Abstract

Spinal myoclonus is a rare form of non-generalized movement disorder. Myoclonus has been defined as sudden, brief, lightninglike jerks, twitching or spasm of a muscle or a group of muscles and can be generated by any area in the central nervous system. Drugs administered through intrathecal and epidural routes can occasionally cause myoclonus. The differential diagnosis of myoclonus is extensive. Local anaesthetic neurotoxicity may be responsible for acute myoclonus in our patient. IMPLICATIONS STATEMENT Spinal myoclonus is a rare form of non-generalized movement disorder. Spinal myoclonus following spinal or epidural anaesthesia is extremely rare. Local anaesthetic neurotoxicity may be responsible for acute myoclonus in our patient. INTRODUCTION Myoclonus has been defined as involuntary, repetitive, instantaneous, irregular contractions of a group of muscles or occasionally of a single muscle. Spinal myoclonus is a rare syndrome that has been reported in association with several types of spinal cord pathology. We report a case of spinal myoclonus possibly induced by intrathecal local anaesthetics. CASE REPORT A 65 yr-old female was admitted for the removal of a Backer s cyst in the right knee. Previous surgeries included an operation of a cholesteatoma in the left ear eleven years ago under general anaesthesia. She had no other significant medical history, any allergies and she had no previous neurological disease. The patient wasn t on any medication and there wasn t any positive neurological family history for myoclonus. Preoperative parameters were within the normal limits (ECG, blood tests and thorax radiology). Midazolam 2 mg was given IV before the initiation of spinal anaesthesia as well as 500 ml of lactated Ringer s solution. The usual monitoring was used (ECG, non invasive blood pressure and pulsioximetry). Spinal anaesthesia with a 25gauge-pencil point Whitacre needle (B.D.) was performed at the L3-L4 interspace with the patient in the seated position. Ten mg of hyperbaric bupivacaine 0.5% was injected through the needle after freely flowing cerebrospinal fluid was obtained. No opioids were added. The spinal procedure was performed without incidences. When adequate sensory block was achieved (T-10), the pneumatic ischemia tourniquet was inflated 300 mm Hg at the level of tight and then the patient was moved to the prone position. Oxigen was administered through a Venturi mask (nominal inspired oxygen (O2) concentrations of 35%). The surgery proceeded uneventful, as well as the intraoperative course. The pneumatic tourniquet was inflated for 50 minutes. When deflated, the patient had an episode of hypotension which reversed with ephedrine (10 mg) and fast infusion of cristalloids. When arriving Post Anaesthetic Care Unit (PACU), the patient developed involuntary jerky movements of both lower limbs. These movements were shock-like, sudden, short burst of muscles contractions with lifting of the legs. They were clinical diagnosed of spinal myoclonus. The patient was alert and conscious and there were no other neurological manifestations. Ten minutes after arriving PACU our patient felt nausea and ondansetron 4 mg was given IV. The motor block resulted in a Bromage score of 1. The sensory block, confirmed by pin-prick and cold sensation, was up to L3 dermatoma. The frequency (every minute) and severity of the myoclunus movements increased gradually. Diazepam 8 mg was administered IV but myoclonus did not subside. Sodium valproate 15mg/kg was given IV and myoclonus disappeared after 15 minutes. The patient was discharged from PACU 90 minutes after her arrival and returned asymptomatic to the Intensive Care Unit. Two more episodes of myoclonus movements occurred during the following five hours, responsive to sodium Spinal myoclonus following spinal anesthesia.

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