Coexistence of Acute Cerebral Infarction and Reversible Posterior Encephalopathy Syndrome in a Patient with Hashimoto's Thyroiditis

A 33-year-old male with a history of hyperthyroidism and diabetes presented 16 hours after the sudden onset of dizziness and aphasia. On physical examination, he exhibited complete motor aphasia and right central facial palsy. A cranial computed tomography scan revealed hypodense lesions in the left frontotemporal-parietal lobes and the brainstem (not shown). Brain magnetic resonance imaging (MRI) showed abnormal signals in the left frontotemporal-parietal lobes, which appeared hypointense on T1-weighted images, hyperintense on T2-weighted, and fluid attenuated inversion recovery (FLAIR) sequences (see Fig 1A–C), with restricted diffusion (see Fig 1D, E). The pons displayed abnormal signals, characterized by T1 hypointensity, T2, and FLAIR hyperintensity, isointensity on diffusion weighted imaging (DWI), and hyperintensity on apparent diffusion coefficient (ADC) (Fig 2A–E). Laboratory investigations revealed elevated free thyroxine (20.49pmol/L), undetectable thyroid-stimulating hormone (<0.005μIU/mL), markedly increased thyroglobulin antibodies (>4,000IU/mL), and anti-thyroid peroxidase antibodies (493.40IU/mL). Electrocardiography indicated atrial fibrillation, whereas cranial magnetic resonance angiography showed no abnormalities (not shown). The patient was diagnosed with acute cerebral infarction accompanied by posterior reversible encephalopathy syndrome (PRES). Treatment included antiplatelet therapy, glycemic control, and thyroid regulation, leading to gradual clinical improvement. Follow-up MRI at 6 weeks showed partial resolution of brainstem abnormalities (see Fig 2F). However, persistent high FLAIR signals and mild cortical atrophy remained in the left frontotemporal-parietal lobes (see Fig 1F). Nine weeks later, the patient was rehospitalized because of persistent atrial fibrillation and heart failure, attributed to hyperthyroid heart disease, as a result of non-compliance with the prescribed oral thyroid medication. Following treatment, his condition improved, and he was subsequently discharged. PRES is typically characterized by a range of neuroimaging findings and neurological symptoms indicative of vasogenic edema. Although hypertension remains the most common trigger for PRES,1 there are documented cases of PRES occurring in the context of autoimmune diseases or thyroid dysfunction1, 2 Among these, autoimmune thyroid disease has been recognized as a contributor to endothelial damage, subsequently leading to reversible vasogenic edema characteristic of PRES.2, 3 Notably, the coexistence of PRES and acute cerebral infarction has been observed in the literature, albeit exclusively in patients with concurrent hypertension.4 This case is particularly remarkable because of the simultaneous occurrence of acute cerebral infarction and reversible brainstem lesions in a normotensive patient with thyroid dysfunction, with clear radiographic evidence differentiating cytotoxic from vasogenic edema. We hypothesize that the metabolic instability caused by hyperthyroidism, combined with cardiovascular abnormalities, played a significant role. Atrial fibrillation, which is known to be associated with hyperthyroidism, likely led to a cardioembolic stroke, contributing to the acute hemispheric infarction. Meanwhile, the significantly elevated thyroid antibodies suggest endothelial dysfunction, which may have contributed to the development of PRES. Therefore, in this patient, hyperthyroidism and the associated autoimmune process likely acted as a common underlying mechanism, precipitating both the acute infarction and the development of PRES. This case underscores the critical importance of early recognition and swift intervention in patients presenting with neurological deficits and a background of thyroid dysfunction. Timely diagnosis and treatment were essential in achieving a favorable outcome in this patient. W.W. contributed to drafting the text. J.Y. contributed to preparing the figure. Nothing to report.