[1] 吴湖炳,王全师,王明芳,等.18F-FDG PET显像对致痫灶的定位及在外科治疗中的价值.中华核医学杂志,2006,26(2):69-72.
[2] 姚涛,邹晓毅.PET在癲痫定位诊断中的应用.华西医学,2005,20(2):257-258.
[3] Giovacchini G,Conant S,Herscovitch P,et al.Using cerebral white matter for estimation of nondisplaceable binding of 5-HT1A receptors in temporal lobe epilepsy.J Nucl Med,2009,50(11):1794-1800.
[4] Benifla M,Sala F Jr,Jane J,et al.Neurosurgical management of intractable rolandic epilepsy in children:role of resection in eloquent cortex.J Neurosurg Pediatr,2009,4(3):199-216.
[5] Richardson EJ,Griffith HR,Martin RC,et al.Structural and functional neuroimaging correlates of depression in temporal lobe epilepsy.Epilepsy Behav,2007,10(2):242-249.
[6] Saeki K,Saito Y,Sugai K,et al.Startle epilepsy associated with gait-induced seizures; Pathomechanism analysis using EEG,MEG,and PET studies.Epilepsia,2009,50(5):1274-1279.
[7] 申广浩,罗二平,路丽华,等.PET、VEEG、MRI癲痫灶定位与病理一致性的研究.中国医学物理学杂志,2008,25(1):481-483.
[8] 李一明,张华,井晓荣,等.比较发作间期PET,M RI和EEG对难治性癲痫的定位价值.第四军医大学学报,2006,27(2):151-154.
[9] Tanriverdi T,Klein D,Mok K,et al.Atypical speech activations:PET results of 92 patients with left-hemispheric epilepsy.Acta Neurochir(Wien),2009,151(10):1175-1190.
[10] Vinton AB,Carne R,Hicks RJ,et al.The extent of resection of FDG-PET hypometabolism relates to outcome of temporal lobectomy.Brain,2007,130(Pt 2):548-560.
[11] Takaya S,Hanakawa T,Hashikawa K,et al.Prefrontal hypopfunction in patients with intractable mesial temporal lobe epilepsy.Neurology,2006,67(9):1674-1676.
[12] Engel J Jr,Kuhi DE,Phelps ME,et al.Interctal cerebral glucose metabolism in patial epilepsy and its relation to EEG changes.Ann Neurol,1982,12(6):510-517.
[13] Joo EY,Hong SB,Han HJ,et al.Postoperative alteration of cerebral glucose metabolism in mesial temporal lobe epilepsy.Brain,2005,128(Pt 8):1802-1810.
[14] Benabid AL,Chabardes S,Torres N,et al.Functional neurosurgery for movement disorders:a historical perspective.Prog Brain Res.2009,175:379-391.
[15] Theodore WH,Giovacchini G,Bonwetsch R,et al.The effect of antiepileptic drugs on 5-HT-receptor binding measured by positron emission tomography.Epilepsia,2006,47(3):499-503.
[16] Hammers A,Asselin MC,Turkheimer FE,et al.Balancing bias,reliability,noise properties and the need for parametric maps in quantitative ligand PET:[11C]diprenorphine test-retest data.Neuroimage,2007,38(1):82-94.
[17] Padma MV,Simkins R,White P,et al.Clinic alutility of 11C-flumazenil positron emission tomography in intractable temporal lobe epilepsy.Neurol India,2004,52(4):457-462.
[18] Bonati MT,Combi R,Asselta R,et al.Exclusion of linkage of nine neuronal nicotinic acetylcholine receptor subunit genes expressed in brain in autosomal dominant nocturnal frontal lobe epilepsy in four unrelated families.J Neurol,2002,249(8):967-974.
[19] Pannell C,Simonian SX,Gillies GE,et al.Hypothalamic somatostatin and growth hormone releasing hormone mRNA expression depend upon GABA(A) receptor expression in the developingmouse.Neuroendocrinology,2002,76(2):93-94.
[20] Duncan JS.Position emission tomography receptor studies.Adv Neuro,1999,79:893-899.
[21] Fowler JS,Volkow ND,Cilento R,et al.Comparison of brain glucose metabolism and monoamine oxidase B(MAO B)in traumatic brain injury.Clin Positron Imaging,1999,2(2):71-79,.
[22] Haut SR,Albin RL.Dopamine and epilepsy:hints of complex subcortical roles.Neurology,2008,71(11):784-785.
[23] Mukherjee J,Shi B,Christian BT,et al.11C-Fallypride:radiosynthesis and preliminary evaluation of a novel dopamine D2/D3 receptor PET radiotracer in non-human primate brain.Bioorg Med Chem,2004,12(1):95-102.