2026 ECNP Congress

PS03-3079

Steroid-responsive autoimmune encephalopathy presenting as treatment-resistant depression

Şeymanur Güven — K.C. Can, Z.R. Köse, F.C. Atalık, B. Çolak, B. Duman, Y. Kır, E.T. Özel Kızıl, M.C. Saka, S. Erdoğan, R. Yılmaz, M. Araz, R.S. İlhan · Ankara University Faculty of Medicine, Department of Psychiatry, Ankara, Türkiye

2026 ECNP Congress

Introduction

Hashimoto encephalopathy (HE), now termed steroid-responsive encephalopathy associated with autoimmune thyroiditis (SREAT), is a rare neuropsychiatric disorder characterised by elevated antithyroid antibodies, diverse neuropsychiatric manifestations, and corticosteroid responsiveness. Its presentation within a chronic psychiatric course poses significant diagnostic challenges. FDG-PET may support the diagnosis by revealing reversible cortical hypometabolism [1,3].

Aims

We report a case of HE presenting as acute neuropsychiatric deterioration superimposed on treatment-resistant depression, highlighting the diagnostic role of FDG-PET and the clinical significance of lorazepam-resistant catatonia as a potential diagnostic signal [2].

Case Presentation

A 57-year-old woman with a 35-year history of treatment-resistant major depressive disorder was evaluated following acute neuropsychiatric deterioration. A comprehensive workup was performed, encompassing blood analysis with thyroid antibody titres, CSF analysis (biochemistry, meningitis panel, oligoclonal bands), serum and CSF limbic encephalitis and paraneoplastic panels, malignancy screening, EEG, brain MRI, and pre- and post-treatment FDG-PET.

Results

Superimposed on her chronic course, a subacute deterioration emerged characterised by confusion, visual hallucinations, Cotard delusions, atypical unilateral parkinsonism, apraxia, and mixed-type catatonia (Bush-Francis Catatonia Rating Scale score:23), with no response to lorazepam. Anti-thyroglobulin (517.0 IU/mL; ref: 0–115) and anti-thyroid peroxidase (313.0 IU/mL; ref: 0–34) antibodies were markedly elevated despite euthyroid status. CSF revealed a Type IV oligoclonal band pattern; all limbic, paraneoplastic, and infectious markers were negative. EEG was normal; brain MRI was inconclusive. Pre-treatment FDG-PET revealed widespread cortical hypometabolism with left-hemispheric predominance(see Table for regional Z-scores). The convergence of acute neuropsychiatric deterioration, focal neurological signs, markedly elevated antithyroid antibodies, widespread FDG-PET hypometabolism, and Type IV oligoclonal bands following thorough exclusion of infectious, paraneoplastic, and other autoimmune aetiologies, collectively prompted empirical immunotherapy. Intravenous methylprednisolone (1g/day for 5 days) induced rapid and complete remission of catatonic and extrapyramidal symptoms. The patient was discharged on prednisolone (80 mg/day) and azathioprine (100mg/day). No recurrence was observed during follow-up.

Conclusions

This case underscores that SREAT should remain in the differential diagnosis of treatment-resistant psychiatric presentations, particularly when acute neuropsychiatric deterioration, including lorazepam-resistant catatonia is superimposed on a chronic course [1,2]. The regionally heterogeneous pattern of metabolic recovery, substantial in sensorimotor, posterior cingulate, and precuneus, corresponding with resolution of catatonia, and least in prefrontal and temporal regions, consistent with only partial improvement in depressive symptoms provides a compelling neuroanatomical correlate of clinical outcomes [4,5]. FDG-PET, may thus guide timely immunotherapy even in the absence of definitive CSF or EEG abnormalities [2,3].

Table.Regional FDG-PET Z-Scores: Pre- and Post-Treatment Comparison

Region Pre-R Pre-L Post-R Post-L ΔR ΔL
Prefrontal-Lateral −3.13 −3.47 −2.80 −3.46 +0.33 +0.01
Prefrontal-Medial −2.20 −2.47 −1.67 −2.10 +0.53 +0.37
Sensorimotor −2.47 −2.69 −1.73 −2.04 +0.74 +0.65
Anterior-Cingulate −0.43 −0.50 −0.08 −0.14 +0.35 +0.36
Posterior-Cingulate −1.72 −1.91 −1.01 −1.40 +0.71 +0.51
Precuneus −2.08 −2.29 −1.40 −1.63 +0.68 +0.66
Parietal-Superior −2.98 −2.85 −2.32 −2.43 +0.66 +0.42
Parietal-Inferior −3.48 −5.04 −3.07 −4.71 +0.41 +0.33
Occipital-Lateral −2.29 −2.88 −1.01 −2.10 +1.28 +0.78
Primary Visual −3.19 −1.06 −2.21 +0.22 +0.98 +1.28
Temporal-Lateral −2.44 −3.98 −2.30 −3.98 +0.14 0.00
Temporal-Medial −0.92 −0.97 −0.54 −0.64 +0.38 +0.33

Positive Δ values indicate metabolic improvement. R = right; L = left hemisphere.

References

  1. Laurent, C., Capron, J., Quillerou, B., Thomas, G., Alamowitch, S., Fain, O., et al., 2016. Steroid-responsive encephalopathy associated with autoimmune thyroiditis (SREAT): characteristics, treatment and outcome in 251 cases from the literature. Autoimmun. Rev. 15 (12), 1129–1133.
  2. İlhan, R.S., Can, K.C., Şahiner, Ş.Y., Duman, B., Çolak, B., Kır, Y., et al., 2025. Hashimoto’s encephalopathy in psychiatric inpatients: neuropsychiatric morbidity, diagnostic challenges and treatment. Front. Psychiatry 16. https://doi.org/10.3389/fpsyt.2025.1639179
  3. Lagström, R.M.B., Østerbye, N.N., Henriksen, O.M., Høgh, P., 2019. Hashimoto’s encephalopathy: follow-up data from neuropsychology, lumbar puncture, and FDG-PET. Clin. Case Rep. 7 (9), 1750–1753.
  4. Duque, L., Ghafouri, M., Nunez, N.A., Ospina, J.P., Philbrick, K.L., Port, J.D., et al., 2024. Functional neuroimaging in patients with catatonia: a systematic review. J. Psychosom. Res. 179, 111640.
  5. Su, L., Cai, Y., Xu, Y., Dutt, A., Shi, S., Bramon, E., 2014. Cerebral metabolism in major depressive disorder: a voxel-based meta-analysis of positron emission tomography studies. BMC Psychiatry 14 (1), 321.