A 37-year-old male patient was admitted to the Second Hospital of Lanzhou University on 23rd July 2019 due to "fever accompanied by progressively deteriorating headache for 3 days and paroxysmal unconsciousness for 1 day." The patient had a history of "herpes zoster" 6 months ago. He developed fever without obvious predisposing factors 3 days before admission. His body temperature was 38.4-39.4 C, accompanied by a headache, mainly a mild intermittent throbbing pain in the temporal region. The symptoms aggravated the next day. The headache spread to the occipital region and the back of the neck and lasted longer. Meanwhile, the patient experienced mild fatigue and sore muscles that were unresponsive to ibuprofen sustained-release capsules. On the morning of 22nd July, the headache became significantly aggravated and more persistent, accompanied by nausea and vomiting of stomach contents two times. The patient suddenly lost consciousness that night, accompanied by involuntary movement of the left limbs, and regained consciousness 0.5 min later. When visiting our hospital on 23rd July, the patient lost consciousness again, accompanied by involuntary movement of the left limbs, and regained consciousness 1 min later.
Physical examination on admission showed a body temperature of 38.2 C, a pulse-93 beats/min, a respiratory rate of 23 times/min, and a blood pressure of 124/82 mmHg. Scattered rice-like scabs caused by previous herpes zoster were observed in the sixth left intercostal space, with old skin lesions and fusion, but without redness or ulceration. The nervous system examination showed consciousness and a poor mental state without obvious abnormalities involving high-level cortical functions or cranial nerves. The muscle strength of the four limbs was graded as 4+. The muscle tension was normal, and tendon reflexes were present without any pathological signs. The neck was rigid, and the mentosternal distance was four fingers. Kernig sign+ and Brudzirnki sign+ were observed. Blood routine on admission plus C-reactive protein (CRP) showed white blood cell (WBC) counts at 9.5 x 109/L, neutrophil ratio (NE%) of 0.51, lymphocyte ratio (LY%) of 0.49, and CRP of 21 mg/L. The rest of the laboratory tests showed no abnormalities (Table 1). Electroencephalography (EEG) showed rhythmic emission of focal slow waves in the right frontal and temporal regions at 2-6 cycles per second, spreading to all leads. Preliminary diagnosis on admission indicated central nervous system infection of suspected viral meningoencephalitis and secondary epilepsy. Acyclovir 0.5 g/8 h, intravenously guttae (ivgtt), dexamethasone 10 mg, ivgtt, and carbamazepine 200 mg orally twice daily. were administered. Lumbar puncture was subsequently performed with the cerebrospinal fluid (CSF) intracranial pressure of 210 mmH2O, WBC counts of 145 x 106/L, mononuclear cell ratio (MN%) of 97.7, and proteins of 0.84 g/L. The rest examinations showed no abnormalities. In addition, 4 mL of CSF was collected for Pathogen Capture Engine Sequence (PACEseq) mNGS (Hugobiotech, Beijing, China) to determine the pathogen. In the meantime, autoimmune encephalitis antibody, infectious disease (including Toxoplasma, rubella virus, cytomegalovirus, herpes simplex virus, and other pathogenic microorganisms), rheumatism, respiratory tract 9-items, and tuberculosis antibody were all tested but showed negative. Brain magnetic resonance imaging (MRI) on July 25th showed patchy long T1 signal and slightly longer T2 signal in the right frontal, temporal, and insular lobes. While on diffusion-weighted imaging (DWI) and fluid-attenuated inversion recovery (FLAIR) sequences, high signals and patchy enhanced shadows in the lesion areas were also observed, and the dura mater adjacent to the lesion areas was enhanced and thickened (Figure 1). On July 26th, the mNGS result came out, and a total of 12,024 unique sequences of HHV-2, with a coverage of 95.44% were detected (Table 1, Figure 2), indicating HHV-2 meningoencephalitis. On 28th July, the patient's autoimmune encephalitis-related antibody was reported negative. After 21 days of antiviral treatment, the re-examination of the CSF showed intracranial pressure of 120 mmH2O, WBC counts of 4 x 106/L, and MN% of 100. No abnormalities were found for the rest items. The patient was discharged and given acyclovir and carbamazepine. One month later, an EEG re-examination on 15th September showed normal results. Head MRI showed irregular long T1 and T2 signal shadows in the right temporal pole. Low signals in FLAIR lesions and patchy high signals in the periphery were also detected by DWI. When compared with previous findings, temporal lobe and hippocampus atrophy adjacent to the lesions were observed. Local necrosis and softening foci were formed, and the right temporal horn was widened (Figure 1). After discharge from the hospital, the patient felt significant memory loss, without other obvious discomforts.