Hostname: page-component-84b7d79bbc-l82ql Total loading time: 0 Render date: 2024-07-25T14:38:28.071Z Has data issue: false hasContentIssue false
  • English
  • Français

Seizure Exacerbation and Developmental Regression with Carbamazepine

Published online by Cambridge University Press:  18 September 2015

A.N. Prasad ,
M. Stefanelli  and
L Nagarajan
A.N. Prasad*
Affiliation:
Discipline of Pediatrics (Neurology), Princess Margaret Hospital Perth, Australia
M. Stefanelli
Affiliation:
The Charles A. Janeway Child Health Centre, and theDiscipline of Medicine(Neurology), Princess Margaret Hospital Perth, Australia Memorial University of Newfoundland, St. John's, Newfoundland and the Division of Pediatric Neurology, Princess Margaret Hospital Perth, Australia
*
Discipline of Pediatrics (Neurology), The Charles A. Janeway Child Health Centre, Memorial University of Newfoundland, Janeway Place, St. John's, Newfoundland, Canada A1A 1R8
Rights & Permissions [Opens in a new window]

Abstract:

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.
Background:

Unexpected exacerbation of seizures may occur following initiation of treatment with carbamazepine (CBZ). We reviewed the occurrence of such reactions in our patient population at a tertiary care children's hospital.

Methods:

A retrospective analysis of our clinic database identified 129/691 (18.6%) patients with epilepsy treated with CBZ, as monotherapy. 38/129 children were later switched to another drug. In 11/38 (28.5 %) clinical and/or EEG deterioration was observed. Two patients identified at another institution with similar exacerbation were also included in our analysis. We report on the findings in these 13 cases.

Results:

Two groups were identified: Group I - 6 patients with normal neurological exam, normal EEG background, and a diagnosis of idiopathic generalized epilepsy. Group II - 7 patients with an abnormal neurological exam and/or abnormal EEG background. Following introduction of CBZ therapy, worsening of preexisting seizures, appearance of new seizure types, behavioral regression, and accompanying EEG deterioration were reported in both groups. Dramatic improvement in seizure control occurred, following withdrawal of CBZ and substitution of another anticonvulsant.

Conclusion:

Physicians treating epilepsy must be aware that CBZ can exacerbate seizures, and cause developmental regression in children. Careful patient selection, when choosing CBZ as treatment, and prompt recognition of clinical deterioration and intervention, may help avoid or reverse these paradoxical reactions.

Résumé:

RÉSUMÉ:Introduction:

Une exacerbation inattendue des crises peut survenir suite au début du traitement avec la carbamazépine (CBZ). Nous avons examiné la fréquence de ces réactions chez notre population de patients dans un hôpital de soins tertiaires pour enfants.

Méthodes:

Une analyse rétrospective de la banque de données de notre clinique a identifié 129/691 (18.6%) patients épileptiques qui ont été traités par la CBZ en monothérapie. On y a substitué une autre médication chez 38/129 enfants. Chez 11/38 (28.5%), une détérioration clinique et/ou EEG a été observée. Deux patients ayant présen¬té une exacerbation similaire, identifiés dans une autre institution, sont également inclus dans notre analyse. Nous rap¬portons les observations chez ces 13 cas.

Résultats:

Deux groupes ont été identifiés: le groupe I - 6 patients ayant un examen neurologique normal, une activité de fond de l'EEG normale et un diagnostic d'épilepsie généralisée idiopathique. Le groupe 11-7 patients ayant un examen neurologique anormal et/ou une activité de fond de l'EEG anormale. Suite à l'introduction du traitement par la CBZ, une exacerbation des crises de même type, l'apparition de nouveaux types de crises, une régression comportementale et une détérioration concomitante de l'EEG ont été rap¬portées dans les deux groupes. Une amélioration dramatique dans le contrôle des crises a été observée suite à l'arrêt de la CBZ et à la substitution d'un autre anticonvulsivant.

Conclusion:

Les médecins qui traitent Pépilepsie doivent être avertis que la CBZ peut exacerber les crises et causer une régression développementale chez les enfants. Une sélection soigneuse des patients qui reçoivent la CBZ et une détection précoce de la détérioration clinique ainsi qu'une intervention précoce peuvent aider à éviter ou à contrer ces réactions paradoxales.

Type
Original Articles
Information
Canadian Journal of Neurological Sciences , Volume 25 , Issue 4 , November 1998 , pp. 287 - 294
Copyright
Copyright © Canadian Neurological Sciences Federation 1998

References

REFERENCES

1. Levy, L, Fenichel, G. Diphenylhydantoin activated seizures. Neurology 1965; 15: 716–722.CrossRefGoogle ScholarPubMed
2. Vallarta, JM, Bell, DB, Reichert, A. Progressive encephalopathy due to chronic hydantoin intoxication. Am J Dis Child 1974; 128: 27–34.Google Scholar
3. Wilder, BJ, Rangel, R. Carbamazepine efficacy in adults with partial and generalized tonic- clonic seizures. Epilepsia 1987; 28 Suppl 3: S25-S28.Google Scholar
4. Dodson, WE. Carbamazepine efficacy and utilization in children. Epilepsia 1987; 28 Suppl 3: S17-S24.CrossRefGoogle ScholarPubMed
5. Shields, WD, Saslow, E. Myoclonic, atonic, and absence seizures following institution of carbamazepine therapy in children. Neurology 1983; 33: 1487–1489.Google Scholar
6. Snead, OC 3rd Hosey, LC. Exacerbation of seizures in children by carbamazepine. N Engl J Med 1985; 313: 916–921.CrossRefGoogle ScholarPubMed
7. Loiseau, P. Do antiepileptic drugs exacerbate seizures? Epilepsia 1998; 39: 2–4.Google Scholar
8. De Silva, M, Macardle, B, Mcgowan, M, et al. Randomised comparative monotherapy trial of phenobarbitone, phenytoin, carbamazepine, or sodium valproate for newly diagnosed childhood epilepsy. Lancet 1996; 347: 709–713.Google Scholar
9. Johnsen, S, Tarby, T, Sidell, A. Carbamezepine induced seizures. Ann Neurol 1984; 16: 392–393.Google Scholar
10. Liporace, JD, Sperling, MR, Dichter, MA. Absence seizures and carbamazepine in adults. Epilepsia 1994; 35: 1026–1028.Google Scholar
11. Horn, CS, Ater, SB, Hurst, DL. Carbamazepine-exacerbated epilepsy in children and adolescents. Pediatr Neurol 1986; 2: 340–345.CrossRefGoogle ScholarPubMed
12. Marescaux, C, Hirsch, E, Finck, S, et al. Landau-Kleffner syndrome: a pharmacologic study of five cases. Epilepsia 1990; 31: 768–777.Google Scholar
13. So, EL, Ruggles, KH, Cascino, GD, Ahmann, PA, Weatherford, KW. Seizure exacerbation and status epilepticus related to carbamazepine-10,11-epoxide. Ann Neurol 1994; 35: 743–746.Google Scholar
14. Sachdeo, R, Chokroverty, S. Enhancement of absence with Tegretol (Abstract). Epilepsia 1985; 26: 534.Google Scholar
15. Callahan, DJ, Noetzel, MJ. Prolonged absence status epilepticus associated with carbamazepine therapy, increased intracranial pressure, and transient MRI abnormalities. Neurology 1992; 42: 198–201.CrossRefGoogle ScholarPubMed
16. Silverstein, FS, Parrish, MA, Johnston, MV. Adverse behavioral reactions in children treated with carbamazepine (Tegretol). J Pediatr 1982; 101: 785–787.Google Scholar
17. Marjerrison, G, Jedlicki, SM, Keogh, RP, Hrychuk, W, Poulakakis, GM. Carbamazepine: behavioral, anticonvulsant and EEG effects in chronically-hospitalized epileptics. Dis Nerv Syst 1968; 29: 133–136.Google Scholar
18. Pryse-Phillips, WE, Jeavons, PM. Effect of carbamazepine (Tegretol) on the electroencephalograph and ward behaviour of patients with chronic epilepsy. Epilepsia 1970; 11: 263–273.Google Scholar
19. Rodin, EA, Rim, CS, Rennick, PM. The effects of carbamazepine on patients with psychomotor epilepsy: results of a double-blind study. Epilepsia 1974; 15: 547–561.Google Scholar
20. Jeavons, P. Carbamazepine and the EEG. In: Wink, C, ed. Tegretol in epilepsy: report of an international clinical symposium. Manchester: C. Nicholls, 1972: 35–39.Google Scholar
21. Wilkus, R, Dodrill, C, Troupin, A. Carbamazepine and the electroencephalogram in epileptics: a double blind study in comparison to phenytoin. Epilepsia 1978; 19: 283–291.Google Scholar
22. Talwar, D, Arora, MS, Sher, PK. EEG changes and seizure exacerbation in young children treated with carbamazepine. Epilepsia 1994; 35: 1154–1159.Google Scholar
23. Swinyard, E, Woodhead, J. Experimental detection, quantification and evaluation of anticonvulsants. In: Woodbury, D, Penry, J, Pippenger, C, eds. Antiepileptic Drugs. New York: Raven Press, 1982: 111–126.Google Scholar
24. Snead, OC 3rd Basic mechanisms of generalized absence seizures. Ann Neurol 1995; 37: 146–157.Google Scholar
25. Lortie, A, Chiron, C, Mumford, J, Dulac, O. The potential for increasing seizure frequency, relapse, and appearance of new seizure types with vigabatrin. Neurology 1993; 43: S24-S27.Google Scholar
26. Dhuna, A, Pascual-Leone, A, Talwar, D. Exacerbation of partial seizures and onset of nonepileptic myoclonus with carbamazepine. Epilepsia 1991; 32: 275–278.Google Scholar
27. Sozuer, D, Atakli, D, Atay, T, Baybas, S, Arpaci, B. Evaluation of various antiepileptic drugs in juvenile myoclonic epilepsy. Epilepsia 1996; 37: 77.Google Scholar
28. Wakai, S, Ito, N, Sueoka, H, et al. Severe myoclonic epilepsy in infancy and carbamazepine [letter]. Eur J Pediatr 1996; 155: 724.Google Scholar
29. Viani, F, Romeo, A, Viri, M, et al. Seizure and EEG patterns in Angelman’s syndrome. J Child Neurol 1995; 10: 467–471.Google Scholar