Neuropediatrics 2006; 37(1): 32-41
DOI: 10.1055/s-2006-923949
Original Article

Georg Thieme Verlag KG Stuttgart · New York

Biphasic Clinical Course and Early White Matter Abnormalities may be Indicators of Neurological Sequelae after Status Epilepticus in Children

R. Okamoto1 , S. Fujii2 , T. Inoue1 , K. Lei1 , A. Kondo1 , 3 , T. Hirata4 , M. Okada4 , I. Suzaki5 , T. Ogawa2 , Y. Maegaki1 , K. Ohno1
  • 1Division of Child Neurology, Institute of Neurological Sciences, Faculty of Medicine, Tottori University, Yonago, Japan
  • 2Division of Radiology, Institute of Neurological Sciences, Faculty of Medicine, Tottori University, Yonago, Japan
  • 3Department of Pediatrics, Tottori Prefectural Central Hospital, Tottori, Japan
  • 4Department of Pediatrics, Matsue Red Cross Hospital, Matsue, Japan
  • 5Department of Pediatrics, Tottori Prefectural Kousei Hospital, Kurayoshi, Japan
Further Information

Publication History

Received: September 6, 2005

Accepted after Revision: January 27, 2006

Publication Date:
15 March 2006 (online)

Abstract

Clinical course and serial neuroimaging findings are not fully described in children who have had neurological sequelae following status epilepticus. We found four patients who had neurological sequelae out of 42 children with status epilepticus in 2004. MRI studies were reviewed with specific attention to diffusion-weighted images (DWI) and the apparent diffusion coefficient (ADC). Proinflammatory cytokines, including tumor necrosis factor-α and interleukin-6, were measured in the cerebrospinal fluid (CSF) (3 patients). The clinical course showed biphasic; initial status epilepticus and neurological exacerbation along with seizure recurrence four to five days after onset. Within three days after initial status epilepticus, CT (all patients) and MRI (2 patients) did not show any abnormalities. From four to ten days after onset, MRI demonstrated diffuse hyperintensity in the cerebral white matter on DWI and hypointensity on ADC maps in all patients. Diffuse brain atrophy progressed thereafter. Tumor necrosis factor-α or interleukin-6 was elevated in all patients. A biphasic clinical course may be a specific feature for neurological sequelae. The preferential white matter involvement on MRI and elevated CSF cytokines indicate that glial dysfunction may play an important role in the pathophysiology of status epilepticus-associated cerebral damage.

References

  • 1 Akasaka M, Sasaki M, Ehara S, Kamei A, Chida S. Transient decrease in cerebral white matter diffusivity on MR imaging in human herpes virus-6 encephalopathy.  Brain Dev. 2005;  27 30-33
  • 2 Chalela J A, Wolf R L, Maldjian J A, Kasner S E. MRI identification of early white matter injury in anoxic-ischemic encephalopathy.  Neurology. 2001;  56 481-485
  • 3 Chu K, Kang D-W, Kim J-Y, Chang K ‐H, Lee S K. Diffusion-weighted magnetic resonance imaging in nonconvulsive status epilepticus.  Arch Neurol. 2001;  58 993-998
  • 4 Diehl B, Najm I, Ruggieri P, Foldvary N, Mohamed A, Tkach J. et al . Periictal diffusion-weighted imaging in a case of lesional epilepsy.  Epilepsia. 1999;  40 1667-1671
  • 5 Evans M, Griffiths T, Meldrum B. Early changes in the rat hippocampus following seizures induced by bicuculline or L-allylglycine: a light and electron microscope study.  Neuropathol Appl Neurobiol. 1983;  9 39-52
  • 6 Flacke S, Wüllner U, Keller E, Hamzei F, Urbach H. Reversible changes in echo planar perfusion- and diffusion-weighted MRI in status epilepticus.  Neuroradiology. 2000;  42 92-95
  • 7 Freeman J L, Coleman L T, Smith L J, Shield L K. Hemiconvulsion-hemiplegia-epilepsy syndrome: characteristic early magnetic resonance imaging findings.  J Child Neurol. 2002;  17 10-16
  • 8 Gurnett C A, Landt M, Wong M. Analysis of cerebrospinal fluid glial fibrillary acidic protein after seizures in children.  Epilepsia. 2003;  44 1455-1458
  • 9 Hisano T, Ohno M, Egawa T, Takano T, Shimada M. Changes in diffusion-weighted MRI after status epilepticus.  Pediatr Neurol. 2000;  22 327-329
  • 10 Hong K-S, Cho Y-J, Lee S K, Jeong S-W, Kim W K, Oh E J. Diffusion changes suggesting predominant vasogenic oedema during partial status epilepticus.  Seizure. 2004;  13 317-321
  • 11 Ichiyama T, Morishima T, Isumi H, Matsufuji H, Matsubara T, Furukawa S. Analysis of cytokine levels and NF-κB activation in peripheral blood mononuclear cells in influenza virus-associated encephalopathy.  Cytokine. 2004;  27 31-37
  • 12 Kassem-Moussa H, Provenzale J M, Petrella J R, Lewis D V. Early diffusion-weighted MR imaging abnormalities in sustained seizure activity.  AJR Am J Roentgenol. 2000;  174 1304-1306
  • 13 Kawada J, Kimura H, Yoshikawa T, Ihira M, Okumura A, Morishima T. et al . Hemiconvulsion-hemiplegia syndrome and primary human herpes virus 7 infection.  Brain Dev. 2004;  26 412-414
  • 14 Kim J ‐A, Chung J I, Yoon P H, Kim D I, Chung T ‐S, Kim E-J. et al . Transient MR signal changes in patients with generalized seizure or status epilepticus: periictal diffusion-weighted imaging.  AJNR. 2001;  22 1149-1160
  • 15 Lansberg M G, O'Brien M W, Norbash A M, Moseley M E, Morrell M, Albers G W. MRI abnormalities associated with partial status epilepticus.  Neurology. 1999;  52 1021-1027
  • 16 Maegaki Y, Kurozawa Y, Hanaki K, Ohno K. Risk factors for fatality and neurological sequelae after status epilepticus in children.  Neuropediatrics. 2005;  36 186-192
  • 17 Maytal J, Shinnar S, Moshé S L, Alvarez L A. Low morbidity and mortality of status epilepticus in children.  Pediatrics. 1989;  83 323-331
  • 18 Mazumdar A, Mukherjee P, Miller J H, Malde H, McKinstry R C. Diffusion-weighted imaging of acute corticospinal tract injury preceding Wallerian degeneration in the maturing human brain.  AJNR. 2003;  24 1057-1066
  • 19 Morimoto T, Fukuda M, Suzuki Y, Kusu M, Kida K. Sequential changes of brain CT and MRI after febrile status epilepticus in a 6-year-old girl.  Brain Dev. 2002;  24 190-193
  • 20 Nakai Y, Itoh M, Mizuguchi M, Ozawa H, Okazaki E, Kobayashi Y. et al . Apoptosis and microglial activation in influenza encephalopathy.  Acta Neuropathol. 2003;  105 233-239
  • 21 Nedelcu J, Klein M A, Aguzzi A, Boesiger P, Martin E. Biphasic edema after hypoxic-ischemic brain injury in neonatal rats reflects early neuronal and late glial damage.  Pediatr Res. 1999;  46 297-304
  • 22 Pantoni L, Garcia J H, Gutierrez J A. Cerebral white matter is highly vulnerable to ischemia.  Stroke. 1996;  27 1641-1647
  • 23 Rizzi M, Perego C, Aliprandi M, Richichi C, Ravizza T, Colella D. et al . Glia activation and cytokine increase in rat hippocampus by kainic acid-induced status epilepticus during postnatal development.  Neurobiol Dis. 2003;  14 494-503
  • 24 Schmidt-Kastner R, Ingvar M. Loss of immunoreactivity for glial fibrillary acidic protein (GFAP) in astrocytes as a marker for profound tissue damage in substantia nigra and basal cortical areas after status epilepticus induced by pilocarpine in rat.  Glia. 1994;  12 165-172
  • 25 Verity C M, Ross E M, Golding J. Outcome of childhood status epilepticus and lengthy febrile convulsions: findings of national cohort study.  BMJ. 1993;  307 225-228
  • 26 Watanabe T, Honda Y, Fujii Y, Koyama M, Tanaka R. Serial evaluation of axonal function in patients with brain death by using anisotropic diffusion-weighted magnetic resonance imaging.  J Neurosurg. 2004;  100 56-60
  • 27 Wieshmann U C, Symms M R, Shorvon S D. Diffusion changes in status epilepticus.  Lancet. 1997;  350 493-494

Yoshihiro Maegaki

Division of Child Neurology, Institute of Neurological Sciences
Faculty of Medicine
Tottori University

36 - 1 Nishi-Cho

Yonago 683 - 8504

Japan

Email: maegaki@grape.med.tottori-u.ac.jp

    >