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Original Contribution |

Clinical Spectrum of Reversible Posterior Leukoencephalopathy Syndrome FREE

Vivien H. Lee, MD; Eelco F. M. Wijdicks, MD; Edward M. Manno, MD; Alejandro A. Rabinstein, MD
[+] Author Affiliations

Author Affiliations: Section of Cerebrovascular Disease and Neurological Critical Care, Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois (Dr Lee); and Division of Critical Care Neurology, Department of Neurology, Mayo Clinic College of Medicine, Rochester, Minnesota (Drs Wijdicks, Manno, and Rabinstein).


Arch Neurol. 2008;65(2):205-210. doi:10.1001/archneurol.2007.46.
Text Size: A A A
Published online

Background  Reversible posterior leukoencephalopathy syndrome (RPLS) is characterized by neuroimaging findings of reversible vasogenic subcortical edema without infarction. The clinical syndrome of RPLS typically involves headache, encephalopathy, visual symptoms, and seizures.

Objective  To retrospectively identify patients with RPLS with a characteristic clinical presentation and neuroimaging abnormalities and documented improvement on repeated neuroimaging.

Design  Retrospective.

Setting  Mayo Clinic.

Patients  Thirty-six patients with RPLS.

Main Outcome Measures  Associated comorbid medical conditions, presenting clinical symptoms, duration of clinical symptoms, diagnostic test results (magnetic resonance imaging, electroencephalography, and lumbar puncture), and time to clinical and neuroimaging recovery.

Results  We identified 38 episodes of RPLS in 36 patients (20 females and 16 males) with a mean age of 44.7 years. Comorbid conditions included hypertension (53%), renal disease (45%), dialysis dependency (21%), malignancy (32%), and transplantation (24%). Presenting symptoms included clinical seizures (87%), encephalopathy (92%), visual symptoms (39%), and headache (53%). Mean peak systolic blood pressure at presentation was 187 mm Hg. Clinical symptoms resolved after a mean of 5.3 days. Atypical neuroimaging features included significant frontal involvement in 22 episodes (58%), gray matter lesions in 16 (42%), unilateral lesions in 2 (5%), hemorrhage in 2 (5%), recurrent RPLS in 2 (5%), confluent lesions in 2 (5%), and foci of permanent injury in 10 (26%). Twenty-two episodes (58%) had brainstem/cerebellar involvement on neuroimaging.

Conclusions  This is the largest clinical series to date of RPLS with confirmed neuroimaging improvement. Clinical recovery occurred in most patients within days. The condition was rarely isolated to the parieto-occipital white matter, and atypical neuroimaging features were frequent.

Figures in this Article

Reversible posterior leukoencephalopathy syndrome (RPLS), also referred to as posterior reversible encephalopathy syndrome, is characterized by neuroimaging findings of reversible vasogenic subcortical edema without infarction. Clinical presentation typically involves global encephalopathy, seizures, headache, or visual symptoms.1 This clinicoradiographic syndrome can be triggered by eclampsia,2 hypertensive emergency,3 or exposure to immunosuppression (most notably the calcineurin inhibitors).47 The clinical presentation of RPLS is often nonspecific, and therefore the diagnosis of RPLS has come to increasingly rely on magnetic resonance imaging (MRI).

With Mayo Clinic institutional review board approval, we retrospectively identified patients with RPLS clinically diagnosed at the Mayo Clinic between January 1, 1999, and December 31, 2006. We used a text-retrieval system (the Mayo Clinic Life Sciences System) that searches the final diagnosis in electronic clinic notes for coded text. Included patients had a clinical presentation and neuroimaging abnormalities consistent with RPLS with documented recovery clinically and on repeated neuroimaging. We collected data on demographics, predisposing conditions, presenting symptoms, documented blood pressure measurements the day of presentation, time to neuroimaging, time to clinical recovery, and time to repeated imaging. In addition, we gathered the results of laboratory studies, including cerebrospinal fluid analysis and electroencephalography.

All neuroimages (including brain computed tomographs and MRIs) were reviewed by study neurologists (V.H.L. and A.A.R.) for identification of atypical RPLS features, including significant frontal involvement, gray matter/cortical lesions, unilateral lesions, presence of hemorrhage, confluent RPLS lesions, brainstem/cerebellar involvement, corpus callosum lesions, recurrent episodes, and foci of permanent injury on repeated neuroimaging. The second neurologist (A.A.R.) was blinded to the clinical aspects of the cases. Permanent injury was operationally defined as lesions that were still present on brain imaging studies 2 weeks after initial MRI.

DEMOGRAPHICS

We identified 38 episodes of RPLS in 36 patients (20 females and 16 males). Mean age at presentation was 44.7 years (range, 14-78 years) (Table). The RPLS etiologies included hypertension (n = 26; 68%), eclampsia (n = 4; 11%), calcineurin inhibitor use (n = 4; 11%), and other (n = 4; 11%). Comorbid conditions were common in this cohort and included hypertension in 20 (53%), kidney disease in 17 (45%), dialysis dependency in 8 (21%), and transplantation (4 bone marrow and 5 solid organ) in 9 (24%). Four patients (11%) were nonambulatory at baseline, and 6 (16%) were alcoholics. Malignancy was present in 32% of the episodes and included squamous cell cancer (n = 2), metastatic sarcoma (n = 2), multiple myeloma (n = 3), lymphoma (n = 4), and cholangiocarcinoma (n = 1).

Table Graphic Jump LocationTable. Clinical Characteristics of the 38 Episodes of Reversible Posterior Leukoencephalopathy Syndrome
CLINICAL PRESENTATION

Clinical seizures occurred in 33 episodes (87%), of which there was focal onset in 10 (26%) and multiple seizures in 14 (37%). One patient presented with status epilepticus (episode 31). Encephalopathy was a presenting symptom in 35 episodes (92%), visual symptoms in 15 (39%), and headache in 20 (53%). Blood pressure data were available in 36 occurrences within the day before presentation, and the mean peak systolic blood pressure was 187 mm Hg (range, 80-240 mm Hg). The mean duration of hospitalization was 20 days (range, 1-140 days). Intubation was performed in 14 episodes (39%), and these patients remained intubated for a mean of 3.1 days (range, 1-11 days). Clinical recovery occurred within a mean of 5.3 days (range, 0-32 days). Of the 36 patients, 5 died and 3 had no follow-up data available. The remaining 28 patients had follow-up data available for a mean of 1.8 years (range, 19 days to 6.8 years), and none had recurrent seizures.

LABORATORY DATA

Cerebrospinal fluid data were available for 18 patients and demonstrated a mean protein level of 92 mg/dL (0.092 g/dL) (reference range, 10-455 mg/dL) [0.010-0.455 g/dL]; (to convert grams per deciliter to grams per liter, multiply by 10.0) and a mean white blood cell count of 1.6/μL (range, 0-5/μL) (to convert to ×109 per liter, multiply by 0.001). Electroencephalographic data were available in 28 patients and showed focal sharp waves in 3 (8%), slowing in 22 (58%), and normal findings in 3 (8%).

The mean delay from the onset of symptoms to neuroimaging was 3 days (range, 0-17 days; median, 2 days), and MRI was performed in 36 episodes (95%). Gadolinium enhancement was seen in 5 of the 15 patients who received contrast. All the patients had significant improvement on repeated neuroimaging (Figure 1). The repeated neuroimaging technique was MRI in 35 episodes (92%). Repeated neuroimaging occurred with a mean delay of 138 days (range, 4-1321 days). Most MRIs (80%) were repeated within 6 months after presentation. Complete neuroimaging resolution of RPLS occurred in 25 episodes (66%), and the earliest complete resolution documented was at 5 days.

Place holder to copy figure label and caption
Figure 1.

Neuroimaging of 38 discrete episodes of reversible posterior leukoencephalopathy syndrome. The top rows represent the initial neuroimages, and the bottom rows represent the repeated neuroimages.

Graphic Jump Location

Atypical neuroimaging features included significant frontal involvement in 22 episodes (58%), gray matter/cortical lesions in 16 (42%), unilateral lesions in 2 (5%), presence of hemorrhage in 2 (5%), and confluent RPLS in 2 (5%) (Figure 2). Corpus callosum involvement in RPLS occurred in 5 episodes (13%). Brainstem and cerebellar neuroimaging involvement were present in more than half of the patients (58%). Recurrent separate episodes of RPLS occurred in 2 patients (episodes 14 and 15 and episodes 25 and 26) (Figure 3). Permanent injury, typically in the form of small lesions, was seen on repeated MRI in 10 episodes (26%).

Place holder to copy figure label and caption
Figure 2.

Fluid-attenuated inversion recovery magnetic resonance images (FLAIR MRIs) showing reversible posterior leukoencephalopathy syndrome atypical features. A, Significant frontal involvement. B, Unilateral lesion. C, Presence of hemorrhage into lesion. D, Confluent leukoencephalopathy. E, Gray matter/cortical lesions. F, Repeated FLAIR MRIs with persistent abnormality.

Graphic Jump Location
Place holder to copy figure label and caption
Figure 3.

Recurrent reversible posterior leukoencephalopathy syndrome episodes in 2 patients. The top row shows episodes 14 and 15, and the bottom row shows episodes 25 and 26. Note that the splenium of the corpus callosum is involved (bottom row, third panel from left).

Graphic Jump Location

As the name implies, RPLS is classically associated with the features of subcortical vasogenic edema, patchy symmetrical bilateral involvement with preferential involvement of the posterior head regions, and complete clinical and radiographic resolution.1 It is postulated to have a pathogenesis similar to hypertensive encephalopathy,8,9 although correlation with elevated blood pressure has not been demonstrated. Schwartz9 suggested that the vertebrobasilar territory, owing to its relatively sparse sympathetic innervation, may experience preferential disruption of autoregulatory mechanisms, leading to increased perfusion and edema. Lesions of RPLS have been associated with increased perfusion on single-photon emission computed tomography, supporting a vasodilatory mechanism.10,11 Encephalopathy and seizures remain the major presenting symptoms in RPLS and can include status epilepticus, as demonstrated in this series.12Whereas treatment with antiepileptic medications is the standard of care for seizures associated with acute episodes of RPLS, this does not necessitate long-term antiepileptic drug therapy. In this limited series, no patients had recurrence of seizures on follow-up, suggesting that most patients with RPLS, including those who present early with multiple seizures, do not routinely progress to chronic epilepsy.

When an easily identifiable trigger is present (eclampsia, a hypertensive episode, or medication use), RPLS is more readily diagnosed than in patients without obvious precipitants. A common feature in the patients in this series was the presence of comorbid medical conditions in nearly all of the patients, including renal disease, malignancy, alcohol use, pregnancy, inflammatory disease, nonambulatory status, and significant infection. As medical advances escalate the use of chemotherapeutic agents, immunosuppressive medications, and cytotoxic treatments for malignancy, the risk and frequency of RPLS can be expected to increase.

TYPICAL NEUROIMAGING FEATURES

Neuroimaging of RPLS is typically associated with high signal intensity on T2-weighted images predominantly in the posterior regions, which is caused by subcortical white matter vasogenic edema.1,13 Abnormalities are more conspicuous on fluid-attenuated inversion recovery imaging, which increases the ability to detect subtle lesions in RPLS.14 Supplemental diffusion-weighted imaging and apparent diffusion coefficient (ADC) map images are helpful in distinguishing vasogenic edema, the predominant abnormality in RPLS, from cytotoxic edema, which can also occur and may represent foci of irreversible ischemia.1420 Because vasogenic rather than cytotoxic edema is the principal basis for the lesions, regions demonstrating high signal intensity on T2-weighted images correspond to slightly increased or isointense signal intensity on diffusion-weighted images.13,21 In ADC mapping, the hyperintense lesions on T2-weighted images correlate with increased ADC values (appear brighter).13,21 Most RPLS lesions do not enhance on T1-weighted images. Contrast enhancement in the areas of T2 signal abnormality occurs in a few patients and may represent a dynamic feature related to the timing of imaging after the onset of symptoms and severity of lesions.22,23 Gadolinium enhancement in areas of T2 abnormality is inconsistent and typically not a striking finding22 and in this series was seen in only 5 patients. Complete reversibility is generally regarded as a defining feature of RPLS. The ideal timing of repeated brain imaging to document recovery is unclear. In this series, the earliest neuroimaging resolution occurred in 5 days (patient 10). Of interest, 4 patients with improved but incomplete MRI resolution at 3 to 7 days went on to demonstrate complete resolution with further serial imaging weeks to years later (patients 18, 20, 32, and 37). Thus, resolution of RPLS neuroimaging abnormalities probably occurs in the range of several days to weeks.

ATYPICAL NEUROIMAGING FEATURES

Although classic neuroimaging features of RPLS with involvement of the posterior head regions are easily recognized, features that may generally be regarded as atypical were often present in our patients, such as significant anterior involvement, cortical lesions, recurrent RPLS episodes, foci of permanent injury, hemorrhage into lesions, and unilaterality (Figure 1). High signal intensity on T2-weighted image lesions can occur in regions other than the parieto-occipital areas, frequently involving the frontal lobes, basal ganglia, thalami, or brainstem.13 The RPLS lesions typically do not exclude the anterior head regions. Frontal lobe involvement is a common feature seen in most of these patients and is consistent with previous studies.22 Similarly, RPLS lesions do not have to be restricted to the white matter. Cortical lesions or gray matter lesions occurred in 42% of these episodes and have been reported at an even higher frequency in other series.14 Although white matter is predominantly involved, gray matter lesions, anterior lesions, and isolated brainstem involvement are becoming increasingly appreciated.2426

Recurrent episodes of RPLS have been reported in the same patient.27 Recurrent discrete episodes of RPLS occurred in 2 different patients in this series (episodes 14 and 15 and episodes 25 and 26). Hemorrhage is recognized as a potential complication of hypertensive encephalopathy, particularly in patients with clotting abnormalities or coagulopathy,9,11,28 and hemorrhage into the RPLS lesion was demonstrated in 2 patients in the present series.

Although RPLS is typically reversible, lesions can progress to irreversible damage and leukomalacia.16,28 Residual foci of abnormalities on follow-up neuroimaging after 2 weeks are suggestive of small residual infarcts and were found in approximately one-fourth of our patients. It is conceivable that some of these lesions may take longer than 2 weeks to resolve. Use of ADC mapping to distinguish cytotoxic edema (indicating acute infarction) from vasogenic edema can be equivocal with small foci. An alternative consideration is that some of these foci of hyperintense lesions on repeated neuroimaging may represent preexisting ischemic disease. This series shares the intrinsic limitations of all retrospective studies, including lack of uniformity in timing of follow-up imaging. The strength of this study arises from the fact that all the patients had repeated neuroimaging documenting recovery, ensuring the diagnosis of RPLS and excluding mimickers.

Correspondence: Vivien H. Lee, MD, Department of Neurological Sciences, Rush University Medical Center, 1725 W Harrison St, Ste 1121, Chicago, IL 60612 (vivien_lee@rush.edu).

Accepted for Publication: March 19, 2007.

Author Contributions: All authors had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis. Study concept and design: Lee, Wijdicks, and Rabinstein. Analysis and interpretation of data: Lee, Wijdicks, Manno, and Rabinstein. Drafting of the manuscript: Lee and Wijdicks. Critical revision of the manuscript for important intellectual content: Wijdicks, Manno, and Rabinstein. Administrative, technical, and material support: Lee. Study supervision: Wijdicks and Manno.

Financial Disclosure: None reported.

Hinchey  JChaves  CAppignani  B  et al.  A reversible posterior leukoencephalopathy syndrome. N Engl J Med 1996;334 (8) 494- 500
PubMed Link to Article
Schwaighofer  BWHesselink  JRHealy  ME MR demonstration of reversible brain abnormalities in eclampsia. J Comput Assist Tomogr 1989;13 (2) 310- 312
PubMed Link to Article
Hauser  RALacey  DMKnight  MR Hypertensive encephalopathy: magnetic resonance imaging demonstration of reversible cortical and white matter lesions. Arch Neurol 1988;45 (10) 1078- 1083
PubMed Link to Article
Appignani  BABhadelia  RABlacklow  SCWang  AKRoland  SFFreeman  RB Neuroimaging findings in patients on immunosuppressive therapy: experience with tacrolimus toxicity. AJR Am J Roentgenol 1996;166 (3) 683- 688
PubMed Link to Article
Small  SLFukui  MBBramblett  GTEidelman  BH Immunosuppression-induced leukoencephalopathy from tacrolimus (FK506). Ann Neurol 1996;40 (4) 575- 580
PubMed Link to Article
Truwit  CLDenaro  CPLake  JRDeMarco  T MR imaging of reversible cyclosporin A-induced neurotoxicity. AJNR Am J Neuroradiol 1991;12 (4) 651- 659
PubMed
Singh  NBonham  AFukui  M Immunosuppressive-associated leukoencephalopathy in organ transplant recipients. Transplantation 2000;69 (4) 467- 472
PubMed Link to Article
Chester  EMAgamanolis  DPBanker  BQVictor  M Hypertensive encephalopathy: a clinicopathologic study of 20 cases. Neurology 1978;28 (9 Pt 1) 928- 939
PubMed Link to Article
Schwartz  RB A reversible posterior leukoencephalopathy syndrome. N Engl J Med 1996;334 (26) 1743
PubMed Link to Article
Antunes  NLSmall  TNGeorge  DBoulad  FLis  E Posterior leukoencephalopathy syndrome may not be reversible. Pediatr Neurol 1999;20 (3) 241- 243
PubMed Link to Article
Schwartz  RBJones  KMKalina  P  et al.  Hypertensive encephalopathy.  AJR Am J Roentgenol 1992;159 (2) 379- 383
PubMed Link to Article
Wartenberg  KEPatsalides  ADYepes  M Transient diffusion-weighted imaging changes in a patient with reversible leukoencephalopathy syndrome. Acta Radiol 2004;45 (6) 674- 678
PubMed Link to Article
Ahn  KJYou  WJJeong  SL  et al.  Atypical manifestations of reversible posterior leukoencephalopathy syndrome. Neuroradiology 2004;46 (12) 978- 983
PubMed Link to Article
Casey  SOSampaio  RCMichel  ETruwit  CL Posterior reversible encephalopathy syndrome. AJNR Am J Neuroradiol 2000;21 (7) 1199- 1206
PubMed
Jarosz  JMHowlett  DCCox  TCBingham  JB Cyclosporine-related reversible posterior leukoencephalopathy: MRI. Neuroradiology 1997;39 (10) 711- 715
PubMed Link to Article
Ay  HBuonanno  FSSchaefer  PW  et al.  Posterior leukoencephalopathy without severe hypertension: utility of diffusion-weighted MRI. Neurology 1998;51 (5) 1369- 1376
PubMed Link to Article
Schwartz  RBMulkern  RVGudbjartsson  HJolesz  F Diffusion-weighted MR imaging in hypertensive encephalopathy: clues to pathogenesis. AJNR Am J Neuroradiol 1998;19 (5) 859- 862
PubMed
Shimono  TMiki  YToyoda  H  et al.  MRI imaging with quantitative diffusion mapping of tacrolimus-induced neurotoxicity in organ transplant patients. Eur Radiol 2003;13 (5) 986- 993
PubMed
Schaefer  PWBuonanno  FSGonzalez  RGSchwamm  LH Diffusion-weighted imaging discriminates between cytotoxic and vasogenic edema in a patient with eclampsia. Stroke 1997;28 (5) 1082- 1085
PubMed Link to Article
Koch  SRabinstein  AFalcone  SForteza  A Diffusion-weighted imaging shows cytotoxic and vasogenic edema in eclampsia. AJNR Am J Neuroradiol 2001;22 (6) 1068- 1070
PubMed
Provenzale  JMPetrella  JRCruz  LC  JrWong  JCEngelter  SBarboriak  DP Quantitative assessment of diffusion abnormalities in posterior reversible encephalopathy syndrome. AJNR Am J Neuroradiol 2001;22 (8) 1455- 1461
PubMed
Covarrubias  DJLuetmer  PHCampeau  NG Posterior reversible encephalopathy syndrome. AJNR Am J Neuroradiol 2002;23 (6) 1038- 1048
PubMed
Ugurel  MSHayakawa  M Implications of post-gadolinium MRI results in 13 cases with posterior reversible encephalopathy syndrome. Eur J Radiol 2005;53 (3) 441- 449
PubMed Link to Article
Bartynski  WSZeigler  ZSpearman  MPLin  LShadduck  RKLister  J Etiology of cortical and white matter lesions in cylosporin-A and FK-506 neurotoxicity. AJNR Am J Neuroradiol 2001;22 (10) 1901- 1914
PubMed
Oliverio  PJRestrepo  LMitchell  SATornatore  CSFrankel  SR Reversible tacrolimus-induced neurotoxicity isolated to the brain stem. AJNR Am J Neuroradiol 2000;21 (7) 1251- 1254
PubMed
Kitaguchi  HTomimoto  HMiki  Y  et al.  A brainstem variant of reversible posterior leukoencephalopathy syndrome. Neuroradiology 2005;47 (9) 652- 656
PubMed Link to Article
Hagemann  GUgur  TWitte  OWFitzek  C Recurrent posterior reversible encephalopathy syndrome (PRES). J Hum Hypertens 2004;18 (4) 287- 289
PubMed Link to Article
Schwartz  RBBravo  SMKlufas  RA  et al.  Cyclosporine neurotoxicity and its relationship to hypertensive encephalopathy: CT and MR findings in 16 cases. AJR Am J Roentgenol 1995;165 (3) 627- 631
PubMed Link to Article

Figures

Place holder to copy figure label and caption
Figure 1.

Neuroimaging of 38 discrete episodes of reversible posterior leukoencephalopathy syndrome. The top rows represent the initial neuroimages, and the bottom rows represent the repeated neuroimages.

Graphic Jump Location
Place holder to copy figure label and caption
Figure 2.

Fluid-attenuated inversion recovery magnetic resonance images (FLAIR MRIs) showing reversible posterior leukoencephalopathy syndrome atypical features. A, Significant frontal involvement. B, Unilateral lesion. C, Presence of hemorrhage into lesion. D, Confluent leukoencephalopathy. E, Gray matter/cortical lesions. F, Repeated FLAIR MRIs with persistent abnormality.

Graphic Jump Location
Place holder to copy figure label and caption
Figure 3.

Recurrent reversible posterior leukoencephalopathy syndrome episodes in 2 patients. The top row shows episodes 14 and 15, and the bottom row shows episodes 25 and 26. Note that the splenium of the corpus callosum is involved (bottom row, third panel from left).

Graphic Jump Location

Tables

Table Graphic Jump LocationTable. Clinical Characteristics of the 38 Episodes of Reversible Posterior Leukoencephalopathy Syndrome

References

Hinchey  JChaves  CAppignani  B  et al.  A reversible posterior leukoencephalopathy syndrome. N Engl J Med 1996;334 (8) 494- 500
PubMed Link to Article
Schwaighofer  BWHesselink  JRHealy  ME MR demonstration of reversible brain abnormalities in eclampsia. J Comput Assist Tomogr 1989;13 (2) 310- 312
PubMed Link to Article
Hauser  RALacey  DMKnight  MR Hypertensive encephalopathy: magnetic resonance imaging demonstration of reversible cortical and white matter lesions. Arch Neurol 1988;45 (10) 1078- 1083
PubMed Link to Article
Appignani  BABhadelia  RABlacklow  SCWang  AKRoland  SFFreeman  RB Neuroimaging findings in patients on immunosuppressive therapy: experience with tacrolimus toxicity. AJR Am J Roentgenol 1996;166 (3) 683- 688
PubMed Link to Article
Small  SLFukui  MBBramblett  GTEidelman  BH Immunosuppression-induced leukoencephalopathy from tacrolimus (FK506). Ann Neurol 1996;40 (4) 575- 580
PubMed Link to Article
Truwit  CLDenaro  CPLake  JRDeMarco  T MR imaging of reversible cyclosporin A-induced neurotoxicity. AJNR Am J Neuroradiol 1991;12 (4) 651- 659
PubMed
Singh  NBonham  AFukui  M Immunosuppressive-associated leukoencephalopathy in organ transplant recipients. Transplantation 2000;69 (4) 467- 472
PubMed Link to Article
Chester  EMAgamanolis  DPBanker  BQVictor  M Hypertensive encephalopathy: a clinicopathologic study of 20 cases. Neurology 1978;28 (9 Pt 1) 928- 939
PubMed Link to Article
Schwartz  RB A reversible posterior leukoencephalopathy syndrome. N Engl J Med 1996;334 (26) 1743
PubMed Link to Article
Antunes  NLSmall  TNGeorge  DBoulad  FLis  E Posterior leukoencephalopathy syndrome may not be reversible. Pediatr Neurol 1999;20 (3) 241- 243
PubMed Link to Article
Schwartz  RBJones  KMKalina  P  et al.  Hypertensive encephalopathy.  AJR Am J Roentgenol 1992;159 (2) 379- 383
PubMed Link to Article
Wartenberg  KEPatsalides  ADYepes  M Transient diffusion-weighted imaging changes in a patient with reversible leukoencephalopathy syndrome. Acta Radiol 2004;45 (6) 674- 678
PubMed Link to Article
Ahn  KJYou  WJJeong  SL  et al.  Atypical manifestations of reversible posterior leukoencephalopathy syndrome. Neuroradiology 2004;46 (12) 978- 983
PubMed Link to Article
Casey  SOSampaio  RCMichel  ETruwit  CL Posterior reversible encephalopathy syndrome. AJNR Am J Neuroradiol 2000;21 (7) 1199- 1206
PubMed
Jarosz  JMHowlett  DCCox  TCBingham  JB Cyclosporine-related reversible posterior leukoencephalopathy: MRI. Neuroradiology 1997;39 (10) 711- 715
PubMed Link to Article
Ay  HBuonanno  FSSchaefer  PW  et al.  Posterior leukoencephalopathy without severe hypertension: utility of diffusion-weighted MRI. Neurology 1998;51 (5) 1369- 1376
PubMed Link to Article
Schwartz  RBMulkern  RVGudbjartsson  HJolesz  F Diffusion-weighted MR imaging in hypertensive encephalopathy: clues to pathogenesis. AJNR Am J Neuroradiol 1998;19 (5) 859- 862
PubMed
Shimono  TMiki  YToyoda  H  et al.  MRI imaging with quantitative diffusion mapping of tacrolimus-induced neurotoxicity in organ transplant patients. Eur Radiol 2003;13 (5) 986- 993
PubMed
Schaefer  PWBuonanno  FSGonzalez  RGSchwamm  LH Diffusion-weighted imaging discriminates between cytotoxic and vasogenic edema in a patient with eclampsia. Stroke 1997;28 (5) 1082- 1085
PubMed Link to Article
Koch  SRabinstein  AFalcone  SForteza  A Diffusion-weighted imaging shows cytotoxic and vasogenic edema in eclampsia. AJNR Am J Neuroradiol 2001;22 (6) 1068- 1070
PubMed
Provenzale  JMPetrella  JRCruz  LC  JrWong  JCEngelter  SBarboriak  DP Quantitative assessment of diffusion abnormalities in posterior reversible encephalopathy syndrome. AJNR Am J Neuroradiol 2001;22 (8) 1455- 1461
PubMed
Covarrubias  DJLuetmer  PHCampeau  NG Posterior reversible encephalopathy syndrome. AJNR Am J Neuroradiol 2002;23 (6) 1038- 1048
PubMed
Ugurel  MSHayakawa  M Implications of post-gadolinium MRI results in 13 cases with posterior reversible encephalopathy syndrome. Eur J Radiol 2005;53 (3) 441- 449
PubMed Link to Article
Bartynski  WSZeigler  ZSpearman  MPLin  LShadduck  RKLister  J Etiology of cortical and white matter lesions in cylosporin-A and FK-506 neurotoxicity. AJNR Am J Neuroradiol 2001;22 (10) 1901- 1914
PubMed
Oliverio  PJRestrepo  LMitchell  SATornatore  CSFrankel  SR Reversible tacrolimus-induced neurotoxicity isolated to the brain stem. AJNR Am J Neuroradiol 2000;21 (7) 1251- 1254
PubMed
Kitaguchi  HTomimoto  HMiki  Y  et al.  A brainstem variant of reversible posterior leukoencephalopathy syndrome. Neuroradiology 2005;47 (9) 652- 656
PubMed Link to Article
Hagemann  GUgur  TWitte  OWFitzek  C Recurrent posterior reversible encephalopathy syndrome (PRES). J Hum Hypertens 2004;18 (4) 287- 289
PubMed Link to Article
Schwartz  RBBravo  SMKlufas  RA  et al.  Cyclosporine neurotoxicity and its relationship to hypertensive encephalopathy: CT and MR findings in 16 cases. AJR Am J Roentgenol 1995;165 (3) 627- 631
PubMed Link to Article

Correspondence

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