Spinal myoclonus

Treatment of palatal myoclonus is often unsuccessful, but phenytoin, carbamazepine, clonazepam, trihexyphenidyl, and baclofen have been effective in some patients. Clonazepam is effective in over half of patients with propriospinal myoclonus, but other anticonvulsants are usually not helpful. Segmental spinal myoclonus is often resistant to drug treatment, but diazepam, carbamazepine, tetrabenazine and, particularly, clonazepam are sometimes effective. 

A 77-year-old woman undergoing hip replacement surgery received spinal anesthesia with bupivacaine 12 mg. On the first postoperative day she suddenly developed shock-like involuntary jerks, which were diagnosed as spinal myoclonus and confirmed by clinical and elec-trophysiological studies. She was given valproate and clonazepam, and the transient myoclonus disappeared after 4 days. 

A report has illustrated the recurrence of spinal myoclonus after a second spinal anesthetic with bupivacaine after 1 year... 

Lee JJ, Hwang SM, Lee JS, Jang JS, Lim SY, Hong SJ. Recurrent spinal myoclonus after two episodes of spinal anesthesia at a 1-year interval. Korean J Anesthesiol 2010 59(Suppl) S62-A. 

Lin CS, Wei-Hung C, Lee YW. Transient spinal myoclonus after spinal anaesthesia with bupivacaine in the perioperation period. Anaesthesist 2008 57 518. 

Batra YK, Rajeev S, Lokesh VC, Rao KL. Spinal myoclonus associated with intrathecal bupivacaine and fentanyl in an infant. Can J Anaesth 2007 54 587-8. 

Spinal anesthesia with intrathecal bupivacaine has been associated with spinal myoclonus [38 ]. 

A 52-year-old woman developed spinal myoclonus 60 minutes after receiving 60 mg of hyperbaric prilocaine 5%. She had involuntary, asymmetrical, brief movements of the legs at a frequency of 10-20/minute. Treatment with intravenous diazepam 5 mg blunted the symptoms but did not abolish them they resolved completely 60 minutes after full recovery from spinal anesthesia. There were no residual signs of neurological impairment. 

Spinal myoclonus is postulated to be caused by reduced activity of inhibitory pathways at the level of motor neurons or intemeu-rons. It is a rare self-limiting adverse event and has so far been evoked by bupivacaine and prilocaine. Diazepam has been reported to be effective in the past, but did not convince in this case. 

Fores Novales B, Aguilera Celorrio L. Spinal myoclonus following intrathecal anaesthesia with prilocaine. Anaesth Intensive Care 2009 37(3) 498-9. 

The tendency for MAO inhibitors to produce symptoms related to neuromuscular excitability, the serotonin syndrome, has been recognized in cases of overdose (SEDA-10, 18) and in interactions with other antidepressants or tryptophan (SEDA-10, 16, 17) (20). The authors of a thorough review of the preclinical and clinical literature have drawn attention to these phenomena, which occur at therapeutic doses with a MAO inhibitor alone, and have speculated that the mechanism is related to a combination of increased serotonergic tone and central disin-hibition of alpha motor neuron-mediated spinal activity (21). They discussed ten previous reports of myoclonus, hyper-reflexia, muscle twitching, and increased muscle tone in patients taking MAO inhibitors. These neuromuscular effects appear to occur in up to 15% or more of patients, and are more likely when tryptophan is given in combination. They usually appear after 10-14 days. Tolerance does not occur, but the effects may abate or... 

There have been no previous reports of propriospinal myoclonus precipitated by marijuana. The etiology was not clear but may have involved cannabinoid receptors located in the brain and spinal cord as well as the peripheral nervous system. 

Myoclonus and opisthotonos, especially in children (38), and choreoathetosis (39) have been attributed to propofol. However, in experimental studies propofol has been shown to be effective against drug-induced seizures (40,41). It has been suggested that propofol inhibits efferent inhibitory neurons in the midbrain and reticular activating system, producing movements that originate subcortically and in the spinal cord (42). 

An otherwise healthy 63-year-old man was anesthetized with propofol 2 mg/kg + fentanyl 1 micrograms/kg followed by an infusion of propofol 6 mg/kg/hour (43). Three minutes after induction he developed myoclonus in his legs. This continued for 10 minutes and the anesthetic was abandoned. When he awoke 10 minutes later, the myoclonus stopped. A repeat anesthetic with propofol soon after caused the same response. When the procedure was performed 12 days later under regional block with propofol infusion for sedation, the myoclonus recurred, and lasted for 2 hours. The patient was alert after each anesthetic and did not appear to be post-ictal. An MRI scan of the spinal cord was normal. 

A 35-year-old woman developed involuntary rhythmic movements of her right leg after recovery from a spinal anesthetic for surgical treatment of peroneal tendonitis. At a second operation within 1 year myoclonus recurred about 100 minutes after intrathecal administration of 9 mg of heavy bupivacaine 0.5%, with bilateral involuntary myoclonic movement of both legs and arms. The symptoms disappeared after 4 hours and there were no abnormal neurological or laboratory findings. 

Fox EJ, Villanueva R, Schutta HS. Myoclonus following spinal anesthesia. Neurology 1979 29 379-80. 

Alfa JA, Bamgbade OA. Acute myoclonus following spinal anaesthesia. Eur J Anaes-thesiol 2008 25 256-7. 

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