The brain’s electrical activity is a finely tuned system, maintaining a balance between excitation and inhibition. The “seizure threshold” describes the level of brain excitability that must be reached for a seizure to occur. Everyone possesses a seizure threshold, representing their individual resistance to seizures. While most people have a sufficiently high threshold to prevent spontaneous seizures, certain factors can lower this threshold, making the brain more susceptible to uncontrolled electrical activity and thus increasing the likelihood of a seizure. This article explores various influences that can reduce the seizure threshold.
Medications and Substances
Many medications, both prescription and illicit, can influence brain chemistry and consequently lower the seizure threshold. These substances often affect neurotransmitters, the chemical messengers that regulate brain activity. The primary excitatory neurotransmitter is glutamate, while gamma-aminobutyric acid (GABA) serves as the main inhibitory neurotransmitter; an imbalance favoring excitation can lead to seizures.
Certain prescription medications are known to reduce the seizure threshold. These include some antidepressants, such as bupropion and tricyclic antidepressants, particularly at higher doses. Antipsychotic medications, especially clozapine, can also increase seizure risk, often in a dose-dependent manner. Stimulants used for conditions like ADHD, as well as some antibiotics like fluoroquinolones, penicillins, and imipenem, have been linked to lowered seizure thresholds. Even commonly used antihistamines found in over-the-counter remedies may carry this risk.
Recreational substances can similarly impact brain excitability. Alcohol, especially during withdrawal, is a common factor that significantly lowers the seizure threshold. Chronic alcohol consumption leads the central nervous system to adapt to its depressant effects; abrupt cessation then causes a rebound hyperexcitability, as GABA receptors are downregulated and NMDA receptors are upregulated. Illicit drugs such as cocaine, amphetamines, and ecstasy can directly stimulate the brain, increasing neuronal excitability. Cannabis use has also been noted to lower the seizure threshold in some individuals.
Lifestyle and Environmental Influences
Daily habits and external surroundings play a significant role in modulating an individual’s seizure threshold. One of the most frequently reported factors is sleep deprivation, which can notably increase brain excitability. Lack of adequate sleep disrupts the brain’s natural electrical rhythms and can impair its ability to inhibit abnormal neuronal firing, making seizures more likely.
Stress, both acute and chronic, can also lower the seizure threshold. Stress activates the hypothalamic-pituitary-adrenal (HPA) axis, leading to the release of hormones like cortisol that can alter brain chemistry and make nerve cells more excitable. Chronic stress, in particular, may promote neuroinflammation and contribute to increased seizure frequency.
Fatigue, distinct from just lack of sleep, also contributes to a lowered threshold. This can involve both mental and physical exhaustion that impairs overall brain function and resilience. Furthermore, certain environmental stimuli can act as triggers for some individuals, particularly those with photosensitive epilepsy. Flickering lights, specific patterns, or even video games can induce seizures by overstimulating the visual cortex.
Extreme temperatures can additionally influence seizure susceptibility. Both overheating and severe cold can disrupt the brain’s delicate balance.
Physiological Changes and Health Conditions
Internal bodily states and underlying medical conditions can significantly impact the seizure threshold. Fever and illness are common precipitants, particularly in children between 6 months and 5 years of age. A rapid increase in body temperature, often above 38°C (100.4°F), can increase neuronal excitability, leading to febrile seizures. Inflammatory responses during infections can release cytokines, such as interleukin-1β, which contribute to fever and can enhance neuronal excitability by affecting the balance of excitatory and inhibitory neurotransmitters in the brain.
Electrolyte imbalances profoundly disrupt normal nerve cell function. Critical electrolytes like sodium, calcium, and magnesium are essential for proper electrical signaling in the brain. For instance, low sodium levels (hyponatremia) can cause brain swelling, leading to impaired electrical signaling and seizures, especially if the drop is rapid. Similarly, low levels of calcium (hypocalcemia) and magnesium (hypomagnesemia) can increase neuromuscular excitability and brain hyperexcitability, respectively, making seizures more likely.
Head injuries and brain trauma are well-recognized causes of a lowered seizure threshold and a significant risk factor for developing epilepsy. Damage to brain tissue can create areas of abnormal electrical activity, and the severity of the injury often correlates with the risk of seizures. Seizures can occur immediately after the injury (“early post-traumatic seizures”) or manifest much later, even years afterward (“late post-traumatic seizures”), due to the lasting disruption of brain networks.
Infections affecting the brain, such such as meningitis (inflammation of the membranes surrounding the brain and spinal cord) or encephalitis (inflammation of the brain itself), can also lower the seizure threshold. These infections can cause direct damage to brain tissue, leading to abnormal electrical activity and increased seizure susceptibility. The risk of seizures after such central nervous system infections can persist for many years. Specific medical conditions like stroke, which results from interrupted blood flow to the brain, or brain tumors, which can exert pressure and disrupt normal brain function, are also known to increase seizure risk by creating areas of abnormal neuronal activity.