Can Thyroid Issues Cause Seizures? Risks and Key Insights

Thyroid disorders affect various bodily systems, yet their impact on neurological function is often overlooked. While fatigue, weight changes, and mood disturbances are well-known symptoms, the potential link between thyroid dysfunction and seizures receives less attention. Understanding this connection is crucial for those managing thyroid conditions or unexplained seizure activity.

Though thyroid issues may not always directly cause seizures, they can increase the risk through various physiological mechanisms. Examining how thyroid imbalances affect brain function provides insight into why some individuals with thyroid disorders experience seizure-like episodes.

Thyroid’s Role In The Nervous System

The thyroid gland plays a key role in neurological stability by regulating hormones that influence brain function. Thyroxine (T4) and triiodothyronine (T3) extend beyond metabolism to impact neuronal activity, synaptic transmission, and brain excitability. These hormones cross the blood-brain barrier, binding to receptors in neurons and glial cells to regulate gene expression involved in neurodevelopment, neurotransmitter balance, and myelination. Disruptions in thyroid levels can alter neural signaling, potentially leading to abnormal electrical activity in the brain.

T3, the more active form of thyroid hormone, regulates neurotransmitters like gamma-aminobutyric acid (GABA), glutamate, and serotonin, which are crucial for maintaining excitatory-inhibitory balance. A deficiency or excess of these hormones can shift this equilibrium, heightening neuronal excitability or impairing inhibitory control, both of which are linked to seizure susceptibility. Studies in The Journal of Clinical Endocrinology & Metabolism indicate that thyroid dysfunction can weaken GABAergic inhibition, a key mechanism in preventing excessive neuronal firing.

Thyroid hormones also support the nervous system’s structural integrity. During fetal development and early childhood, they facilitate neuronal differentiation, axonal growth, and myelin formation. Even in adulthood, these hormones promote neuroprotection by sustaining oligodendrocyte function and white matter integrity. Research in Brain Research Reviews has shown that hypothyroidism can result in demyelination, disrupting electrical signal transmission and increasing seizure risk. Conversely, hyperthyroidism has been associated with oxidative stress in neural tissues, contributing to excitotoxicity and neuronal hyperactivity.

Hyperthyroid-Related Seizures

Excess thyroid hormones can significantly enhance neural excitability, increasing seizure risk. Hyperthyroidism accelerates metabolic processes, including those in the brain, amplifying synaptic transmission and disrupting the balance between excitatory and inhibitory signaling. Research in Epilepsy & Behavior has found that hyperthyroid individuals exhibit a higher prevalence of abnormal electroencephalographic (EEG) patterns, suggesting increased cortical excitability.

This heightened excitability is largely attributed to neurotransmitter imbalances. Elevated thyroid hormone levels enhance glutamate activity while reducing GABA function, creating a hyperexcitable cortical state. A study in Neuropharmacology demonstrated that hyperthyroidism-induced reductions in GABAergic inhibition led to spontaneous seizure activity in animal models, reinforcing the link between thyroid hormone excess and seizure susceptibility.

Hyperthyroidism also affects cerebral blood flow and metabolic demand. Increased thyroid hormone levels elevate cerebral oxygen consumption, potentially leading to transient hypoxia in vulnerable brain regions. Additionally, hyperthyroid patients often experience fluctuations in glucose metabolism, with some studies indicating periods of hypoglycemia that may further contribute to neuronal instability. A clinical case series in The Journal of Neurology documented patients with poorly controlled hyperthyroidism experiencing seizure episodes linked to metabolic disturbances.

Cardiovascular changes associated with hyperthyroidism may further exacerbate seizure risk. The condition increases heart rate and can induce arrhythmias, leading to intermittent cerebral hypoperfusion. In extreme cases, this can trigger seizure-like activity due to insufficient oxygen delivery to the brain. Case reports in Circulation highlight instances where patients with hyperthyroid-induced atrial fibrillation experienced transient ischemic attacks or seizure-like episodes, demonstrating the broader neurological impact of thyroid hormone dysregulation.

Hypothyroid-Related Seizures

Reduced thyroid hormone levels can impair brain function, lowering the seizure threshold. Hypothyroidism slows central nervous system metabolism, disrupting neuronal signaling and neurotransmitter balance. Severe thyroid hormone deficiency can lead to cognitive slowing, depression, and, in some cases, seizure-like episodes. These disturbances stem from diminished T3 availability, which is crucial for synaptic function and neuronal excitability.

Hypothyroidism also affects electrolyte homeostasis. Thyroid hormones regulate sodium-potassium pump activity, essential for maintaining neuronal stability. When thyroid levels drop, this regulation weakens, leading to intracellular sodium and potassium imbalances. Hypothyroid patients may develop hyponatremia, a condition linked to seizure activity. Clinical observations show that individuals with myxedema, a severe form of hypothyroidism, can present with confusion and, in extreme cases, generalized seizures due to metabolic slowing and electrolyte disturbances.

Additionally, hypothyroidism influences cerebral blood flow, further increasing seizure risk. Imaging studies reveal that untreated hypothyroid individuals exhibit reduced perfusion in key brain regions, particularly the temporal and frontal lobes. This decline in oxygen and nutrient delivery can lead to localized ischemia, fostering erratic neuronal activity. Case reports have documented patients experiencing focal seizures that resolved with thyroid hormone replacement, emphasizing the role of blood flow deficits in seizure development. Prolonged hypothyroidism has also been linked to increased blood-brain barrier permeability, allowing neurotoxic substances to accumulate and trigger abnormal electrical discharges.

Potential Mechanisms Leading To Seizure

Thyroid dysfunction can contribute to seizure susceptibility through multiple physiological pathways, including ion transport disruption, neuronal excitability changes, and hormone receptor sensitivity.

Ion Transport Disruption

Thyroid hormones regulate ion channel function, critical for neuronal stability. The sodium-potassium ATPase pump, responsible for maintaining resting membrane potential, is particularly sensitive to thyroid levels. In hyperthyroidism, excessive hormones enhance sodium influx and potassium efflux, increasing neuronal excitability. In contrast, hypothyroidism weakens this regulation, leading to intracellular sodium buildup and potassium deficiency, impairing action potential propagation. Research in Neuroscience Letters suggests that altered ion gradients in thyroid disorders can lead to spontaneous depolarization events, increasing seizure likelihood. Additionally, calcium channel dysfunction has been observed, with hyperthyroidism promoting excessive calcium influx that can trigger excitotoxicity, while hypothyroidism reduces calcium availability, impairing synaptic transmission.

Brain Excitability Changes

Thyroid hormones modulate the balance between excitatory and inhibitory neurotransmitters. Elevated thyroid hormone levels enhance glutamatergic activity, increasing excitatory postsynaptic potentials and making neurons more prone to hyperactivity, particularly in the hippocampus—a key region for seizure generation. Hypothyroidism reduces excitatory neurotransmission while impairing inhibitory GABAergic signaling, leading to an environment where neurons struggle to suppress aberrant electrical activity. A study in Brain Research found that thyroid hormone deficiency decreases GABA receptor expression, weakening the brain’s ability to counteract excessive excitatory input.

Hormone Receptor Sensitivity

The brain’s response to thyroid hormones depends on nuclear receptors that regulate gene expression related to neuronal function. In hyperthyroidism, an overabundance of thyroid hormones can desensitize receptors, reducing the brain’s ability to regulate excitability. This may contribute to persistent neural hyperactivity, increasing seizure susceptibility. Conversely, hypothyroidism results in insufficient receptor activation, leading to inadequate transcription of genes involved in synaptic stability and neuroprotection. Research in Endocrinology indicates that thyroid hormone receptor dysfunctions can lead to neurological symptoms, including seizures, due to impaired neuronal excitability regulation.

Comorbidities That May Exacerbate Seizures

Thyroid dysfunction often coexists with other medical conditions that can further increase seizure susceptibility. The interplay between thyroid disorders and additional health issues can amplify neurological instability, complicating the identification of seizure triggers.

Autoimmune conditions frequently accompany thyroid disorders, especially in cases of Hashimoto’s thyroiditis or Graves’ disease. Patients with autoimmune thyroiditis have a higher likelihood of developing central nervous system inflammation, which can contribute to seizure activity. Research in Autoimmunity Reviews has identified a link between autoimmune encephalitis and thyroid antibodies, suggesting immune-mediated mechanisms could exacerbate neuronal excitability. Individuals with multiple autoimmune disorders, such as lupus or type 1 diabetes, may experience systemic inflammation that affects brain function, increasing seizure risk.

Metabolic disorders also play a role in worsening seizure risk in those with thyroid dysfunction. Diabetes mellitus, particularly when poorly managed, can cause blood glucose fluctuations that impact neuronal stability. Hypoglycemia, a common complication in individuals on insulin therapy, can trigger seizures, and thyroid dysfunction may further impair glucose regulation. Similarly, electrolyte imbalances, often observed in thyroid disorders, can contribute to abnormal neuronal firing. Addressing these comorbid conditions is essential to reducing seizure risk and improving overall neurological health.