HASHIMOTO’S ENCEPHALOPATHY: A FORGOTTEN CAUSE OF ACUTE ALTERED SENSORIUM

Abstract

Hashimoto’s encephalopathy (HE), or steroid-responsive encephalopathy associated with autoimmune thyroiditis (SREAT), is a rare, underrecognized autoimmune neuro-endocrine disorder. It presents with acute or subacute neuropsychiatric features, ranging from altered sensorium and stroke-like episodes to status epilepticus. Because patients are frequently euthyroid, diagnosis is often delayed. A 48-year-old female presented to the emergency department with a 3-day history of acute onset altered sensorium, visual hallucinations, and generalized tonic-clonic seizures. Physical examination revealed an agitated patient with fluctuating consciousness (Glasgow Coma Scale 11/15) and hyperreflexia. Routine metabolic panels, toxicological screens, and contrast-enhanced brain magnetic resonance imaging (MRI) were unremarkable. Cerebrospinal fluid (CSF) analysis demonstrated elevated protein (68 mg/dL) with normal cellularity and negative infectious PCR panels. Electroencephalography (EEG) showed diffuse bi-frontal theta-delta slowing. Thyroid function testing revealed euthyroid status (TSH 2.10 mIU/L), but serum anti-thyroid peroxidase (anti-TPO) antibodies were markedly elevated at >1,000 IU/mL. After excluding infectious, metabolic, toxic, and vascular etiologies, a diagnosis of HE was established. High-dose pulse methylprednisolone (1 g/day intravenously) was initiated for 5 consecutive days. The patient exhibited rapid neurological recovery within 48 hours, regaining baseline orientation with resolution of seizure activity. An oral prednisone taper was maintained, and follow-up at 3 months confirmed complete cognitive recovery without recurrence. HE remains a forgotten differential diagnosis in acute altered sensorium. Normal thyroid function does not rule out the disease. Early recognition and prompt administration of high-dose corticosteroids yield remarkable clinical recovery, preventing unnecessary invasive interventions and permanent neurological damage.