A 54-year-old Chinese woman with a history of poorly managed hypertension was admitted to the hospital due to a 5-day history of vertigo, nausea, vomiting, diarrhea, altered mental status, and progressive left-sided weakness. She denied having a headache, fever, chills, visual disturbances, or weight loss. The patient was employed as a cake shop salesperson and denied any history of unsafe sex. Upon admission, her vital signs were within normal limits, and the general physical examination was unremarkable, with no rash, skin lesions, or joint swelling. Neurological examination showed an awake and oriented patient with slow psychomotor response to questions and commands, impaired attention, calculation, and short-term memory, but normal speech. The patient's left pupil was irregular with a sluggish response to light, and the left nasolabial fold was mildly flattened. There was no dysphagia or dysarthria, and tongue movements were normal. The patient had muscle strength of 4/5 (Frankel grade) with a positive Chaddock sign on the left side and reduced light touch and pinprick sensation in the left arm and leg without extinction. There was no right-side impairment, and no meningismus was observed. The routine blood test and chemistry analysis were unremarkable, including evaluations of liver, renal, and thyroid function, as well as C-reactive protein levels. Cranial MRI revealed high signal changes in the right cingulate gyrus and nearby frontal lobe on T2-weighted imaging (T2WI) and fluid-attenuated inversion recovery (FLAIR) images, as depicted in Figure 1. These lesions appeared hyperintense on diffusion-weighted imaging (DWI) with increased apparent diffusion coefficient (ADC) values, suggestive of vasogenic edema. Brain magnetic resonance angiography (MRA) demonstrated no abnormalities. The lesion displayed partial contrast enhancement on the enhanced T1-weighted image. Herpes simplex encephalitis was considered the most likely diagnosis, and empirical treatment with acyclovir was initiated while awaiting laboratory results. On the third day of admission, the patient experienced a generalized body jerking episode, and Levetiracetam was administered to treat seizures. On the sixth day of admission, an electroencephalogram revealed mild diffuse slowing with rare sharp waves on the right hemisphere. Additionally, the serum Toluidine Red Unheated Serum Test (TRUST) was positive at 1:32 dilutions, but the HIV test was negative, which prompted a lumbar puncture. The patient's cerebrospinal fluid (CSF) was clear and colorless, with no erythrocytes, 10 cells/mm3 leukocytes (lymphocytes 80%), 3.26 mmol/L glucose (range 2.5-4.4 mmol/L), and 84 mg/dL protein (range 15-45 mg/dL). The CSF viral polymerase chain reaction (PCR) test was negative for varicella-zoster virus, herpes simplex virus (HSV) 1 and 2.
An extensive CSF workup for autoimmune encephalitis, including anti-glial fibrillary acidic protein (GFAP), anti-N-methyl-D-aspartate receptor (NMDAR), antibodies to glutamic acid decarboxylase (anti-GAD) , and other autoimmune encephalitis antibodies, yielded negative results. Furthermore, the CSF bacterial and fungal cultures and skin purified protein derivative of tuberculin remained negative. However, subsequent testing of the CSF showed positive results for Treponema pallidum particle agglutination (TPPA) (titer greater than 1:320) and TRUST (titer 1:32). As a result, acyclovir was discontinued, and the patient received intravenous penicillin G for 2 weeks. Following hospital discharge, the patient received 2.4 million units of intramuscular benzathine penicillin for 1 month as an outpatient. At the 2-month follow-up, the patient demonstrated signs of cognitive recovery, becoming able to live independently but remaining slightly forgetful. Subsequent imaging showed resolution of the signal change, with mild focal atrophy of the right cingulate gyrus and adjacent frontal lobe (Figure 2).
