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Case Report |
1
Department of Neurology, Duke University Medical Center, Box 2905, Durham, NC
27710.
2
Department of Radiology, Duke University Medical Center, Durham, NC
27710.
3
Department of Pediatric Neurology, Duke University Medical Center, Durham, NC
27710.
Received July 22, 1999;
accepted after revision October 13, 1999.
Address correspondence to H. Kassem-Moussa.
Introduction
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MR imaging was performed 4 hr after obtundation. The patient was noted to have a generalized convulsive seizure while in the MR scanner. The seizure was aborted by IV diazepam, followed within minutes by an increased level of alertness, the resolution of gaze deviation, and normalization of the neurologic examination findings. At this point it became apparent that the obtundation was caused by prolonged complex partial seizure activity.
MR imaging showed subcortical regions of hyperintense signal on T2-weighted and FLAIR images (Fig. 1A) in the right posterior temporal lobe and left occipital lobe, consistent with the suspected diagnosis of PLES. Diffusion-weighted images showed increased signal intensity within the right parietal and occipital cortices in addition to the right temporal lobe (Fig. 1B), in areas that appeared normal on T2-weighted and FLAIR images. Apparent diffusion coefficient (ADC) values from the areas of increased signal intensity were reduced approximately 25-30% compared with that from normal white matter (Fig. 1C).
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Electroencephalography performed 2 hr after MR imaging showed right hemisphere slowing, and sharp- and slow-wave discharges at 0.8-1.5 Hz emanating from the right parietal—temporal—occipital cortex, compatible with a postictal state. These findings corresponded to the sites of altered water diffusibility seen on diffusion-weighted images. Repeated MR imaging 5 weeks later showed no evidence of infarction on T2-weighted (Fig. 1D) and coronal FLAIR (Fig. 1E) images and the return of ADC values to normal; axial FLAIR imaging was not performed.
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TopIntroductionCase ReportDiscussionReferences |
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In our patient, diffusion-weighted imaging findings with no permanent clinical or radiographic lesions were seen in regions of the right hemispheric cortex in the presence of relatively normal T2-weighted and FLAIR imaging findings. We propose that the diffusion-weighted imaging signal abnormalities were caused by the prolonged seizure activity, estimated to be at least 4 hr in duration, before MR imaging. The neurologic examination finding of leftward gaze deviation with left-beating nystagmus is consistent with a seizure discharge arising in the right parietal-temporal-occipital lobe [6], corresponding to the regions of abnormality seen on the electroencephalogram and to the region of abnormality seen on diffusion-weighted images [6].
An ischemic insult was considered unlikely to be the cause of the abnormality seen on initial diffusion-weighted images in our patient because diffusion-weighted signal changes did not correspond to particular vascular territories and because no evidence of infarction was seen on follow-up imaging. Moreover, the results of neurologic examination substantially improved after administration of diazepam.
Although PLES was contributory to the seizures in our patient, it is unlikely to be the direct cause of the cytotoxic edema and the decreased ADC values because this syndrome primarily causes vasogenic edema and elevated ADC values (compared with normal white matter) [7]. In fact, our patient had ADC values that were elevated on the order of 30% in areas affected by PLES not involved in seizure activity, such as the left temporal and occipital regions. In the right temporal lobe, focal areas affected by PLES showed ADC reduction on the order of 5%; this finding was thought to reflect the combined effect of vasogenic edema and cytotoxic edema.
Our patient differed from those described in previous reports [1, 2] in a number of ways. First, T2-weighted and FLAIR imaging signal abnormalities were lacking at sites of decreased ADC values in our patient. The lack of T2-weighted or FLAIR imaging signal abnormalities corresponding to these diffusion-weighted imaging abnormalities suggests that the diffusion-weighted imaging abnormalities in our patient were seen at an early stage. This stage presumably preceded development of cytotoxic edema sufficient to produce T2 prolongation (and presumably before neuronal and glial cell death) in a manner analogous to that seen in the first few hours of cerebral ischemia.
Another unique finding in our patient is that low ADC values were seen essentially throughout the entire temporal cortical and subcortical regions, whereas in most previous reports reduction in ADC values was confined mainly to brain cortex. One report did describe subcortical involvement, which was documented as an approximately 30% increase, rather than decrease, in ADC values in the white matter underlying affected cortex [2]. This finding occurred with coexisting hyperintense T2 changes and was seen after numerous days of continuous seizures. Finally, evidence of permanent injury, manifested by volume loss on subsequent imaging, was noted in a previous report [1]. However, such abnormalities were not seen on follow-up imaging in our patient, perhaps reflecting the relatively short duration of seizure activity compared with that of other reported cases.
In conclusion, at a time of heightened interest in consideration of the use of diffusion-weighted imaging in the setting of acute stroke [8], it is important to remember that abnormal processes other than ischemia can cause acute diffusion-weighted imaging changes.
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