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Case report |
Departments of 1 Diagnostic Radiology, 2 Neurology and 3 Haematology, The Catholic University of Korea, Seoul, Korea
Correspondence: Dr S T Hahn, Department of Radiology, St Mary's Hospital, #62 Youido-Dong, Yongdeungpo-Gu, Seoul 150–713, Korea
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Abstract |
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Introduction |
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Both diffusion-weighted MRI and apparent diffusion coefficient (ADC) mapping make it possible to differentiate between a vasogenic oedema and a cytotoxic oedema [4–6]. We report a FK506 neurotoxicity patient in whom diffusion-weighted MRI and ADC mapping were used to differentiate the cause of the high signal intensity observed in T2 weighted images.
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Case report |
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On the next day after onset of patient's manifestations, brain MRI (1.5 T Magnetom Vision Plus; Siemens, Erlangen, Germany) was performed. On T2 weighted images (repetition time (TR)/echo time (TE)=4000/99, slice thickness 6 mm, number of slices 19, field of view 230 x 230 mm, matrix size 198 x 512) multiple cortical and subcortical high signal intensities were revealed in both parieto-occipital lobes and both frontal watershed zones (Figure 1a
). These results strongly suggested posterior reversible leukoencephalopathy syndrome. On diffusion-weighted images (single-shot spin-echo echo-planar pulse sequence with b-value=1000 s mm-2, superior–inferior direction of diffusion encoding gradient, TR/TE=4000/110, field of view 230 x 230 mm, matrix size 128 x 128, number of slices 17, slice thickness 5 mm, and number of excitation 1) isosignal or high signal intensities were shown on the areas of increased signal intensities indicated by the T2 weighted images (Figure 1b). ADC mapping (3 different b-values: 0 s mm-2, 500 s mm-2, 1000 s mm-2, and 3 orthogonally directed diffusion encoding gradients for each b-value) was performed to elucidate the cause of the increased signal intensity on the diffusion-weighted images. On the ADC maps, the areas corresponding to the increased signal intensities on diffusion-weighted images showed increased signal intensity, even in the frontal watershed zones, when compared with the adjacent brain parenchymal signal intensity (Figure 1c). The areas of increased signal intensity on ADC maps appeared to be larger compared with those on the diffusion-weighted images. From both the clinical and radiological findings, FK506 neurotoxicity was strongly suspected, and thus FK506 was discontinued. The patient's condition greatly improved over the next few days after cessation of FK506 and he was discharged after 4 weeks.
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Discussion |
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These neurological symptoms and signs in association with the signal abnormalities on the T2 weighted MRI involving the posterior white matter have been described as a complication of cyclosporine therapy [1, 2, 9]. The neuroimaging findings in FK506-induced neurotoxicity are similar to those reported with cyclosporine-induced toxicity. Both cause abnormalities predominantly affecting the parieto-occipital lobes, although other regions of the brain may also be affected. These symptoms generally resolve over time [10]. Both cyclosporine and FK506 neurotoxicity can be included in reversible posterior leukoencephalopathy [11].
Schwartz et al [12] suggested that the neurotoxic effects of cyclosporine appear to be identical to those with hypertensive encephalopathy, which may be induced by a breakdown of autoregulation preferentially affecting the posterior circulation. According to their study, hypertension plays a pivotal role in the pathogenesis of cyclosporine neurotoxicity.
Vasculopathy also has been suggested as a main pathogenic mechanism. Lesion locations in the brain anastomotic border zones and the high co-existence of neurological symptoms with bone marrow-associated thrombotic microangiopathy indicate an underlying cerebral vasculopathy [13]. Diffuse vessel injury can lead to regional cerebral hypoperfusion, with the most severe flow reduction expected in the anastomotic border zones. Although mechanism for vasculopathy was different, Truwit et al [9] also suggested that endothelin, a potent vasoconstrictor, may play an important role in the pathogenesis of cyclosporine neurotoxicity by vasospam.
Ultimately, the pathophysiology of both cyclosporine and FK506 neurotoxicity remain unclear. Two pathogenic mechanisms have been suggested. One is that a cerebral vasospasm results in ischaemia and consequent cytotoxic oedema. This is supported by angiographic findings of a diffuse or focal vasospasm and by infarctions in posterior leukoencephalopathy patients. Pathological findings of widespread arteriolar vasospasm and thrombosis and multifocal infarctions also support this theory [14]. An alternative theory is that acute hypertension in posterior leukoencephalopathy induces a loss of autoregulation with passive dilatation of the cerebral arterioles; the hydrostatic pressure results in the extravasation of proteins and fluid into the interstitium [15, 16]. Multiple reports of reversible T2 hyperintense white matter lesions with predominance in the posterior circulation as well as increased perfusion with SPECT scanning in patients with posterior leukoencephalopathy support this latter theory.
Diffusion-weighted imaging provides a means of identifying a cytotoxic oedema caused by acute ischaemia or infarction through a reduction in the diffusibility of protons [4, 5]. This elicits a bright signal on the heavily diffusion-weighted images, and is believed to reflect increased intracellular and decreased extracellular fluid resulting from sodium pump failure.
However, on diffusion weighted images a vasogenic oedema can also be visualized as increased signal intensity-T2 shine through effect [17]. Consequently, ADC mapping is necessary to differentiate a cytotoxic oedema from a vasogenic oedema.
Our patient's findings of increased signal intensity on both diffusion-weighted images and ADC mapping indicate that not cytotoxic oedema but vasogenic oedema was the main cause of increased signal intensities on T2 weighted images. A vasogenic oedema can develop in the course of cerebral ischaemia and also secondary to increased interstitial fluid by breakdown of autoregulation.
In our case the MRI was taken just 1 day after patient's manifestations. In acute ischaemic stroke diffusion coefficients are initially decreased, and usually normalized similar to those of normal brain tissue 1 week after onset of symptoms [18]. Thus it may not be academic to regard this vasogenic oedema as a manifestation of vasculopathy induced ischaemia. Our patient's findings are consistent with the hypothesis that FK506 neurotoxicity results from a breakdown of autoregulation.
In conclusion, we have reported the findings of diffusion-weighted MRI and ADC mapping in a FK506 neurotoxicity patient who showed increased signal intensities in both parieto-occipital lobes on T2 weighted images. On ADC mapping, there was no area with decreased signal intensity. Otherwise, the areas showing increased signal intensity on T2 weighted images were demonstrated with increased signal intensity on ADC mapping. These findings suggest that a vasogenic oedema was the main cause of high signal intensities on T2 weighted images, and breakdown of autoregulation rather than vasculopathy induced ischaemia played a pivotal role in FK506 neurotoxicity pathogenesis.
Received for publication August 30, 2002. Revision received February 4, 2003. Accepted for publication March 25, 2003.
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This article has been cited by other articles:
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  C. M. Lavigne, D. A. Shrier, M. Ketkar, and J. M. Powers Tacrolimus leukoencephalopathy: A neuropathologic confirmation Neurology, September 28, 2004; 63(6): 1132 - 1133. [Full Text] [PDF]
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