Complex partial seizures refer to focal seizures that start in one hemisphere of the brain and are associated with impairment in consciousness. Complex partial seizures are now preferably called "focal impaired awareness seizure" or "focal onset impaired awareness seizure." International League Against Epilepsy (ILAE) 2017 classification has categorized seizures based on three key features: the location of seizure onset, level of awareness during a seizure, and other features of seizures. Focal seizures refer to the epileptiform activity starting in one area on one side of the brain. If awareness is impaired or affected at any time during the seizure, it is called focal impaired awareness seizure. Focal seizures are further classified into motor onset (automatisms, atonic, clonic, myoclonic, tonic, epileptic spasms, hyperkinetic) and nonmotor onset (autonomic, emotional, sensory, cognitive, behavior arrest) types. A seizure that starts on one side or one part of the brain and then spreads to both sides, earlier referred to secondarily generalized seizures, is now preferably termed as "focal to bilateral seizure."[1]

Focal seizures with impaired consciousness can present with or without an aura. Auras can last from a few seconds to as long as 1 to 2 minutes before the consciousness is impaired. Consciousness is maximally impaired in the beginning typically. Most of the seizures with automatisms last longer than 30 seconds, up to 1 to 2 minutes and sometimes can be as long as 10 minutes. Absence seizures can sometimes present with the same symptomatology however ictal EEG will show generalized 3-Hz spike-wave complexes. Symptoms of focal seizures with impaired awareness depend on the area of the brain it is arising from. Most of the complex partial seizures arise from the temporal lobe. Extratemporal origin has been reported in at least 10% to 30% of patients.[2]

Seizures of Temporal Lobe Origin

These are the most common type of focal impaired awareness seizures. Stereotyped automatisms occur in about 40% to 80% of patients with temporal lobe epilepsies. Seizures with predominantly oral and manual automatisms in addition to some other motor manifestations are highly suggestive of temporal lobe origin. About 60% of temporal lobe seizures have a secondary generalization. Gradual recovery after several minutes of confusion occurs postictally in most patients, however, in some patients automatic behavior like running, walking about, the nondirected violent behavior may occur. Temporal lobe focal impaired seizures can have features similar to frontal seizures, but temporal lobe focal impaired seizures typically have slower onset and progression, and more pronounced confusion. Certain features can help in localizing the seizure onset to one hemisphere. Ictal vomiting, ictal speech, urinary urge, and automatisms with intact consciousness suggest seizure onset in the non-dominant hemisphere, and speech disturbance postictally is suggestive of seizure onset in the dominant hemisphere. Upper limb dystonia lateralizes seizure to the opposite hemisphere.

In young children with focal seizures of temporal lobe onset, behavioral arrest and unresponsiveness are common. Oroalimentary automatisms tend to occur in children older than age 5. In younger children, the symmetric motor movement of the limbs and head nodding is typical. In infants, these seizures may be subtle with few automatisms. In very young infants, central apnea can occur. Temporal focal impaired seizures can be confused with absence seizures as both may have automatisms, but temporal seizures are usually longer in duration and are associated with postictal confusion.

Seizures arising from the mesial temporal lobe are characterized by auras such as epigastric sensation, deja vu, a feeling of fear, and unpleasant smells. Autonomic features like tachycardia, flushing, and pallor are common. Auras may be followed by impaired awareness and manual and oroalimentary automatisms. Automatisms in the upper limb and /or pupillary dilatation unilaterally may lateralize seizure to the ipsilateral hemisphere. Dystonia in the upper limbs and head and eye version on the opposite side can occur.

Lateral temporal seizures may have vertigo, auditory (buzzing, ringing), or visual symptoms as initial aura symptoms. Auditory aura in only one ear may lateralize seizure to the contralateral hemisphere. Initial aura is usually not prolonged, and impaired awareness is an early feature. Seizures are of shorter duration and progression to bilateral convulsions is more common than those arising from the mesial temporal lobe.[3]

Seizures of Frontal Lobe Origin

Up to 30% of the patients with focal epilepsy have seizures arising from the frontal lobe. It is the most common extratemporal type. Seizures are accompanied by loss of consciousness in about half of the patients with frontal lobe epilepsy. Focal impaired awareness seizures can arise from various locations within the frontal lobe, except the rolandic strip. These seizures typically are brief, lasting about 30 seconds, occurring in clusters, multiple times a day, are often nocturnal occurring during sleep and have minimal postictal confusion. Motor symptoms are predominant and range from hypermotor thrashing episodes like pelvic thrusting, bicycling movements to asymmetric tonic posturing. Sexual automatisms, bizarre behavior, and vocalizations are common. These seizures often have a stereotypical pattern for each patient. Nocturnal frontal lobe seizures may be mistaken for parasomnias. The ictal EEG may be difficult to interpret because of movement artifacts. Identification based on semiology alone and differentiating from mesial temporal lobe epilepsy may be difficult, however earliest signs and symptoms and their order of appearance may help in distinction. Seizures with hypermotor features are more likely to have an ictal focus in the orbitofrontal and frontopolar regions. Temporal lobe seizures have more oroalimentary automatisms, gesturing and fumbling semiology.

Epileptiform activity in frontal convexity can cause clonic seizures, and in the supplementary motor area can cause tonic seizures. Unique semiology of the supplementary sensorimotor cortex includes deviation of head and eye to the side contralateral to seizure onset, the asymmetrical posturing of upper limbs with an extension of arm contralateral to the side of seizure onset and flexion of ipsilateral arm. Orbitofrontal region seizures are automotor type and manifest prominently with autonomic phenomena like flushing, vocalization, and automatisms. Anterior cingulate gyrus seizures have predominant motor manifestations like hypermotor seizures and complex motor seizures. Posterior cingulate cortex epilepsies predominantly have altered consciousness and automotor seizures as main clinical manifestations. Antero-lateral dorsal convexity seizures may manifest with auras such as dizziness, epigastric sensation, behavioral arrest and speech arrest.

Seizures of Parietal Lobe Region

Seizures arising from the parietal lobe may be difficult to diagnose because of their subjective nature. Positive and /or negative sensory features are common. Sensorimotor phenomenon and vestibular hallucinations suggest onset in the parietal lobe. Paresthesias, visual hallucinations, visual illusions, somatic illusions, vertiginous features can occur. Seizures arising from the dominant hemisphere can cause receptive language impairment. Parietal lobe complex partial seizures can have auras like epigastric sensations, visual hallucinations, panic attacks, and behavioral arrest. Often there is an involvement of other lobes as the seizure spreads. When focal seizures from the parietal lobe spread and involve the temporal lobe, loss of consciousness and automatisms may occur.

Seizures of occipital lobe origin

Seizures with ictal origin in the occipital lobe are characterized by a visual aura and are difficult to diagnose especially in young children. Visual auras, typically of elementary sensations, ictal blindness, versions of the head and eyes to the opposite side, rapid and forced blinking, oculoclonic activity are some features suggesting occipital lobe as an origin of focal seizure with impaired consciousness. Seizures from the primary visual cortex can cause bilateral loss of vision in the form of white-out or black-out. Shorter duration of the visual aura (less than 2 minutes) can help to differentiate from migraine aura which is typically longer (5 to 15 minutes). Complex, formed visual hallucinations like pictures of people, animals, etc. are associated with seizure onset in the extra-striate cortex. Other symptoms may result from spread to temporal or parietal lobes.

Seizures of Insular Lobe Origin

Seizures arising from the insula can mimic frontal, temporal, parietal lobe seizures. Origin from the insula is suspected when viscerosensitive symptoms (nausea, vomiting, salivation), motor symptoms (tonic, hypermotor or generalized tonic-clonic movements), and/or sensory symptoms (numbness, tightness, vibration, pain, vertigo) occur at seizure onset.[4][5][6]

Some known causes of seizures include:

• Infectious: The most common cause of epilepsy in developing countries and overall worldwide is infectious. Infections can cause both acute seizures and epilepsy. Tuberculosis, neurocysticercosis, cerebral toxoplasmosis, HIV, cerebral malaria, SSPE, and bacterial and viral meningoencephalitis are some infections known to cause seizures.
• Structural: Any structural brain abnormality like stroke, trauma, infection, tumor, hippocampal sclerosis, AVM, postsurgical changes can increase the risk of seizures and epilepsy
• Metabolic: Several inherited enzymatic disorders like GLUT-1 deficiency, cerebral folate deficiency, among others can cause seizures. Other acquired disorders like electrolyte imbalance - hyponatremia, hypocalcemia, and hypoglycemia can cause seizures.
• Genetic/chromosomal abnormalities: Several chromosomal disorders (e.g., AKT3, Fragile X syndrome) and gene defects (e.g., Down's syndrome, Klinefelter's syndrome, Angelman syndrome) have been associated with epilepsy.
• Traumatic brain injury
• Hypoxic brain injury

Etiology cannot be determined in more than half of all individuals with epilepsy. A congenital anomaly is the most common known etiology in children, and head trauma in young adults. In people, age 35 to 64 years, head trauma, tumors, and vascular disorders are common causes. In people age 65 years or more, cerebrovascular disease, and degenerative disorders are the most commonly known etiologies.

Certain situations or triggers cause seizures. Some common triggers include tiredness and lack of sleep, stress, alcohol, fever, acute medical illness, hormonal changes, substance abuse, certain medications, bright and flashing lights, and medication noncompliance.[1][7][8]

After the first year of life, complex partial seizures are the most common seizure type in patients with epilepsy. It is estimated that around 36% of people with epilepsy have complex partial seizures. It affects all ages. Incidence is highest in children and older adults. No predilection for gender or race is known.

The most common pathological feature of temporal lobe epilepsy is hippocampal sclerosis. Hippocampal sclerosis (HS) consists of neuronal loss and gliosis in the dentate nucleus and pyramidal layer of the hippocampus. Mechanism of damage in HS is glutamate discharge during the seizure episode. The most frequent site of damage is in the CA1 area of the hippocampus. It is controversial whether HS is a result of seizures or a cause of seizures.

Both cortical and subcortical structures play an important role in controlling the level of consciousness. Higher-order association cortices on both sides have a role in maintaining an overall level of attention and awareness, and they interact reciprocally with the subcortical arousal structures. Subcortical arousal systems contain numerous neurotransmitter systems that act in conjunction to maintain the level of consciousness.

The characteristic feature of the complex partial seizure (focal impaired awareness seizure) is impaired awareness, referring to decreased overall arousal and responsiveness. These seizures most commonly arise from the temporal lobe. Simple responses like visual tracking may be preserved in complex partial seizures. However higher-order processing tasks like a verbal response, decision making are profoundly impaired.

Several mechanisms of altered consciousness in the setting of focal seizures have been proposed.

Network Inhibition Hypothesis

Focal ictal activity in the temporal lobe produces abnormal polyspike discharges. Abnormal seizure activity is carried to subcortical structures with pools of GABAergic inhibitory neurons via known anatomical connections. This may inhibit the subcortical arousal systems in the upper brainstem, thalamus, hypothalamus and basal forebrain. Inhibition of subcortical arousal leads to slow-wave activity in regions of the frontoparietal association cortex bilaterally, producing impaired consciousness.

Epileptic Activation of Subcortical Structures, Mainly Thalamus and Upper Brainstem

The prefrontal cortex and the nonspecific thalamic nucleus and the midline regions of the intralaminar thalamic complex have close connections. It is hypothesized that the rapid epileptic spread from all the frontal regions of the reticular formation may be responsible for the impaired consciousness observed in frontal lobe epilepsy. A similar mechanism has been suggested in temporal lobe epilepsy with additional spread to the upper brainstem structures.

Epileptic Disturbance of the Normal Balance Between Excitation and Inhibition of Cortical/Subcortical Networks

Interference with the normal activity of primary motor cortex or epileptic activation of the negative motor areas during frontal lobe involvement, or both, may be responsible for the arrest of activity during a seizure, has been suggested by some authors.[9][10]