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Focal Onset Seizure

Editor: Sandeep Sharma Updated: 9/24/2023 9:20:16 PM


A focal onset seizure refers to abnormal neural activity in only one brain area within one brain hemisphere with a fixed focal or localized onset. Focal onset seizures are divided into 2 subtypes: motor onset and nonmotor onset.[1] Both focal motor and focal nonmotor onset seizures can be further classified based on level of awareness: aware, impaired, and unknown awareness. The motor manifestations of focal motor onset seizures can be characterized as automatism, atonic, clonic, epileptic spasms, hyperkinetic, myoclonic, or tonic movements. The behavioral manifestations of focal nonmotor onset seizures can be described by autonomic, behavioral arrest, cognitive, emotional, or sensory symptoms.

Some focal onset seizures can be preceded by an "aura," which refers to symptoms and signs that occur before the onset of seizure activity. These symptoms may include vision changes, dyspepsia, déjà vu, paresthesias, hearing disturbances, and sensation of abnormal taste or smell.[2][3][4]

A seizure is a sign that refers to a transient occurrence of signs and symptoms due to episodic, excessive, and disorderly neuronal activity within the brain. Epilepsy is a brain disorder "characterized by an enduring predisposition to generate epileptic seizures and by this condition's neurobiological, cognitive, psychological, and social consequences. The definition of epilepsy requires the occurrence of at least one epileptic seizure."[2][3] These events have traditionally been classified into partial and generalized seizures. However, the International League Against Epilepsy (ILAE) in 2017 reclassified seizures into 3 types: generalized onset seizures (formerly known as grand-mal seizures), focal onset seizures (formerly known as simple partial seizures or complex partial seizures), and unknown onset seizures.[1] 

Focal Motor Seizures (Formerly Simple Partial Seizures, Complex Partial Seizures)

Focal motor seizures occur due to an epileptogenic lesion on the contralateral frontal lobe. They usually originate from the supplementary motor area. The excitatory focus is generally around the rolandic (motor) cortex. Temporal lobe seizures can also have motor symptoms. These symptoms include turning the head and neck to the opposite side and sometimes tonic contractions of the limbs and trunk. The motor manifestations of focal motor onset seizures can be characterized by tonic, clonic, atonic, myoclonic, hyperkinetic, epileptic spasms, and automatisms.[5] 

Motor manifestations of focal motor onset seizures include the following:

  • Abnormal sustained contractions and posturing of the limbs characterize tonic movements.
  • Clonic movements are characterized by repeated, short contractions of various muscle groups characterized by twitching movements or rhythmic jerking.
  • Atonic movements are characterized by loss of tone in a limb.
  • Myoclonic movements are characterized by irregular, nonrhythmic jerking of the limbs.
  • Abnormal regular or irregular excess involuntary movements of the limbs characterize hyperkinetic movements.
  • Epileptic spasms are characterized by repetitive flexion of the waist and flexion or extension of the arms.
  • Automatisms are characterized by coordinated, repetitive motor activities such as lip-smacking, tapping, or swallowing.

Following focal motor seizures, patients may have transient, functional, and localized paralysis of the affected muscles, known as Todd paralysis. This paralysis can last minutes to hours, usually in proportion to the duration of the focal motor seizure. This postepileptic paralysis occurs due to persistent focal dysfunction of the affected epileptogenic area and is the signature of a focal seizure. The significant clinical value lies in lateralizing the hemisphere of seizure onset, and it is often mistaken for a stroke.[6][7][8][9]

Focal Nonmotor Seizures

The clinical manifestations of focal nonmotor seizure include autonomic, behavioral arrest, cognitive, emotional, or sensory symptoms.

  • Autonomic seizures are characterized by changes in blood pressure, heart rate, sweating, skin color, or gastrointestinal upset.
  • Behavioral arrest seizures are characterized by cessation of movement.
  • Cognitive seizures are characterized by abnormal language or thinking, eg, jamais vu, déjà vu, hallucinations, and visualization of illusions.
  • Emotional seizures are characterized by emotional changes such as fear, dread, anxiety, or pleasure. Nonmotor seizures that manifest as laughing are called gelastic, and those that manifest as crying are called dacrystic.[10]
  • Sensory seizures are characterized by changes in sensation, such as abnormal sensations of vision, paresthesias, hearing, smell, or pain.

At times, focal motor and focal nonmotor seizures can evolve into bilateral tonic-clonic seizures. 


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Specific clinical pathologies and conditions can predispose individuals to have seizures. Etiology should always be investigated alongside the type of focal seizure. According to the ILAE, the causes of seizures can be classified into the 6 categories below:[11]

  • Genetic
  • Structural
  • Metabolic
  • Immune
  • Infectious
  • Unknown

A common cause of childhood seizures is a perinatal hypoxic brain injury. In adolescents, seizures are most commonly caused by head trauma and infections. In adults, the most common cause of seizures is stroke.[12][13]

At times, the underlying etiology of seizures is unknown. Certain environmental triggers increase the frequency of seizure onset in patients predisposed to having seizures. Common environmental triggers include sleep deprivation, stress, photosensitive imagery, drug use, infection, and medication noncompliance.[12][13]


An estimated 52.5 million people worldwide are affected by epilepsy.[14][15] The incidence of epilepsy has a bimodal age distribution, mainly affecting infants and older individuals.[16] The prevalence of epilepsy differs by country, ethnicity, race, socioeconomic status, and access to healthcare.[17][18] Focal onset seizures are more prevalent than generalized onset seizures.[19] The most common type of focal onset seizure is focal onset seizure with impaired awareness.[14]


Seizures occur when a disruption in the stability of the neuronal membrane leads to hyperexcitability. For example, hyponatremia alters the ion concentration surrounding the neuronal membrane, decreasing the intracellular to extracellular gradient; this affects the neuron's stability, which can lead to hyperexcitability of neurons. Withdrawing from certain medications (eg, alcohol, benzodiazepines, barbiturates) causes GABAA, an inhibitory neurotransmitter, to be sensitized, thus leading to neuronal hyperexcitability and seizures. Hypoglycemia alters neuronal metabolism and impairs subcellular function. Abnormalities affecting any central nervous system component (eg, ions, receptors, cells, networks, or brain regions) can lead to seizures.[20]

History and Physical

When a patient presents with seizure-like activity, it is important to determine if the underlying etiology is due to electrographic seizures. During seizures, patients may lose consciousness, have difficulty communicating, or be in a postictal state. Therefore, it is important to obtain clinical information from a bystander who witnessed the event and not solely rely on the patient's recollection of the clinical history. Establishing a timeline of events is vital to help with seizure diagnosis and classification.[2][4] A clinician should ask about prodromal symptoms, including lightheadedness, dizziness, GI upset, changes in taste or smell, visual disturbances, or tinnitus. Clinicians should also inquire about loss of consciousness or impaired awareness during the episode.

Of note, interictal awareness does not involve knowledge that a seizure has occurred but awareness and the ability to interact with the surroundings during the seizure. Motor movements, including jerking, twitching, or stiffening of the face or limbs, should be characterized. Other clinical symptoms that can occur during a seizure include bowel or urinary continence, tongue biting, drooling, and forced gaze deviation. Obtaining a thorough clinical history and timeline can aid in the localization of epileptogenic focus.[2][4]

  • Temporal lobe focal onset seizures can cause autonomic or psychological symptoms, including dyspepsia, auditory hallucinations, and olfactory sensations. 
  • Frontal lobe focal onset seizures have prominent motor manifestations like twitching or stiffness of the face or limbs.
  • Parietal lobe focal onset seizures present with paresthesias, visual disturbances, lack of awareness of a body part, vertigo, and language disturbances.
  • Occipital lobe seizures can present with visual obscuration (eg, scotoma, amaurosis, flashing lights) or hallucinations.

When performing a neurological exam on a patient with seizures, it is important to assess their level of consciousness. If a patient is awake, one can evaluate their speech, memory, and ability to follow commands. It is also important to look for signs of continued seizure activity, including abnormal face or limb movements, forced gaze deviation, tongue biting, and bowel or urinary incontinence. Hemibody weakness may be a sign of Todd paralysis.[3][6][7]


In addition to obtaining clinical information, EEG is needed to accurately diagnose seizures and aid in the localization of seizure focus.[21] If an EEG contains focal epileptiform discharges, it is imperative to obtain brain imaging with magnetic resonance imaging (MRI) to determine the presence and location of structural abnormalities. Of note, EEG sensitivity significantly increased with the EEG's duration and 24-hour EEGs that capture diurnal variation in seizure activity.

Unless contraindicated, an MRI is usually performed after a first seizure to evaluate the brain, vasculature, and meningeal structures. MRI brain scans have several imaging modalities and sequences; therefore, MRIs provide higher sensitivity for detecting structural abnormalities than CT scans. In addition, CT scans often have suboptimal visualization of the posterior fossa due to bony structures.[22][23] 

Routine laboratory studies, including electrolytes, complete blood count, liver function tests, renal function tests, urine analysis, lactate, creatinine phosphokinase, and toxicology tests, should also be performed to evaluate for toxic and metabolic etiologies. If there is a suspicion of cerebral infection or an autoimmune process, a lumbar puncture (LP) followed by cerebrospinal fluid analysis (CSF) is indicated to identify the underlying cause.[21] 

An important distinction is the differentiation of true epileptic seizures from psychogenic nonepileptic seizures (formerly called pseudoseizures). Psychogenic nonepileptic seizures (PNES) are episodic motor, sensory, mental, or autonomic manifestations resembling epileptic seizures without corresponding neuronal activity on EEG. They are often related to a history of abuse or trauma and are considered a form of conversion disorder. PNES affects 20% to 30% of patients at epilepsy centers, and patients can be on high doses of antiepileptics with corresponding adverse effects if incorrectly diagnosed with epilepsy. In addition, between 5% to 40% of patients with PNES also have epilepsy, further confounding the diagnosis.[24] Please see our corresponding StatPearls article, "Psychogenic Nonepileptic Seizures."[25]

Treatment / Management

Pharmacological Treatments 

The first step in the management of a seizure patient is to asses for continued seizure activity and abort it using first-line abortive seizure medications, eg, benzodiazepines, levetiracetam, valproic acid, phenytoin, fosphenytoin, lacosamide.[26][27] If a patient continues to seize after dispensing first-line abortive seizure medications, then continuous IV infusions, including propofol, midazolam, and ketamin,e should be considered. Once the seizure has been stopped, the addition of a long-acting oral seizure medication should be initiated. The appropriate seizure medication is chosen based on the type of seizure, adverse effect profile of the medication, the patient's age, use of other medications, and medical comorbidities. Carbamazepine and lamotrigine are the first-line antiepileptic drugs (AED) for focal onset seizures. Alternative agents include valproate, oxcarbazepine, and levetiracetam. Adjunctive therapy for focal onset seizures includes carbamazepine, lamotrigine, levetiracetam, oxcarbazepine, sodium valproate, gabapentin, topiramate, and clonazepam. If adjunctive therapy is ineffective or not tolerated, referral to a tertiary epilepsy center should be considered.[28](A1)

Nonpharmacological Treatments

For patients with focal epilepsy refractory to medications, nonpharmacological treatments should be considered, including ketogenic diet, vagal nerve stimulator implantation, and epilepsy surgery. The ketogenic diet is a specialized high-fat, low-carbohydrate, and controlled protein diet that should be considered in children with intractable seizures when at least 2 AEDs have been ineffective. Certain genetic disorders are also highly responsive to the ketogenic diet. Surgery should be considered as an option for refractory seizures when a specific epileptogenic locus has been identified and is in a location amenable to removal. Neurologists and neurosurgeons often perform neural mapping in which different areas of the brain will be sequentially stimulated to identify a focus for seizure activity.[29] (B3)

Vagus nerve stimulation (VNS) involves an electric stimulator inside the body connecting to the neck's left vagus nerve, which helps to decrease irregular electrical activity in the brain. VNS can reduce the frequency, severity, and length of seizures. VNS therapy should be considered in patients whose seizures are not controlled with AEDs and who are not candidates for surgery.[30] 

Differential Diagnosis

Some conditions that can present similarly to focal onset seizures include the following:

  • Psychogenic nonepileptic seizures
  • Movement disorders
  • Migraine disorders
  • Psychiatric disorders 
  • Headache disorders

When a patient presents with seizure-like activity, obtaining a video EEG (vEEG) to capture the clinical events is important. vEEG monitoring allows the clinician to determine if the epileptogenic activity is associated with the seizure-like activity and can aid in appropriate management. An alternative diagnosis should be considered if the vEEG report does not show epileptogenic activity.[31][32] 


In patients with focal onset seizures, it is essential to treat identifiable etiologies to reduce seizure recurrence. Common modifiable exacerbating factors include sleep deprivation, dehydration, medication noncompliance, drug or alcohol use, and photostimulatory images. Patients tend to have a higher risk of seizure recurrence if a seizure etiology is not identified. Therefore, prescribing a long-term antiseizure medication is imperative for patients with these seizures.[33]  


If a patient with focal onset seizures is left untreated, focal status epilepticus can develop. Immediate complications of focal status epilepticus include coma, brain damage, cardiac arrhythmia, respiratory failure, aspiration, and death.[34][35] Status epilepticus (SE) is more likely with focal seizures, which develop into generalized-tonic-clonic seizures, than with generalized onset of seizures. SE can be convulsive or nonconvulsive, and convulsive SE is considered a medical emergency. Two minutes is often the threshold after which permanent damage or death is possible. The long-term effects of nonconvulsive SE are less well-defined.

Long-term complications of focal onset seizures include depression, anxiety, cognitive impairment, insomnia, bone fractures, and premature mortality. Screen for these conditions in patients with a history of focal onset epilepsy is essential.[35] 

Deterrence and Patient Education

Patients with focal onset seizures and their families should be educated on necessary seizure precautions to reduce the risk of injury during a seizure event. Depending on the patient's state of residence, there are varying driving restrictions for patients with seizures. Healthcare providers should routinely review driving restrictions with patients, especially if their seizures are uncontrolled. Patients should use caution when cooking, operating heavy machinery or power tools, climbing tall structures, and working at heights. Patients should also avoid unsupervised baths and swimming alone.[36][37]

Pearls and Other Issues

Some special focal epileptic syndromes include self-limiting epilepsy with centrotemporal spikes, self-limiting epilepsy with autonomic seizures, and childhood occipital visual epilepsy. These are discussed below. 

Self-limited Epilepsy With Centrotemporal Spikes (Benign Epilepsy with Centrotemporal Spikes)

Self-limited epilepsy with Ccentrotemporal spikes (SeLECTS), formerly known as benign epilepsy with centrotemporal spikes (BECTS), is a benign form of focal motor epilepsy in children featuring centrotemporal spikes. SeLECTS accounts for 6% to 10% of all childhood epilepsies and is more common in boys than girls. The age of onset is 3 to 13 years, with a peak at 7 to 8 years. Centrotemporal spikes are characteristic of SeLECTS but not pathognomic, as seen in other epilepsy syndromes. Seizures typically occur during sleep, either shortly after falling asleep or just before awakening.

Classically, the unilateral lower face is involved with facial twitching, paresthesia, and dysarthria. Hemiconvulsions may occur, especially in young children. They can rarely become generalized. The seizures are brief, occurring in clusters and followed by prolonged seizure-free intervals. Typical EEG findings are high amplitude diphasic spikes or sharp waves followed by prominent slow waves in the contralateral centrotemporal area. SeLECTS has an excellent prognosis, and most children achieve remission by puberty regardless of antiepileptic drug therapy. Pharmacotherapy is not needed in most cases. Antiseizure drugs like valproate may be used in severe cases or with frequent symptoms.[38][39]

Self-limited Epilepsy With Autonomic Seizures (Early-Onset Benign Occipital Epilepsy, Panayiotopoulos Syndrome)

Self-limited epilepsy with autonomic seizures (SeLEAS), formerly known as early-onset benign occipital epilepsy or Panayiotopoulos syndrome, accounts for 1% to 2% of children with focal epilepsy and is more common in girls than boys. The age of onset is 3 to 8 years, peaking at 5 years. Seizures are often nocturnal and present with autonomic symptoms, most commonly nausea and vomiting. The seizure frequently lasts longer than 30 minutes, and about one-third of patients may develop focal status epilepticus. SeLEAS may evolve into generalized onset seizures, and consciousness may be impaired. Ictal EEG shows rhythmic theta or delta activity with intermixed spikes that start posteriorly. Most children have occasional seizures and do not require pharmacological treatment.[40]

Childhood Occipital Visual Epilepsy (Late-Onset Benign Occipital Epilepsy, Gastaut-Type Epilepsy)

Childhood occipital visual epilepsy (COVE), formerly known as late-onset benign occipital epilepsy or Gastaut-type epilepsy) presents in mid-to-late childhood with a peak age of 8 years. COVE manifests as frequent, often more than 15, brief visual seizures resulting in visual hallucinations or blindness. Typically, no impairment in consciousness occurs unless there is generalization.[38][40]

Enhancing Healthcare Team Outcomes

Patients with focal onset seizures are at high risk of seizure recurrence. Early identification and management of patients with focal onset seizures are imperative in reducing morbidity and mortality. The care of patients with focal onset seizures necessitates a collaborative approach among healthcare professionals to ensure patient-centered care and improve overall outcomes. Neurologists, emergency medicine physicians, critical care physicians, advanced practitioners, nurses, pharmacists, and other health professionals involved in the care of these patients should possess the essential clinical skills and knowledge to diagnose and manage focal onset seizures accurately. This includes expertise in recognizing the varied clinical presentations and understanding the nuances of diagnostic techniques such as electroencephalography and neuroimaging. These teams have been shown to improve early detection and cessation of seizures. Patient and caregiver education about triggering factors, medication compliance, auras, and other ictal symptoms are essential to prevent morbidity from focal seizures.[41]

A strategic approach is equally crucial, involving evidence-based strategies to optimize treatment plans and minimize adverse effects. Ethical considerations must guide decision-making, ensuring informed consent and respecting patient autonomy in treatment choices. Each healthcare professional must be aware of their responsibilities and contribute their unique expertise to the patient's care plan, fostering a multidisciplinary approach. Effective interprofessional communication is paramount, allowing seamless information exchange and collaborative decision-making among the team members. Care coordination plays a pivotal role in ensuring that the patient's journey from diagnosis to treatment and follow-up is well-managed, minimizing errors and enhancing patient safety. By embracing these principles of skill, strategy, ethics, responsibilities, interprofessional communication, and care coordination, healthcare professionals can deliver patient-centered care, ultimately improving patient outcomes and enhancing team performance in the management of focal onset seizures.



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