Hashimotos thyroiditis with associated neurological deficits (Hashimotos encephalopathy)
Elin Owen, Stella Woodward, Avril Wayte, Sarah Wenham & Antony Wilton
A 48-year-old female received radioiodine ablation therapy for thyrotoxicosis secondary to a solitary toxic nodule. The subsequent unexpected requirement for replacement thyroxine was explained by Hashimotos thyroiditis with an anti-thyroid peroxidase antibody level of 692.3 IU/ml. Thirty months later she presented with debilitating left facial pain and painful sensory symptoms of her left arm and leg. She was euthyroid taking thyroxine 75 μg daily with a fT4 of 19.2 pmol/l, fT3 4.2 pmol/l and TSH 2.15 mU/l. Anti-thyroid peroxidase level was 826.9 IU/ml.
Examination revealed an absent left corneal reflex and impaired sensation over the second and third divisions of the fifth cranial nerve and the left arm and leg. An MRI of brain and lumbar puncture were normal. EEG was abnormal with temporal sharp and slow waves. A diagnosis of Hashimotos encephalopathy was considered and treatment with prednisolone 30 mg daily commenced. At one month she was symptom free and neurological examination was normal. EEG was also normal. She remained symptom free for 3 months at which time there was a relapse of symptoms and signs with the left corneal reflex being present but impaired. She remained euthyroid with fT4 of 17.6 pmol/l, fT3 3.4 pmol/l and TSH 0.79 mU/l taking thyroxine 100 μg daily. EEG again demonstrated right temporal sharp and slow waves and anti-thyroid peroxidase antibody level was >500 IU/ml. Her prednisolone dose of 2.5 mg was not increased as symptoms were not troublesome and was stopped one month later. Over the ensuing six months symptoms resolved completely and a repeat EEG was normal. Anti-thyroid peroxidase antibodies however remained strongly positive at >500 IU/ml. This case describes a rare complication of Hashimotos thyroiditis with debilitating neurological deficits which responded to treatment with prednisolone. The condition is regarded as an uncommon associated auto-immune encephalopathy not caused by thyroid dysfunction (she was euthyroid throughout) or thyroid auto-antibody titres which remained elevated.