# When Autoimmunity and Vascular Events Collide: A Unique Presentation of Hashimoto’s Encephalopathy and Ischemic Stroke

**Authors:** Marilhia C Cornejo Leon, Nariman Noorbakhsh-Sabet

PMC · DOI: 10.7759/cureus.98423 · Cureus · 2025-12-03

## TL;DR

A rare case of Hashimoto’s encephalopathy and ischemic stroke is presented, highlighting the importance of considering autoimmune thyroiditis in patients with thyroid disease and acute neurological symptoms.

## Contribution

This paper reports a rare case linking autoimmune thyroiditis with watershed strokes, emphasizing the need for early diagnosis and treatment.

## Key findings

- The patient showed clinical improvement after immunotherapy, suggesting an autoimmune mechanism.
- Thyroid disorders, particularly autoimmune thyroiditis, may increase stroke risk through multiple pathways.
- Hypotension episodes in the patient raised concerns about cerebral hypoperfusion linked to Hashimoto’s encephalopathy.

## Abstract

Hashimoto’s encephalopathy (HE) encompasses an umbrella of symptoms, including cognitive decline, seizures, neurological focal deficits, stroke, psychosis, dementia, and coma. Its pathogenesis is not clear, nor is its mechanism by which it causes strokes.

A 56-year-old African American female with nodular thyroid disease presented with subacute encephalopathy, amnesia, and bilateral symmetric cerebral watershed strokes in the setting of elevated antithyroid antibodies that clinically improved after immunotherapy. This is a rare reported case of possible autoimmune thyroiditis (AT) presenting with watershed strokes.

Thyroid disorders are a risk factor for cerebrovascular disease. Autoimmune thyroiditis increases the risk of stroke in patients with hypothyroid AT due to the higher frequency of atrial fibrillation, large artery atherosclerosis, and hypertension. The pathogenesis of HE is uncertain, but it is believed that it could be autoimmune, vasculitis, and/or hypoperfusion-related. Our patient had three episodes of hypotension, raising concern for global cerebral hypoperfusion due to the microvascular disruption that takes place in HE.

HE has a low prevalence but good response to steroids. Considering it as a differential diagnosis in cases of thyroid disease and acute stroke is crucial to promptly make a diagnosis and start treatment.

## Linked entities

- **Diseases:** Hashimoto’s encephalopathy (MONDO:0019385), ischemic stroke (MONDO:1060198), autoimmune thyroiditis (MONDO:0005623), atrial fibrillation (MONDO:0004981)

## Full-text entities

- **Diseases:** seizures (MESH:D012640), Thyroid disorders (MESH:D013959), dementia (MESH:D003704), neurological focal deficits (MESH:D009461), amnesia (MESH:D000647), atrial fibrillation (MESH:D001281), cognitive decline (MESH:D003072), cerebral hypoperfusion (MESH:D002547), Ischemic Stroke (MESH:D002544), encephalopathy (MESH:D001927), vasculitis (MESH:D014657), acute stroke (MESH:D020521), atherosclerosis (MESH:D050197), hypertension (MESH:D006973), hypotension (MESH:D007022), psychosis (MESH:D011618), autoimmune (MESH:D001327), hypothyroid AT (MESH:C562768), AT (MESH:D013967), cerebrovascular disease (MESH:D002561), HE (MESH:C535841), coma (MESH:D003128)
- **Chemicals:** antithyroid (-), steroids (MESH:D013256)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

15 references — full list in the complete paper: https://tomesphere.com/paper/PMC12759291/full.md

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Source: https://tomesphere.com/paper/PMC12759291