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Rapid Responses: Rapid Responses published:
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Cogwheel Rigidity : A forgotten diagnostic clue ?
- Salvador Vale (4 September 1999)
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Acute Dystonia And Anaesthesia
- Samer Abdalla (17 September 1999)
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Response
- Sophia John (21 September 1999)
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A patient''s perspective
- Collissa Weber (29 October 1999)
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Metoclopramide and extrapyramidal reactions
- Martin R Tramer (22 December 1999)
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Changing trends in acute dystonia in children in India
- Edwin Dias (27 December 1999)
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Salvador Vale, Research Psychiatrist Antiguo Hospital Concepcion Beistegui, Regina 7, CP 06080, Mexico
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In the "Acute Dystonia induced by Drug Treatment" review, van Harten and colleagues (1) do not mention other relevant, associated extrapyramidal side effects of the Dopamine-2 Receptor-blocking drugs. These consist in drug-induced Parkinsonian syndrome and Akathisia (a harmless but extremely unpleasant restlessness where the patient feels that he or she must move continuously). The acute dystonic syndrome is usually accompanied by these additional extrapyramidal side-effects, but the inverse is not true. The importance of these complications for the drug-induced Acute Dystonic treatment, rests in its diagnostic value. In a patient treated with dopamine-2 receptor blocking drugs, the presence of a Parkinsonian syndrome or akathisia in addition to an Acute Dystonic syndrome, points clearly toward the extrapyramidal origin of the Dystonia. Moreover, the so-called "cogwheel phenomenon" (where parkinsonian rigidity is associated with a static tremor generating a rhythmical jerk when the hypertonic muscle is passively stretched, which is easily revealed during limb manipulation) in most cases accompanies the dyskinetic-dystonic subtype of drug-induced extrapyramidal reactions. Eliciting the cogwheel sign, a simple diagnostic manoeuvre, will indicate that the observed Acute Dystonia is a drug extrapyramidal side-effect and that it will be dramatically responsive to anticholinergic medication. 1.- van Harten PN, Hoek HW, Kahn RS. Acute Dystonia induced by Drug Treatment. BMJ 1999 ; 319 : 623 - 626 |
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Samer Abdalla, Anaesthetic SHO The North Hampshire Hospital, Basingstoke, Hampshire, England
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In the interesting review article 'Acute dystonia induced by drug treatment' Peter Harten and Colleagues [1] do not mention the anaesthetic drugs as possible causes of acute dystonia. There are several published reports where different anaesthetic agents, for example; thiopentone , fentanyl and propofol administration has been associated with opisthotonous and other abnormal neurologic sequalae [2], [3], [4] . In many of these reports it is difficult to establish a causal relationship between the anaesthetic drug and the reported neurologic sequalae, but it is equally hard to disprove it. I think such unusual side effects of the anaesthetic agents should deserve more attention to be paid particularly by Day Case Anaesthetists, as many of these side effects can happen postoperatively when the patient has been discharged from close medical care. 1 - Van Harten PN, Hoek HW, Kahn RS. Acute Dystonia induced by Drug Treatment. BMJ 1999; 319: 623 – 626. 2 - Hooda S, Kiran S, Thapa D, Chhabra B. Opisthotonus and thiopental. Anesth Analg 1995; 81(6): 1309-10. 3 - Dehring DJ, Gupta B, Peruzzi WT. Postoperative opisthotonus and torticollis after fentanyl, enflurane, and nitrous oxide. Can J Anaesth. 1991; 38(7): 919-25. Review 4 - Saunders PR, Harris MN. Opisthotonus and other unusual neurological sequelae after outpatient anaesthesia. Anaesthesia. 1990; 45(7): 552-7. |
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Sophia John
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EDITOR I read with interest van Harten et al's excellent review of drug induced dystonia1. I would like to point out a few factual inaccuracies. Dystonias respond better to lorazepam and diazepam than to clonazepam or amantidine2. It is the antimuscarinic (M1) and not the anticholinergic properties of antiparkinsonian drugs that help dystonia. Prophylactic bed time antimuscarinic drug is not useful because dystonia and other drug-induced extrapyramidal side-effects do not occur in sleep. Moreover, the stimulant effect of antimuscarinic drugs can interfere with sleep. There have been reports of clozapine-induced3 and clozapine withdrawal-induced4 dystonia. The lower incidence of clozapine-induced dystonia could be due to the fact that clozapine is introduced much more slowly, over a period of 2-3 weeks, compared to other antipsychotic drugs which may be initiated in full therapeutic doses within a period of hours in acutely unwell patients. Feigned dystonia is suspected when the dystonia is intermittent, rather than when static as authors have suggested. Unfortunately, the suspicion is increased when the dystonia is apparently bizarre, for example a patient who may not be able to walk properly, may be able to walk backwards or run and dance. Sophia John 1 van Harten PN, Hoek HW, Khan R. Acute dystonia induced by drug treatment. BMJ, 1999; 319: 623-626 (4 September). 2 Kaplan HI, Sadock BJ. Comprehensive Textbook of Psychiatry, 6th Edition, Baltimore: Williams & Wilkins, 1995. 3 Kastrup O, Gastpar, M, Schwartz M. Acute dystonia due to clozapine. J Neurol Neurosurg Psychiat, 1994; 57: 119. 4 Ahmed S, Chengappa KNR, Naidu VR, Baker RW, Parepally H, Schooler NR. Clozapine withdrawal-emergent dystonias and dyskinesias: A case series. J Clin Psychiat, 1998; 59; 472-477. |
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Collissa Weber
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I read with great interest your response to Fortnightly review: Acute dystonia induced by drug treatment by Peter N van Harten, Hans W Hoek, and Rene S Kahn, BMJ 1999; 319: 623-626 [Full text] due to the fact that you suggested that diazepam was the best line of treatment for the dystonias. I have done months of research into this neurological disorder and the dyskinesias, as I have contracted both. I was exposed to the drug bupropion for a period of 3.5 days one year ago this August. I experienced an acute dystonic reaction which initially threw me to the floor, my limbs pulling in and my diaphragm refusing to go through the motions of inhaling. I landed in ER via 911. I was given diazepam IV and released, with a tentative diagnosis of possible drug reaction as opposed to underlying psychiatric problems. I remained on oral diazepam, 2mg every 4 hours around the clock and attempted to return to work. My back would lock, my legs would turn in, my arms would pull in, and often, my speech would cut off in mid sentence. I fought it with all I had, but less than a month later, as I was attempting to wean as per doctor's orders from the diazepam, I experienced a complete collapse and the inability to articulate, my right eye dropping and my body uncontrollable. I remained confined to a couch, jerking at times, in and out of consciousness for nearly three months. I have since been on diazepam, approximately 4mg, 4 times per day since that time. I have attempted to wean on numerous occasions with the ensuing results being an exacerbation of the dyskinetic and dystonic symptoms. Initially, I was labeled psychiatric, although a review by a psychiatrist/neurologist revealed "cogwheeling" and recommendations for further neuro follow up. After a misdiagnosis of MS, and my refusal to be submitted to immediate home administered cortisone IV treatments, and refusal to take Cogentin after much research I had done, I was diagnosed by UCLA as having dyskinesia secondary to the drug, and have since been diagnosed as having dystonia in combination with akathesia. An MRI showed multiple lesions consistent with dystonia/dyskinesia and ishemia. My question to you is how could this drug have affected me in such a serious, life changing way, and what are my chances of reversal of the symptomology? My doctor has said that I did not experience a stroke, and I am wondering if it was a TIA. Is there any way to know if the lesions were caused by the drug, or that the lesions already were there and contributed to my reaction? At present, under situational stress, my legs and arms turn in, and sometimes my neck jerks to the side and I collapse, even on diazepam maintenance. The severe symptoms have only happened two times since the initial reaction. Most often, the akathesia gets the best of me and I consciously attempt to stay calm and move more slowly to help alleviate the discomfort. I often walk with my legs inward, and sometimes find my hands pulling in. Is what happened to me rare? According to the product insert information 1 in 100 people experienced my symptoms in the reported open and uncontrolled clinical trials. I had been exposed years ago (in my twenties, I am now in my mid 40's) to Ativan and did not like it's effects and so did not continue on it after about 2 weeks. Any information you can provide, or any other direction you can provide me with would be greatly appreciated. Had I known that this drug could do such a thing, I would have never taken it. I told the prescribing physician that I did not do well on antidepressant drugs, but was prescribed it nonetheless by the internal medicine doctor for unusual extreme exhaustion and ongoing long term diarrhea. His tentative diagnosis was depression vs perimenopause. It has since been discovered that I have Hashimoto's thyroiditis which now requires the use of Thyrolar, which appears to have been the problem all along (not depression which the bupropion was prescribed for), as well as perimenopausal symptoms which I now take Prometrium (micronized progesterone) for. Collissa Weber |
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Martin R Tramer, Staff Anaesthetist Division of Anesthesiology, Geneva University Hospitals, CH-1211 Geneva, Switzerland
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We read with great interest the review on drug-induced acute dystonia by van Hartne et al.1 The authors mentioned metoclopramide as a cause of dystonia; they cited an estimated frequency of dystonia with that antiemetic of 28.6 per 1,000,000 prescriptions. We have systematically reviewed the literature on the antiemetic efficacy and potential for harm of prophylactic metoclopramide in the surgical setting.2 We analysed data of 66 randomised trials; 3,260 patients received 18 different regimens of metoclopramide. In adults, the most frequently used dose was 10 mg iv, in children it was 0.25 mg/kg iv. We combined data on extrapyramidal reactions and abnormal movements of all studies which mentioned these adverse effects. With metoclopramide 6 of 537 patients (all adults) had extrapyramidal reactions or abnormal movements, with placebo there were 5 of 640 (all adults). These numbers suggest that about 550 surgical patients will have to be treated with a single prophylactic dose of metoclopramide for one to show such an adverse reaction. We did not consider this additional risk to be of clinical relevance. The fact that in these trials metoclopramide did not show any clinically relevant antiemetic efficacy, suggested strongly that the doses which have been used by anaesthetists for almost 40 years are too low. Higher doses may be more efficacious but may also increase the risk of dystonic reactions. Martin R. Tramèr Division of Anaesthesiology,
Department APSIC,
Geneva University Hospitals,
CH-1211 Geneva 14,
Switzerland
References 1. van Harten PN, Hoek HK, Kahn RS. Acute dystonia induced by drug treatment. BMJ 1999;319:623-6. 2. Henzi I, Walder B, Tramèr MR. Metoclopramide in prevention of postoperative nausea and vomiting. A quantitative systematic review of randomised placebo-controlled trials. Br J Anaesth 1999;83:761-71. |
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Edwin Dias, Assistant professor Kasturba hospital manipal
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Dear Sir, The last decade has seen newer antiemetics,antipyschotic drugs.It was so common to admit patients with an acute dystonia due to Stemetil or Largactil given for vomiting. The present trend of ORS and use of domperidone and ondansetron for vomiting in the different clinical situations has brought down the ases of acute dystonia due to drugs and there are fewer cases beig admitted to the emergency care clinics. In children ,this strategy for preventing a troublesome complication of drug use in vomiting has been succesful. |
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