|Year : 2014 | Volume
| Issue : 1 | Page : 74-76
Acute dyskinesia: A rare adverse effect of oxcarbazepine in epilepsy with neurobehavioral symptoms
Amita Bhargava, Bharat Bhushan, Subhakaran Khichar, Gaurav Kasundra
Department of Neurology, Dr. S. N. Medical College and M. G. Hospital, Jodhpur, Rajasthan, India
|Date of Submission||09-Oct-2013|
|Date of Acceptance||18-Nov-2013|
|Date of Web Publication||8-Jan-2014|
H. No. 21/267, Chopasani Housing Board, Jodhpur - 340 008, Rajasthan
Source of Support: None, Conflict of Interest: None
| Abstract|| |
We are reporting an 11-year-old female child of febrile partial seizure since age of 3 months and transient neurobehavioral changes of psychic, gelastic semiology since childhood. She had no history of continued febrile seizure, but had 3 admissions for 3 episodes of status epilepticus in last 3 years. She experienced acute generalized dyskinesia (torticollis, oromandibular dystonia, spasmodic dysphonia, right lower limb eversion plantarflexed type feet dystonia) soon after oxcarbazepine (OXC) therapy from last episode of status epilepsy on 15 April 2013 with similar semiology. We failed to explain the considered infectious, non-convulsive state and hyponatremic extra pyramidal syndrome. We used the Naranjo adverse drug reaction probability scale and stopped OXC. After state intravenous diazepam 2 nd day, she was starting to improve and over a period of 4 days she was asymptomatic. We shifted on clonazepam, sodium valproate for further. She was asymptomatic until 1 month follow-up.
Keywords: Acute dyskinesia, adverse effect, oxcarbazepine
|How to cite this article:|
Bhargava A, Bhushan B, Khichar S, Kasundra G. Acute dyskinesia: A rare adverse effect of oxcarbazepine in epilepsy with neurobehavioral symptoms. Int J Nutr Pharmacol Neurol Dis 2014;4:74-6
|How to cite this URL:|
Bhargava A, Bhushan B, Khichar S, Kasundra G. Acute dyskinesia: A rare adverse effect of oxcarbazepine in epilepsy with neurobehavioral symptoms. Int J Nutr Pharmacol Neurol Dis [serial online] 2014 [cited 2020 Nov 27];4:74-6. Available from: https://www.ijnpnd.com/text.asp?2014/4/1/74/124618
| Introduction|| |
Oxcarbazepine (OXC) is an anticonvulsant and mood stabilizing drug used primarily in the treatment of epilepsy. It is also used to treat anxiety and benign motor tics. OXC is a structural derivative of carbamazepine, with a ketone in place of the carbon-carbon double bond on the dibenzazepine ring at the 10 position (10-keto). This difference helps reduce the impact on the liver of metabolizing the drug and also prevents the serious adverse effects which are associated with carbamazepine. Aside from this reduction in side-effects, it is thought to have the same mechanism as carbamazepine but has a more favorable pharmacokinetic profile. The most common adverse events are usually related to the central nervous or gastrointestinal systems. Here, we are reporting rare adverse effect of acute generalized dyskinesia by OXC to support the few others observations.  The most important problem in assessing adverse drug reactions (ADRs) is whether there is a causal relationship between the drug and the untoward clinical event. Naranjo ADR Probability Scale assigned to a probability category after certain questionnaires from the total score. In this scale four category were defined in the form of "definite" if score > 9, "probable" 5-8, "possible" 1-4 and "doubtful" if score zero. We applied this scale to endorse our observation regarding adverse effect of OXC.
| Case Report|| |
This was a case report of a 11-year old weighing 20 kg female child fifth standard student average scholastic performer. She is first issue to non-consanguineous healthy parents. Her healthy mother's and father's age is 30 and 37 years respectively. She was born at term by normal vaginal delivery at hospital, normal birth weight and there was no history suggestive of perinatal asphyxia. She was asymptomatic until 3 months of age. She evaluated for multiple episodes of febrile partial seizures (left frontal/limbic, sometime psychic and gelastic semiology) since the age of 3 months with no history of continued febrile seizure. She had mild global developmental delay with normal cognition. Has been admitted thrice for seizures landing into status epileptics in last 3 year but parents had very poor compliance. She has never been on regular antiepileptic drug (AED). Last episode of seizure on 15-April 2013 with similar semiology and landed into status epilepticus. After control of status epilepticus, only OXC therapy was begun at 15 mg/kg daily for 1 week and then 30 mg/kg/d (300 mg B.I.D).
Within a week, she developed insidious onset progressive generalized dyskinesia (torticollis, oromandibular dystonia, spasmodic dysphonia, right lower limb eversion plantiflxed type feet dystonia) and sometime of choreodystonic movement of pelvic girdle and drooling of saliva. She came to us after 1 month of illness and she did not take orally since 4 days. On examination, she is conscious, comprehending verbal command, unable to speak and swallow (due to loss of tongue movement) but continent. Other than abnormal involuntary movement she did not have any cranial nerve, motor, sensory, cerebellar, bladder, peripheral, autonomic function impairment and meningeal irritation. No preceding history of infectious, metabolic and other system impairment. We failed to explain the considered infectious, non-convulsive state and hyponatremic extra pyramidal syndrome [Table 1]. We used of the Naranjo ADR Probability Scale indicated a probable (the score was 7) relationship between generalized acute dyskinesia and OXC therapy in this patient for adverse drug effect.  We stopped OXC and treated with single-dose intravenous diazepam then oral difenhydramine, baclofen, trihexiphenidyl, clonazepam. On 2 nd day, she was starting to improve and over a period of 4 days she was asymptomatic. We discharged to her on clonazepam, sodium valproate. She was asymptomatic until 1 month follow-up. The free informed consent was got from the patient for this publication.
| Discussion|| |
Time tested adverse effects of AED have limitations due to paucity of drugs trial. Hence we are exploring acute dyskinesia due to OXC in epilepsy patients with neurobehavioral presentation. Acute dyskinesia caused by myriads of drugs frequently encountered by neuroleptics and antiemetic. , Acute dystonic reactions occur after exposure to dopamine (DA) receptor blocking agents, a class that includes neuroleptic agents and antiemetic agents. It is well recognized that some anticonvulsant therapy may also be associated with various dyskinesias, including chorea, choreoathetosis, dystonia and asterixis. Phenytoin, primidone, phenobabitone, phenobarbital, ethosuximide and carbamazepine have been implicated as offending agents.  Dyskinesias due to anticonvulsants usually result from toxicity and initial exposure of drug or, more commonly during chronic uses.
OXC and its active metabolite, monohydroxy derivative, have effects on sodium channels and possibly potassium and calcium channels. The results of clinical trials suggest that it is better tolerated than carbamazepine. The most common adverse events are usually related to the central nervous (dizziness, diplopia, ataxia, headache, weakness, nystagmus, slurred speech) or gastrointestinal systems (nausea, vomiting, epigastric distress, diarrhoea). The other adverse events are hypersensitivity and hyponatremia. 
Acute dyskinesia is not a common adverse reaction after OXC treatment.  There are rare reports about carbamazepine-induced tic disorders and tardive dyskinesia-like syndrome.  It was thought that the presence of striatal DA receptor super sensitivity serves as the prevailing hypothesis regarding the underlying neurobiological mechanism for tics. This is based on the following observations: DA receptor antagonists are the most effective drugs for suppressing tics and that tics may be worsened by drugs that enhance dopaminergic neurotransmission, such as amphetamins. ,,
The possible mechanism of OXC-induced dyskinesia may be similar to that of carbamazepine (dopaminergic effect of carbamazepine). This dopaminergic effect of carbamazepine may be responsible for the induction of tics, but the drug has a multiplicity of other central neurochemical effects that may be involved as well. Epilepsy with neurobehavioral symptoms have some abnormalities in the central dopaminergic and other neurotransmitter system. ,
Although there are conflicting results in the literature, carbamazepine has been reported to be useful in the treatment of tardive dyskinesia related to chronic neuroleptic use.  It is not clear, whether it is the result of a state-dependent condition rather than the action of carbamazepine. Due to this, it is important to be careful when using agents that induced the dopaminergic system in these patients. ,
| Conclusion|| |
Based on the above report it can be concluded that acute dyskinesia is a rare adverse reaction during OXC therapy, also seen in the early phase of therapy. It is not due to overdose and hyponatremic extrapyramidal effect but our proposed hypothesis of DA receptor supersensitivity by OXC. OXC should be used cautiously in those patients who have epilepsy with neurobehavioral symptoms. Keep OXC in differentials of acute dyskinesia presentation of extrapyramidal syndrome.
| Acknowledgments|| |
The authors would like to thank Dr. Banakar Basavaraj and Dr. Pujar Guruprashad S.
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