Multiple intracranial lesions as the unusual imaging features of Hashimoto's encephalopathy: A case report

Abstract

Rationale: Hashimoto's encephalopathy (HE) is associated with autoimmune thyroid disease and is complex, diverse, and easily misdiagnosed. However, if HE is diagnosed and treated in a timely manner, an optimal prognosis may be achieved.

Patient concerns: We presented a case of a 63-year-old female patient with paroxysmal dizziness, unsteady gait, emotion apathy, progressive cognitive impairment, and unusual magnetic resonance imaging (MRI) findings.

Diagnoses: After suffering for almost 8 years, the patient was diagnosed with HE based on clinical manifestation, abnormal electroencephalogram, unusual MRI findings, sensitivity to cortisol treatment, and characteristic high antithyroid peroxidase antibody (TpoAb) titer.

Interventions: The patient continued regular glucocorticoids therapy after intravenous methylprednisolone pulse therapy, neurotrophic drugs, traditional Chinese medicine and rehabilitation to relieve hypermyotonia and cognitive impairment.

Outcomes: After combined treatment, the patient's symptoms, electroencephalogram (EEG), MRI, and the TpoAb titer gradually improved. However, the patient had to stop glucocorticoids treatment because of severe osteoporosis, fractures and other adverse reactions. Her symptoms fluctuated, and her TpoAb titer increased again.

Lessons: HE may cause highly heterogeneous clinical features, particularly MRI findings. Withdrawal of the systematic glucocorticoids treatment can lead to varied outcomes in these patients.

Figure 1

April 2015 brain CT scan (A, B): Symmetry visible image density is slightly flaky, and the bilateral basal ganglia and semioval center exhibit multiple punctate low density white matter, bilateral basal ganglia with visible symmetry punctate calcification. September 2015 brain CT scan (C, D): Bilateral symmetry visible ventricle white matter halo density changes and right basal ganglia visible low density strips. CT = computed tomography.

Figure 2

Magnetic resonance evolution of the case. Brain MRI of the case obtained for the first time in April 2015 (A–F) indicates the left basal ganglia, thalamus and cerebellum have multiple small circular abnormal signals, the T1WI, T2WI, and FLAIR exhibited low signals in the bilateral basal ganglia and thalamus, and an enhanced scan indicated lesion visible edge enhancements. Semioval center bilateral basal ganglia and other T1WIs indicate multiple punctate or low signals, T2WI high signals, and a FLAIR sequence with a clear display. On the FLAIR sequence, next to the bilateral lateral symmetry, a large sheet of white matter high signal was identified. Next brain MRI obtained in September 2015 (G–K) indicates which compared with April 2015, the right thalamus T2 high signal disappeared. The third MRI obtained in April 2016 (L–Q) indicates multiple punctate susceptibility effects on the SWI sequence in the basal ganglia, which is similar findings with 2015s. FLAIR = fluid-attenuated inversion recovery, MRI = magnetic resonance imaging, SWI = susceptibility-weighted imaging, T2WI = T2-weighted image.

Figure 3

Electroencephalogram evolution of the case.