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Figure.
Clinical and imaging review of 6 patients. MRI indicates magnetic resonance imaging; FLAIR, fluid-attenuated inversion recovery; DWI, diffusion-weighted imaging; LP, lumbar puncture; ADC, apparent diffusion coefficient; and D50, dextrose (25 g) in 50 mL of buffered water.

Clinical and imaging review of 6 patients. MRI indicates magnetic resonance imaging; FLAIR, fluid-attenuated inversion recovery; DWI, diffusion-weighted imaging; LP, lumbar puncture; ADC, apparent diffusion coefficient; and D50, dextrose (25 g) in 50 mL of buffered water.

Table 1. 
Causes Associated With Splenium Damage
Causes Associated With Splenium Damage
Table 2. 
Findings Associated With Magnetic Resonance Imaging–Defined Splenium Changes
Findings Associated With Magnetic Resonance Imaging–Defined Splenium Changes
1.
Kawamura  MShiota  JYagishita  THirayama  K Marchiafava-Bignami disease: computed tomographic scan and magnetic resonance imaging. Ann Neurol 1985;18103- 104
PubMedArticle
2.
Delangre  THannequin  DClavier  E  et al.  Marchiafava-Bignami disease with favorable development [in French]. Rev Neurol 1986;142933- 936
PubMed
3.
Inagaki  TSaito  K A case of Marchiafava-Bignami disease demonstrated by MR diffusion-weighted image [in Japanese]. No To Shinkei 2000;52633- 637
PubMed
4.
Gass  ABirtsch  GOlster  MSchwartz  AHennerici  MG Marchiafava-Bignami disease: reversibility of neuroimaging abnormality. J Comput Assist Tomogr 1998;22503- 504
PubMedArticle
5.
Ruiz-Martinez  JMartinez Perez-Balsa  ARuibal  M  et al.  Marchiafava-Bignami disease with widespread extracallosal lesions and favourable course. Neuroradiology 1999;4140- 43
PubMedArticle
6.
Chang  KHCha  SHHan  MH  et al.  Marchiafava-Bignami disease: serial changes in corpus callosum on MRI. Neuroradiology 1992;34480- 482
PubMedArticle
7.
Gambini  AFalini  AMoiola  L  et al.  Marchiafava-Bignami disease: longitudinal MR imaging and MR spectroscopy study. AJNR Am J Neuroradiol 2003;24249- 253
PubMed
8.
Hayashi  TTanohata  KKunimoto  MInoue  K Marchiafava-Bignami disease with resolving symmetrical putaminal lesion. J Neurol 2002;249227- 228
PubMedArticle
9.
Celik  YKaya  MSengun  SUtku  U Marchiafava-Bignami disease: cranial MRI and SPECT findings. Clin Neurol Neurosurg 2002;104339- 341
PubMedArticle
10.
Helenius  JTatlisumak  TSoinne  LValanne  LKaste  M Marchiafava-Bignami disease: two cases with favourable outcome. Eur J Neurol 2001;8269- 272Article
11.
Yamamoto  TAshikaga  RAraki  YNishimura  Y A case of Marchiafava-Bignami disease: MRI findings on spin-echo and fluid attenuated inversion recovery (FLAIR) images. Eur J Radiol 2000;34141- 143
PubMedArticle
12.
Baron  RHeuser  KMarioth  G Marchiafava-Bignami disease with recovery diagnosed by CT and MRI: demyelination affects several CNS structures. J Neurol 1989;236364- 366
PubMedArticle
13.
Caparros-Lefebvre  DPruvo  JPJosien  E  et al.  Marchiafava-Bignami disease: use of contrast media in CT and MRI. Neuroradiology 1994;36509- 511
PubMedArticle
14.
Pasutharnchat  NPhanthumchinda  K Marchiafava-Bignami disease: a case report. J Med Assoc Thai 2002;85742- 746
PubMed
15.
Takayama  HKobayashi  MSugishita  MMihara  B Diffusion-weighted imaging demonstrates transient cytotoxic edema involving the corpus callosum in a patient with diffuse brain injury. Clin Neurol Neurosurg 2000;102135- 139
PubMedArticle
16.
Mendelsohn  DBLevin  HSHarward  HBruce  D Corpus callosum lesions after closed head injury in children: MRI, clinical features and outcome. Neuroradiology 1992;34384- 388
PubMedArticle
17.
Kato  ZKozawa  RHashimoto  KKondo  N Transient lesion in the splenium of the corpus callosum in acute cerebellitis. J Child Neurol 2003;18291- 292
PubMedArticle
18.
Cordoliani  YSSarrazin  JLFelten  D  et al.  MR of cerebral malaria. AJNR Am J Neuroradiol 1998;19871- 874
PubMed
19.
Kobata  RTsukahara  HNakai  A  et al.  Transient MR signal changes in the splenium of the corpus callosum in rotavirus encephalopathy. J Comput Assist Tomogr 2002;26825- 828
PubMedArticle
20.
Mito  YYoshida  KKikuchi  S Measles encephalitis with peculiar MRI findings: a report of two adult cases. Neurol Med 2002;56251- 256
21.
Kobuchi  NTsukahara  HKawamura  Y  et al.  Reversible diffusion-weighted MR findings of Salmonella enteritidis-associated encephalopathy. Eur Neurol 2003;49182- 184Article
22.
Ogura  HTakaoka  MKishi  M  et al.  Reversible MR findings of hemolytic uremic syndrome with mild encephalopathy. AJNR Am J Neuroradiol 1998;191144- 1145
PubMed
23.
Signorini  ELucchi  SMastrangelo  M  et al.  Central nervous system involvement in a child with hemolytic uremic syndrome. Pediatr Nephrol 2000;14990- 992
PubMedArticle
24.
Kieburtz  KDKetonen  LZettelmaier  AE  et al.  Magnetic resonance imaging findings in HIV cognitive impairment. Arch Neurol 1990;47643- 645
PubMedArticle
25.
Ochi  HYamashita  Y A case of adult type adrenoleukodystrophy with an acute onset and repeated episodes of ataxic dysarthria [in Japanese]. Rinsho Shinkeigaku 1996;361229- 1233
26.
Oster  JDoherty  CGrant  PE  et al.  Diffusion-weighted imaging abnormalities in the splenium after seizures. Epilepsia 2003;44852- 854
PubMedArticle
27.
Mirsattari  SMLee  DHJones  MWBlume  WT Transient lesion in the splenium of the corpus callosum in an epileptic patient. Neurology 2003;601838- 1841
PubMedArticle
28.
Wong  SHTurner  NBirchall  D  et al.  Reversible abnormalities of DWI in high-altitude cerebral edema. Neurology 2004;62335- 336
PubMedArticle
29.
Kim  SSChang  KHKim  ST  et al.  Focal lesion in the splenium of the corpus callosum in epileptic patients. AJNR Am J Neuroradiol 1999;20125- 129
PubMed
30.
Cohen-Gadol  AABritton  JWJack  CR  JrFriedman  JAMarsh  WR Transient postictal magnetic resonance imaging abnormality of the corpus callosum in a patient with epilepsy. J Neurosurg 2002;97714- 717
PubMedArticle
31.
Polster  THoppe  MEbner  A Transient lesion in the splenium of the corpus callosum: three further cases. J Neurol Neurosurg Psychiatry 2001;70459- 463
PubMedArticle
32.
Gimeno  MJLasierra  RPina  JI Marchiafava Bignami disease: four case reports. Rev Neurol 2002;35596- 598
PubMed
33.
Hackett  PHYarnell  PRHill  R  et al.  High-altitude cerebral edema evaluated with magnetic resonance imaging: clinical correlation and pathophysiology. JAMA 1998;2801920- 1925
PubMedArticle
34.
Johnson  MMaciunas  RDutt  P  et al.  Granulomatous angiitis masquerading as a mass lesion: magnetic resonance imaging and stereotactic biopsy findings in a patient with occult Hodgkin's disease. Surg Neurol 1989;3149- 53
PubMedArticle
35.
Pekala  JSMamourian  ACWishart  HA  et al.  Focal lesion in the splenium of the corpus callosum on FLAIR MR images: a common finding with aging and after brain radiation therapy. AJNR Am J Neuroradiol 2003;24855- 861
PubMed
36.
Tha  KKTerae  SSugiura  M  et al.  Diffusion-weighted magnetic resonance imaging in early stage of 5-fluorouracil-induced leukoencephalopathy. Acta Neurol Scand 2002;106379- 386Article
37.
Miyake  KKamimura  TGondo  HOkamura  TNiho  Y Tacrolimus administration to a patient with cyclosporine-induced encephalopathy after allogeneic bone marrow transplantation [in Japanese]. Rinsho Ketsueki 2000;41585- 590
PubMed
38.
Epstein  MAZimmerman  RARorke  LBSladky  JT Late-onset globoid cell leukodystrophy mimicking an infiltrating glioma. Pediatr Radiol 1991;21131- 132
PubMedArticle
39.
Suwanwela  NCLeelacheavasit  N Isolated corpus callosal infarction secondary to pericallosal artery disease presenting as alien hand syndrome. J Neurol Neurosurg Psychiatry 2002;72533- 536
PubMed
40.
Kollar  JPeter  MFulesdi  BSikula  J Is every sharply defined, symmetrical, necrotic-demyelinating lesion in the corpus callosum an actual manifestation of Marchiafava-Bignami disease? Eur J Radiol 2001;39151- 154
PubMedArticle
41.
Ito  TSakai  TInagawa  SUtsu  MBun  T MR angiography of cerebral vasospasm in preeclampsia. AJNR Am J Neuroradiol 1995;161344- 1346
PubMed
42.
Marchiafava  BBignami  A Sopra una alterazione del corpo calloso osservata in suggetti alcoolistis. Riv Pat Med 1903;8544- 599
43.
Grant  PEHe  JHalpern  EF  et al.  Frequency and clinical context of decreased apparent diffusion coefficient reversal in the human brain. Radiology 2001;22143- 50
PubMedArticle
44.
Schaefer  PWGrant  PEGonzalez  RG Diffusion-weighted MR imaging of the brain. Radiology 2000;217331- 345
PubMedArticle
45.
Whittall  KPMacKay  ALGraeb  DA  et al.  In vivo measurement of T2 distributions and water contents in normal human brain. Magn Reson Med 1997;3734- 43
PubMedArticle
46.
Rosenthal  RBigelow  LB Quantitative brain measurements in chronic schizophrenia. Br J Psychiatry 1972;121259- 264
PubMedArticle
47.
Casanova  MFZito  MBigelow  LB  et al.  Axonal counts of the corpus callosum of schizophrenic patients. J Neuropsychiatry Clin Neurosci 1989;1391- 393
PubMed
48.
Nasrallah  HAMcCalley-Whitters  MBigelow  LB  et al.  A histological study of the corpus callosum in chronic schizophrenia. Psychiatry Res 1983;8251- 260
PubMedArticle
49.
Keshavan  MSDiwadkar  VAHarenski  KRosenberg  DRSweeney  JAPettegrew  JW Abnormalities of the corpus callosum in first episode, treatment naive schizophrenia. J Neurol Neurosurg Psychiatry 2002;72757- 760Article
50.
Motomura  NSatani  SInaba  M Monozygotic twin cases of the agenesis of the corpus callosum with schizophrenic disorder. Psychiatry Clin Neurosci 2002;56199- 202
PubMedArticle
Original Contribution
March 2005

Clinical Implications of Splenium Magnetic Resonance Imaging Signal Changes

Author Affiliations

Author Affiliations: Departments of Neurology (Drs Doherty, Jayadev, and Watson) and Radiology (Drs Konchada and Hallam), The University of Washington, and the Swedish Epilepsy Center (Dr Doherty), Seattle.

Arch Neurol. 2005;62(3):433-437. doi:10.1001/archneur.62.3.433
Abstract

Background  Magnetic resonance imaging (MRI) may show discrete splenium abnormalities; however, the implications of this radiologic finding are unclear.

Objective  To describe causes, clinical presentations, and prognoses of midline splenium changes evident on MRI.

Design  Retrospective case series.

Setting  Teaching hospital.

Patients  Medical records of 9 patients with MRI-noted splenium changes were studied; 60 additional published cases were accessed.

Interventions  Sixty-nine cases were reviewed.

Main Outcome Measures  Clinical and imaging findings, causes, and prognosis.

Results  Confusion (35 patients), ataxia (25 patients), and recent seizure (23 patients) were common. Causes included alcohol use, infections, hypoglycemia, trauma, salt abnormalities, and seizure. Twenty-eight patients had complete resolution, 23 improved, and 1 died. Diffusion-weighted imaging showed splenium abnormalities the best. Eleven of 12 patients showed decrease in apparent diffusion coefficient. Most improved clinically, as did their subsequent MRI studies.

Conclusions  Midline splenium changes are commonly seen on MRI diffusion-weighted imaging sequences. Multiple causes can result in splenium changes. Physicians should evaluate for glucose and electrolyte abnormalities, seizure risk, ongoing infectious or parainfectious process, and traumatic causes.

Magnetic resonance imaging (MRI) studies suggest splenium injury is common, reversible, and associated with multiple origins and presentations (Table 1); however, the implications of this radiologic finding are unclear. In this series of MRI-evident splenium injuries, causes are recorded with clinical findings and outcomes. We evaluate records of patients with midline splenium changes incidentally noted on brain MRI to determine if they share a characteristic presentation or common cause. The results are discussed and evaluation strategies proposed.

METHODS

This retrospective case series study was performed in a teaching hospital. Using MEDLINE keywords splenium and MRI, we accessed and reviewed published cases of splenium changes. Studies in which radiologic changes were markedly asymmetric and extended beyond the splenium, as seen with vascular infarction or malignancy, were not studied. Symmetric, bilateral involvement was not excluded. Clinical findings and outcomes were collected. No statistical hypothesis testing occurred.

RESULTS

Medical records of 9 patients along with 60 published cases with MRI splenium changes were studied. Of 69 patients evaluated, 52 had clinical outcomes recorded: 28 had complete resolution, 23 improved, and 1 died. Causes are given in Table 1. The vignettes and imaging of unique patients evaluated by the authors appear in the Figure. Clinical findings of 58 patients are given in Table 2. The most consistent splenium changes evident from MRI were reduced T1 signal intensities, increased T2 and fluid-attenuated inversion recovery signals, and, if performed, increased diffusion-weighted imaging (DWI) (Figure). Splenium abnormalities were easiest to see with DWI in 8 of 9 original cases. Seven of our 9 patients had DWI changes in posterior limbs of the internal capsules. No splenium abnormalities were evident in computed tomograms of the 9 patients reviewed from our institution. Of those same patients, 3 had elevations of creatine kinase levels, necessitating directed treatment and surveillance.

The DWI was reported with apparent diffusion coefficient (ADC) values in 12 patients; all but 1 was reduced.3,15,19,21,2628 Of those with reductions, 8 of 11 had complete clinical recovery. In 16 of 18 patients, splenium abnormalities resolved on follow-up MRI. The DWI changes and ADC values related to convulsions showed no residual MRI or clinical abnormalities. The patient with increased ADC values had complete resolution of MRI and clinical findings.28

COMMENT

The MRI-documented splenium changes may be associated with confusion, ataxia, seizure, hemispheric disconnection findings, and dysarthria. The most common clinical finding was altered mental status. The triad of tremor, dementia, and death as described in patients with Marchiafava-Bignami disease was not seen.42 Diagnoses associated with splenium abnormalities varied markedly (Table 1). More important, DWI often showed other areas of involvement, particularly the posterior limbs of the internal capsules. The DWI demonstrated splenium changes markedly better than other MRI sequences or computed tomograms.

Reporting bias limits the usefulness of the study. Descriptions of patient symptoms, particularly of hemispheric disconnection or psychiatric findings, were sparse. In a literature-based case series, reported causes or clinical findings may not parallel what is most common. Follow-up MRI was rare, and few reports documented ADC values.

POSSIBLE INJURY MECHANISMS

The DWI signal changes suggest restricted movement of free water. The ADC values help clarify this restriction: reduced ADC values, as seen in 11 patients, suggest cytotoxic edema; ADC value increases (1 patient) suggest vasogenic edema.28,43,44 Patients with increased and decreased splenium ADC values may normalize with additional imaging, perhaps implying an absence of cytotoxic edema. Both ADC reduction and subsequent reversal are uncommon; associated diagnoses include hemiplegic migraine, venous sinus occlusion, and seizure.26,44 Splenium injuries should be added to this list.

In healthy patients who underwent MRI T2 relaxation studies, the splenium and posterior limb of the internal capsule displayed heterogeneity in water content; however, comparison tissue myelin water content was higher.45 The splenium may have easily perturbed cellular fluid mechanics when compared with surrounding tissues. Origins associated with splenium injury, including renal failure, hyponatremia, hypernatremia, hypoglycemia, infection, altitude sickness, and thiamine deficiency and alcoholism, can compromise cellular fluid regulation. How generalized convulsions might contribute to splenium DWI and ADC changes is harder to explain.

Convulsions might transiently impair available glucose, leading to brief, reversible failures of cellular fluid regulation. A similar mechanism could explain why hypoglycemic patients develop reversible splenium changes. Alternatively, antiepileptic drug toxicity or level fluctuations combined with changes in salt homeostasis and resultant myelin edema are other suggested mechanisms.2629

Not all MRI findings reversed. Persisting changes included cystic lesions within the splenium, although pathologic correlation was limited.5,6 Magnetic resonance spectroscopy suggests that lactate levels can be abnormal and may resolve over time; in patient 5, however, no spectroscopic changes were seen.7

CONFUSION, MUTISM, AND HALLUCINATIONS: WHAT IS THE ROLE OF THE SPLENIUM?

Thirty-five of the patients had confusion and delirium, and hallucinations occurred in at least 4 patients. Patient 2 is unique, because the presentation included catatonia, increased muscle tone, waxy posturing, and an amobarbital response, features similar to catatonic schizophrenia. Splenium pathologic findings from patients with schizophrenia may show increased fiber thickness and preservation of axonal fiber density.4648 Neuroimaging of new-onset schizophrenia demonstrates differing splenium size and diffusion tensor imaging anisotropy.49 Both agenesis of the corpus callosum and schizophrenia in patients suggest that disrupted interhemispheric communication predisposes to behavioral change and psychosis.50

Mutism, hallucinations, psychosis, and hemispheric disconnection are potentially more specific findings of splenium compromise. Still unclear is if and how the splenium regulates mutism or hallucinations. Perhaps the right and left hemispheres generate independent nonsense, the censure of which is necessary and normal and requires an intact splenium.

IS THERE A SPLENIUM SYNDROME?

From this series, nonspecific common findings, such as ataxia, dysarthria, increased tone, and delirium, do not easily localize. More important, splenium injuries in 7 of 9 patients occurred, with subtle changes evident in the posterior limbs of the internal capsule. Damage to these corticospinal pathways could result in marked dysarthria, ataxia, and increased tone. What surprised us was that findings of hemispheric disconnection were not common, potentially illustrating reporting bias. Prospective, descriptive studies that used DWI inclusion criteria might clarify this concession.

PROPOSED EVALUATION

Splenium changes evident on MRI are not incidental. Although infrequently associated with death, the finding can suggest treatable causes. A detailed history with regard to travel, trauma, medications, seizure activity, or substance abuse is essential. At minimum, understanding prior medical and psychiatric history, serum salt and glucose levels, renal functions, creatine kinase levels, trauma surveys, seizure risk, possible ongoing infectious or parainfectious processes, and blood pressure would be appropriate. Whether thiamine administration helps improve outcomes remains unknown. Further descriptive studies of splenium abnormalities are needed, particularly in the setting of new-onset altered mental status.

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Article Information

Correspondence: Michael J. Doherty, MD, Swedish Epilepsy Center, 801 Broadway, Suite 901, Seattle, WA 98122 (michael.doherty@swedish.org).

Accepted for Publication: May 25, 2004.

Author Contributions:Study concept and design: Doherty. Acquisition of data: Doherty, Jayadev, and Watson. Analysis and interpretation of data: Doherty, Konchada, and Hallam. Drafting of the manuscript: Doherty and Watson. Critical revision of the manuscript for important intellectual content: Doherty, Jayadev, Konchada, and Hallam. Administrative, technical, and material support: Jayadev and Watson. Study supervision: Doherty and Hallam.

References
1.
Kawamura  MShiota  JYagishita  THirayama  K Marchiafava-Bignami disease: computed tomographic scan and magnetic resonance imaging. Ann Neurol 1985;18103- 104
PubMedArticle
2.
Delangre  THannequin  DClavier  E  et al.  Marchiafava-Bignami disease with favorable development [in French]. Rev Neurol 1986;142933- 936
PubMed
3.
Inagaki  TSaito  K A case of Marchiafava-Bignami disease demonstrated by MR diffusion-weighted image [in Japanese]. No To Shinkei 2000;52633- 637
PubMed
4.
Gass  ABirtsch  GOlster  MSchwartz  AHennerici  MG Marchiafava-Bignami disease: reversibility of neuroimaging abnormality. J Comput Assist Tomogr 1998;22503- 504
PubMedArticle
5.
Ruiz-Martinez  JMartinez Perez-Balsa  ARuibal  M  et al.  Marchiafava-Bignami disease with widespread extracallosal lesions and favourable course. Neuroradiology 1999;4140- 43
PubMedArticle
6.
Chang  KHCha  SHHan  MH  et al.  Marchiafava-Bignami disease: serial changes in corpus callosum on MRI. Neuroradiology 1992;34480- 482
PubMedArticle
7.
Gambini  AFalini  AMoiola  L  et al.  Marchiafava-Bignami disease: longitudinal MR imaging and MR spectroscopy study. AJNR Am J Neuroradiol 2003;24249- 253
PubMed
8.
Hayashi  TTanohata  KKunimoto  MInoue  K Marchiafava-Bignami disease with resolving symmetrical putaminal lesion. J Neurol 2002;249227- 228
PubMedArticle
9.
Celik  YKaya  MSengun  SUtku  U Marchiafava-Bignami disease: cranial MRI and SPECT findings. Clin Neurol Neurosurg 2002;104339- 341
PubMedArticle
10.
Helenius  JTatlisumak  TSoinne  LValanne  LKaste  M Marchiafava-Bignami disease: two cases with favourable outcome. Eur J Neurol 2001;8269- 272Article
11.
Yamamoto  TAshikaga  RAraki  YNishimura  Y A case of Marchiafava-Bignami disease: MRI findings on spin-echo and fluid attenuated inversion recovery (FLAIR) images. Eur J Radiol 2000;34141- 143
PubMedArticle
12.
Baron  RHeuser  KMarioth  G Marchiafava-Bignami disease with recovery diagnosed by CT and MRI: demyelination affects several CNS structures. J Neurol 1989;236364- 366
PubMedArticle
13.
Caparros-Lefebvre  DPruvo  JPJosien  E  et al.  Marchiafava-Bignami disease: use of contrast media in CT and MRI. Neuroradiology 1994;36509- 511
PubMedArticle
14.
Pasutharnchat  NPhanthumchinda  K Marchiafava-Bignami disease: a case report. J Med Assoc Thai 2002;85742- 746
PubMed
15.
Takayama  HKobayashi  MSugishita  MMihara  B Diffusion-weighted imaging demonstrates transient cytotoxic edema involving the corpus callosum in a patient with diffuse brain injury. Clin Neurol Neurosurg 2000;102135- 139
PubMedArticle
16.
Mendelsohn  DBLevin  HSHarward  HBruce  D Corpus callosum lesions after closed head injury in children: MRI, clinical features and outcome. Neuroradiology 1992;34384- 388
PubMedArticle
17.
Kato  ZKozawa  RHashimoto  KKondo  N Transient lesion in the splenium of the corpus callosum in acute cerebellitis. J Child Neurol 2003;18291- 292
PubMedArticle
18.
Cordoliani  YSSarrazin  JLFelten  D  et al.  MR of cerebral malaria. AJNR Am J Neuroradiol 1998;19871- 874
PubMed
19.
Kobata  RTsukahara  HNakai  A  et al.  Transient MR signal changes in the splenium of the corpus callosum in rotavirus encephalopathy. J Comput Assist Tomogr 2002;26825- 828
PubMedArticle
20.
Mito  YYoshida  KKikuchi  S Measles encephalitis with peculiar MRI findings: a report of two adult cases. Neurol Med 2002;56251- 256
21.
Kobuchi  NTsukahara  HKawamura  Y  et al.  Reversible diffusion-weighted MR findings of Salmonella enteritidis-associated encephalopathy. Eur Neurol 2003;49182- 184Article
22.
Ogura  HTakaoka  MKishi  M  et al.  Reversible MR findings of hemolytic uremic syndrome with mild encephalopathy. AJNR Am J Neuroradiol 1998;191144- 1145
PubMed
23.
Signorini  ELucchi  SMastrangelo  M  et al.  Central nervous system involvement in a child with hemolytic uremic syndrome. Pediatr Nephrol 2000;14990- 992
PubMedArticle
24.
Kieburtz  KDKetonen  LZettelmaier  AE  et al.  Magnetic resonance imaging findings in HIV cognitive impairment. Arch Neurol 1990;47643- 645
PubMedArticle
25.
Ochi  HYamashita  Y A case of adult type adrenoleukodystrophy with an acute onset and repeated episodes of ataxic dysarthria [in Japanese]. Rinsho Shinkeigaku 1996;361229- 1233
26.
Oster  JDoherty  CGrant  PE  et al.  Diffusion-weighted imaging abnormalities in the splenium after seizures. Epilepsia 2003;44852- 854
PubMedArticle
27.
Mirsattari  SMLee  DHJones  MWBlume  WT Transient lesion in the splenium of the corpus callosum in an epileptic patient. Neurology 2003;601838- 1841
PubMedArticle
28.
Wong  SHTurner  NBirchall  D  et al.  Reversible abnormalities of DWI in high-altitude cerebral edema. Neurology 2004;62335- 336
PubMedArticle
29.
Kim  SSChang  KHKim  ST  et al.  Focal lesion in the splenium of the corpus callosum in epileptic patients. AJNR Am J Neuroradiol 1999;20125- 129
PubMed
30.
Cohen-Gadol  AABritton  JWJack  CR  JrFriedman  JAMarsh  WR Transient postictal magnetic resonance imaging abnormality of the corpus callosum in a patient with epilepsy. J Neurosurg 2002;97714- 717
PubMedArticle
31.
Polster  THoppe  MEbner  A Transient lesion in the splenium of the corpus callosum: three further cases. J Neurol Neurosurg Psychiatry 2001;70459- 463
PubMedArticle
32.
Gimeno  MJLasierra  RPina  JI Marchiafava Bignami disease: four case reports. Rev Neurol 2002;35596- 598
PubMed
33.
Hackett  PHYarnell  PRHill  R  et al.  High-altitude cerebral edema evaluated with magnetic resonance imaging: clinical correlation and pathophysiology. JAMA 1998;2801920- 1925
PubMedArticle
34.
Johnson  MMaciunas  RDutt  P  et al.  Granulomatous angiitis masquerading as a mass lesion: magnetic resonance imaging and stereotactic biopsy findings in a patient with occult Hodgkin's disease. Surg Neurol 1989;3149- 53
PubMedArticle
35.
Pekala  JSMamourian  ACWishart  HA  et al.  Focal lesion in the splenium of the corpus callosum on FLAIR MR images: a common finding with aging and after brain radiation therapy. AJNR Am J Neuroradiol 2003;24855- 861
PubMed
36.
Tha  KKTerae  SSugiura  M  et al.  Diffusion-weighted magnetic resonance imaging in early stage of 5-fluorouracil-induced leukoencephalopathy. Acta Neurol Scand 2002;106379- 386Article
37.
Miyake  KKamimura  TGondo  HOkamura  TNiho  Y Tacrolimus administration to a patient with cyclosporine-induced encephalopathy after allogeneic bone marrow transplantation [in Japanese]. Rinsho Ketsueki 2000;41585- 590
PubMed
38.
Epstein  MAZimmerman  RARorke  LBSladky  JT Late-onset globoid cell leukodystrophy mimicking an infiltrating glioma. Pediatr Radiol 1991;21131- 132
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