Seizures After Brain Surgery: Postoperative Insights

Seizures are a known complication following brain surgery, affecting some patients in the days, weeks, or even months after their procedure. While not everyone experiences them, seizures may indicate underlying neurological changes that require medical attention. Understanding why they occur and how they are managed is essential for both patients and healthcare providers.

Several factors contribute to postoperative seizures, including surgical techniques, pre-existing conditions, and brain tissue responses. Recognizing these influences helps guide treatment and prevention strategies.

Timeline Of Seizure Occurrence

The onset of seizures after brain surgery varies, influenced by factors such as procedure type, surgical site location, and the patient’s neurological history. Some seizures emerge within the first 24 to 48 hours postoperatively, often due to acute surgical trauma, metabolic disturbances, or localized inflammation. These early seizures may not indicate long-term epilepsy but rather a temporary disruption in neuronal stability. Studies show that up to 15% of patients undergoing craniotomy for tumor resection or vascular procedures experience seizures in the first few days, with higher risk in those with pre-existing cortical irritation (Englot et al., 2016, J Neurosurg).

Seizures can also develop in the subacute phase, typically within the first few weeks. This period is associated with gliosis, delayed neuronal excitability, and blood-brain barrier breakdown. Research suggests that patients who experience seizures in this window have a higher likelihood of recurrent episodes, particularly if structural abnormalities persist. A retrospective analysis found that nearly 30% of patients who had their first seizure within one month of surgery later developed chronic epilepsy (de Tisi et al., 2011, Brain).

For some, seizures do not appear until months or even years after surgery, often due to long-term neuroplastic changes and scar tissue formation. Late-onset seizures, occurring beyond six months postoperatively, are commonly linked to permanent alterations in cortical networks and epileptogenic foci. The risk is higher in cases involving traumatic brain injury, tumor resections, or vascular malformations, where gliotic scarring and synaptic reorganization contribute to sustained hyperexcitability. A longitudinal study in Epilepsia (Herman, 2020) found that nearly 50% of patients who developed late-onset seizures after brain surgery eventually met the criteria for post-surgical epilepsy, highlighting the need for long-term monitoring.

Key Surgical And Neuropathological Factors

The likelihood of postoperative seizures is closely tied to surgical intervention and the underlying neuropathological landscape. Procedures involving direct manipulation of gray matter—such as tumor resections, epilepsy surgery, or vascular lesion removal—can lead to localized hyperexcitability. Resections in the perirolandic or mesial temporal regions have a particularly high association with seizure development due to dense neuronal connectivity and excitatory imbalances (Englot et al., 2016, J Neurosurg). Surgical precision, hemostatic control, and minimizing cortical traction are crucial in reducing seizure risk.

Neuropathological changes also contribute to long-term seizure susceptibility. Gliosis, where reactive astrocytes proliferate in response to injury, can disrupt normal neuronal signaling and promote epileptogenesis. A study in Brain (de Tisi et al., 2011) found that extensive gliotic scarring significantly increases the risk of recurrent seizures, particularly after tumor resection or traumatic brain injury. Hemosiderin deposits from intraoperative microhemorrhages further exacerbate seizure propensity by altering ion homeostasis and promoting chronic neuroinflammation.

Disruption of the blood-brain barrier (BBB) during surgery can lead to transient or persistent leakage of serum proteins into the extracellular space, triggering excitotoxic cascades. Elevated albumin levels in the parenchyma activate astrocytes and increase neuronal excitability, fostering epileptiform activity (Friedman et al., 2009, Ann Neurol). Prolonged BBB dysfunction may also facilitate infiltration of pro-inflammatory mediators, compounding seizure risk in vulnerable cortical regions.

Types Of Seizures Observed Postoperatively

Seizures after brain surgery vary in presentation, influenced by surgical site location, cortical involvement, and underlying neurological conditions. Focal seizures, originating in a specific brain region, are among the most common. Focal aware seizures may involve localized motor twitching, sensory disturbances, or autonomic symptoms like flushing or gastrointestinal discomfort. Focal impaired awareness seizures, more frequent in temporal lobe resections, can cause transient confusion, staring spells, or repetitive movements like lip-smacking or hand rubbing.

When seizure activity spreads beyond the initial focal point, secondary generalization can occur, leading to tonic-clonic seizures. These episodes, marked by sudden unconsciousness, muscle stiffening (tonic phase), and rhythmic jerking (clonic phase), pose risks such as aspiration pneumonia or prolonged postictal confusion. Patients with a preoperative seizure history are at higher risk of generalized seizures, suggesting that pre-existing epileptogenic circuits may be further destabilized by surgery.

Some individuals develop non-convulsive seizures, which lack dramatic motor symptoms but can significantly affect cognitive function and recovery. These seizures, often detected only through electroencephalographic (EEG) monitoring, may present as confusion, slowed responsiveness, or sudden lapses in awareness. Non-convulsive status epilepticus, a prolonged state of seizure activity without overt convulsions, is particularly concerning post-surgery, as it can delay neurological recovery and contribute to secondary brain injury if untreated. Given the difficulty in recognizing these seizures, continuous EEG monitoring is sometimes required for patients with unexplained cognitive fluctuations.

Brain Edema And Swelling Effects

Brain edema and swelling after surgery can impact neurological recovery and increase complications. Excess fluid disrupts normal cellular function, raising intracranial pressure (ICP) and impairing cerebral perfusion. Swelling can be classified as vasogenic edema, caused by BBB disruption and fluid leakage into the extracellular space, or cytotoxic edema, where intracellular swelling results from ionic imbalances and metabolic failure. The severity of post-surgical edema varies based on surgical technique, pre-existing pathology, and the brain’s ability to regulate fluid dynamics.

Swelling near critical brain areas can worsen neurological deficits, particularly when edema compresses adjacent structures. Patients may experience temporary cognitive changes, motor impairments, or speech difficulties due to pressure on nearby neural circuits. In cases where deep brain structures are affected, complications such as hydrocephalus or brainstem compression may arise, requiring prompt intervention. Clinicians monitor these changes using MRI with diffusion-weighted sequences to distinguish between reversible swelling and permanent ischemic injury.

Diagnostic Methods For Seizure Confirmation

Accurately identifying postoperative seizures requires clinical assessment and specialized diagnostic tools. Seizure manifestations range from overt convulsions to subtle, non-motor symptoms, necessitating thorough evaluation to differentiate epileptic events from other postoperative neurological changes. Physicians rely on patient history, witness accounts, and neurological examinations to establish suspicion, but definitive confirmation often requires electrophysiological and imaging studies.

Electroencephalography (EEG) is the gold standard for detecting abnormal cortical activity. Routine EEG can capture interictal epileptiform discharges, indicating neuronal hyperexcitability even without active seizures. For unconfirmed cases, prolonged video EEG monitoring allows correlation of electrical disturbances with clinical symptoms. If standard EEG fails to detect abnormalities, high-density EEG or intracranial electrode placement may be used, particularly in patients undergoing reoperation for epilepsy management.

Advanced imaging techniques, such as MRI with fluid-attenuated inversion recovery (FLAIR) sequences, help identify structural changes like gliosis, hemosiderin deposition, or cortical dysplasia that contribute to seizure susceptibility. Positron emission tomography (PET) and single-photon emission computed tomography (SPECT) scans may also be employed to assess metabolic or perfusion abnormalities in regions prone to epileptogenesis.