the masseter and temporalis muscles. This should probably be done early in the course of tetanus to reduce the risk of pulmonary aspiration, involuntary tongue biting, anorexia and dental caries. Other muscle groups are also amenable to botulinum toxin treatment. Six tetanus patients have been successfully treated with botulinum toxin A. This review discusses the use of botulinum toxin for tetanus in the context of the pathophysiology, symptomatology, and medical treatment of Clostridium tetani infection.

Effect of low-level laser therapy on the post-surgical inflammatory process after third molar removal: study protocol for a double-blind randomized controlled trial.

BACKGROUND: Low-level laser therapy (LLLT) has been shown to modulate the inflammatory process without adverse effects , by reducing pain and swelling and promoting the repair of damaged tissues. Because pain, swelling and muscle spasm are complications found in virtually all patients following oral surgery for the removal of impacted teeth, this model has been widely used to evaluate the effects of LLLT on the inflammatory process involving bone and, connective tissue and the muscles involved in mastication. METHODS/DESIGN: After meeting the eligibility criteria, 60 patients treated at a Specialty Dental Center for the removal of impacted lower third molars will be randomly divided into five groups according to the type of laser therapy used at the end of surgery (intraoral irradiation with 660 nm laser; extraoral irradiation with 660 nm laser; intraoral irradiation with 808 nm laser; extraoral irradiation with 808 nm laser and no irradiation). To ensure that patients are blinded to the type of treatment they are receiving, the hand piece of the laser apparatus will be applied both intraorally and extraorally to all participants, but the device will be turned on only at the appropriate time, as determined by the randomization process. At 2 and 7 days after surgery, the patients will be evaluated by three blinded evaluators who will measure of swelling, mouth opening (muscle spasm evaluation) and pain (using two different pain scales). The 14-item Oral Health Impact Profile (OHIP-14) will be used to assess QOL. All data will be analyzed with respect to the normality of distribution using the Shapiro-Wilk test. Statistically significant differences between the experimental groups will be determined using analysis of variance, followed by a suitable post hoc test, when necessary. The significance level will be set at α = 0.05. DISCUSSION: The lack of standardization in studies with regard to the samples, methods and LLLT parameters complicates the determination of the actual effect of laser therapy on this model. The present study aims to provide a randomized, controlled, double-blind trial to compare four different LLLT parameters in relation to the outcomes of pain, swelling and muscle spasm following surgery for the extraction of impacted third molars and evaluate the effects os surgery on patients' quality os life (QOL). TRIAL REGISTRATION: Brazilian Registry of Clinical Trials - Rebec (RBR-6XSB5H).

Clinical characteristics of lateral pterygoid myospasm: a retrospective study of 18 patients.

The available scientific literature on masticatory myospasm-induced oromandibular dystonia is limited. The objective of this study was to determine the clinical characteristics of lateral pterygoid myosapsm in a series of 18 patients. Clinical and electromyographic (EMG) data of 36 patients diagnosed with masticatory muscle myospasm were reviewed, and data from 18 patients with needle EMG-confirmed lateral pterygoid myospasm were extracted for retrospective study. The study population included 6 men and 12 women with a mean age of 53.2 ± 15.3 years. Patients' chief complaints, severity and frequency of myospasm, clinical observations, video recordings, and surface/needle EMG recordings were analyzed. Despite the variety of manifestations, 3 characteristic signs and symptoms of lateral pterygoid myospasm were observed. These were: 1) jaw function disabilities; 2) difficulty in jaw closing after wide opening; and 3) involuntary jaw movements. A differential diagnosis of lateral pterygoid myospasm should be included when oromandibular dystonia is accompanied by the fore mentioned.

[Classification and clinical characteristics of masticatory myospasm].

OBJECTIVE: To determine the classification of masticatory myospasm by analyzing characteristics of clinical appearances. METHODS: Thirty-six cases of masticatory myospasm from 2000 to 2010 were included. The clinical data of these patients were analyzed, including patient information, patient history, clinical characteristics, severity and the frequency of myospasmodic movement, electromyogram (EMG), and the efficacy of botulinum toxin injection treatment. RESULTS: There were 11 males and 25 females, aged from 15 to 71. According to the clinical manifestation and EMG findings, patients could be divided into two groups: 18 cases were classified as jaw closing type which involved masseter and/or temporalis muscles presenting as trismus and acute pain, the other 18 cases were jaw opening type which involved lateral pterygoid muscles complaining difficulty in jaw closing and teeth clenching. The jaw closing type was often seen in patients of 20 to 50 years old, the jaw opening was frequently seen in patients over 50 years old. Jaw closing type was attacked intermittently and unilaterally, but jaw opening was often attacked continually and bilaterally. The rating scale of the severity of spasmodic movement was not different between the two types, but the frequency of spasmodic attack was much higher for jaw opening type (P < 0.05). The EMG of jaw closing type was classified into persistent, rhythmic and irregular type. The EMG of jaw opening type was classified into spontaneous and exercise-induced type. Twelve cases were treated by botulinum toxin injection that could significantly relieve symptoms. CONCLUSIONS: Masticatory myospasm can be classified into jaw closing and jaw opening types. Jaw closing type involves masseter and/or temporalis muscles and jaw opening type involves lateral pterygoid muscles. Botulinum toxin injection was the most effective therapy for the masticatory myospasm.