Propopol in myotonic dystrophyA 37-year-old, slightly mentally retarded woman with Steinert myotonic dystrophy was admitted for cholecystectomy. Premedication consisted of midazolam 4 mg intramuscularly and I hour later an epidural catheter was inserted at the T,,-Tll interspace and 15 ml 0.5% bupivacaine injected. Ringer's lactate solution 500 ml and two doses of ephedrine 15 mg were required to maintain a normal arterial blood pressure. When the block was fixed and the haemodynamic status had stabilised, general anaesthesia was induced with propofol 2 mg/kg.Immediately following the propofol injection myoclonic movements occurred in the extremities and appeared to provoke a myotonic state which began in the upper limbs and extended to the trunk. It was possible to intubate the trachea easily without muscle relaxants and the myotonia resolved with the introduction of isoflurane. Anaesthesia was maintained thereafter with isoflurane in 50% nitrous oxide and oxygen; the lungs were mechanically ventilated without the use of muscle relaxants. Recovery from anaesthesia was uneventful; analgesia was provided by an infusion of fentanyl into the epidural space.Propofol has been used previously in a patient with myotonic dystrophy without a problem,' although in another case exaggerated physiological responses were reported.* In our patient, the myotonic response followed an episode of myoclonia and may have been due to a centrally mediated increase in muscle stimulation.
The involuntary blink rate is a clinical monitor of dopaminergic activity. Since there is disagreement in the literature on the relative neurochemical hemispheric asymmetry or laterality of dopamine, we studied the effects of differential forced unilateral nostril breathing on blink rate. This technique has been demonstrated to induce selective contralateral hemispheric stimulation as measured by relative increases in the EEG amplitude as well as alternating lateralization of plasma catecholamines. We used the artifact of the two-channel electro-oculogram to measure the endogenous eyeblink in an N = 1 design with 11 reversals of left vs. right hemisphere activation. There was a significant increase in blink rate (p less than .01) with right hemisphere activation, and this suggests that dopamine may be lateralized to the right cerebral hemisphere.
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