LETTER TO EDITOR
Year : 2012 | Volume
: 28 | Issue : 3 | Page : 407--408
Masseteric muscle spasm following neostigmine
S Bala Bhaskar, N Kiran Chand, B Devanand
Department of Anaesthesiology and Critical Care, Vijayanagar Institute of Medical Sciences, Bellary, India
S Bala Bhaskar
Department of Anaesthesiology and Critical Care, Vijayanagar Institute of Medical Sciences, Cantonment, Bellary - 583 104
|How to cite this article:|
Bhaskar S B, Chand N K, Devanand B. Masseteric muscle spasm following neostigmine.J Anaesthesiol Clin Pharmacol 2012;28:407-408
|How to cite this URL:|
Bhaskar S B, Chand N K, Devanand B. Masseteric muscle spasm following neostigmine. J Anaesthesiol Clin Pharmacol [serial online] 2012 [cited 2019 Sep 16 ];28:407-408
Available from: http://www.joacp.org/text.asp?2012/28/3/407/98371
A 42-year-old woman was scheduled for hemithyroidectomy for simple nodular goitre. Anesthesia was induced with intravenous (IV) fentanyl, midazolam, thiopentone sodium, and the trachea intubated after administration of suxamethonium (SCH). Anesthesia was maintained with oxygen (O 2 ), nitrous oxide (N 2 O), isoflurane, and vecuronium. Supplemental fentanyl was administered after one hour and adequate anesthetic depth ensured throughout. After stopping isoflurane and confirming patient's spontaneous breathing attempts, neostigmine 2.5 mg and atropine 1.2 mg were administered IV. N 2 O-O 2 mixture was continued to allow for inspection of vocal cords post thyroidectomy. Although adequate chest expansion and reservoir bag movements were observed, the laryngoscope could not be introduced as the jaw was clenched tightly with taut masseters; rest of the body was relaxed. Endotracheal tube (ETT) was seen in the gap between the empty socket of the absent right lower 2 nd molar tooth and the upper teeth and was partially compressed. On auscultation, breath sounds were satisfactory, peripheral O 2 saturation and end-tidal CO 2 were normal. Emergence associated rise in blood pressure and heart rate was observed. Even 5 minutes after patient started breathing spontaneously the masseteric spasm remained. The patient was not responding to verbal commands. Except for chest wall movements, there were no movements in other parts of the body or extremities, as expected in lighter planes of anesthesia. There was no increased tone or stiffness in any part of the body except the masseters.
SCH 25 mg was administered, which relieved the spasm in 30 sec. The patient started responding to oral commands and trachea was extubated after 10 min. Serum electrolytes, creatinine phosphokinase, and thyroid hormones estimated postoperatively were found to be normal. Postoperative period was otherwise uneventful. On re-evaluation, the patient admitted to have had episodes of bruxism at night since 6 months and her mother was known to suffer chronically from similar episodes.
Masseteric spasm is commonly attributed to SCH, as a normal response or heralding onset of malignant hyperthermia. SCH-induced myotonic response in masseters when severe, represents 'masseteric spasm'.  Masseteric spasm has been reported following administration of non-depolarising relaxants pancuronium, atracurium, and vecuronium but no specific reason could be attributed in any of them. ,,[ 4] Masseteric spasm has been observed at induction of anesthesia and has been attributed to extreme preoperative anxiety. 
Masseteric spasm after administration of neostigmine has not been reported earlier. In the present case, vecuronium effectively maintained motor paralysis, till neostigmine administration. Light plane of anesthesia was ruled out as adequate depth was ensured throughout the procedure. As the ETT was stuck in the empty lower molar socket, lungs could be ventilated and this prevented hypoxia. We did not use a neuromuscular monitor as it was not available.
Bruxism involves involuntary jaw muscle contraction, which may occur during day time or in sleep, with clenching and tooth grinding. An interplay among several brainstem structures and neurochemicals (acetylcholine, serotonin, dopamine, GABA, noradrenaline) may be involved in modulation of muscle tone during normal sleep and in sleep bruxism.  The increase in acetyl choline levels due to neostigmine and in sympathetic amines associated with recovery from anesthesia may have precipitated the masseteric spasm in this patient. We used SCH 25 mg as it was more likely to relieve spasm and its effect would last for 10 to 15 minutes.
Masseteric spasm may occur in patients with bruxism. Neostigmine and emergence associated release of neurochemicals may have contributed to development of masseteric spasm in the present case.
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