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The clinical and electrophysiological features of a case of hemimasticatory spasm are presented. The findings are in many respects similar to those described in hemifacial spasm. A peripheral cranial neuropathy as proposed in hemifacial spasm also may be responsible for hemimasticatory spasm.
This investigation used a model of increased skeletal muscle contractile activity to evaluate whether the adenylate cyclase-adenosine 3',5'-cyclic monophosphate (cAMP) pathway and/or the high-energy phosphate state of the muscle might be temporally related to the contraction-induced increase in skeletal muscle GLUT-4 protein concentration. Plantaris and gastrocnemius muscles of Sprague-Dawley rats were subjected to 3, 7, 14, or 28 days of chronic low-frequency electrical stimulation (10 Hz, 24 h/day). GLUT-4 protein concentration was slightly reduced after 3 days of electrical stimulation, similar to control values at 7 days and significantly elevated above control at 14 days (53%, P < 0.05) and 28 days (338%, P < 0.05) of stimulation. ATP, creatine phosphate, creatine, and P, were inversely related to GLUT-4 protein concentration. Adenylate cyclase activity increased with electrical stimulation and was significantly related to the increased GLUT-4 protein. cAMP was significantly increased at 14 days of stimulation and remained elevated through 28 days. These results demonstrate that both the adenylate cyclase-cAMP pathway and the high-energy phosphate state of the muscle are temporally related to elevations in skeletal muscle GLUT-4 protein concentration in response to chronic low-frequency electrical stimulation and, as such, suggest that both may comprise a component of the intracellular signal that regulates the contraction-induced increase in skeletal muscle GLUT-4 protein concentration.
1. During chewing, little muscle activity is required to make open-close movements with the mandible, and much additional muscle activity (AMA) of the closing muscles is needed to overcome the resistance of food. The neuromuscular control of the AMA was investigated. 2. Subjects made rhythmic open-close movements at their natural chewing frequency controlled by a metronome. Food resistance was simulated by an external force, acting on the jaw in a downward direction during part of the closing movement. Sequences of cycles with a force were unexpectedly alternated with sequences of cycles without a force. Jaw movement, and surface electromyograph (EMG) of the masseter, temporalis, and digastric muscles on both sides were recorded during cycles before and after the transition from force to no force (Disappear experiment) and vice versa (Appear experiment). 3. The movement trajectory of the second and following cycles after the transition from force to no force or vice versa were similar. Thus adaptation to the changed circumstances occurred in both types of experiments within two open-close cycles. 4. In the first cycle with force in the Appear experiments, the AMA started, on average, 129 ms after the onset of the force. In all other cycles with force, the AMA started, on average, 70 ms before the onset of the force at a low level and steeply increased 23 ms after the onset of the force. 5. In the first cycle without force in the Disappear experiments, the AMA started, on average, 69 ms before the moment at which the force would have started. However, the large contribution to the AMA had disappeared.(ABSTRACT TRUNCATED AT 250 WORDS)
Cross-sections of normal digastric, temporalis and masseter muscles from 7- and 30-week-old mice were studied for centrally positioned nuclei. Such nuclei were inhomogeneously distributed throughout each muscle and varied markedly between specimens. The incidence of centrally positioned nuclei in the digastric muscle (mean +/- SD: 0.029 +/- 0.015, n = 25) was significantly higher (p less than 0.001) than that in the temporalis (mean +/- SD: 0.011 +/- 0.010, n = 25) and masseter muscles (mean +/- SD: 0.005 +/- 0.007, n = 9), but did not differ between the two latter muscles (p = 0.41). Furthermore, the frequency in a given muscle was apparently age-independent. A connection between fiber type and centrally positioned nuclei is suggested.
Masticatory forces or bite forces applied to the teeth are known to generate a compressive force on the temporomandibular joint (TMJ). This intra-articular force is referred to as TMJ loading. TMJ loading is considered to be controlled to a certain extent by the stomatognathic system, so as not to exceed a certain limit. In order to clarify the control mechanism of the TMJ during biting, the controllability of TMJ loading through coordinated activities of the masticatory muscles has been numerically analyzed using a static two-dimensional jaw model. This model consists of a rigid-body model of the jaws and a spring model of the articular disk, which includes three dominant muscle force vectors representing the masseter, temporalis and lateral pterygoid muscles. The bite force vector is assumed to be applied solely at the first molar. Static equilibrium analyses suggest that coordinated activities of the masseter muscle and anterior portion of the temporalis muscle can minimize TMJ loading and concentrate the stress within the articular disk to the intermediate zone of the disk, and that the activity of the posterior portion of the temporalis muscle has the possibility of reducing TMJ loading.
The aim of the present study was to gain an insight into the influence of a vertical bite-rise (clenching in intercuspal occlusion vs. clenching on an occlusal stabilization splint), the mode of visual feedback (VF; obtained from the compound masseter signal, from the compound anterior temporalis signal, or from the compound signal of both masseter and anterior temporalis muscles) and the EMG clenching level (10% MVC and 50% MVC) on the muscle balance between the masseter and the anterior temporalis muscles. The muscle balance was quantified as the logarithmic value of the ratio between the summated mean rectified EMG activity of the masseter muscles and this activity of the anterior temporalis muscles. The muscle balance was influenced significantly by the mode of VF (p < 0.01), the muscle balance shifting toward the group of muscles from which VF was obtained. When VF was obtained from the masseter muscles, a decrease in the anterior temporalis EMG activity was observed when the vertical dimension was increased (p < 0.05-0.01). When VF was obtained from the anterior temporalis muscles, the activity of the masseter muscles was raised with respect to that of the anterior temporalis muscles during clenching with a vertical bite-rise (p < 0.05-0.01). When VF was obtained from both groups of muscles, the masseteric EMG activity increased, whereas the anterior temporalis EMG activity decreased. Hence, regardless of the mode of VF, a relatively lower activity level of the anterior temporalis muscles was achieved after insertion of an occlusal stabilization splint.(ABSTRACT TRUNCATED AT 250 WORDS)
Both experimental and retrospective studies suggest a link between parafunctions and pain in temporomandibular disorder (TMD) patients. To investigate the role of parafunctions in TMD, experience sampling methodology was used as a prospective test of the hypothesis that patients with TMD have higher levels of tooth contact and tension than non-TMD controls. Three groups of TMD patients and a group of normal controls carried pagers for one week, were contacted approximately every two hours by an automated calling system, and completed questionnaires assessing tooth contact, tension, and pain at each contact. Results showed that tooth contact was much more frequent among normal controls than is commonly presumed. Patients with myofascial pain with/without arthralgia reported more frequent contact, higher intensity contact, and more tension than patients with disk displacement or normal controls. Increased masticatory muscle activity responsible for tooth contact and tension may be an important mechanism in the etiology and maintenance of the myofascial pain and arthralgia of TMD.
We report a successful treatment of bruxism in a patient with anoxic brain injury using botulinum toxin-A (BTX-A). On examination the mouth opening was 0 mm, no feeding was possible through the mouth. Botulinum toxin was injected into the masseter and temporalis; great improvement in trismus and bruxism was noted after 3 weeks. One further treatment improved the mouth opening on the following week and the patient was discharged from our care to be reviewed when required.
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OBJECTIVE: This anatomic study was carried out in a bid to decrease damage of the temporal branch of the face nerve in endoscopic temporal lifting. METHODS: We dissected the frontal-temporal region and located the temporal branch on 36 sides of adult head specimens. RESULTS: It was found that the temporal branch is deep to the temporoparietal fascia and frontal muscle. The temporal branch has one to four branches in general. The first one is 8.1 +/- 2.1 mm anterior to articular tubercle and 33.8 +/- 4.9 mm superior to the bony lateral canthus. The temporal branches locate below a line drawn from the articular tubercle to 40 mm above the bony lateral canthus. CONCLUSION: It is suggested that the operation incisions in the temporal region be selected above this line.
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A number of diverse symptoms, conventionally diagnosed and treated as individual problems, exist in combination in the craniomandibular pain and dysfunction patient. This chapter explores musculoskeletal dysfunction of the area as a common etiologic factor for head and neck pain. The electronically derived data, reported in 68 case histories, indicate that a common measurable etiology is responsible for the many ostensibly diverse manifestations of craniomandibular pain and dysfunction. Both quantitative and subjective data support the etiologic validity of the diagnosis. The basis for the effectiveness of the reported therapy rests on diagnosis of a skeletal malrelation of the mandible to the cranium that poses sustained accommodative demand on the neuromusculature.
Muscle biopsies of the mandible adductors of the Wistar rat (Rattus norvegicus Berkenhout) have been analyzed enzyme-histochemically for the investigation of the postnatal development (42.-126. d post partum) of their muscle fibers with special regards to the fiber types. The following methods have been used in this investigation: myofibrillar adenosine triphosphatase (ATP-ase) with different pre-incubations, Sudan black B (triglycerides), periodic acid-Schiff reagent (PAS) (glycogen), Gomori modified Trichrome staining. Quantitative analysis of muscle fibre-type composition and muscle fibre size was done from different regions of muscle sections. Estimation of the fiber size was carried out by measuring the minimum diameter of each type of muscle fibre.
A 49-year old man developed myositis of the left masticatory muscles followed by myositis of the right supinator longus; these two lesions were histologically confirmed. Blood and bone marrow eosinophilia was present. Cure was obtained with systemic corticosteroids. Only one similar case was found in the literature. These cases differ from the various localized or focal forms of myositis as well as from eosinophilic polymyositis. Despite some similarities with masseteric myopathies in animals, no hypothesis can be formulated concerning the cause of the disease.
Young adult albino rats of Wistar strain were used for the present study. 0.5 to 15 microliters of 20-50% of horseradish peroxidase (HRP) were injected into each individual muscle of mastication to label neurons in the trigeminal motor nucleus (TMON) for light microscopic study. The results reveal that: (1) Many HRP-labeled, multipolar neurons are observed in the motor nucleus in each jaw-closing muscle (JCM) with less in each the jaw-opening muscle (JOM). (2) The motor neurons innervating each masticatory muscle in the motor nucleus show a somatotopic arrangement: (a) those innervating the temporalis muscle are located in the medial and dorsomedial parts; (b) those innervating the masseter muscle are located in the intermediate and lateral; (c) those innervating the medial and lateral pterygoid muscles are located in the lateral, ventrolateral and ventromedial parts, respectively; and (d) those innervating the mylohyoid and the anterior belly of the digastric muscles are located in the most ventromedial part of the caudal one-third of the nucleus. Axons of most masticatory motor neurons run ventrolaterally in between the motor and the chief sensory nuclei of the trigeminal nerve. However, those of the mylohyoid and anterior belly of the digastric muscles ascend dorsally to the dorsal aspect of the caudal nucleus and then turn ventrolaterally to join the motor root of the trigeminal nerve. Furthermore, the dendrites of the motor neuron of JCM converge dorsocaudally to the supratrigeminal region. The diameters of neurons of each JCM display a bimodal distribution. However, an unimodal distribution is present in the motor neurons from each JCM. It is suggested that the motor nucleus innervating the JCM is comprised of comprised of alpha- and gamma-motor neurons. It, thus, may provide a neural basis for the regulation of the muscle tone and biting force.
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Disruption of the erythrocyte flow occurred more frequently in microvessels of the brain (2-3/sec) than in those of muscles (1/sec), and the amplitude of the blood flow oscillations was greater in the former (150-450 mu/sec) than in the latter (0-300 mu/sec). Besides, the average blood flow velocity was greater in the brain microvessels (1830 +/- 680 mu/sec) than in those of muscles (1460 +/- 630 mu/sec), the diameter of the erythrocyte flow being about 5-8 mu in the former and about 10-13 mu in the latter. The differences seem to be due to different spatial organization of the microvessel beds.
Silent periods were elicited in the electromyographic activity of the masseter and temporalis muscles from six normal subjects, by electrical stimulation of the skin over the contralateral masseter during clenching. Pairs of suprathreshold square pulses with varied time intervals were delivered using surface electrodes. It was found that the silent periods, which were mostly of the long latency (about 53 ms) type, had a refractory period, during which a new silent period could be evoked only by increasing the strength of the second stimulus. This refractory period could last for up to 1.5 s. During the first 200 ms after the first stimulus a second silent period was almost impossible to evoke with the moderately painful stimuli used in the present experiments. It is suggested that the refractory period should be considered as significant for the methodology when recording the silent period duration. It is also suggested that the long latency silent period should be recorded as a separate parameter and differentiated from the short latency (10-12 ms) silent period. This may be of special importance to recognize when a short latency silent period and a long latency silent period merge.