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• Clinical Article •
The correlation study of seizure and cerebral hemodynamics in Sturge-Weber syndrome
ZHENG Cheng-cheng  CAI Zhao-cheng  FENG Jie  NIU Tian-li  MIAO Yan-wei 

DOI:10.3969/j.issn.1674-8034.2013.02.003.


[Abstract] Objective: To evaluate the perfusion status of involved white matter in Sturge-Weber syndrome (SWS) using dynamical susceptibility contrasted perfusion imaging (DSC-PI), and then to compare the perfusion data and seizure variables, including age of first seizure, seizure frequency (score of seizure frequency, SSF) and duration of epilepsy, for reasonable explaining the hemodynamics and seizure variables in SWS.Materials and Methods: 14 patients (8 girls and 6 boys; age range, 0.8-10.0 years; median age, 4.0 years) with Sturge-Weber syndrome were recruited and performed MRI examination. All patients with unilateral lesions were located in one side of the cerebral hemispheres. MR protocols included axial and sagittal T1-weighted, axial fast spin-echo (FSE) T2-weighted, DSC-PI and contrasted T1-weighted. All raw data of DSC-PI were processed through the SPIN software (signal process in neuroimage). After determining the location and realm of SWS lesions, the CBF, CBV and MTT value of the affected and contralateral white matter were measured, and then the ratio of perfusion data, including CBFr, CBVr and MTTr were calculated. According to the CBFr values, all cases were divided into hyperperfusion group (HP) and hypoperfusion group (LP). The comparison of CBF, CBV and MTT values between the affected and contralateral hemispheres was tested by Mann-Whitney U analysis. The correlations of all perfusion data and seizure variables (age of first seizure, SSF and duration of epilepsy) were analyzed by Spearman correlation analysis.Results: In all, nine cases belonged to the LP group according to the significantly decreased CBF and CBV in the affected white matter compared to those in the contralateral’s (CBFr=-0.37±0.24, CBVr=-0.22±0.25, P<0.01), and the other 5 cases were in the HP group based on the significantly increased CBF and CBV of affected white matter (CBFr=0.31±0.05; CBVr=0.40±0.17, P<0.01). The age and SSF of LP group were slightly higher than HP group (age were 63.80 months & 48.83 months; SSF were 2.50 & 1.33), but no significant difference was present respectively (P=0.36, 0.12). Longer duration of epilepsy was related to lower CBF (more negative CBFr, r=-0.58, P<0.05) and low CBV (r=-0.55, P<0.05) on the affected side. Lower perfusion was associated with more frequent seizures (CBFr: r=-0.56, CBVr: r=-0.63, P<0.05).Conclusions: The perfusion of affected white matter in Sturge-Weber syndrome did not decrease continuously as illustrated by previous studies, whiles the relatively hyperperfusion was considered as a common phenomena. There are relationships between brain perfusion status and seizure severity in SWS.
[Keywords] Sturge-Weber syndrome；Epilepsy；Magnetic resonance imaging；Perfusion, regional

ZHENG Cheng-cheng Deparment of Radiology, The First Affiliated Hospital, Dalian Medical University, Dalian 116011,China

CAI Zhao-cheng Deparment of Radiology, Zhongshan Hospital of Dalian University, dalian 116001, China

FENG Jie Deparment of Radiology, The First Affiliated Hospital, Dalian Medical University, Dalian 116011,China

NIU Tian-li Deparment of Radiology, The First Affiliated Hospital, Dalian Medical University, Dalian 116011,China

MIAO Yan-wei* Deparment of Radiology, The First Affiliated Hospital, Dalian Medical University, Dalian 116011,China

*Correspondence to: MIAO Yan-wei, E-mail: ywmiao716@yahoo.com.cn

Conflicts of interest   None.

Received  2012-10-15
Accepted  2012-11-20
DOI: 10.3969/j.issn.1674-8034.2013.02.003
DOI:10.3969/j.issn.1674-8034.2013.02.003.

[1]
Juhasz C, Lai Ch, Behen ME, et al. White matter volume as a major predictor of cognitive function in Sturge-Weber Syndrome. Arch Neurol, 2007, 64(8): 1169-1174.
[2]
Deary IJ, Bastin ME, Pattie A, et al. White matter integrity and cognition in childhood and old age. Neurology, 2006, 66(4): 505-512.
[3]
Sivaswamy L, Rajamani K, Juhasz C, et al. The corticospinal tract in Sturge-Weber syndrome: a diffusion tensor tractography study. Brain Dev, 2008, 30(7): 447-453.
[4]
Juhasz C, Haacke EM, Hu J, et al. Multimodality imaging of cortical and white matter abnormalities in Sturge-Weber Syndrome. AJNR Am J Neuroradiol, 2007, 28(5): 900-906.
[5]
Pinton F, Chiron C, Enjolras O, et al. Early single photon emission computed tomography in Sturge-Weber syndrome. J Neurol Neurosurg Psychiatry, 1997, 63(5): 616-621.
[6]
Duncan DB, Herholz K, Pietrzyk U, et al. Regional cerebral blood flow and metabolism in Sturge-Weber disease. Clin Nucl Med, 1995, 20(6): 522-523.
[7]
Maria BL, Neufeld JA, Rosainz LC, et al. High prevalence of bihemispheric structural and functional defects in Sturge-Weber syndrome. J Child Neurol, 1998, 13(12): 595-605.
[8]
Lin DD, Barker PB, Kraut MA, et al. Early characteristics of Sturge-Weber syndrome shown by perfusion MR imaging and proton MR spectroscopic imaging. AJNR Am J Neuroradiol, 2003, 24(9): 1912-1915.
[9]
Evans AL, Widjaja E, Connolly DJ, et al. Cerebral perfusion abnormalities in children with Sturge-Weber Syndrome shown by dynamic contrast bolus magnetic resonance perfusion imaging. Pediatrics, 2006, 117(6): 2119-2125.
[10]
Lin DD, Barker PB, Hatfield LA, et al. Dynamic MR perfusion and proton mr spectroscopic imaging in Sturge-Weber syndrome: correlation with neurological symptoms. J Magn Reson Imag, 2006, 24(2): 274-281.
[11]
Oguz KK, Senturk S, Ozturk A, et al. Impact of recent seizures on cerebral blood flow in patients with sturge-weber syndrome: study of 2 cases. J Child Neurol, 2007, 22(5): 617-620.
[12]
Thomas-Sohl KA, Vaslow DF, Maria BL. Sturge-Weber syndrome: a review. Pediar Neurol, 2004, 30(5): 303-310.
[13]
Kelley TM, Hatfield LA, Lin Doris DM, et al. Quantitative analysis of cerebral cortical atrophy and correlation with clinical severity in unilateral Sturge-Weber syndrome. J Child Neurol, 2005, 20(11): 867-870.
[14]
Pfund Z, Kagawa K, Juhász C, et al. Quantitative analysis of gray- and white-matter volumes and glucose metabolism in Sturge-Weber syndrome. J Child Neurol, 2003, 18(2): 119-126.
[15]
Bentson JR, Wilson GH, Newton TH. Cerebral venous drainage pattern of the Sturge-Weber syndrome. Radiology, 1971, 101(1): 111-118.
[16]
Rhoton AL Jr. The cerebral veins. Neurosurgery, 2002, 51(4Suppl): 159-205.
[17]
Namer IJ, Battaglia F, Hitsch E, et al. Subtraction Ictal SPECT co-registered to MRI (SISCOM) in Sturge-Weber syndrome. Clin Nucl Med, 2005, 30(1): 39-40.
[18]
Juhasz C, Chugani DC, Muzik O. et al. Is epileptogenic cortex truly hypometabolic on interictal position emission tomography? Ann Neurol, 2000, 48(1): 88-96.
[19]
Lee JS, Asano E, Muzik Q. Sturge-Weber syndrome: correlation between clinical course and FDG PETfinding. Neurology, 2001, 57(2): 189-195.
[20]
Okudaira Y, Arai H, Sato K. Hemodynamic compromise as a factor in clinical progression of Sturge-Weber syndrome. Child’s Nerv Syst, 1997, 13(4): 214-219.
[21]
Yu TW, Liu HM, Lee WT. The correlation between motor impairment and cerebral blood flow in Sturge-Weber syndrome. Eur J Paediatr Neurol, 2007, 11(2): 96-103.
[22]
Miao Y, Juhasz C, Wu J, et al. Clinical correlates of white matter blood flow perfusion changes in Sturge-Weber syndrome: a dynamic MR perfusion-weighted imaging study. AJNR Am J Neuroradiol, 2011, 32(7):1280-1285.
[23]
Comi AM. Pathophysiology of Sturge-Weber syndrome. J Child Neurol, 2003, 18(8): 509-516.
[24]
Alkonyi B, Miao Y, Wu J, et al. A perfusion-metabolic mismatch in Sturge-Weber syndrome: a multimodality imaging study. Brain Dev, 2012, 34(7): 553-562.

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