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Focal Impaired Awareness Seizure
Introduction
The 2017 classification by the International League Against Epilepsy has categorized seizures based on 3 key features: the location of seizure onset, level of awareness during a seizure, and other features of seizures. Focal impaired awareness seizures refer to focal seizures that start in one hemisphere of the brain and are associated with impairment in consciousness. Formerly known as "complex partial seizures," they are now called "focal impaired awareness seizure" or "focal onset impaired awareness seizure" and are typically referred to as a "focal onset seizure."
Focal onset seizures refer to 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 a focal impaired awareness seizure. Focal seizures are further classified into:
- Motor onset (automatisms, atonic, clonic, myoclonic, tonic, epileptic spasms, hyperkinetic)
- Nonmotor onset (autonomic, emotional, sensory, cognitive, behavior arrest)
A seizure that starts on one side or one part of the brain and then spreads to both sides, previously referred to as secondarily generalized seizures, is now preferably termed a "focal to bilateral seizure."[1]
Focal onset impaired awareness seizures can present with or without an aura. Auras can last from a few seconds to 1 to 2 minutes before consciousness is impaired. Consciousness is maximally impaired in the beginning. Most of the seizures with automatisms will last longer than 30 seconds, up to 1 to 2 minutes, and sometimes can be as long as 10 minutes. Absence seizures can occasionally present with the same symptomatology; however, ictal electroencephalogram (EEG) will show generalized 3-Hz spike-wave complexes.
The characteristic feature of the focal impaired awareness seizure is impaired awareness, referring to decreased overall arousal and responsiveness. Symptoms of focal onset seizures with impaired awareness depend on the area of the brain it is arising from. Simple responses like visual tracking may be preserved in focal impaired awareness seizures; however, higher-order processing tasks like verbal response decision-making are profoundly impaired. Most focal impaired awareness seizures originate in the temporal lobe, although extratemporal origin has been reported in at least 10% to 30% of patients.[2]
Seizures of Temporal Lobe Origin
Temporal lobe seizures 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 automatism and some other motor manifestations suggest temporal lobe origin. About 60% of temporal lobe seizures spread to involve both cerebral hemispheres. Gradual recovery after several minutes of confusion occurs postictally in most patients; however, in some patients, automatic behavior like running or walking about and non-directed 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 with more pronounced confusion. Certain features can help in localizing the seizure onset to 1 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 5. The symmetric motor movement of the limbs and head nodding is typical in younger children. 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 more prolonged and are associated with postictal confusion.
Seizures arising from the medial 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 oroalimentary automatisms. Automatisms in the upper limb with or without unilateral pupillary dilatation may lateralize the seizure to the ipsilateral hemisphere. Dystonia in the upper limbs, 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. An auditory aura in only one ear may lateralize a 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 medial temporal lobe.[3]
Seizures of Frontal Lobe Origin
Up to 30% of the patients with focal epilepsy have seizures arising from the frontal lobe; therefore, this 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 nocturnally occurring during sleep, and have minimal postictal confusion. Motor symptoms are predominant and range from hypermotor thrashing episodes like pelvic thrusting and 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 can cause tonic seizures in the supplementary motor area. 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 the ipsilateral arm. Orbitofrontal region seizures are auto-motor 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 the 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 from the parietal lobe may be difficult to diagnose because of their subjective nature. Sensorimotor phenomenon and vestibular hallucinations suggest onset in the parietal lobe. Positive and/or negative sensory features are common. Paresthesias, visual hallucinations, visual illusions, somatic illusions, and vertiginous features can occur. Seizures arising from the dominant hemisphere can cause receptive language impairment. Parietal lobe focal impaired awareness 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
A visual aura characterizes seizures with ictal origin in the occipital lobe but is 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, and oculoclonic activity are some features suggesting the occipital lobe as an origin of focal seizure with impaired consciousness. Seizures from the primary visual cortex can cause bilateral vision loss in the form of white-out or black-out. A shorter duration of the visual aura (less than 2 minutes) can help to differentiate from a migraine aura, which is typically longer (5-15 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 the spread of the seizure to the temporal or parietal lobes.
Seizures of Insular Lobe Origin
Seizures arising from the insula can mimic frontal, temporal, and 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]
Etiology
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Etiology
Etiology cannot be determined in more than half of all individuals with epilepsy. Some known causes of seizures include:
- Infectious: The most common cause of epilepsy worldwide is infection. Infections can cause both acute seizures and epilepsy. Tuberculosis, neurocysticercosis, cerebral toxoplasmosis, human immunodeficiency virus, cerebral malaria, and bacterial and viral meningoencephalitis are infections known to cause seizures.
- Structural: Any structural abnormality of the brain, such as stroke, trauma, infection, tumor, hippocampal sclerosis, vascular malformations, or postsurgical changes, can increase the risk of seizures and epilepsy.
- Metabolic: Several inherited enzymatic disorders like GLUT-1 deficiency and cerebral folate deficiency, among others, can cause seizures. Acquired disorders like electrolyte imbalance, such as hyponatremia, hypocalcemia, and hypoglycemia, can cause seizures.
- Genetic/chromosomal abnormalities: Several chromosomal disorders (eg, AKT3, Fragile X syndrome) and gene defects (eg, Down syndrome, Klinefelter syndrome, Angelman syndrome) have been associated with epilepsy.
- Traumatic brain injury
- Hypoxic brain injury
The most common etiology of seizures in children is congenital anomalies. In young adults, head traumas are the most common cause of seizures. Common etiologies in those 35 to 64 are head trauma, tumors, and vascular disorders. In people 65 or older, cerebrovascular disease and degenerative disorders are the most commonly known etiologies.
Certain situations or triggers can provoke seizures. Common triggers include tiredness and lack of sleep, stress, alcohol, fever, acute medical illness, hormonal changes, substance use, certain medications, bright flashing lights, and medication noncompliance.[1][7][8]
Epidemiology
After the first year of life, focal impaired awareness seizures are the most common seizure type in patients with epilepsy. Approximately 36% of people with epilepsy have focal impaired awareness-type seizures. While all ages can be affected, incidence is highest in children and older adults with no known predilection for sex or race.
Pathophysiology
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. There is controversy about whether HS is a result of seizures or a cause of seizures. The 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.
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.
In the setting of focal seizures, there have been several mechanisms of altered consciousness 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 gamma-aminobutyric acid-ergic 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, the nonspecific thalamic nucleus, and the midline regions of the intralaminar thalamic complex have close connections. A hypothesis states 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
Some authors have suggested that interference with the normal activity of the 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.[9][10]
History and Physical
With any seizure, it is most important to ensure the episode is genuinely a seizure. Diagnosing focal impaired awareness seizure is based on clinical history, and epilepsy is a clinical diagnosis. Obtaining a detailed history from the patient and witnesses is important; therefore, a thorough description of the episode, including the sequence of events, nature of onset, any loss of consciousness, motor or convulsive activity, bilateral involvement, tongue bite, incontinence, stare, automatisms, eye movements, postictal confusion, recovery, and duration of events are essential to elicit. Further, detailed medical history is important to identify possible risk factors.
The clinical details may provide clues to the location of a seizure focus, and a detailed neurological examination is essential. Even subtle findings on the neurological exam can support the diagnosis of seizures; any specific lateralizing abnormalities on the neurological exam can help predict the epileptic focus.
Specific features associated with focal seizures can help in lateralizing the seizure origin to 1 hemisphere. These features provide a good clue for lateralization but can be falsely lateralizing.
Dystonic limb posturing: Unilateral dystonic posturing is the most reliable lateralizing sign in temporal lobe automotor seizures. Unilateral hand/arm dystonic posturing in conjunction with automatisms of the opposite limb and head-turning is highly suggestive of temporal lobe onset contralateral to the dystonic upper extremity.
Head version: The classical head version (a tonic, unnatural, forced lateral gyratory head movement) highly suggests seizure onset to the contralateral side. This version can occur in both temporal and extratemporal seizures. Seizures that spread to the premotor areas may be the cause.
Automatisms: Most automatisms are usually accompanied by impaired consciousness and have no lateralizing value, but preserved responsiveness during automatisms lateralize to the non-dominant hemisphere. Eye blinking or fluttering at seizure onset may indicate occipital lobe onset. Aversion of the eyes to the opposite side suggests seizures arising from the occipital region. Oroalimentary automatisms like lip-smacking, chewing, or swallowing may occur without loss of consciousness at seizure onset in temporal lobe seizures, with seizures confined to the amygdala and anterior hippocampus. Focal seizures with impaired consciousness arising from mesial frontal and orbitofrontal regions can cause bicycling or pedaling movements of the leg. Mimetic automatisms and crying have been reported in focal seizures with impaired consciousness arising from the non-dominant temporal lobe. Vomiting during seizure lateralizes to the non-dominant hemisphere. Sexual or genital automatisms (like pelvic thrusting and masturbation) can occur in focal seizures with impaired consciousness of frontal and temporal lobe origin.
Postictal nose-wiping: Postictal nose-wiping may occur within 60 seconds of the seizure and occurs in about 50% to 85% of temporal lobe epilepsy patients and is performed with the ipsilateral hand in most cases.[1][6]
Evaluation
Clinical data are often insufficient to diagnose and localize focal seizures precisely. Other testing includes:
- A comprehensive metabolic profile, complete blood count, urine analysis, and urine toxicology screen are usually initially observed to rule out metabolic causes and infections.
- Electroencephalography (EEG) is an essential test for evaluating patients with seizures. Some patients may require video EEG or prolonged EEG monitoring.
- Neuroimaging is often needed to rule out structural causes.
Interictal EEG: Thirty to 40% of patients may have normal interictal findings on a single routine EEG recording. Temporal intermittent rhythmic delta activity is predictive of temporal lobe epilepsy. Bitemporal sharp wave foci may be noted in 25% to 30% of the patients. Intermittent rhythmic slowing may be the only clue, as mesial temporal spikes may not be seen well at the surface. The amplitude of mesial temporal spikes is maximal at the anterior temporal scalp electrodes and nasopharyngeal and sphenoidal electrodes when used. Sharp wave foci are seen in the mid-temporal and posterior temporal regions less frequently. Extratemporal focus (most commonly frontal lobes) is seen in 10% to 30% of patients who experience focal seizures with impaired consciousness. The interictal discharge may take the form of a bifrontal spike and wave discharge in some patients with mesial frontal foci.
Ictal EEG: Ictal EEG is abnormal in about 95% of patients with focal impaired awareness seizures. About two-thirds of patients with focal seizures with impaired consciousness have an electrodecremental pattern at the onset. A prototype pattern of 5 to 7 Hz rhythmic theta discharge in the temporal regions is seen in about 50% to 70% of patients with temporal lobe epilepsy. This pattern has shown high accuracy in localizing the onset to the ipsilateral mesial temporal structures on depth electrode studies. Lateralization from scalp EEG is usually satisfactory; however, localization within a lobe may sometimes be incorrect. Scalp ictal changes are difficult to appreciate, with some frontal lobe seizures because of movement artifacts.
Neuroimaging: Magnetic resonance imaging (MRI) of the head is a sensitive and specific imaging technique for localization-related epilepsy. The use of high-resolution MRI and specific seizure protocols can enhance the detection of abnormalities like hippocampal atrophy. The likelihood of finding an epileptic focus on neuroimaging studies is higher in patients with focal seizures than in generalized seizures. Common MRI findings are mesial temporal sclerosis, congenital anomalies, brain tumors, sequelae of head injury, vascular lesions, and neurocysticercosis. Many head MRI findings may be nonspecific and should be interpreted in a clinical context.
Sometimes, further imaging with positron emission tomography scan, ictal, and interictal single photon emission computed tomography scan may be utilized to identify the ictal onset zone, especially in patients with refractory seizures.[11][12][13]
Treatment / Management
The goal of treatment is to cease seizure activity without adverse events or with at least an acceptable level of adverse events. Antiepileptic medications (AEDs) are the mainstay of treatment, but other approaches are available for refractory seizures.
Medications
Except for ethosuximide, all other currently available AEDs can be used to treat focal impaired awareness seizures. The choice of medication depends on the patient's preference, comorbid conditions, drug interactions, and adverse effect profile; monotherapy is preferred initially. An increased dose of a single agent may be required to achieve seizure control before adding another agent. Classical AEDs used for focal impaired awareness seizures include carbamazepine, valproate, phenytoin, and phenobarbital. Newer agents available are levetiracetam, topiramate, lamotrigine, gabapentin, oxcarbazepine, zonisamide, felbamate, tiagabine, pregabalin, and lacosamide. The most common first-line drugs are carbamazepine, phenytoin, valproic acid, and oxcarbazepine.
More than half of patients with focal impaired awareness seizures will require more than 1 AED. Using more than 1 antiepileptic drug creates a potential for drug interactions, often necessitating constant monitoring and adjustment in doses. Seizures are considered refractory when 2 or more AEDs have failed to control the seizures. Only about half of the patients with focal impaired awareness seizures have epilepsy fully controlled with medications.
Ketogenic Diet
The ketogenic diet is a specialized high-fat, low-carb, and controlled protein diet that should be considered in children with intractable seizures when at least 2 AEDs have been ineffective.
Surgery
Surgical intervention is considered for refractory focal impaired awareness seizures. Resection surgery is considered when the seizure focus is localized and solo. An ideal candidate for respective surgery is a patient with refractory focal impaired awareness seizures who has failed a trial of at least 2 or 3 AEDs, has features suggesting mesial temporal onset, and MRI shows mesial temporal sclerosis. Surgical procedures for refractory focal impaired awareness seizures include amygdalohippocampectomy, temporal lobectomy, and gamma knife radiation.
Vagus Nerve Stimulation
Patients with refractory seizures who are not candidates for surgery should be considered for the implantation of a vagal nerve stimulation device. Response rates of 35% to 45% have been reported with vagal nerve stimulation therapy. Antiepileptic drugs should always be used in conjunction with this therapy. If vagal nerve stimulation therapy is effective, it may be possible to reduce the medications slowly.[14][15]
Differential Diagnosis
Some conditions that can initially present similarly to focal impaired awareness seizures include the following:
- Absence seizures
- Benign childhood epilepsy
- Benign neonatal convulsions
- Complicated migraine
- Juvenile myoclonic epilepsy
- Parasomnias
- Paroxysmal movement disorders
- Psychogenic nonepileptic seizures
- Vasovagal syncope
Prognosis
Patients with focal seizures have a higher risk of seizure recurrence than those with generalized seizures. Recurrence rates of simple and focal impaired awareness seizures appear to be the same. Loss of consciousness can cause trauma, aspiration, burns, and accidents. Associated anxiety, limitations in work, and driving add to significant morbidity. The mortality rate in patients with epilepsy is 2 to 3 times higher than in the general population. Most deaths are due to underlying etiology and accidents. Sudden unexpected death in epilepsy is more common in patients with medically intractable seizures.
Complications
Focal impaired awareness seizures can lead to significant morbidity and mortality. If left untreated, these seizures can develop into focal status epilepticus, which can be difficult to abort. Immediate complications of focal status epilepticus include coma, brain damage, cardiac arrhythmia, respiratory failure, aspiration, and death. Long-term complications of focal impaired awareness seizures include cognitive impairment, depression, anxiety, head injury, and premature mortality. Screening for these conditions in patients with a history of focal onset epilepsy is essential.[16][17]
Deterrence and Patient Education
Patients with focal impaired awareness seizures and their families should be educated on seizure precautions to reduce morbidity and mortality. Driving restrictions vary depending on the patient's state of residence; healthcare providers should routinely review driving restrictions with patients. Patients should use caution when working at heights, cooking, and operating heavy machinery or power tools. Patients should also avoid swimming alone or unsupervised baths.[18]
Enhancing Healthcare Team Outcomes
Seizures are best managed by an interprofessional team that includes a nurse practitioner, primary care provider, neurologist, pharmacist, and neurosurgeon. Once treated, the primary care provider often follows the patient as an outpatient. The nurse and primary care provider must educate the patient on safety and compliance with treatment. Depending on the medication, drug levels may need to be obtained regularly to ensure they are within therapeutic levels. In addition, the pharmacist should keep track of the patient's medications to ensure no drug interactions occur. The outlook for patients with seizures depends on the chronicity.[19][20]
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