Diffusion tensor tractography in a patient with memory impairment following encephalitis

A 45-year-old male was admitted to the neurology department of a university hospital due to drowsiness, fever (38.5 C), and headache, which had persisted for 3 days. Cerebrospinal fluid (CSF) analysis performed on the day of admission showed 200 cells/lL, which were predominantly lymphocytic (70 %), and an increased protein level (221 mg/dL, normal range 15–45 mg/dL). CSF tests for herpes simplex virus (HSV)-polymerase chain reaction (PCR), HSV immunoglobulin-M, tuberculosis-PCR, acidfast bacillus stain, cryptococcus antigen, and cultures for bacteria and fungus were all negative. Brain MRI [T2 Fluid attenuated inversion recovery (FLAIR)] performed on the day of admission showed increased signal intensity (diffusion restrictive) in the left temporal lobe and insula, however, this increased signal intensity had disappeared on follow-up MRI performed 1-week after admission. Sleep electroencephalography (EEG) showed continuous theta waves on the left temporal lobe. After intravenous administration of acyclovir (2160 mg/day) for 2 weeks, the patient’s symptoms had almost disappeared. Although the causative organism could not be identified, a tentative diagnosis of herpes encephalitis was made based on the clinical manifestations and the results of CSF analysis, EEG, and brain MRI. Since the onset of encephalitis, the patient complained of memory impairment. Results of the neuropsychological test performed 3 months after onset showed verbal memory impairment on the Memory Assessment Scale [68 (2 %)]. The patient’s total score on the Memory Assessment Scale [84 (14 %)] was relatively low compared with his total intelligence quotient on the Wechsler Adult Intelligence Scale [123 (94 %)]. On conventional brain MRI at 3 months after onset no sequellary macroscopic brain damage (Fig. 1b). Diffusion tensor images were acquired at 3 months after onset using a sensitivity encoding head coil on a 1.5-T. Each neural tract (the thalamocingulate tract, fornix, cingulum, and mammillothalamic tract) of the Papez circuit was determined by selection of fibers passing through seed and target regions of interest (ROI), as in previous studies [1–4]. The various neural tracts of the Papez circuit (fornix, cingulum, mamillothalamic tract, and thalamocingulate tract) were reconstructed in both hemispheres and a disruption in the right thalamocingulate tract was observed (Fig. 1c). Encephalitis, a diffuse or focal inflammatory process of the brain parenchyma, is often followed by various neurological sequelae, including memory impairment [5, 6]. Memory impairment following encephalitis is the result of damage to the frontal lobe, temporal lobe, or the Papez circuit of the limbic system [6]. However, the pathogenic mechanism of memory impairment has not been clearly elucidated so far. The Papez circuit plays important roles in control of episodic memory and emotion. Partial reconstruction of the neural tracts of the Papez circuit in three dimensions has & Sung Ho Jang strokerehab@hanmail.net