Seizures and Sleep

Amy Korn-Reavis

David A. Davis

A seizure is a sudden abnormal discharge of electrical activity in the brain, usually affecting how a person acts or feels for a short time. These involuntary actions or sensations can range from a brief muscle twitch to a distorted vision to a staring spell to complete loss of consciousness with tonic-clonic activity (see Table 24-1). One in 10 Americans will have a seizure at some point in their lifetime, with 3% of those developing epilepsy, or seizure disorder, by the age of 80 (1). Epilepsy is defined as two or more unprovoked seizures (2), and is the third most common brain disorder after Alzheimer disease and stroke (3). Epilepsy affects 50 million people worldwide (3). The chances of having a seizure are greatest during early childhood or after the age of 65, with men slightly more at risk than women.

The known causes of seizures include birth trauma, brain injury, brain tumor, cerebral hemorrhage, anoxic event, brain infection (meningitis or encephalitis), stroke, cerebral palsy, mental handicap, high fever, toxins (lead), and illegal drug use (cocaine). When no underlying cause is found for the seizure, which happens in 7 out of 10 people (3), it is referred to as idiopathic.

“EEGs are known to capture approximately 50% of people with seizures however with repeat recording and recordings that include sleep the capture rate increases to 80% to 90% range” (4). It therefore becomes important to record patients during sleep. Many of the symptoms that are indications for a sleep study such as sleep paralysis, memory loss, confusional arousals, and fatigue are also symptoms of seizures. This can bring to the sleep laboratory patients who may not be aware they are having seizures. Therefore, it is essential for the technologist to be familiar with seizure activity and how
to identify it on electroencephalogram (EEG) and with video recording (5, 6).

Table 24-1 Terminology

Aura	A sensation experienced by some people with epilepsy before a seizure. Commonly described auras include copper taste, distorted vision, burning sensation, dizziness, headache, déjá vu, and jamais vu (5)
Déjá vu	A feeling that you have experienced something before (5)
Jamais vu	The familiar seems unfamiliar (5)
Ictal	During the time a seizure is occurring (6)
Interictal	The time between seizures (6)
Preictal	The time before a seizure occurs (6)
Postictal	The time after a seizure occurs (6)
Spike	Transient electroencephalography wave with pointed peak and duration of 20-70 ms (5)
Polyspikes	Multiple spike complexes (5)
Sharp wave	Same morphology as a spike but with duration of >70 and <200 ms (5)
Spike and slow wave	Spike followed by a high-amplitude slow wave (5)

CLINICAL OBSERVATIONS

Clinical observations during a seizure will vary depending on the location and size of the seizure focus (area of the brain where the seizure originates) and how the seizure is classified (Table 24-2) (7, 8, 9).

Location

Functions of the frontal lobe include speech and language skills, reasoning, and problem solving (7). Seizure activity in this area may present with difficulty speaking, hollering profanities, or laughing inappropriately. Parietal lobe functions are perception of stimuli (touch, pressure, and taste), recognition, orientation, and motor control (7). Presentation may include face or upper extremity numbness or twitching. Visual processing is the primary function of the occipital lobe of the brain (6). Clinical presentation may include distorted vision or visual hallucinations. Functions of the temporal lobe include recognition of auditory stimuli, memory, language skills, and emotional responses (6). Impairments during a seizure may include not being able to respond to auditory stimuli, impaired memory, or fear. The functions of each lobe of the brain are specific, and the clinical observations indicated are simplistic and may represent other medical conditions.

Table 24-2 Seizure Classifications

Generalized seizures	Event begins as widespread epileptiform activity over both hemispheres of the brain associated with sudden movement or loss of consciousness (6, 7, 8).
• Tonic-clonic	Occurs without warning with loss of consciousness, can be associated with injury (tongue biting or from initial fall), usually lasts up to 2-3 min, consciousness returns slowly, respirations may be absent during the tonic phase and may be labored during the clonic phase. Confusion, sleepiness, agitation, headache, and nausea all can be present postictal (6).
• Absence	Most commonly seen in children aged 4-14, has a duration of 5-15 s, begins and ends abruptly, described as a blank stare, appears to be daydreaming, and can be associated with rapid eye blinking (6).
• Myoclonic	Abnormal brief jerk-like movements involving both sides of the body lasting a second or two (8).
• Atonic (drop attack)	Complete loss of muscle tone, including falling to the ground, usually associated with injury and often noticed by head drop (8).
Partial seizures	Event begins as an electrical discharge over a localized area of the brain (one hemisphere). Note: Partial seizures can evolve, spreading to involve both hemispheres (6, 7, 8).
• Simple partial	Consciousness is not impaired, memory remains intact, awareness is preserved, may exhibit face twitching, eye blinking, odd smiling, or unexplained emotions (6).
• Complex partial	At least one of the following is present: impaired consciousness, memory, or awareness. Presents with trance-like appearance, may appear afraid and exhibit random undirected movements like walking, lip smacking, or picking at clothing (8).
Psychogenic nonepileptic seizures	These events are defined as clinical events that appear to be an epileptic seizure without correlating electroencephalogram changes. Other terminology used in the past for this type of activity has been pseudoseizure, psychological, or psychosomatic. It is important to recognize that many precipitating factors can lead to this diagnosis including past or present abuse, depression, and mental disorders (9).

Standard Nomenclature for the Description of EEG Discharges

The American Clinical Neurophysiology Society provides specific nomenclature for documentation of discharges seen in the EEG. They are defined by the area that is affected: generalized, lateralized, bilateral independent, and multifocal. When describing discharges, document
which lobes are predominant and whether the discharges are symmetrical or asymmetrical. In addition, describe the frequency and pattern of the discharge, such as rhythmic discharges, periodic discharges, or spike-and-wave discharges. The morphology and the shape of the discharge should also be described. Discharges can consist of sharp waves 70 to 200 ms, spikes 20 to 70 ms, sharp- and slow-wave complexes, and multiple spike- and slow-wave complexes that are similar to spike and slow wave but include multiple spikes associated with one or more slow waves (10), and paroxysmal slow-wave discharges.

It can be difficult to identify these discharges using a 30-second epoch; utilize a 10-second page to assist with identification. It can also be difficult to identify interictal epileptiform discharges (IEDs). Some normal variants can be mistaken for IEDs. An example is Mu rhythm, which is a rhythmic discharge of 8 to 11 Hz that has a sharp and comb-like shape. Mu rhythm can be suppressed with movement of the contralateral limb. Positive sharp transients of sleep are 4 to 6 Hz discharges seen in the occipital region. These can be confused with IEDs. However, most IEDs are of negative polarity (4). Electrocardiogram (ECG) artifact can also be mistaken for spikes. If a technologist is suspicious that a wave looks like a spike, one of the first steps would be to rule out artifact.

The technologist should also be aware of interictal changes that can be seen in the EEG such as voltage attenuation or augmentation, burst-suppression activity, or electrocerebral inactivity. These patterns can occur as well and should be documented (11).

EEG and patient activity (video) must be recorded. IEDs can be either electroclinical in nature or purely electrographic; therefore, the behavior of the patient and what occurred pre- and postevent must be clearly documented.

SLEEP AND EPILEPSY OVERVIEW

The sleep-wake cycle significantly affects the frequency of interictal epileptiform activity (IEA) as well as epileptic seizures. The two neurophysiologic states that characterize sleep (nonrapid eye movement [NREM] and rapid eye movement [REM]) have opposite consequences on both. According to most studies, generalized discharges and clinical seizures mostly occur in NREM sleep (12), which may be considered a natural “convulsive agent” (13), when brain activity is relatively more synchronous. The majority of EEG discharges are seen in stage N2, whereas REM sleep, with its asynchronous cell discharge patterns and atonia, is resistant to epileptic EEG potentials (14). NREM sleep activates IEDs in both partial and generalized syndromes (15).

For a patient with epilepsy presenting with EDS, several possible causes need to be considered. These include, but are not limited to, nocturnal seizure activity, side effects from medications used for seizure control, an underlying sleep disorder fragmenting sleep, or poor sleep hygiene (16). If multiple causes are present, one can feed off the other and the patient can be caught in a vicious cycle. For example, untreated obstructive sleep apnea is associated with increased arousals, increased NREM sleep, and decreased REM sleep. All of these lower the threshold for the appearance of seizure discharges and seizures during sleep. The disruption in sleep quality leads to daytime symptoms, which can include sleepiness, increased frequency of seizures, and memory impairment.

EPILEPTIFORM DISCHARGES DURING SLEEP IN GENERALIZED EPILEPSY

Primary Generalized Tonic-Clonic Seizures

Sleep has a well-documented influence on this class of seizure that tends to occur during NREM sleep (17, 18). Generalized IEA increases in NREM (18, 19, 20) and is most prominent at sleep onset and during the first part of the night. Interestingly, the morphology of IEA changes during sleep (21). In NREM sleep, generalized bursts of spike-wave complexes may become fragmented, polyspikes may appear, and the discharges may occur in a focal distribution (usually in a frontocentral region; Fig. 24-1).

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