Amnesic syndrome with bilateral mesial temporal lobe involvement in Hashimoto’s encephalopathy

Abstract

A 25-year-old woman presented with a subacute confusional state, headaches, unsteadiness, myoclonus, seizures, and an amnesic syndrome as a manifestation of Hashimoto's encephalopathy. Investigations showed biochemical hypothyroidism, raised thyroid microsomal antibodies, and weakly positive antineuronal antibodies. A T2-weighted MRI of the brain showed bilateral symmetric areas of increased signal in the mesial temporal lobes and hippocampi that had a low signal intensity on T1-weighted imaging. Despite clinical and radiologic improvement after steroid and thyroid hormone replacement therapy, a severe amnesic syndrome with associated localized MRI abnormalities persists.

Reversible white matter alterations in encephalopathy associated with autoimmune thyroid disease

“…Nevertheless there is another report of irreversible white matter abnormalities in a case of an amnesic syndrome related to bilateral mesial temporal involvement, which does not exactly resemble our case [8]. In our patient white matter abnormalities were more diffuse than in the case mentioned above, involving a large part of both hemispheres and the brainstem.…”

A case of autoimmune thyroid disease presenting posterior reversible encephalopathy syndrome

“…6,13 The cerebellar hemisphere, temporal lobe, brainstem, and hippocampus were also involved in some cases. 4,7,8 In a limited number of the cases of EAATD, cor tical involvement was observed, as in our case. 5 It has been suggested that these signal abnormalities reflect either edema or inflammation.…”

Anti-neuronal autoantibody in Hashimoto's encephalopathy: neuropathological, immunohistochemical, and biochemical analysis of two patients

“…It is therefore unlikely that CNS vasculitis could cause the symptoms, which are serious but can be quickly overcome, that are usually seen in HE. The second theory, on the other hand, which postulates direct harmful action of antineuronal antoantibodies, constitutes a more likely explanation of the pathogenesis of HE because of the non-focal neurological symptoms and diffuse background slowing on EEG, which imply diffuse encephalopathy [7,8], and the usually normal, or occasionally diffuse and/or symmetric abnormal findings in neuroradiological studies of HE patients [7,8,10,[25][26][27]. All of these findings are thought to indicate the involvement of humoral immunity.…”