Can Hypothyroidism Really Cause Seizures?

The effects of hypothyroidism extend beyond metabolism and energy levels, potentially influencing brain function in unexpected ways. While seizures are not commonly listed as a primary consequence, some cases suggest a possible link that warrants further exploration.

Understanding how low thyroid hormone levels might contribute to seizure activity requires examining their role in brain physiology and electrical stability.

Thyroid Hormones And Brain Physiology

Thyroid hormones play a fundamental role in brain development, neuronal function, and synaptic regulation. Triiodothyronine (T3) and thyroxine (T4) influence neurogenesis, myelination, and neurotransmitter balance, all of which contribute to the brain’s electrical stability. During fetal and early postnatal development, they regulate neural differentiation and synaptic formation. Deficiencies during these periods can lead to irreversible cognitive impairments, but even in adulthood, imbalances can disrupt neural communication and excitability.

One key way thyroid hormones affect brain physiology is by modulating ion channels and neurotransmitter systems. T3 regulates voltage-gated sodium and potassium channels, essential for action potential propagation. A reduction in thyroid hormones can alter neuronal excitability, potentially leading to hyperexcitability or impaired synaptic transmission. Additionally, they influence gamma-aminobutyric acid (GABA) and glutamate signaling, which maintain the balance between excitation and inhibition in the brain. A disruption in this balance can predispose neural circuits to abnormal firing patterns, increasing seizure susceptibility.

Cerebral blood flow and energy metabolism are also closely linked to thyroid hormone activity. Studies using functional imaging have shown that hypothyroidism reduces glucose metabolism in brain regions like the cerebral cortex and hippocampus, which are involved in cognitive processing and seizure generation. Furthermore, thyroid hormones regulate mitochondrial activity, and deficiencies can lead to oxidative stress and impaired ATP production, both of which are implicated in seizure pathophysiology.

Possible Mechanisms Linking Hypothyroidism To Seizures

The relationship between hypothyroidism and seizures likely stems from multiple physiological disruptions that collectively alter neuronal excitability. One significant factor is the effect of thyroid hormone deficiency on ion channels, which govern neuronal electrical activity. Reduced T3 and T4 levels can alter the expression and function of voltage-gated sodium, potassium, and calcium channels, all crucial for maintaining proper firing patterns. When these channels are dysregulated, neurons may become more susceptible to erratic depolarization, increasing the likelihood of seizures, particularly in the hippocampus.

Beyond ion channel modulation, thyroid hormone deficiency also impacts neurotransmitter dynamics. GABA, the brain’s primary inhibitory neurotransmitter, plays a central role in preventing excessive neuronal firing. Research suggests hypothyroidism reduces GABAergic inhibition by decreasing receptor expression and impairing synthesis. A reduction in inhibitory signaling allows excitatory neurotransmitters like glutamate to exert a stronger influence, increasing the risk of hyperexcitability. Elevated glutamatergic activity has been implicated in seizure generation, as excessive NMDA and AMPA receptor stimulation can lead to excitotoxicity and neuronal damage.

Mitochondrial dysfunction further compounds the risk by disrupting neuronal energy homeostasis. Thyroid hormones regulate mitochondrial biogenesis and oxidative phosphorylation, ensuring adequate ATP production to sustain neuronal function. Studies show hypothyroidism decreases mitochondrial enzyme activity, resulting in impaired energy metabolism and increased oxidative stress. Neurons, which have high metabolic demands, are particularly vulnerable to energy deficits. A lack of ATP can impair ion pump activity, leading to intracellular ion imbalances and increased excitability. Additionally, oxidative stress can damage neuronal membranes and proteins, further destabilizing electrical signaling.

Cerebral hypoperfusion, another consequence of hypothyroidism, may also contribute to seizure susceptibility. Functional imaging studies have shown reduced cerebral blood flow in individuals with hypothyroidism, particularly in regions involved in cognition and motor control. Decreased perfusion can lead to localized hypoxia, disrupting neuronal function and lowering the seizure threshold. Hypoxic conditions can trigger seizures by promoting anaerobic metabolism, increasing lactate accumulation, and altering ion gradients that regulate excitability. This mechanism may be particularly relevant in severe hypothyroidism, where prolonged reductions in cerebral blood flow exacerbate dysfunction.

Distinguishing Thyroid-Related Events From Epilepsy

The overlap between neurological symptoms caused by hypothyroidism and those seen in epilepsy presents a diagnostic challenge. Seizures linked to thyroid dysfunction often lack the hallmark features of primary epilepsy, making it essential to differentiate between metabolic disturbances and true epileptic activity. Unlike epilepsy, where seizures originate from abnormal, synchronized neuronal firing, thyroid-related seizure-like episodes may stem from transient neurotransmitter imbalances, ion channel dysfunction, or cerebral perfusion deficits. These differences influence both the presentation and the response to conventional antiepileptic treatments, which may be ineffective if thyroid hormone deficiency is the underlying cause.

Electroencephalography (EEG) is a valuable tool in this distinction, as epileptic seizures typically produce characteristic spike-wave discharges or focal abnormalities. In contrast, individuals experiencing seizure-like events due to hypothyroidism may exhibit nonspecific slowing of background rhythms rather than paroxysmal activity. This diffuse slowing reflects the broader impact of thyroid hormone deficiency on neuronal function rather than localized hyperexcitability. Additionally, restoring normal thyroid hormone levels often resolves seizure-like activity, whereas epilepsy generally requires long-term management with antiepileptic drugs.

Clinical history further aids in differentiation. Patients with thyroid-related seizures frequently report other systemic hypothyroid symptoms, such as cognitive slowing, depression, or muscle weakness, which are not typically associated with epilepsy. Furthermore, thyroid dysfunction tends to progress gradually, in contrast to the sudden, unprovoked nature of epileptic seizures. Laboratory findings provide additional clarity, with elevated thyroid-stimulating hormone (TSH) and low free T4 levels pointing to endocrine dysfunction. In cases where patients with epilepsy also have hypothyroidism, careful assessment is needed to determine whether thyroid dysfunction is exacerbating seizure frequency or if the seizures are unrelated.

Evaluating Neurological Symptoms In Clinical Settings

Assessing neurological disturbances in individuals with hypothyroidism requires a comprehensive approach. Patients often present with cognitive impairment, slowed reflexes, and altered mental status, making it essential to differentiate between thyroid-related dysfunction and primary neurological disorders. Clinicians typically begin with a detailed history, noting the onset, duration, and progression of symptoms. A gradual cognitive decline or intermittent confusion may suggest metabolic involvement, whereas abrupt neurological events raise concerns for stroke or epilepsy.

Neurological examination plays a central role in identifying patterns consistent with thyroid dysfunction. Reflex testing often reveals delayed relaxation of deep tendon reflexes, a hallmark of hypothyroid myopathy absent in many primary neurological conditions. Muscle weakness, often proximal, may mimic neuromuscular disorders but improves with thyroid hormone replacement. In suspected seizure-like episodes, clinicians assess for accompanying signs such as myoclonus, altered consciousness, or focal deficits to refine the diagnosis.