Seizures in Lung Transplant Recipients

Vaughn, Bradley V.; Ali, Izna; Olivier, Kenneth N.; Lackner, Rudy P.; Robertson, Kevin; Messenheimer, John A.; Paradowski, Linda J.; Egan, Thomas M.

doi:10.1111/j.1528-1157.1996.tb00549.x

Cited by 49 publications

(27 citation statements)

References 22 publications

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“…Seizures have been described in organ transplant recipients during rejection episodes and steroid use, and have been attributed to the focal breakdown of the blood-brain barrier. 13 The use of other drugs and peripherally involving the cortex and subcortical area and expanding with effacement of the sulci; contrast-enhanced T1W SE (TR/TE; 550/15) image showed that the lesion did not enhance and axial FLAIR (TR/TE/TI; 5000/100/1900) image displayed hyperintense lesion, respectively. metabolic problems that arise in patients with GvHD may also be contributory factors.…”

Section: Discussionmentioning

confidence: 99%

Life-threatening neurological complications after bone marrow transplantation in children

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Çetin

Yigitkanli

et al. 2004

Bone Marrow Transplant

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Summary:Neurological complications may occur in BMT recipients (11-59%), frequently contributing to morbidity or mortality. They are the main causes of death in 10-15%. Lifethreatening neurological complications were seen in 11 out of 113 (9.7%) children who underwent BMT from HLAmatched family (n ¼ 7) or mismatched donors (n ¼ 4) at our institution. Diagnoses of patients with neurological complications were acute myeloblastic leukemia (AML) (five), thalassemia major (two), Fanconi anemia (two), Omenn syndrome (one) and leukodystrophy (one), and the neurological events were seen between days þ 13 and þ 85 after transplantation. Minor symptoms including reversible, nonrepetitive seizures were excluded. Cyclosporine A toxicity was diagnosed in six children. The rest of the complications were brain abscess/meningoencephalitis (two), severe hypomagnesemia (one), busulfan toxicity (one), sustained hypertension (three), and intracranial hemorrhage (three). Six patients with neurological complications suffered from 4grade II graft-versus-host disease (GvHD), and all were high risk for transplantrelated complications. In this study, risk status of the underlying disease, mismatched transplantation, a diagnosis of AML (advanced stage), older age and 4grade II GvHD were important adverse factors for the development of severe life-threatening neurological complications. Bone Marrow Transplantation (2005) 35, 71-76.

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Section: Discussionmentioning

confidence: 99%

Life-threatening neurological complications after bone marrow transplantation in children

Uçkan

Çetin

Yigitkanli

et al. 2004

Bone Marrow Transplant

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“…Minimal data exist concerning the correlation of cerebrospinal fluid (CSF) CSA levels with serum levels in patients with or without CSA toxicity. Limited evidence suggests that CSA may normally have lower concentrations in CSF compared with serum (15), presumably because of poor permeability across the blood-brain barrier. It has been hypothesized that a transient disruption of the blood-brain barrier, such as with hypertension, may predispose to CSA toxicity by allowing increased concentrations of CSA into the brain.…”

Section: Cyclosporine-induced Epileptiform Activitymentioning

confidence: 99%

Cyclosporine Induces Epileptiform Activity in an In Vitro Seizure Model

Wong

Yamada

2000

Epilepsia

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Summary: Purpose: Cyclosporine (CSA) toxicity represents a common cause of seizures in transplant patients, but the specific mechanisms by which CSA induces seizures are unknown. Although CSA may promote seizure activity by various metabolic, toxic, vascular, or structural mechanisms, CSA also has been hypothesized to modulate neuronal excitability directly. The objective of this study was to determine if CSA exerts direct epileptogenic actions on neurons in an in vitro seizure model. Methods: Combined hippocampal‐entorhinal cortex slices from juvenile rats were exposed directly to artificial cerebro‐spinal fluid (ACSF) containing either (a) 1.0 mM magnesium sulfate (control), (b) 1.0 mM sodium sulfate (low‐magnesium), or (c) 1.0 mM magnesium sulfate + CSA (1,000–10,000 ng/ml). Spontaneous and evoked extracellular field potentials were recorded simultaneously from the dentate gyrus (DG) and CA3 hippocampal regions. Evoked synaptic responses were elicited by stimulation of the entorhinal cortex/perforant pathway. Results: CSA elicited spontaneous or stimulation‐induced epileptiform activity in the DG or CA3 region of –40% of slices, consisting of brief repetitive “interictal” discharges or prolonged stereotypical “ictal” discharges. Mean latency to epileptiform activity was –100 min after onset of CSA application. The interictal discharges were inhibited by the non‐NMDA antagonist, NBQX. Similar epileptiform activity was observed in low‐magnesium ACSF without CSA. In control ACSF alone, epileptiform activity was not seen, except for rare spontaneous potentials in the DG. Conclusions: Direct effects of CSA on neuronal excitability and synaptic transmission may contribute to seizures seen in clinical CSA neurotoxicity.

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“…The authors went on to speculate that exaggerated neuronal excitability in individuals with CF might contribute to an increased incidence of seizures following lung transplantation. 66 A role for CFTR in modulating ATP release from dorsal root ganglion neurons was reported. 53 Given the important role of ATP in pain responses, it is possible that CFTR in the dorsal root ganglia might modify nociception.…”

Section: Cftr Expression and Function In The Nervous Systemmentioning

confidence: 99%

Cystic Fibrosis and the Nervous System

Reznikov

2017

Chest

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Seizures in Lung Transplant Recipients

Cited by 49 publications

References 22 publications

Life-threatening neurological complications after bone marrow transplantation in children

Life-threatening neurological complications after bone marrow transplantation in children

Cyclosporine Induces Epileptiform Activity in an In Vitro Seizure Model

Cystic Fibrosis and the Nervous System

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