To assess how thyroid and immune fluctuations relate to neurological symptoms, especially vestibular dysfunction, and the role of meningioma in an elderly Graves’ disease patient.

Graves’ disease is an autoimmune disorder that primarily affects the thyroid gland but may also involve extrathyroidal and neurological manifestations through complex neuro-immune-endocrine interactions. Patients may develop ophthalmopathy, vestibular dysfunction, and neurological symptoms that are multifactorial and difficult to interpret clinically. These challenges become more significant when intracranial abnormalities, such as meningioma, coexist. Understanding the relationship between thyroid dysfunction, immune activity, and neurological symptoms is essential for accurate diagnosis and management.

We report a 74 year old woman with Graves’ disease status post radioiodine ablation, complicated by Graves’ ophthalmopathy, a left parietal extra axial meningioma, and vestibular dysfunction. A descriptive longitudinal evaluation was performed using detailed history taking, serial neurological examinations, brain imaging, and repeated thyroid function tests, including thyroid stimulating hormone (TSH) and free thyroxine (FT4), over more than one year. The analysis focused on correlating fluctuations in thyroid function with neurological symptom dynamics.

The patient demonstrated marked variability in thyroid function, ranging from severe hyperthyroidism (TSH <0.01 µIU/mL with FT4 up to 5.17 ng/dL) to hypothyroid phases (TSH up to 12.10 µIU/mL with low FT4). Periods of hyperthyroidism and increased autoimmune activity were associated with episodic vertigo consistent with vestibular migraine, along with balance disturbances and recurrent falls. As thyroid function stabilized and ophthalmopathy became inactive, vestibular symptoms improved significantly. The meningioma remained stable without progressive focal deficits and was considered a structural comorbidity. Residual balance impairment was likely related to chronic small vessel disease and peripheral polyneuropathy.

This case illustrates a neuro-immune-endocrine interplay in Graves’ disease, where autoimmune dysregulation creates a proinflammatory, hormone sensitive environment influencing multiple systems. An integrated approach is crucial for managing complex neurological presentations in such patients