Parkinsonism and Related Disorders 18 (2012) 115–116
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Editorial
Propofol-induced paroxysmal dystonia
1. Introduction Propofol (2,6-diisopropylphenol) is a short acting intravenous anesthetic agent used for induction and maintenance of general anesthesia. Rapid recovery and lack of postoperative nausea have made it particularly valuable for patients undergoing surgery as well as in emergency and intensive care units where brief periods of sedation are required. Propofol provides anesthetic effects through a potentiation of GABAA transmission. It also appears to inhibit glutamate release, possibly as a result of a complex activation on the GABAergic system. Since its introduction, almost 30 years ago, excitatory neurological reactions (ENR), mainly seizure-like events and abnormal involuntary movements have been recognized as side effects. Although uncommon, they are well recognized and appear during induction, maintenance and emergence from propofol anesthesia, both in adults and children [1]. We describe a case of delayed onset and unusually prolonged abnormal dystonic movements after anesthesia with propofol. 2. Case report A 28 year-old woman underwent an umbilical hernioplasty under anesthesia with propofol 230 mg and fentanyl 150 mg. She had no history of seizures, psychiatric or previous neurological conditions forepart from migraine. The surgical procedure lasted for 30 min and was uncomplicated. She was transferred to the ward fully awake and 2 h later she complained of moderate abdominal pain which was well controlled with pethidine 30 mg. Six hours after surgery the patient was noticed to have facial spasms, hand tremor, jerky movements of her neck and mild opisthotonus. Some minutes later she developed tonic-clonic-like spells without loss of consciousness. following this she developed repeated cervical dystonic crises with right laterocollis and retrocollis with tonic spasms in her upper limbs particularly in her hands. During an episode speech was impaired; however she remained fully conscious. These episodes lasted for one or 2 min and were repeated several times during the first day. There were no factors that either exacerbated or relieved the episodes. A CT scan and an EEG performed during the first day were normal. Cerebral and cervical MRI performed some days later were also normal. Sodium valproate was started at 1500 mg/d. Over the few first days, the frequency of episodes began to improve with an average of four episodes per day and over the following days the episodes became both more infrequent and shorter. Over the next weeks, episodes were reduced to approximately two to three a week and then three to four per month. 1353-8020/$ – see front matter Ó 2011 Elsevier Ltd. All rights reserved. doi:10.1016/j.parkreldis.2011.11.027
They lasted for 20–30 s and were always painless. The episodes resolved completely after 3 months and the sodium valproate was stopped. We were unable to determine whether her recovery was due to sodium valproate or to the natural history of the condition. 3. Discussion Excitatory neurological reactions (ENR) secondary to propofol administration manifests in several forms including: dystonia, choreoathetosis [2], myoclonus [3], opisthotonus, masseter spasm, generalized tonic-clonic seizures, and exacerbation or resolution pre-existing movement disorders. These abnormal motor activities have been described in all phases of the perioperative period, i.e. induction, maintenance, emergence and delayed (>30 min often after cessation of anesthesia or sedation). A review of the reported cases over a period of more than 30 years revealed that most cases occur in young females and on the day of surgery [4]. Another systematic review indicated that these reactions occurred most often during induction of, emergence from, or following anesthesia, with a few occurrences during maintenance, probably because propofol plasma and cerebral concentrations remain stable during maintenance, suggesting that ENR are likely to occur during changes of propofol levels in the blood or brain [1]. Patients were also classified as those with seizure-like activity (generalized tonic-clonic seizures, focal motor seizures and events presenting as increased muscle tone with twitching and rhythmic movements not considered to be generalized tonicclonic seizures), opisthotonos and involuntary movements. The mechanism by which propofol induces these reactions is unknown but it is assumed that by causing an imbalance in basal ganglia transmitters that in turn produces an increase in excitatory cholinergic output resulting in abnormal motor activity that would be subcortical in origin [5]. Additionally, Borgeat et al. showed that spontaneous motor movements during induction of propofol did not produce any EEG focal abnormalities, arguing against cortical epileptiform origin and supporting the concept of a subcortical origin. An intriguing related feature is that while propofol has proconvulsant properties in susceptible patients, it is also used to treat intractable status epilepticus. This apparently paradoxical feature of both pro- and anticonvulsant activity in a single drug may be due to misinterpretation of the true nature of what are apparently epileptic seizures. The majority of previously published case reports did not have simultaneous EEG monitoring to determine whether each propofol-related seizure-like event was actually caused by cortical epileptiform activity. There are also some paradoxical features regarding the relationship between propofol and movement disorders. Many types
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Editorial / Parkinsonism and Related Disorders 18 (2012) 115–116
of involuntary movements have been well described including our case. There are some reports of patients with Parkinson’s disease developing propofol-induced dyskinesias during stereotactic pallidotomy and bilateral subthalamic nucleus deep brain stimulator placement. Nevertheless, propofol has also been used in managing some movement disorders such as status dystonicus, seizure-like movements, myoclonus and tremor [5]. Propofol’s ability to both cause and treat movement disorders suggests a complex, central-mediated effect and remains an area for future research. Abnormal involuntary movements following anesthesia may be difficult to differentiate and the differential diagnosis includes: adverse drug reaction, emergence delirium, hysterical response and post-anesthesic shivering, nevertheless as was pointed out by others the association of abnormal involuntary movements, as part of ENR, and propofol are not well known in neurology as only a few are published in neurological journals. Furthermore, there is insufficient clinical data to suggest any specific treatment but spontaneous recovery often follows. Therefore, clinicians need to be aware of this potential adverse effect so that rational treatment, reassurance and explanation can be given.
References [1] Walder B, Tramer MR, Seeck M. Seizure-like phenomena and propofol: a systematic review. Neurology 2002;58:1327–32. [2] Borgeat A, Dessibourg C, Popovic V, Meier D, Blanchard M, Schwander D. Propofol and spontaneous movements: an EEG study. Anesthesiology 1991;74: 24–7. [3] Dearlove J, Dearlove O. Cortical reflex myoclonus after propofol anaesthesia. Anaesthesia 2002;57(8):834–5. [4] Schramm B, Orser B. Dystonic reaction to propofol attenuated by benztropine (Cogentin). Anesth Analg 2002;94:1237–40. [5] Lardizabal D, Sabharwal V, Jahan A, Jain S, Snyder C, Popovich M, et al. Use of propofol to control refractory involuntary movements. Neurocritical Care 2004;3:367–9.
Carlos Cosentino*, Luis Torres Neurology Section, Complejo Hospitalario San Pablo, El Polo 780 (406). Surco, Lima 33, Peru * Corresponding author. Tel.: þ51 14366087. E-mail address:
[email protected] (C. Cosentino) 25 September 2011
