PRES Mimicking Ischaemic Stroke in Severe Autoimmune Hyperthyroidism: A Case Report

Cortical Visual Loss and Seizures Emerge in Severe Autoimmune Hyperthyroidism

Posterior reversible encephalopathy syndrome (PRES) has been documented in a patient experiencing severe autoimmune hyperthyroidism, presenting with profound cortical visual loss that initially mimicked a posterior cerebral artery infarction, as reported in a medical case study.

Thyroid Crisis Caused Brain Swelling and Temporary Blindness

• What happened: A patient with severe overactive thyroid function developed brain swelling in the areas responsible for vision, leading to temporary blindness and seizures.
• Why it mattered: Medical teams initially mistook the brain scan results for a standard stroke caused by a blocked blood vessel in the brain.
• The outcome: Recognizing that the condition was actually PRES—a brain disorder that can reverse itself—allowed doctors to treat the underlying thyroid crisis and seizures successfully.

Clinical Manifestations and Diagnostic Challenges of Thyrotoxic PRES

The patient presented to the emergency department after being found collapsed, exhibiting confusion, a fever of 38.7°C, and tachycardia. Initial blood tests revealed severe thyrotoxicosis, with a suppressed thyroid-stimulating hormone (TSH) alongside markedly elevated free thyroxine (FT4) and free triiodothyronine (FT3). Strongly positive thyroid peroxidase and TSH receptor antibodies confirmed Graves’ disease. While thyroid storm was suspected due to the combination of severe biochemical thyrotoxicosis, fever, and altered mental status, clinicians noted these findings lacked absolute specificity for thyroid storm in the presence of suspected systemic infection and hypercapnic respiratory failure.

As the inpatient stay progressed, the patient developed recurrent focal and generalized seizures. Serial electroencephalogram (EEG) monitoring demonstrated focal epileptiform activity over the right hemisphere, indicating ongoing focal-onset seizure activity. Antiepileptic therapy was escalated to achieve seizure control.

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Simultaneously, neurological deficits expanded to include profound visual impairment. The patient progressed from general visual disturbance to an absolute inability to detect hand movements despite preserved pupillary responses. While initial CT and CTA scans showed no acute intracranial abnormalities, a subsequent brain MRI revealed cortical and subcortical T2/FLAIR hyperintensity involving the right occipital lobe with associated diffusion restriction.

Pathophysiological Mechanisms Linking Thyroid Storm to Cerebral Edema

Posterior reversible encephalopathy syndrome is characterized by acute neurological symptoms including encephalopathy, seizures, headaches, and visual disturbances, accompanied by posterior cerebral vasogenic edema on MRI. Vasogenic edema involves fluid accumulation in brain tissue driven by increased blood-brain barrier permeability. The syndrome is thought to stem from a disruption of cerebral autoregulation—the mechanism stabilizing blood flow despite systemic blood pressure shifts—alongside endothelial dysfunction.

While severe or rapidly developing hypertension typically drives PRES, the syndrome can also manifest without marked blood pressure elevations in patients experiencing renal dysfunction, sepsis, autoimmune disease, or cytotoxic therapies.

Trajectory of Recovery and Diagnostic Resolution

The patient’s recovery trajectory hinged on treating both the underlying autoimmune hyperthyroidism and the secondary neurological complications. The substantial interval improvement observed on follow-up neuroimaging confirmed the reversibility of the occipital white matter abnormalities, distinguishing the presentation from permanent ischemic stroke and showing that doctors must identify metabolic triggers in atypical presentations of posterior reversible encephalopathy syndrome.

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References

• Posterior Reversible Encephalopathy Syndrome Associated With Severe Autoimmune Hyperthyroidism: A Case of Cortical Visual Loss Mimicking Posterior Cerebral Artery Infarction.