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This report describes a 15-year-old woman presenting posterior reversible encephalopathy syndrome (PRES) due to azathioprine. She was under treatment for ulcerative colitis. She was prescribed azathioprine seven days before admission. Four days after, she complained of headache. Then, she disturbed consciousness and showed generalized convulsive seizure on the day of admission. Magnetic resonance imaging (MRI) revealed vasogenic edema in both hemispheres. She was discontinued azathioprine and treated by anticonvulsant. Her symptoms were recovered and the MRI findings were disappeared. We diagnosed as PRES due to azathioprine because of clinical course and MRI findings. Only one case of PRES due to azathioprine is reported previously. Our case is the first report that showed the changes and improvement of MRI findings along the clinical course.

We describe a 31-year-old, right-handed man who exhibited pure word deafness (PWD) due to a localization-related seizure. The patient was suddenly unable to comprehend spoken words, whereas he had no difficulty in speaking, comprehending written language, or discriminating non-verbal sounds. Diffusion-weighted imaging and fluid-attenuated inversion recovery on brain magnetic resonance imaging revealed hyperintense lesions in the left superior temporal gyrus (STG) and left superior marginal gyrus (SMG). Furthermore, brain single-photon emission computed tomography showed that these lesions were hyperperfused. An electroencephalogram (EEG) showed multiple spike-and-slow-wave complexes spreading to the left temporal regions. Immediately after administering midazolam intravenously, the patient was able to comprehend spoken words, and the epileptiform discharges in the left temporal regions disappeared. These findings indicate that he suffered from PWD resulting from a dysfunction of the left hemisphere alone. Furthermore, they suggest that the left STG and left SMG play an important role in the recognition of spoken words.

A 57 year-old man developed broad-based unsteady gait and memory loss over a period of one year. On admission, bradykinesia and impairment of postural reflex were evident. Mini-mental state examination scored 27/ 30. Urinary control was normal. MRI revealed symmetric dilatation of lateral and 3rd ventricles, but the 4th ventricle appeared normal. Partial obstruction of the aqueduct with a membranous structure was disclosed by fast imaging employing steady state acquisition (FIESTA), and the diagnosis of late-onset aqueductal membranous occlusion (LAMO) was made. The symptoms were ameliorated shortly after endoscopic aqueductoplasty (EAP) and endoscopic third ventriculostomy (ETV). Membranous occlusion of the aqueduct can be detected by FIESTA and it can be cured by neuro-endoscopic measures.

We report two patients of status epilepticus, in which detailed brain magnetic resonance image (MRI) studies were performed. In one patient apparent diffusion coefficient (ADC) increased in the right temporopareital regions in the acute phase. This patient finally has good clinical course without neurological deficits, and abnormal findings on MRI also disappeared. In another patient ADC increased in the similar regions in the acute phase, and an MRI demonstrated cortical laminar necrosis on T1-weighted scans in the same regions in the posticteric phase about 3 months later. The patient had a poorer prognosis with moderate dementia. It has been demonstrated that increased ADC reflects extracellular edema, while decreased ADC indicates cytotoxic edema. ADC mapping appears to be useful for predicting the reversibility of brain damages due to status epilepticus.