Cyclosporine neurotoxicity and its relationship to hypertensive encephalopathy: CT and MR findings in 16 cases.

Schwartz, Richard B.; Bravo, Stephen M.; Klufas, Roman A.; Hsu, Liangge; Barnes, Patrick D.; Robson, Caroline D.; Antin, Joseph H.

doi:10.2214/ajr.165.3.7645483

Cited by 307 publications

(234 citation statements)

References 14 publications

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“…The mechanism behind the brain edema development is controversial. The failure of auto‐regulation caused by severe hypertension or direct toxic insult to endothelium is the most popular theory for pathophysiology (Bartynski, 2008b; Dinsdale, 1983; Schwartz et al., 1995; Strandgaard, Olesen, Skinhoj, & Lassen, 1973). One of the unsettled questions about PRES is the correlation between the brain lesion distribution patterns and blood pressure (BP).…”

Section: Introductionmentioning

confidence: 99%

The effect of presymptomatic hypertension in posterior reversible encephalopathy syndrome

et al. 2018

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ObjectiveThe effect of blood pressure (BP) on the lesion distribution of posterior reversible encephalopathy syndrome (PRES) is controversial. The aim of this study was to identify the relationship between brain lesion distribution patterns and BP.MethodsSixty‐five patients with PRES were selected from the database. Data regarding brain MRI findings, clinical symptoms, medical conditions, and BP at the presymptomatic period (24 hr before the symptom onset) and at the symptom onset were collected. The brain lesion distribution degree was numerically calculated (lesion scoring point [LSP]) and compared with BP and medical conditions.ResultsMean onset‐MAP was higher than mean pre‐MAP. Pre‐MAP correlated with onset‐MAP. The LSP was significantly correlated with pre‐MAP (p = 0.009, correlation coefficient [cc] = 0.323), whereas no significant correlation was found between LSP and onset‐MAP (p = 0.159, cc = 0.177). Similarly, when patients were grouped by mean MAP values, LSP was significantly higher in the patients with high MAP at the presymptomatic period (p = 0.004), whereas no difference was found in the LSP value between patients with low MAP and high MAP at the symptom onset (p = 0.272).ConclusionThe patient with PRES who has relatively higher BP in the presymptomatic period would be more likely to have wider lesion distribution than the patient with lower BP. BP elevation during presymptomatic period may be a heralding sign of impending PRES and a factor affecting the severity of PRES although BP was not investigated at earlier time points.

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Section: Introductionmentioning

confidence: 99%

The effect of presymptomatic hypertension in posterior reversible encephalopathy syndrome

et al. 2018

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“…8 Also, the high concentration of CsA might have been one of the causes of encephalopathy, although it has been reported that neurotoxicity does not always occur in the presence of a high concentration of CsA. 1,2 We conclude that accurate diagnosis, and prompt substitution of tacrolimus for CsA and careful monitoring of serum drug concentrations in this case prompted the good clinical outcome.…”

Section: Discussionmentioning

confidence: 75%

“…Considering the above reported findings, [1][2][3][4][5][6][7] we suspected that there were various factors closely related to the encephalopathy in this patient, such as acute hypertension, a high serum concentration of CsA, atypical metabolism induced by chronic hepatitis B, co-administration of FLCZ, and PSL used for prevention of allergic reaction to ATG (days −6 to day 0). Moreover, we had to reduce the dose of CsA on day −1, because of the history of a high concentration of CsA before BMT.…”

Section: Discussionmentioning

confidence: 96%

“…Hypertension has been reported to occur in more than 90% of allo-BMT recipients receiving CsA for prevention of GVHD, and neurotoxicity has been reported to occur in 3ෂ5% of such patients. 1,2 Although the etiology of CsAinduced encephalopathy is unclear, it has been reported that there is the possibility of CsA causing endothelial injury directly or indirectly through its products and disrupting the blood-brain barrier. 3 Since there is a tendency for CsA to disrupt the vertebrobasilar system and its branches, lesions in the occipital lobes are frequently observed on MR images.…”

Section: Discussionmentioning

confidence: 99%

“…3 Since there is a tendency for CsA to disrupt the vertebrobasilar system and its branches, lesions in the occipital lobes are frequently observed on MR images. 1 This may be partly related to the regional density of adrenergic receptors on intracranial vessels, 1 but the precise mechanism of the disruption is unknown. CsA is also known to disrupt the endothelium of renal vessels.…”

Section: Discussionmentioning

confidence: 99%

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Cyclosporin A-induced encephalopathy after allogeneic bone marrow transplantation with prevention of graft-versus-host disease by tacrolimus

Takahata

Hashino

Izumiyama

et al. 2001

Bone Marrow Transplant

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Summary:A 21-year-old woman with severe aplastic anemia received an allogeneic bone marrow transplant (allo-BMT) from an HLA-matched and ABO-matched sibling donor after conditioning with cyclophosphamide, rabbit ATG (Lymphoglobuline; Aventis-Pharma), and total lymphoid irradiation. She had a long history of cyclosporin A (CsA) therapy before conditioning. She complained of severe headache and convulsions on day 0, and findings on magnetic resonance images suggested CsA-induced encephalopathy. CsA was immediately stopped, and tacrolimus for prevention of graft-versushost disease (GVHD) was started on day 2. Hematological engraftment was observed on day 14 without serious GVHD. Prompt diagnosis, replacement of immunosuppressive agents, and careful monitoring of serum drug concentrations are thought to have contributed to the patient's good clinical course, since CsA-induced encephalopathy tends to be recurrent but to improve completely without any sequelae. Bone Marrow Transplantation (2001) 28, 713-715.

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Clinical Spectrum of Reversible Posterior Leukoencephalopathy Syndrome

et al. 2008

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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.

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Cyclosporine neurotoxicity and its relationship to hypertensive encephalopathy: CT and MR findings in 16 cases.

Cited by 307 publications

References 14 publications

The effect of presymptomatic hypertension in posterior reversible encephalopathy syndrome

The effect of presymptomatic hypertension in posterior reversible encephalopathy syndrome

Cyclosporin A-induced encephalopathy after allogeneic bone marrow transplantation with prevention of graft-versus-host disease by tacrolimus

Clinical Spectrum of Reversible Posterior Leukoencephalopathy Syndrome

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