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Infantile Spasms: a serious neurological disorder following whole-cell pertussis vaccine
Last modified: 2014-04-03
Abstract
Introduction
The adversed events following the whole-cell pertussis vaccination (WCPV) among children, include, infantile spasms (IS), or West Syndrome(1). The IS is an important epileptic encephalopathy of childhood, with a eletroencephalographic (EEG) pattern (hypsarrhythmia) and psycomotor delay (2). The cessation of spasms and normalization of the EEG, implicates in better response and prognosis. It consists of corticosteroids (ACTH, prednisone) and antiepileptic drugs(AED) as vigabatrin(VGB), topiramate(TPM), valproic acid(VPA), and pyridoxine (2). High dosage of pyridoxine, following the japanese and finish protocoles for ACTH (3)(4)(6) has been used. There is a trend in using ACTH in smaller dosage(5).
Case report
A child at 2 months, received the WCPV and developed after 20 days IS. She underwent pyridoxine, ACTH, clonazepan, valproic acid, nitrazepan, topiramate and clobazam. The recent MRI showed subtle slowing of myelination at the right frontal and temporal. She is now with a normal neurological and psycomotor development. A partial epilepsy is present now, controled with lamotrigine, oxcarbazepine and nitrazepan.
Discussion
We think that the WCPV represent a harmfull instrument to develop the spasms (1). Several protocoles have been atributted to IS. Beside the other AED the ACTH was used. We conclude in this case, probably broken out by the WCPV, the rational politherapy, according to universal protocoles was worthy. Despite a partial epilepsy has developed, her neurological exam and development are normal. Findings with delays in myelination are not uncommon in patients with West Syndrome (7)(8) .
The adversed events following the whole-cell pertussis vaccination (WCPV) among children, include, infantile spasms (IS), or West Syndrome(1). The IS is an important epileptic encephalopathy of childhood, with a eletroencephalographic (EEG) pattern (hypsarrhythmia) and psycomotor delay (2). The cessation of spasms and normalization of the EEG, implicates in better response and prognosis. It consists of corticosteroids (ACTH, prednisone) and antiepileptic drugs(AED) as vigabatrin(VGB), topiramate(TPM), valproic acid(VPA), and pyridoxine (2). High dosage of pyridoxine, following the japanese and finish protocoles for ACTH (3)(4)(6) has been used. There is a trend in using ACTH in smaller dosage(5).
Case report
A child at 2 months, received the WCPV and developed after 20 days IS. She underwent pyridoxine, ACTH, clonazepan, valproic acid, nitrazepan, topiramate and clobazam. The recent MRI showed subtle slowing of myelination at the right frontal and temporal. She is now with a normal neurological and psycomotor development. A partial epilepsy is present now, controled with lamotrigine, oxcarbazepine and nitrazepan.
Discussion
We think that the WCPV represent a harmfull instrument to develop the spasms (1). Several protocoles have been atributted to IS. Beside the other AED the ACTH was used. We conclude in this case, probably broken out by the WCPV, the rational politherapy, according to universal protocoles was worthy. Despite a partial epilepsy has developed, her neurological exam and development are normal. Findings with delays in myelination are not uncommon in patients with West Syndrome (7)(8) .
Keywords
Infantile Spasms; Eletrencephalography; antiepileptic drugs; psycomotor delay
References
1-Geier DA et al. Brain & Development 2004;26:296-300.
2-Watemberg N. Infantile Spasms: Treatment Challenges. Current Treatment Options in Neurology 2012.;14:322-331.
3-Ohtahara S et al. Brain & Development 2011; 33: 783-789.
4-Riikonen R. Brain& Development 2001;23:642-646.
5-Heiskala H et al.. Brain& Developement 1996;18:456-460.
6-Chang-Yang Tsao. Neuropsychiatric Disease and Treatment 2009;5:289-299..
7-Schropp C et al. Neuropediatrics 1994;25(3):116-20.
8-Takano T et al. Pediatr Neurol 2007;37(6):417-20
2-Watemberg N. Infantile Spasms: Treatment Challenges. Current Treatment Options in Neurology 2012.;14:322-331.
3-Ohtahara S et al. Brain & Development 2011; 33: 783-789.
4-Riikonen R. Brain& Development 2001;23:642-646.
5-Heiskala H et al.. Brain& Developement 1996;18:456-460.
6-Chang-Yang Tsao. Neuropsychiatric Disease and Treatment 2009;5:289-299..
7-Schropp C et al. Neuropediatrics 1994;25(3):116-20.
8-Takano T et al. Pediatr Neurol 2007;37(6):417-20
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