Excessive Beta Activity Due to Benzodiazepine. EEG of a 12-year-old boy with epilepsy who was treated with clonazepam. There is excessively high-voltage, 18- to 22-Hz, beta activity with anterior predominance. ”Beating” appearance caused by waxing and waning in amplitude of beta activity is noted.

Rhythmic 15- to 25-Hz beta activity increases with therapeutic doses of benzodiazepines (BZP) and phenobarbital and is most prominent during drowsiness. BZP produce a decrease in alpha activity and general voltage and a slight increase of 4- to 7-Hz theta activity. Beta activity is more pronounced and acute in children. In adults, it is more common in chronic treatment. Generalized slowing related to the decreased level of consciousness occurs with a higher dose of BZP. Paroxysmal rhythmic slow waves have been reported in chronic treatment.^1–3

Excessive Beta Activity; Benzodiazepine & Phenobarbital. EEG of a 7-year-old boy with mental retardation and generalized epilepsy caused by traumatic brain injury who was on chronic phenobarbital and clonazepam. There is persistently high-voltage (>20 μV), 20- to 25-Hz beta activity with anterior predominance.

Beta activity in normal children and adults always has a voltage less than 20 μV. Benzodiazepines and barbiturates most prominently and commonly produce this effect. Other agents or medications causing excessive beta activity but with lower voltage include cocaine, amphetamines, methylphenidates, and tricyclic antidepressants.² Excess beta is also seen in rare normal individuals, chronic encephalopathy, hyperthyroidism, anxiety, and alcohol or barbiturate withdrawal. The effect is more prominent in children than in adults.

Type 1 Lissencephaly (Miller-Dieker Syndrome); Generalized High-Amplitude Fast Activity (Beta Frequency Band). A 6-year-old boy with spastic quadriparesis, severe mental retardation, and medically intractable epilepsy (atonic, atypical absence, and generalized tonic-clonic seizures) resulting from Miller-Dieker syndrome. Deletion of the short arm of chromosome 17 (p13.3) containing lissencephaly type 1 gene (LIS1) was found. MRI reveals a nearly smooth cerebral surface with abnormally thick cortex (typically 10–20 mm) and primitive sylvian fissures giving the ”hourglass” configuration.^4,5 EEG shows diffuse high-amplitude fast activity in alpha and beta frequency bands.

The EEG in type 1 lissencephaly is characterized by generalized high-amplitude fast activity in alpha and beta frequency bands (8–18/sec), burst of slow spike-wave complexes, high-amplitude slow rhythms, hypsarrhythmia-like pattern, and alternating patterns consisting of bursts of sharp/spike waves alternating with periods of electrocerebral depression. The EEG does not react to sleep or medication.^6–9

Lissencephaly-Pachygyria Associated with Congenital CMV Infection; Excessive Beta Activity. EEG of a 7-year-old girl with lissencephaly-pachygyria associated with congenital CMV infection. Brain CT shows smooth, flat gyri with thickened cortex and calcification (open arrow) adjacent to the right frontal horn of lateral ventricle. The EEG shows excessively diffuse, medium-voltage beta activity with posterior predominance. The patient did not take any sedative medication.

Patients with lissencephaly suffer injury before 16 or 18 weeks gestational age, whereas those with polymicrogyria are injured between approximately 18 and 24 weeks gestational age. Those with normal gyral patterns are probably injured during the third trimester. Cerebella hypoplasia and myelination delay in association with diffuse lissencephaly or cortical dysplasia should suggest the diagnosis of congenital cytomegalovirus infection.¹⁰

Excessive and high-voltage beta activity (amplitude > 20 μV) with no history of sedative drug usage is a nonspecific finding but can be seen in patients with mental retardation and also lissencephaly.⁷

Type 1 Lissencephaly (Miller-Dieker Syndrome); Generalized High-Amplitude Fast Activity (Alpha Frequency Band). A 6-year-old boy with spastic quadriparesis, severe mental retardation, and medically intractable epilepsy (atonic, atypical absence, and generalized tonic-clonic seizures) resulting from Miller-Dieker syndrome. Deletion of the short arm of chromosome 17 (p13.3) containing lissencephaly type 1 gene (LIS1) was found. MRI reveals a nearly smooth cerebral surface with abnormally thick cortex (typically 10–20 mm) and primitive sylvian fissures giving the ”hourglass” configuration.^4,5 EEG shows generalized high-amplitude fast activity in the alpha frequency band.

The EEG in type 1 lissencephaly is characterized by generalized high-amplitude fast activity in alpha and beta frequency bands (8–18/sec), burst of slow spike-wave complexes, high-amplitude slow rhythms, hypsarrhythmia-like pattern, and alternating patterns consisting of bursts of sharp/spike waves alternating with periods of electrocerebral depression. The EEG does not react to sleep or medication.^6–9

Hypsarrhythmia; Lissencephaly Type 1 (Classical LIS). EEG of a 15-month-old with infantile spasm and global developmental delay due to Lissencephaly type 1 (LIS 1). Hypsarrhythmic pattern is noted.

Classical lissencephaly (LIS) is a neuronal migration disorder resulting in brain malformation, epilepsy and mental retardation. Deletions or mutations of LIS1 on 17p13.3 and mutations in XLIS (also called DCX) on Xq22.3-q23 produce LIS. Whereas the brain malformation due to LIS1 mutations was more severe over the parietal and occipital regions (posterior-to-anterior gradient), XLIS mutations produced the reverse gradient, which was more severe over the frontal cortex (anterior-to-posterior gradient). The distinct LIS patterns suggest that LIS1 and XLIS may be part of overlapping, but distinct, signaling pathways that promote promote neuronal migration. Hypoplasia of the cerebellar vermis is seen more common with XLIS mutations.^11,12

Most children with LIS1 mutation have severe developmental delay and infantile spasms. DCX mutations usually cause lissencephaly in males and SBH in female patients. Mutations of DCX have also been found in male patients with anterior SBH and in female relatives with normal brain MRI. Autosomal recessive lissencephaly with cerebellar hypoplasia, accompanied by severe delay, hypotonia, and seizures, has been associated with mutations of the reelin (RELN) gene. X-linked lissencephaly with corpus callosum agenesis and ambiguous genitalia in genotypic males is associated with mutations of the ARX gene. Affected boys have severe delay and seizures with suppression-burst EEG. Carrier female patients can have isolated corpus callosum agenesis.¹³

Generalized High-Voltage Fast Activity (Alpha Band); Type 1 Lissencephaly. EEG of a 3-year-old boy with mental retardation and intractable epilepsy due to lissencephaly. There is generalized high-voltage 8- to 10-Hz rhythmic alpha activity with frontal-central predominance. MRI is compatible with lissencephaly type 1.

The typical EEG in lissencephaly is characterized by abnormally high-voltage rhythmic EEG activity, predominantly in the alpha and beta frequency bands (8–18 Hz). This pattern is seen in the waking period with high-amplitude slow rhythms and simulates slow spike-wave complexes or hypsarrhythmia. It has been suggested that this is associated with the unusual orientation of the anomalous neuronal columns.⁷ This high-amplitude rhythmic EEG activity associated with lissencephaly has high specificity. Typical features of this EEG pattern include high voltage increasing with age, missing topographic structuring, no reactivity to sleep or medication, and unusually high-voltage, sharp, slow-wave complexes.^8,14,15 They correlate with the severity of the brain malformation and the epilepsy.¹⁶ On sleep EEG, 14-Hz sleep spindles are found from early infancy but poorly observed after 1 year of age. Fourteen-hertz sleep spindles are replaced with high-amplitude rhythmic activity (HARA). The frequency of HARA is in the 5- to 11-Hz bands, and its amplitude is abnormally high. HARA may represent the extreme spindles reported in patients with central nervous system disorders.¹⁷ In an experimental study of lissencephaly, the extent of the extreme spindle activity, longer epileptiform after discharges, and seizure duration are dependent on the degree of cerebellar dysplasia, whereas the EEG focal abnormalities were related to lesions in the cerebral hemispheres.¹⁸

The above-described EEG pattern is not seen in type II lissencephaly. In type II lissencephaly, initially theta or delta waves of somewhat lower amplitude are initially observed. Sharp- and slow-wave complexes of very high amplitude are found more often in type I lissencephaly. They seem to correlate with the severity of the brain malformation and the epilepsy.^16,19 The EEGs in the lissencephaly patients showed the following patterns: (a) generalized fast activity (8–18/sec) with an amplitude higher than 50 mV, (b) sharp- and slow-wave complexes with an amplitude higher than 500 μV, (c) an alternating pattern consisting of bursts of sharp waves alternating with periods of electrocerebral depression. Ninety-five percent show patterns (a) or (b) or both compared to only 5% of the patients with an atypical cortical dysplasia and 0.4% in the controls. EEG appears to be valuable in the diagnosis of lissencephaly type I.²⁰

The EEG features and their evolution change with age. In early or middle infancy when infantile spasms begin, the EEG shows very high-amplitude (more than 400 mV) slow waves mixed with sharp theta waves. In late infancy, the EEG shows extreme spindles and a tendency toward bilaterally synchronous discharges of high-amplitude sharp and slow waves. The very high voltage of hypsarrhythmic patterns and the very low frequency of sharp-wave discharges seem to be typical in the most severe cases of lissencephaly or agyria.²¹

Type 1 Lissencephaly; Infantile Spasm in Remission. (Same patient as in Figure 5-6) The patient was in remission after the treatment with antiseizure medications. EEG shows very frequent sharp waves, maximally expressed in the left midtemporal region without hypsarrhythmia.

Glossokinetic Artifact. Glossokinetic artifact is caused by movement of the tongue, which produces a DC potential. The tip of the tongue has a negative electrical charge with respect to the root. The activity can be either unilateral or bilateral, depending on the direction of tongue movement. The electrical field can be widely distributed, although it is most often noted in the temporal electrodes. Sometimes it can simulate cerebral slow-wave activity, especially when the mouth remains closed during tongue movements.

Excessive Photic Response at High Frequency Stimulation (H response); Migraine. The ”H-response” is a prominent photic driving response at flash rates beyond 20 Hz. In a critical review of the literature, the reported sensitivity of the H-response varied from 25% to 100%, and the specificity from 80% to 91%. Although the relatively high sensitivities and specificities reported suggest that the H-response may be effective in distinguishing migraine patients from controls, and possibly migraineurs from tension headache sufferers, the Quality Standards Subcommittee (QSS) of the American Academy of Neurology concluded that the H-response was not more effective than the neurological history and examination in diagnosing headaches and was not recommended in clinical practice. However, in the presence of complex or prolonged aura, visual hallucinations, disorders of consciousness, history of recent trauma, and in infants vomiting with ocular and head deviation, the EEG may be useful for clinical diagnosis and help to monitor therapeutic response.^22,23

Anterior Slow Dysrhythmia & Frontal Sharp Transients. A 38-week CA girl with hypoxic-ischemic encephalopathy and generalized clonic seizures on the first day of life. She received a loading dose of intravenous phenobarbital a few hours prior to this EEG. The EEG shows bilaterally synchronous and symmetric, rhythmic 1.5-Hz delta activity with frontal predominance, admixed with board frontal sharp transients. Excessive degree of anterior dysrhythmia is indicative of diffuse encephalopathy.

Excessive Anterior Slow Dysrhythmia & Frontal Sharp Transients. (Same patient as in Figure 5-11) EEG is similar to that on the previous page except that the frontal sharp transients and anterior slow dysrhythmia are more continuous. Excessive degree of anterior dysrhythmia is indicative of diffuse encephalopathy.

Hyperventilation Effect; Sobbing Artifact. EEG of a 17-month-old boy with a history of febrile convulsions. There is diffuse rhythmic 5-Hz theta slowing with posterior predominance noted during sobbing. The rest of the EEG was unremarkable. Diffuse theta slowing caused by hyperventilation effect from sobbing should not be interpreted as mild diffuse encephalopathy.

Diffuse Theta Slowing With Central-Parietal Predominance; Myoclonic Astatic Epilepsy (MAE). EEG during wakefulness of a 5-year-old boy with myoclonic astatic epilepsy (MAE) showing diffuse monorhythmic 5- to 6-Hz theta activity with frontal-central-parietal predominance.

Monorhythmic 4- to 7-Hz rhythm is a characteristic background EEG activity seen in almost all instances early in the course of MAE. This rhythm is usually parietally predominant. This EEG pattern is falsely attributed to drowsiness. During active seizures, the rhythm is more irregular and slower, than in a period of remission.^24,25

Diffuse Monomorphic Theta Rhythm; Myoclonic Astatic Epilepsy. Background EEG during wakefulness of a 6-year-old girl with myoclonic astatic epilepsy (MAE) showing monorhythmic 5- to 6-Hz theta activity. The prolonged video-EEG over a 3-day period showed rare bursts of generalized epileptiform activity, activated by sleep.

Monorhythmic 4- to 7-Hz rhythm is a characteristic background EEG activity seen in almost all instances early in the course of MAE. This rhythm is usually parietally predominant. This EEG pattern is falsely attributed to drowsiness. During active seizures, the rhythm is more irregular and slower, than in a period of remission.^24,25

Slow Background Activity & Diffuse Theta Slowing; Lamotrigine Toxicity. A 12-year-old girl with juvenile myoclonic epilepsy (JME) who had been treated with lamotrigine. She developed acute sinusitis and was treated with azithromycin. One day after the treatment, she developed alteration of mental status and exacerbation of migraine. She showed marked improvement of her seizures and a decrease in EEG epileptiform activity. EEG during wakefulness shows slow background activity, diffuse theta activity, and occasional epileptiform activity. She returned back to normal within a few days, and EEG was normalized (not shown) within 1 week after stopping azithromycin.

Therapeutic doses of lamotrigine did not affect the background EEG activity in patients with Lennox-Gastaut syndrome and partial epilepsies with secondary bilateral synchrony.²⁶ There is only little information available about the effect of new AEDs on the EEG record.²

Diffuse Rhythmic Theta Activity; Rett Syndrome. A 12-year-old girl with Rett syndrome. EEG in Rett syndrome is invariably abnormal when recorded during clinical stage II (regression) after age 2 years. The changes in the EEG parallel the clinical course of Rett syndrome. Three characteristic EEG changes have been reported: (1) loss of expected developmental features during wakefulness and NREM sleep and generalized background slowing; (2) epileptiform abnormalities, initially, characterized by central-temporal spike- and/or sharp-wave discharges activated by sleep and, later, multifocal spikes and/or sharp waves and generalized spike- and slow-wave discharges; and (3) rhythmic theta activity in the central or frontal-central regions during clinical stages III (post-regression) and IV (late motor regression). Less frequent EEG patterns, including periodic patterns and hypsarrhythmia, can also be seen. For some older female individuals and adults in clinical stages III and IV, the EEG can be minimally slow, with expected awake and sleep developmental features and an absence of epileptiform abnormalities.²⁷

Diffuse Rhythmic 4-Hertz Delta Activity With Fronto-Central and Vertex Predominance; Rett Syndrome. A 10-year-old girl who presented at 14 months with developmental delay and hypotonia. The first EEG done at 16 months was normal. Subsequently, she developed typical features of Rett syndrome, and the diagnosis was confirmed by the gene test. EEG shows diffuse rhythmic 4-Hz delta activity with frontal-central and frontal vertex predominance.

Rhythmical 3- to 5-Hz theta or delta slowing is the most common EEG abnormality (30/44 patients) in patients with Rett syndrome. Diffuse/bisynchronous spikes or sharp waves or slow spike-wave complexes were found in 22/44 and 9/44 patients, respectively. With advancing age, the EEG abnormalities improve and a low-voltage EEG may develop. These changes parallel the clinical course of Rett syndrome.²⁸

Electroretinogram (ERG). The amplitude of ERG is usually low and obscured by normal EEG activity in Fp1 and Fp2. ERG can be confused with an electrode artifact generated by an exposed silver metal of chipped EEG electrode during photic stimulation. These physiological and art factual potentials can be differentiated by using a high photic stimulus frequency. With 30-Hz photic stimulus frequency, the amplitude of ERG diminishes but the amplitude of electrode artifact is constant.

Sobbing: Hyperventilation Effect. EEG of a 9-year-old boy with mental retardation who sobbed during most of this EEG recording. There is diffuse rhythmic 3-Hz delta activity with posterior predominance noted.

Occipital intermittent rhythmic delta activity (OIRDA) is a physiologic finding seen during hyperventilation.

Migraine; Frontal Intermittent Rhythmic Delta Activity (FIRDA). A 17-year-old girl with migraine and a transient episode of confusion, aphasia, and right hemiparesis, followed by her typical migraine headache. EEG during the headache and mild confusion (2 hrs after the resolution of aphasia and right hemiparesis) shows bursts of bisynchronous high-voltage 2.5-Hz rhythmic delta activity with frontal predominance (FIRDA). MRI/MRA, CT angiography, and hypercoagulation study were unremarkable.

EEG during or shortly after the episodes of basilar migraine showed FIRDA, which appears to be a sign of the rostral basilar artery ischemia. EEG gradually normalizes within 1–3 days after the acute stage.^29–31 Recurrent prolonged episodes of coma, varying from 3 to 14 days, due to basilar artery migraine have been reported. Severe spasm of the basilar artery was demonstrated by arteriography. EEGs during the comatose episodes showed suppression-burst, marked generalized slow-wave delta activity or FIRDA patterns.^{32, 33} Both the EEG and clinical findings subsided within the following weeks. Chronic ischemic structural brain lesions may predispose FIRDA during acute metabolic derangement.³⁴ The EEG changes during hyperventilation in migraine patients include theta activity and FIRDA.³⁵

Confusional Migraine; Frontal Intermittent Rhythmic Delta Activity (FIRDA). The ictal EEG during the prolonged video-EEG monitoring in a 9-year-old boy with confusional migraine. There is bisynchronous rhythmic delta activity, intermixed with low-amplitude spikes, with frontal predominance consistent with FIRDA (frontal intermittent rhythmic delta activity).

EEG during or shortly after the basilar migraine episodes showed FIRDA, which appears to be a sign of ischemia of the rostral basilar artery region. The EEG gradually normalizes after the acute stage, usually within 1–3 days.^29–31 FIRDA may have a slight notch on the descending phase of the delta waves (arrow) and should not be misinterpreted as spike-wave activity.³⁶

Occipital Intermittent Rhythmic Delta Activity (OIRDA); Chronic Renal Failure with Chronic Dialysis. EEG of a 12-year-old boy with chronic renal failure requiring intermittent dialysis. He developed his first GTCS. There are trains of bisynchronous high-amplitude 3-Hz delta activity with a maximum in the occipital regions.

Intermittent rhythmic delta activity (IRDA) is a burst or run of high-voltage, bisynchronous (sinusoidal or sawtooth wave), and rhythmic delta activity of fixed frequency (close to 2.5 Hz) with more rapid ascending than descending phase. It may have a slight notch on the descending phase of the wave form (in this EEG page, the small notches are noted during the ascending phase of the OIRDA). OIRDA is seen in children less than 10–15 years, and FIRDA is always seen in older children or adults. This is a maturation-related spatial EEG feature. The main association of IRDA is diffuse gray matter disease (both cortical and subcortical) or overactive thalamocortical circuits. It is indicative of mild to moderate encephalopathy and is usually seen in active fluctuating, progressing, or resolving diffuse brain dysfunction. It is nonspecific in etiology and is also seen in normal individuals during hyperventilation.

HIV Meningoencephalitis; Frontal Intermittent Rhythmic Delta Activity (FIRDA). An 18-year-old boy with HIV infection due to blood transfusion and a recent episode of recurrent HIV meningoencephalitis. Cranial CT shows bilateral frontal and basal ganglia calcifications. Also note metallic artifact from cochlear implantation. EEG during lethargic state shows frequent bursts of frontal intermittent rhythmic delta activity (FIRDA). This EEG pattern is indicative of diffuse encephalopathy but is nonspecific for etiology. FIRDA can be seen in association with a wide variety of pathologic processes varying from systemic, toxic, or metabolic disturbances to focal intracranial lesions. Even when associated with focal lesions, FIRDA by itself is nonfocal.³⁷

HIV Meningoencephalitis; Occipital Intermittent Rhythmic Delta Activity (OIRDA). (Same patient as in Figure 5-24) EEG shows asymmetrical, bilateral synchronous, rhythmic 2-Hz delta activity with occipital and left-hemispheric predominance.

OIRDA occurs almost exclusively in children and is associated with idiopathic generalized epilepsy and, less commonly, focal epilepsy. Occasionally, it can also be seen in patients with diffuse encephalopathy, as in this patient.^38–41

Frontal Intermittent Rhythmic Delta Activity (FIRDA); Postictal State. EEG of a 20-year-old boy with intractable epilepsy caused by a low-grade tumor in the right occipital region. There is a run of frontal intermittent rhythmic delta activity (FIRDA) appearing immediately after his typical seizure, which is described as a secondarily generalized tonic-clonic seizure.

FIRDA is indicative of a mild to moderate degree of encephalopathy. It is seen in active fluctuating, progressing, or resolving widespread brain dysfunction and is less likely to be associated with chronic, stable brain dysfunction. It is nonspecific in etiology and can be seen in postictal state. OIRDA is seen in children under 10–15 years of age, and FIRDA is always seen in older children and adults. This represents a maturation-related spatial EEG feature.

Occipital Intermittent Rhythmic Delta Activity (OIRDA); Diffuse Encephalopathy Caused by Moyamoya Disease. An 8-year-old boy with a new right frontal infarction resulting in slurred speech and mild left hemiparesis. MRI/MRA shows bilateral supraclinoid carotid occlusion with lenticulostriate collateral vessels reconstituting bilateral middle cerebral and anterior cerebral arteries. These findings are supportive of the diagnosis of moyamoya disease. Hypercoagulation study was positive for heterozygote PT 20210 mutation. EEG shows bilateral synchronous, rhythmic delta activity with peak amplitude localized over the occipital area, which is consistent with an occipital intermittent rhythmic delta activity (OIRDA) pattern.

OIRDA was first described in 1983.⁴² It was concluded that it was only seen in children and was not found to be helpful. in diagnosing a seizure disorder or structural abnormality. Subsequent publications show that OIRDA is seen almost exclusively in children with epilepsy and is rarely seen in children with diffuse encephalopathy.^38–41

Occipital Intermittent Rhythmic Delta Activity (OIRDA); Acute Viral Encephalopathy. A 4-year-old girl with congenital blindness due to congenital CMV infection who developed acute encephalopathy due to enteroviral infection (hand-foot-mouth syndrome). EEG shows asymmetric, bilateral synchronous, rhythmic 2-Hz delta activity with occipital and left-hemispheric predominance.

OIRDA occurs almost exclusively in children and is associated with idiopathic generalized epilepsy and, less commonly, focal epilepsy. Occasionally, it can also be seen in patients with diffuse encephalopathy, as in this patient.^38–41

Occipital Intermittent Rhythmic Delta Activity (OIRDA); Idiopathic Generalized Epilepsy. A 13-year-old boy with a history of idiopathic generalized epilepsy. EEG shows bilateral synchronous, rhythmic delta activity with peak amplitude localized over the occipital area, consistent with the OIRDA pattern.

OIRDA occurs almost exclusively in children and is associated with idiopathic generalized epilepsy and, less commonly, focal epilepsy. Occasionally, it can also be seen in patients with diffuse encephalopathy.^38,39,41,43

Notch Delta Pattern in Angelman Syndrome. An 11-month-old boy with a new-onset myoclonic seizure. His clinical phenotype was not definitely suggestive of Angelman syndrome (AS). MRI was normal. EEG shows frequent bursts of diffuse rhythmic notched delta with posterior predominance. The diagnosis was subsequently confirmed by a genetic test, which showed a deletion of chromosome 15.

The notched delta pattern is the hallmark EEG feature in AS. It was described in AS children as young as 12–14 months.^44,45 It often precedes the seizures and the suggestive phenotype for AS, and therefore allows an early detection of these patients.^44–48 Majority (78%) of the notched delta patients had a clinical phenotype consistent with AS,⁴⁹ and 88% of patients with AS had the notched delta EEG.⁴⁵

Notched Delta Pattern in Angelman Syndrome. A 12-year-old girl with Angelman syndrome (AS) with intractable epilepsy and multiple seizure types, including myoclonic, generalized tonic-clonic, absence, and atonic seizures. Interictal EEG shows frequent bursts of diffuse high-voltage notched delta pattern with frontal predominance.

The notched delta pattern is the hallmark EEG feature in AS. It was described in AS children as young as 12–14 months.^44,45It often precedes the seizures and the suggestive phenotype for AS, and therefore allows an early detection of these patients.^44–48 Majority (78%) of the notched delta patients had a clinical phenotype consistent with AS,⁴⁹ and 88% of patients with AS had the notched delta EEG.^45,50 This EEG pattern is also seen in other genetic conditions such as Rett syndrome^45,51–53 and 4p(–) syndrome.⁵⁴ At times, AS can be very difficult to distinguish from LGS. Absence of paroxysmal fast activity (PFA) during sleep in AS can help differentiate these two conditions. PFA is not seen in AS.

Triphasic Waves (TWs); Hepatic Encephalopathy. EEG of a 28-year-old man with hepatic encephalopathy caused by hepatitis. EEG shows bursts of diffuse moderate amplitude 2-Hz TWs.

TWs are high-voltage positive sharp transients (open arrow) that are preceded and followed by negative waves of lower voltage (double arrows). Anterior-posterior lag (20–140 msec) is inconsistently seen (<—>). TWS predominate in the anterior head regions but can be seen posteriorly, more diffusely, or in mixed dominance. TWs are etiologically nonspecific and are associated with a wide variety of etiologies with hepatic, renal, and anoxic accounting for over 75%. Other conditions such as hyperosmolarity; hyponatremia; Hashimoto thyroiditis; ifosfamide, metrizamide, lithium, tricyclic, baclofen toxicity; CJD; neuroleptic malignant syndrome; serotonin syndrome; Lyme disease; and West Nile disease have been reported. When occur at a frequency faster than 1 Hz, they are very difficult to differentiate from NCSE. The prognosis is mainly dependent on the etiology. TWs can also be seen in patients with cerebral atrophy and diffuse white matter disease. They are rarely seen in patients less than 20 years old.^55–59