# Beyond Pediatric Sleep Disorders: A Case of Hypersomnia Revealing Hashimoto’s Encephalopathy

## TL;DR

A teenage girl with long-term hypersomnia was diagnosed with Hashimoto’s encephalopathy, highlighting the need for thyroid screening in pediatric sleep disorders.

## Contribution

This case emphasizes that hypersomnia in adolescents may indicate Hashimoto’s encephalopathy and advocates for thyroid antibody testing in such cases.

## Key findings

- The patient showed marked clinical improvement with corticosteroid therapy, supporting the diagnosis of Hashimoto’s encephalopathy.
- Thyroid antibody levels were significantly elevated, while other tests ruled out alternative causes of hypersomnia.
- No clinical relapse occurred despite a moderate increase in antibody levels after treatment discontinuation.

## Abstract

Hypersomnia is uncommon in children and is often misinterpreted as fatigue, which may lead to delayed diagnosis and management of underlying conditions. We present a case of steroid-responsive encephalopathy associated with autoimmune thyroiditis (SREAT), also known as Hashimoto’s encephalopathy (HE), in an adolescent, with a clinical picture dominated by hypersomnia. A 15-year-old girl presented with an 18-month history of hypersomnia, associated with sleep paralysis, suspected cataplexy, auditory and visual hallucinations, and tremor. A large diagnostic workup was performed to distinguish between central hypersomnia, including narcolepsy, and secondary causes (obstructive sleep apnea, underlying neurological, psychiatric, or medical disorders). Polysomnography followed by a multiple sleep latency test (MSLT) and human leukocyte antigen (HLA) typing did not support a narcolepsy diagnosis. Brain and spinal cord magnetic resonance imaging (MRI), a 24-hour continuous electroencephalogram (EEG), and a neuropsychological evaluation were all unremarkable. Biological workup, including blood tests and cerebrospinal fluid (CSF) analysis, was also unremarkable, excluding infectious, toxic, metabolic, neoplastic, and autoimmune causes, except for significantly elevated anti-thyroid antibodies (ATA). The patient received corticosteroid therapy (high-dose followed by a maintenance dose), and the marked clinical improvement reinforced Castillo and Graus’s diagnostic criteria for HE. Treatment was stopped after one year due to disabling side effects and disappearance of complaints. At present, there is no clinical relapse despite a moderate increase in ATA levels. This case highlights that hypersomnia can be a potential early manifestation of SREAT in adolescents that can often be overlooked. Pediatric hypersomnia should prompt a comprehensive evaluation, including systematic thyroid screening with the assessment of ATA. Early recognition and early therapeutic management may impact the disease course and reduce the risk of long-term complications.