Masseter muscle

Tetanus is a disease caused by the release of neurotoxins from the anaerobic, spore-forming rod Clostridium tetani. The clostridial protein, tetanus toxin, possesses a protease activity which selectively degrades the pre-synaptic vesicle protein synaptobrevin, resulting in a block of glycine and y-aminobutyric acid (GABA) release from presynaptic terminals. Consistent with the loss of neurogenic motor inhibition, symptoms of tetanus include muscular rigidity and hyperreflexia. The clinical course is characterized by increased muscle tone and spasms, which first affect the masseter muscle and the muscles of the throat, neck and shoulders. Death occurs by respiratory failure or heart failure. 

Masseter muscle spasm, which sometimes is a warning sign of MH, was found in 1 12,000 anesthetics. However, masseter muscle spasm is not diagnostic of an impending MH crisis. Even though approximately 50% of patients with masseter muscle spasm have tested positive for MH by muscle biopsy, this does not reflect the true incidence of MH. Incidence of masseter spasm is reported to be as high as 1% in pediatric patients, yet MH occurs in only about one in 15,000 pediatric patients. 

Signs and Symptoms Symptoms include acute behavioral changes [anorexia, signs of apprehension or nervousness, irritability, hyperexcitability, incoordination (ataxia), altered phonation, aggression] and unexplained progressive paralysis (initially throat and masseter muscles, leading to profuse salivation and inability to swallow but progressing rapidly to all parts of the body). 

Mastication of foods. Most foods in their natural state require prolonged activity of the masseter muscles involved in closing the jaws. 

Increase in intraocular pressure Increase in intracranial pressure Masseter muscle spasm Hyperkalaemia in susceptible patients Cardiovascular effects Prolonged block Anaphylaxis Malignant hyperpyrexia... 

Fig 3. Electromyographs showing differences in patterns for foods and between individuals. Patterns only from left and right masseter muscles are shown. Horizontal axis - time (sec). Vertical axis - EMG units I EMG unit = 0.5mvolts. 

Muller, F., Heath, M.R., Kazazoglu, E. and Hector, M.P. (1993). Contribution of periodontal receptors and food quality to masseter muscle inhibition in man. J. Oral Rehab. 20, 281-290. 

Four women with CREST syndrome or systemic sclerosis had pain and eventually contracture of the masseter muscles during infusion of iloprost for severe attacks of Raynaud s phenomenon (9). The adverse effect was quickly reversed by reducing the infusion rate. There were no electrocardiographic or cardiac enzyme changes. The mechanism of this effect is obscure. 

Kaplan R, Becker M, Broadman L. Isolated masseter muscle spasm versus generalized rigidity Anesth Analg 1992 141 156... 

Littleford JA, Patel LR, Bose D, Cameron CB, McKillop C. Masseter muscle spasm in children implications of continuing the triggering anesthetic. Anesth Analg 1991 72(2) 151-60. 

Allen GC, Rosenberg H. Malignant hyperthermia suscept-ibihty in adult patients with masseter muscle rigidity. Can J Anaesth 1990 37(l) 31-5. 

Rosenberg H, Fletcher JE. Masseter muscle rigidity and malignant hyperthermia susceptibility. Anesth Analg 1986 65(2) 161. ... 

Lazzell VA, Carr AS, Lerman J, Burrows FA, Creighton RE. The incidence of masseter muscle rigidity after succinylcholine in infants and chUdren. Can J Anaesth 1994 41(6) 475-9. 

Ummenhofer WC, BQndler C, Tschaler G, Hampl BfF, Drewe J, Urwyler A. Propofol reduces succinylcholine induced increase of masseter muscle tone. Can J Anaesth 1998 45(5 Pt l) 417-23. 

Jenkins JG. Masseter muscle rigidity after vecuronium. Eur J Anaesthesiol 1999 16(2) 137-9. 

Albrecht A, Wedel DJ, Gronert GA. Masseter muscle rigidity and nondepolarizing neuromuscular blocking agents. Mayo Chn Proc 1997 72(4) 329-32. 

Schwartz N, Eisenkraft JB, Raab EL. Masseter muscle spasm, succinylchohne, and strabismus surgery. Anesthesiology 1988 69(4) 635-6. 

Figure 8.1-3. Perceived pain intensity measnred on a 0-10 NRS in response to varions jaw functions before and after injection of NGF into the masseter muscle. Each point indicates mean + SEM (n = 12). The symbol ( ) indicates significantly higher NRS pain scores compared with baseline (Dunnett p < 0.05). (Reproduced from Ref. 134, with the permission of the International Association for the Study of Pain.)...

Figure 8.1-4. An example of a collision between an orthodromic (activated by mechanical stimulation of the masseter muscle) and an antidromic (activated by electrical stimulation of the caudal brain stem) is illustrated. Collision resulted in the disappearance of the antidromic spike. This method was used to confirm the projection of the masseter afferent fiber from the masseter muscle to the caudal brain stem, a region believed to be responsible for the integration of muscle pain input.

Figure 8.1-5. (A) The shape of a single action potential is shown. (B) The top trace shows the action potentials recorded from the trigeminal ganglion. The bottom trace shows an increase in the force applied with an electronic von Frey (VF) hair on the masseter muscle until the fiber started firing action potentials. The threshold of the fiber (7.71 g) was determined by subtracting the baseline from the minimum force required to activate the fiber.

Figure 8.1-6. The vertical bar graph illustrates the mean relative mechanical threshold of afferent fibers at various time points after a 10- xL injection of phosphate-buffered saline control (black bars, n = 10) or 25- xg/mL human NGF (gray bars, n = l) into the masseter muscle. The error bars represent the standard error of the mean. p < 0.05 ANOVA and post hoc Holm-Sidak method compared with the baseline relative mechanical threshold.

Intramuscular injection of human NGF into the rat masseter muscle failed to evoke afferent discharge however, it decreased the MT of masseter afferent fibers compared with the baseline (Figure 8.1-6). There was a significant decrease in the MT 1 hour postinjection (as compared with the baseline), which lasted for 3 hours. The postinjection MT of saline-injected fibers was not significantly different from the baseline. There was no significant difference between the level of plasma protein extravasation between control saline and human NGF groups. 

The results of this study suggested that intramuscular injection of human NGF at a concentration equivalent to that which resulted in mechanical sensitization in humans [134] caused a significant decrease in the mechanical threshold of rat masseter muscle afferent fibers. Therefore, the method of injecting human NGF into the rat masseter muscle could be used to study peripheral mechanisms associated with the development of NGF-induced masseter muscle sensitization in humans. 

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