Medline ® Abstracts for References 3-21

of 'Magnetic resonance imaging changes related to acute seizure activity'

3
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MRI abnormalities associated with partial status epilepticus.
AU
Lansberg MG, O'Brien MW, Norbash AM, Moseley ME, Morrell M, Albers GW
SO
Neurology. 1999;52(5):1021.
 
OBJECTIVE: To report neuroimaging findings in patients with complex partial status epilepticus.
BACKGROUND: During status epilepticus, neuroimaging may be used to exclude other neurologic conditions. Therefore, it is important to identify the neuroimaging features that are associated with status epilepticus. In addition, MRI characteristics may provide insight into the pathophysiologic changes during status epilepticus.
METHODS: The history and neuroimaging examination results of three patients with complex partial status epilepticus were reviewed. Studies obtained during status epilepticus included diffusion-weighted MRI (DWI), MR angiography (MRA), postcontrast T1-weighted MRI, T2-weighted MRI, and CT. Follow-up MRI was obtained in two patients, and autopsy results were available for the third.
RESULTS: Some of the MRI and CT findings during partial status epilepticus mimicked those of acute ischemic stroke: DWI and T2-weighted MRI showed cortical hyperintensity with a corresponding low apparent diffusion coefficient,and CT showed an area of decreased attenuation with effacement of sulci and loss of gray-white differentiation. However, the lesions did not respect vascular territories, there was increased signal of the ipsilateral middle cerebral artery on MRA, and leptomeningeal enhancement appeared on postcontrast MRI. On follow-up imaging, the abnormalities had resolved, but some cerebral atrophy was present.
CONCLUSIONS: The radiologic characteristics of status epilepticus resemble those of ischemic stroke but can be differentiated based on lesion location and findings on MRA and postcontrast MRI. The MRI abnormalities indicated the presence of cytotoxic and vasogenic edema, hyperperfusion of the epileptic region, and alteration of the leptomeningeal blood-brain barrier. These changes reversed, but they resulted in some regional brain atrophy.
AD
Stanford Stroke Center, UCSF Stanford Health Care, Palo Alto, CA 94304-1705, USA.
PMID
4
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Seizure-associated abnormalities in epilepsy: evidence from MR imaging.
AU
Briellmann RS, Wellard RM, Jackson GD
SO
Epilepsia. 2005;46(5):760.
 
Acute seizure-associated changes have been described in the animal and human literature. Controversy exists over whether seizures cause permanent damage to the brain, and whether a (prolonged) seizure can induce changes that lead to an epileptic lesion, resulting in habitual seizures and epilepsy. Current magnetic resonance imaging (MRI) offers a variety of imaging tools and is capable of detecting acute seizure-associated changes. In contrast to the histologic examination, serial MRI studies are possible and allow longitudinal observation of the fate of these changes. This report reviews the literature on acute seizure-associated effects emphasizing the MRI evidence.
AD
Brain Research Institute, Austin and Repatriation Medical Centre, Victoria, Australia.
PMID
5
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Multimodal longitudinal imaging of focal status epilepticus.
AU
Doherty CP, Cole AJ, Grant PE, Fischman A, Dooling E, Hoch DB, White TH, Cosgrove GR
SO
Can J Neurol Sci. 2004;31(2):276.
 
BACKGROUND: Little is understood about the evolution of structural and functional brain changes during the course of uncontrolled focal status epilepticus in humans.
METHODS: We serially evaluated and treated a nine-year-old girl with refractory focal status epilepticus. Long-term EEG monitoring, MRI, MRA, SPECT, intraoperative visualization of affected cortex, and neuropathological examination of a biopsy specimen were conducted over a three year time span. Imaging changes were correlated with simultaneous treatment and EEG findings.
RESULTS: The EEG monitoring showed almost continuous spike discharges emanating initially from the right frontocentral area. These EEG abnormalities were intermittently suppressed by treatment with anesthetics. Over time, additional brain areas developed epileptiform EEG abnormalities. Serial MRI studies demonstrated an evolution of changes from normal, through increased regional T2 signal to generalized atrophy. An MRA demonstrated dilatation of the middle cerebral artery stem on the right compared to the left with a broad distribution of flow-related enhancement.An 18FDG-PET scan showed a dramatically abnormal metabolic profile in the same right frontocentral areas, which modulated in response to treatment during the course of the illness. A right frontotemporal craniotomy revealed a markedly hyperemic cortical focus including vascular shunting. A sample of resected cortex showed severe gliosis and neuronal death.
CONCLUSIONS: The co-registration of structural and functional imaging and its correlation with operative and pathological findings in this case illustrates the relentless progression of regional and generalized abnormalities in intractable focal status epilepticus that were only transiently modified by exhaustive therapeutic interventions. Increased flow through large vessels appeared to be shunted and did not translate into increased microvascular perfusion.
AD
Epilepsy Service, Neurology Service, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA.
PMID
6
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Magnetic resonance imaging evidence of hippocampal injury after prolonged focal febrile convulsions.
AU
VanLandingham KE, Heinz ER, Cavazos JE, Lewis DV
SO
Ann Neurol. 1998;43(4):413.
 
Magnetic resonance imaging (MRI) was performed after complex febrile convulsions (CFCs) in 27 infants. Definite MRI abnormalities were seen in 6 of the 15 infants with focal or lateralized CFCs and in none of the 12 infants with generalized CFCs. In 2 of the 6 infants with lateralized CFCs and abnormal MRIs, the MR images showed preexisting bilateral hippocampal atrophy consistent with the history of perinatal insults in these infants. However, the remaining 4 infants with MRI abnormalities and lateralized CFCs had significantly longer seizures than other infants and had MRI changes suggesting acute edema with increased hippocampal T2-weighted signal intensity and increased volume predominantly in the hippocampus in the hemisphere of seizure origin. Of those with acute edema, 1 had electrographical seizure activity recorded in the temporal region and another had a choroid fissure cyst displacing the affected hippocampus; both infants had follow-up MRIs showing that hippocampal atrophy had developed. These patients demonstrate that prolonged and focal CFCs can occasionally produce acute hippocampal injury that evolves to hippocampal atrophy. Finally, evidence of preexisting hippocampal abnormalities in several infants and electrographical temporal lobe seizure activity in 1 suggests the possibility that CFCs actually originated in the temporal lobes in some patients.
AD
Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA.
PMID
7
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Reversible periictal MRI abnormalities: clinical correlates and long-term outcome in 12 patients.
AU
Raghavendra S, Ashalatha R, Krishnamoorthy T, Kesavadas C, Thomas SV, Radhakrishnan K
SO
Epilepsy Res. 2007;73(1):129.
 
Although a wide spectrum of reversible periictal magnetic resonance imaging (MRI) abnormalities (RPMA) are being increasingly identified, the clinicians are often in a dilemma about their localization significance. This prompted us to analyze the clinical, MRI, electroencephalographic (EEG) and follow-up data of 12 patients with RPMA seen in a tertiary referral epilepsy center. RPMA occurred after a single or a cluster of focal seizures with or without secondary generalization. The interictal and ictal EEG abnormalities were localized to the site of RPMA in nine patients. RPMA involved areas remote from the site of EEG abnormalities in four patients. We have developed a comprehensive classification to account for the wide spectrum of RPMA involving gray matter, white matter and leptomeninges with or without contrast enhancement or mass effect. Follow-up MRIs showed complete resolution of RPMA in all, except in four patients, who developed residual focal atrophy. During median follow-up period of 3 years, recurrence of RPMA was observed in two patients. Diffusion weighted MRI in two patients and histopathological finding in one patient favored causal role of hypoxia in the pathogenesis of RPMA. Our observations help to understand the electroclinical profile, radiological spectrum, localization significance and natural history of RPMA better.
AD
Department of Neurology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum 695011, Kerala, India.
PMID
8
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Postictal diffusion-weighted imaging for the localization of focal epileptic areas in temporal lobe epilepsy.
AU
Diehl B, Najm I, Ruggieri P, Tkach J, Mohamed A, Morris H, Wyllie E, Fisher E, Duda J, Lieber M, Bingaman W, Lüders HO
SO
Epilepsia. 2001;42(1):21.
 
PURPOSE: Diffusion-weighted MR imaging (DWI) is a novel technique to delineate focal areas of cytotoxic edema of various etiologies. We hypothesized that DWI may also detect the epileptogenic region and adjacent areas during the ictal and early postictal periods in patients with temporal lobe epilepsy (TLE).
METHODS: We studied patients with intractable TLE (n = 9), due to hippocampal sclerosis (HS, n = 7), left mesial temporal lobe tumor (n = 1), and of unknown etiology (n = 1). Informed consent was obtained before inclusion in the study. All patients with single short seizures were scanned immediately after EEG-documented seizures (between 45 and 150 min); one of two patients in status was scanned 14 h after cessation of seizures. DWI results were analyzed visually and by calculating apparent diffusion coefficient (ADC) maps.
RESULTS: We found significant decreases in ADC postictally in one of six patients with TLE due to HS and single short seizures. One patient with an incompletely resected temporal lobe tumor also exhibited ADC abnormalities. One patient in focal status epilepticus revealed a decrease in ADC, and one patient with a continuous aura had no DWI abnormality.
CONCLUSIONS: Postictal DWI technique may occasionally help delineate epileptic areas in some patients with TLE. Yield is low in patients with HS and single short seizures: it may be higher in patients with tumor or status epilepticus.
AD
Department of Neurology, The Cleveland Clinic Foundation, 9500 Euclid Ave., Cleveland, Ohio 44195, U.S.A. diehlb@ccf.org
PMID
9
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Brain diffusion after single seizures.
AU
Hufnagel A, Weber J, Marks S, Ludwig T, De Greiff A, Leonhardt G, Widmann G, Stolke D, Forsting M
SO
Epilepsia. 2003;44(1):54.
 
PURPOSE: Diffusion-weighted magnetic resonance imaging (DWI) after focal status epilepticus has demonstrated focal alterations of the apparent diffusion coefficient (ADC) in the epileptogenic zone. We hypothesized that localized dynamic alterations of brain diffusion during the immediate postictal state will be detectable by serial DWI and correlate with the epileptogenic zone.
METHODS: Nine adult patients (four men, five women) with medically intractable epilepsy were prospectively examined with a total of 25 DWI scans taken 2-210 min after a seizure.
RESULTS: The interictal ADC was significantly (p<0.05) elevated in the ictogenic hippocampus in all patients with temporal lobe epilepsy. The following postictal changes of the ADC were seen: (a) decreases by maximally 25-31%, which were most pronounced in the epileptogenic zone (n = 2); (b) generalized ADC changes after generalized seizures (n = 1) or prolonged complex partial seizures (n = 2); (c) no major changes after short-lived seizures or if the time to first DWI scan was>15 min or both (n = 3); and (d) widespread bilateral ADC increases after a flumazenil-induced seizure (n = 1).
CONCLUSIONS: ADC changes seen during serial postictal DWI are complex and appear to reflect origin and spread of the preceding seizure. A delineation of the epileptogenic zone appears to be possible only in complex-partial seizures of>60 s duration that do not secondarily generalize.
AD
Department of Neurology, University of Essen, Essen, Germany. aa.hufnagel@uni-essen.de
PMID
10
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Efficacy of surgical treatment of de novo, adult-onset, cryptogenic, refractory focal status epilepticus.
AU
Costello DJ, Simon MV, Eskandar EN, Frosch MP, Henninger HL, Chiappa KH, Cole AJ
SO
Arch Neurol. 2006;63(6):895.
 
BACKGROUND: There have been few published reports of successful surgical treatment of focal status epilepticus. Surgical intervention is considered a last resort after medical strategies have been exhausted.
OBJECTIVE: To report a case of an adult who was initially seen with de novo, medically refractory, cryptogenic focal status epilepticus and underwent resection of an electrographically defined portion of the left middle frontal gyrus with multiple subpial transections of the adjacent cortex resulting in termination of the electroclinical seizure activity.
DESIGN: Report of a case of successful surgical treatment of cryptogenic focal status epilepticus.
INTERVENTION: After an initial 35 days of oral antiepileptic drug therapy and subsequent 16 days of continuous electroencephalography-guided intravenous antiepileptic drug therapy in an intensive care unit setting, and after extensive preoperative and intraoperative characterizationof the epileptogenic zone, a tailored resection of the left middle frontal gyrus with multiple subpial transections of the surrounding cortex was performed.
RESULTS: The restricted surgical resection and multiple subpial transections terminated the seizure activity. Neuropathological examination of the resected tissue revealed moderate inflammatory changes and a few abnormally located neurons without any definitive evidence of dysplasia, which was suspected preoperatively.
CONCLUSIONS: We suggest that focal cortical resection may be an appropriate intervention in medically refractory focal status epilepticus even when an overt structural etiology is not evident preoperatively and should be considered as an option at the onset of intractability.
AD
Epilepsy Service, Department of Neurology, Massachusetts General Hospital, Boston 02114, USA. djcostello@partners.org
PMID
11
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Periictal diffusion-weighted imaging in a case of lesional epilepsy.
AU
Diehl B, Najm I, Ruggieri P, Foldvary N, Mohamed A, Tkach J, Morris H, Barnett G, Fisher E, Duda J, Lüders HO
SO
Epilepsia. 1999;40(11):1667.
 
PURPOSE: Diffusion-weighted MR imaging (DWI) has been used for the early diagnosis of acute ischemic lesions in humans and in animal models of focal status epilepticus. We hypothesized that DWI may be a sensitive, noninvasive tool for the localization of the epileptogenic area during the periictal period.
METHODS: A periictal DWI study was performed on a 35-year-old patient during focal status epilepticus with repetitive prolonged focal motor seizures originating from a lesion in the right frontal lobe. DWI results were analyzed visually and by calculating apparent diffusion coefficient (ADC) maps.
RESULTS: On DWI, a single area of signal increase (decrease in ADC) was found in the region of focal electrocorticographic seizures that was mapped intraoperatively.
CONCLUSIONS: Ictal/postictal DWI may be a useful technique for seizure localization in patients with lesional epilepsy.
AD
Department of Neurology, The Cleveland Clinic Foundation, Ohio, USA. diehlb@ccf.org
PMID
12
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Magnetic resonance imaging and spectroscopy findings after focal status epilepticus.
AU
Fazekas F, Kapeller P, Schmidt R, Stollberger R, Varosanec S, Offenbacher H, Fazekas G, Lechner H
SO
Epilepsia. 1995;36(9):946.
 
The etiology of cerebral abnormalities after focal status epilepticus (SE) is unknown. Possible causes include hypoxia and the excessive release of excitatory amino acids. Magnetic resonance imaging (MRI) of a 21-year-old patient with "cryptogenic" continuous motor seizures showed swelling and signal hyperintensity of the contralateral parietotemporal cortex, the thalamus, and the ipsilateral cerebellum on T2-weighted images. These regions are connected by glutamatergic pathways. Proton magnetic resonance spectroscopy (MRS) of the cortical lesion yielded a signal peak at the resonance frequency of 2.29 ppm, suggesting a focal increase of glutamate or its degradation product glutamine. At 3-month follow-up, structural alterations had disappeared, but the N-acetyl-aspartate/choline ratio was still reduced in the previously abnormal area. These findings are the first to demonstrate the contribution of MRS to pathophysiologic studies of focal SE in humans and, in combination with the pattern of imaging abnormalities, support a major role of glutamate for seizure-related brain damage.
AD
Department of Neurology, Karl-Franzens University, Graz, Austria.
PMID
13
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Ipsilateral thalamic MRI abnormality in an epilepsy patient.
AU
Nagasaka T, Shindo K, Hiraide M, Sugimoto T, Shiozawa Z
SO
Neurology. 2002;58(4):641.
 
In a 19-year-old patient with status epilepticus arising in the right parietal neocortex, unenhanced ictal MRI showed abnormalities mainly in the right cerebral cortex, contralateral cerebellum, and ipsilateral thalamus. The thalamus is considered a key site of functional abnormality in this patient.
AD
Department of Neurology, Yamanashi Medical University, Japan. nagat@res.yamanashi-med.ac.jp
PMID
14
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Structural consequences of status epilepticus demonstrated with serial magnetic resonance imaging.
AU
Meierkord H, Wieshmann U, Niehaus L, Lehmann R
SO
Acta Neurol Scand. 1997;96(3):127.
 
OBJECTIVES: To investigate MRI changes during tonic-clonic and focal motor status epilepticus.
MATERIAL AND METHODS: Serial MRI-investigations with saggital, coronal and axial spin-echo (SE) T1-weighted 500/15 (repetition time [TR]msec/echo time [TE]msec) with and without application of gadolinium-DTPA, proton-density-SE 2100/30 and SE T2-weighted 2100/90 images. Correlation with seizure frequency and general clinical state and by using constant EEG recordings as well as video-EEG monitoring.
RESULTS: Initially, images were normal but several days after onset of status epilepticus focal hyperintensive signal changes on T2-weighted images consistent with focal oedema were seen. The oedema produced a local mass effect as demonstrated with angiography. These changes occurred at a time when there were massive epileptic discharges registered by EEG monitoring in both cases. On subsequent images the oedema resolved but atrophy in combination with a high signal on T2-weighted images suggestive of gliosis were noted in identical regions. In the 1st case it could not completely be ruled out that the signal changes were caused by an encephalitis.However, the signal changes occurred in close time correlation with the epileptic seizure activity rendering the assumption less likely that the signal changes were caused by the encephalitis. In the 2nd case the signal changes could not be attributed to cortical dysplasia or any other condition than the epileptic activity itself.
CONCLUSION: Prolonged epileptic seizure activity may cause neuronal damage associated with a typical pattern of MRI signal changes.
AD
Universitätsklinikum Charité, Humboldt-Universität Berlin, Germany.
PMID
15
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Reversible MRI abnormalities following seizures.
AU
Yaffe K, Ferriero D, Barkovich AJ, Rowley H
SO
Neurology. 1995;45(1):104.
 
We describe eight patients with reversible MRI changes following seizures. The patients were mostly young with a serious underlying medical problem; MRI abnormalities were localized primarily in the posterior vascular boundary zones. A likely mechanism for these lesions is edema secondary to disruption in the blood-brain barrier. Recognition of the transient radiologic changes may aid in the diagnostic and therapeutic management of seizures.
AD
Department of Psychiatry, University of California, San Francisco 94143.
PMID
16
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Diffusion-weighted and perfusion MRI demonstrates parenchymal changes in complex partial status epilepticus.
AU
Szabo K, Poepel A, Pohlmann-Eden B, Hirsch J, Back T, Sedlaczek O, Hennerici M, Gass A
SO
Brain. 2005;128(Pt 6):1369.
 
Diffusion-weighted MRI (DWI) and perfusion MRI (PI) have been mainly applied in acute stroke, but may provide information in the peri-ictal phase in epilepsy patients. Both transient reductions of brain water diffusion, namely a low apparent diffusion coefficient (ADC), and signs of hyperperfusion have been reported in experimental and human epilepsy case studies. We studied 10 patients with complex partial status epilepticus (CPSE) with serial MRI including DWI and PI. All patients showed regional hyperintensity on DWI, and a reduction of the ADC in (i) the hippocampal formation and the pulvinar region of the thalamus (six out of 10 patients), (ii) the pulvinar and cortical regions (two out of 10), (iii) the hippocampal formation only (one out of 10), and (iv) the hippocampal formation, the pulvinar and the cortex (one out of 10). In all patients a close spatial correlation of focal hyperperfusion with areas of ADC/DWI change was present. In two patients hyperperfusion was confirmed in additional SPECT (single photon emission computed tomography) studies. All patients received follow-up MRI examinations showing partial or complete resolution of diffusion and perfusion abnormalities depending on the length of the follow-up interval. The clinical course, EEG and SPECT results all indicate that MRI detected changes related to prolonged epileptic activity. Combined PI and DWI can visualize haemodynamic and tissue changes after CPSE in the hippocampus, thalamus and affected cortical regions.
AD
Department of Neurology, Universitätsklinikum Mannheim, University of Heidelberg, Mannheim, Germany.
PMID
17
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Transient MR signal changes in patients with generalized tonicoclonic seizure or status epilepticus: periictal diffusion-weighted imaging.
AU
Kim JA, Chung JI, Yoon PH, Kim DI, Chung TS, Kim EJ, Jeong EK
SO
AJNR Am J Neuroradiol. 2001;22(6):1149.
 
BACKGROUND AND PURPOSE: Our purpose was to investigate transient MR signal changes on periictal MR images of patients with generalized tonicoclonic seizure or status epilepticus and to evaluate the clinical significance of these findings for differential diagnosis and understanding of the pathophysiology of seizure-induced brain changes.
METHODS: Eight patients with MR images that were obtained within 3 days after the onset of generalized tonicoclonic seizure or status epilepticus and that showed seizure-related MR signal changes had their records retrospectively reviewed. T1- and T2-weighted images were obtained of all eight patients. Additional diffusion-weighted images were obtained of five patients during initial examination. After adequate control of the seizure was achieved, follow-up MR imaging was performed. We evaluated the signal changes, location of the lesions, and degree of contrast enhancement on T1- and T2-weighted images and the signal change and apparent diffusion coefficient (ADC) on diffusion-weighted images. We also compared the signal changes of the initial MR images to those of the follow-up MR images.
RESULTS: The initial MR images revealed focally increased T2 signal intensity, swelling, and increased volume of the involved cortical gyrus in all eight patients. The lesions were located in the cortical gray matter or subcortical white matter in seven patients and at the right hippocampus in one. T1-weighted images showed decreased signal intensity at exactly the same location (n = 6) and gyral contrast enhancement (n = 4). Diffusion-weighted images revealed increased signal intensity at the same location and focally reduced ADC. The ADC values were reduced by 6% to 28% compared with either the normal structure opposite the lesion or normal control. Follow-up MR imaging revealed the complete resolution of the abnormal T2 signal change and swelling in five patients, whereas resolution of the swelling with residual increased T2 signal intensity at the ipsilateral hippocampus was observed in the other two patients. For one of the two patients, hippocampal sclerosis was diagnosed. For the remaining one patient, newly developed increased T2 signal intensity was shown.
CONCLUSION: The MR signal changes that occur after generalized tonicoclonic seizure or status epilepticus are transient increase of signal intensity and swelling at the cortical gray matter, subcortical white matter, or hippocampus on periictal T2-weighted and diffusion-weighted images. These findings reflect transient cytotoxic and vasogenic edema induced by seizure. The reversibility and typical location of lesions can help exclude the epileptogenic structural lesions.
AD
Department of Diagnostic Radiology, the Research Institute of Radiological Science, Yonsei University College of Medicine, Seoul, South Korea.
PMID
18
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MRI findings in aphasic status epilepticus.
AU
Toledo M, Munuera J, Sueiras M, Rovira R, Alvarez-Sabín J, Rovira A
SO
Epilepsia. 2008;49(8):1465.
 
Ictal-MRI studies including diffusion-weighted imaging (DWI), perfusion-weighted imaging (PWI), and MR-angiography (MRA) in patients with aphasic status epilepticus (ASE) are lacking. In this report, we aim to describe the consequences of the ASE on DWIs and its impact on cerebral circulation. We retrospectively studied eight patients with ASE confirmed by ictal-EEG, who underwent ictal-MRI shortly after well-documented onset (mean time delay 3 h). ASE consisted in fluctuating aphasia, mostly associated with other subtle contralateral neurological signs such as hemiparesia, hemianopia, or slight clonic jerks. In MRI, six patients showed cortical temporoparietal hyperintensity in DWI and four of them had also ipsilateral pulvinar lesions. Five patients showed close spatial hyperperfusion areas matching the DWI lesions and an enhanced blow flow in the middle cerebral artery. Parenchymal lesions and hemodynamic abnormalities were not associated with seizure duration or severity in any case. The resolution of DWI lesions at follow-up MRI depended on the length of the MRIs interval. In patients with ASE, lesions on DWI in the temporo-parietal cortex and pulvinar nucleus combined with local hyperperfusion can be observed, even when they appear distant from the epileptic focus or the language areas.
AD
Neurology Department, Institute Diagnostic per la Imatge, Hospital Universitari Vall d'Hebron, Barcelona, Spain. mtoledo75@hotmail.com
PMID
19
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Diffusion changes in status epilepticus.
AU
Wieshmann UC, Symms MR, Shorvon SD
SO
Lancet. 1997;350(9076):493.
 
AD
PMID
20
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A case of hippocampal laminar necrosis following complex partial status epilepticus.
AU
Heinrich A, Runge U, Kirsch M, Khaw AV
SO
Acta Neurol Scand. 2007;115(6):425.
 
Cortical laminar necrosis (CLN) is a metabolic injury pattern usually observed after cerebral hypoxia, hypoglycemia, or ischemia. We report serial magnetic resonance imaging findings in a patient with complex partial status epilepticus (SE) developing a band-like, T1-hyperintense lesion consistent with CLN along the surface of the left hippocampus without concurrent other causes of CLN. This observation suggests a direct pathogenetic link between SE and CLN involving combined damage to neurons and glia.
AD
Department of Neurology, University of Greifswald, Greifswald, Germany. alexander.heinrich@bkh-guenzburg.de
PMID
21
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New-onset refractory status epilepticus with restricted DWI and neuronophagia in the pulvinar.
AU
Boyd JG, Taylor S, Rossiter JP, Islam O, Spiller A, Brunet DG
SO
Neurology. 2010;74(12):1003.
 
AD
Division of Neurology, Department of Medicine, Queen's University, Kingston General Hospital, Kingston, ON, K7L 2V7, Canada. 2jgb1@queensu.ca
PMID