Hashimoto’s thyroiditis is a condition where the body’s immune system mistakenly attacks the thyroid gland, leading to hypothyroidism. While the primary effect of Hashimoto’s is on metabolism and energy, the condition has been linked to neurological symptoms, including seizures, under rare and specific circumstances. The connection between this autoimmune process and brain instability can occur through two distinct mechanisms: a direct autoimmune attack on the central nervous system or as a consequence of severe, untreated thyroid hormone deficiency.
The Direct Autoimmune Link (SREAT)
The most direct, though uncommon, connection between Hashimoto’s and seizures is through a rare condition termed Steroid-Responsive Encephalopathy Associated with Autoimmune Thyroiditis (SREAT). SREAT is an autoimmune disorder causing inflammation in the brain (encephalopathy). Seizures are one of its common manifestations, occurring in an estimated 60% to 70% of patients. The condition was historically known as Hashimoto’s Encephalopathy.
The underlying cause of SREAT is believed to be an autoimmune attack on brain tissue, although the specific target remains under investigation. Researchers suspect that certain autoantibodies cross-react with brain cells, leading to inflammation and brain dysfunction. This inflammatory process disrupts the brain’s normal electrical signaling, which manifests as seizures.
The severity of neurological symptoms often does not correlate with the degree of thyroid dysfunction. Patients with SREAT can have high levels of thyroid autoantibodies, specifically Anti-TPO and Anti-Tg, while maintaining normal or near-normal thyroid hormone levels. This disconnect suggests that the central nervous system symptoms result from the direct autoimmune process in the brain, separate from the hormonal effects of hypothyroidism. Symptoms of SREAT can also include cognitive decline, confusion, personality changes, and stroke-like episodes, often following a relapsing-remitting course.
Indirect Seizure Triggers from Thyroid Dysfunction
Severe, uncontrolled hypothyroidism resulting from Hashimoto’s disease can indirectly create metabolic conditions that trigger seizures. Hypothyroidism affects multiple organ systems, and in its most extreme form, it can progress to a life-threatening state known as myxedema coma. This severe metabolic derangement, rather than the autoimmune antibodies themselves, can lead to neurological instability.
One primary indirect trigger is severe hyponatremia. Hypothyroidism can cause the body to retain excess water, leading to a dilution of the blood’s sodium levels, often resulting in a condition known as syndrome of inappropriate antidiuretic hormone secretion (SIADH) or an SIADH-like state. When the sodium level drops rapidly, the brain cells swell as water moves into them, which can disrupt electrical activity and precipitate generalized seizures.
Severe hypoglycemia, or low blood sugar, may occur due to impaired glucose production, which deprives the brain of its primary energy source and can induce seizures. Additionally, the generalized slowing of metabolic processes can lead to cerebral edema and hypoxemia, where oxygen levels in the blood are low. Both cerebral edema and hypoxemia increase the brain’s susceptibility to epileptic activity. These metabolic seizures are a consequence of the physiological fallout from severe hormone deficiency.
Diagnosis and Management of Thyroid-Related Neurological Issues
When a patient with Hashimoto’s presents with new or unexplained seizures, diagnosis involves systematically ruling out other possible causes, such as infection, stroke, tumors, or other forms of autoimmune encephalitis. High titers of antithyroid antibodies, particularly Anti-TPO and Anti-Tg, raise suspicion for a thyroid-related neurological issue in the context of encephalopathy.
Diagnostic tools include electroencephalogram (EEG), which often shows non-specific diffuse slowing of brain activity, and magnetic resonance imaging (MRI) of the brain, which may be entirely normal or show subtle, non-specific abnormalities. The most defining characteristic, however, is the patient’s clinical response to treatment.
The management of SREAT involves a two-pronged approach. Neurological symptoms, including seizures, are typically treated with high-dose corticosteroids, such as intravenous methylprednisolone, to suppress the underlying autoimmune inflammation. The rapid and significant improvement in symptoms following steroid administration is a hallmark of the condition and helps confirm the diagnosis. For the underlying thyroid condition, thyroid hormone replacement therapy is given to manage any associated hypothyroidism. In cases that do not respond sufficiently to steroids, other immunosuppressive therapies, such as plasma exchange or intravenous immunoglobulin (IVIg), may be considered.