PMC8777188_01
Laboratory data. (A) Changes in anti-thyroid antibody levels in the patient's blood. On day 2, TGAb was 751.40 IU/mL (0-115), and on re-examination on day 19 of onset, TGAb was 504 IU/mL, TPO-Ab was 136 IU/mL (0-34), and TRAb was 1.88 IU/L (0-1.75). PAIA was started on day 36. On day 47, TGAb was 112 IU/mL, TPO-Ab was 20.8 IU/mL, and TRAb was 1.07 IU/L, all of which were in normal ranges. At the 12-month follow-up after treatment,TGAb was 103 IU/mL, TPO-Ab was 17 IU/mL, and TRAb was 1.41 IU/L, all of which were in normal ranges. (B) Changes in cytokine levels in the patient's cerebrospinal fluid. On day 7 of onset, IL-8 was 642.09 pg/mL, IFN-gamma was 279.12 pg/mL, and IL-6 was 28.55 pg/mL, which were significantly increased. After treatment with antivirals, glucocorticoids, and IVIG, these values were significantly decreased: IL-8 was 51.59 pg/mL, IFN-gamma was 0.22 pg/mL, and IL-6 was 2.06 pg/mL, but IL-8 remained at a high level and decreased slowly. (C) Changes in IgG and IgM in the patient's blood. On day 6 of onset, blood IgG was 19.54 g/L (7-16) and IgM was 1.06 g/L (0.4-2.3). With progression of the disease and after IVIG treatment, IgG continued increasing, and IgM also increased but very rapidly returned to the normal range. On day 31 of onset, IgG was 47.8 g/L. PAIA was started on day 36, and IgG began to decrease and gradually returned to the normal range. On day 58, IgG was 8.8 g/L and IgM was 0.87 g/L. (D) Changes in IgG levels in the cerebrospinal fluid. On day 7 of onset, IgG was 6.59 mg/dL (1-4), which increased to 19.7 mg/dL on day 21, and then decreased on day 30. After PAIA was started, cerebrospinal fluid IgG continued decreasing at a greater rate than before. The line labeled PAIA represents the time of the first PAIA treatment (day 36), the treatment was continued for 5 days, there was an obvious urinary tract infection, and PAIA was suspended; after improvement, PAIA was resumed on day 51,the treatment was continued for 3 days. TGAb, anti-thyroglobulin antibody; TPO-Ab, anti-thyroid peroxidase antibody; TRAb, anti-thyroid stimulating hormone receptor antibody; IVIG, intravenous immunoglobulin; PAIA, protein A immunoadsorption.
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Blood anti-thyroglobulin antibody level was 751.4 IU/mL ( Figure 1A ), hemoglobin level was 70 g/L, and cerebrospinal fluid (CSF) white blood cell count was 120x 106/L (see  Supplementary Table 1 ). Figure 1B ). Free triiodothyronine, free thyroxine, and thyroid stimulating hormone in the blood were 2.79 pmol/L, 7.84 pmol/L, and 0.08microlU/mL. On day 31, GCS was E3TM1, the patient was breathing spontaneously without ventilation, cytokines decreased during the treatment ( Figure 1B ). Blood IgG and IgM levels are shown in  Figure 1C .
Magnetic resonance imaging (MRI), computed tomography (CT) and diffusion tensor imaging (DTI) scans of the patient. (A, B) T2 MRI on day 6 of onset shows hyperintense signals in the thalamus and caudate nucleus (white arrows) and cerebral peduncles (white arrows). (C) CT performed on day 19 of onset, when the patient fell back into a coma, shows right thalamus hemorrhage (white arrow). (D-F) T2 MRI re-examination at month 6 of the course of disease shows extensive brain atrophy and the lesion area was smaller than before. (G) T1MRI examination at month 14 of the course of disease shows brain atrophy. (H) DTI at month 14 of the course of disease shows partially broken corpus callosum tract.
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Table 1 ). T2WI head MRI indicated hyperintense signals in the thalamus and caudate nucleus, and new-onset lesions in the bilateral cerebral peduncles (substantia nigra) ( Figures 2A   , B ). On day 19, the patient suddenly became unconscious, and head computed tomography (CT) indicated hemorrhage in the right thalamus ( Figure 2C ). Montreal Cognitive Assessment score of 20. MRI indicated extensive brain atrophy, but the lesion area was smaller than before ( Figures 2D   -F, 4 ). However, MRI still indicated brain atrophy ( Figure 2G ) and DTI showed that the patient's corpus callosum tract was partially broken ( Figure 2H ).
Timeline of hospitalisation in the neurological intensive care unit.
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Intravenous infusion of penciclovir 5mg/kg and glucocorticoid 80 mg every 12 h, intravenous immunoglobulin (IVIG) provided at 0.4g/kg/d for 5 days, and palliative treatment were administered ( Figure 3 ). Considering the EMG and clinical symptoms of the patient, we believed that the disease was progressing and treatment strategies need to be changed ( Figure 3 ). Montreal Cognitive Assessment score of 20. MRI indicated extensive brain atrophy, but the lesion area was smaller than before ( Figures 2D   -F, 4 ).
Comparison of the patient's MRI. (A-D) MRI on day 6 of onset. (E-H) MRI re-examination at month 6 of the course of disease. (I-L) MRI examination at month 14 of the course of disease.
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Montreal Cognitive Assessment score of 20. MRI indicated extensive brain atrophy, but the lesion area was smaller than before ( Figures 2D   -F, 4 ).