Posterior Slow Wave of Youth. EEG of an 11-year old girl with a new onset of insomnia, weight loss, and depression shows occipital slow theta and delta slow waves (arrows) mixed with and briefly interrupting the alpha rhythm on both sides.

Posterior slow waves of youth (youth waves or polyphasic waves) are physiologic theta or delta waves accompanied by the alpha rhythm and creating spike-wave-like phenomenon. They are most commonly seen in children aged 8–14 years but are uncommon in children under 2 years. They have a 15% incidence in persons aged 16–20 years but are rare in adults after age 21 years. They are typically seen both unilaterally and bilaterally in a single recording. They are always accompanied by the alpha rhythm, and are attenuated with eye opening, disappear with the alpha rhythm during drowsiness and light sleep, and may be accentuated by hyperventilation.^1–3

Posterior Slow Wave of Youth. EEG of a 10-year old boy with recurrent syncope shows occipital slow waves (arrows) mixed with and briefly interrupting the alpha rhythm on the right side.

Posterior slow waves of youth (youth waves or polyphasic waves) are physiologic theta or delta waves accompanied by the alpha rhythm and creating spike-wave-like phenomenon. They are most commonly seen in children aged 8–14 years but are uncommon in children under 2 years. They have a 15% incidence in persons aged 16–20 years but are rare in adults after age 21 years. They are typically seen both unilaterally and bilaterally in a single recording. They are always accompanied by the alpha rhythm, and are attenuated with eye opening, disappear with the alpha rhythm during drowsiness and light sleep, and may be accentuated by hyperventilation.^1–3

Posterior Slow Wave of Youth; Attenuated with Eye Opening. EEG of a 10-year-old boy with syncope showing occipital slow theta and delta waves (arrows) mixed with and briefly interrupting the alpha rhythm in both occipital regions but maximally expressed in the left hemisphere. This is so-called “posterior slow waves of youth” that are physiologic findings seen commonly in children aged 8–14 years. They are always accompanied by the alpha rhythm, and are attenuated with eye opening (open arrow), and disappear with the alpha rhythm during drowsiness and light sleep.^1–3

Posterior Slow Wave of Youth; Activated with Eye Closure. (Same EEG as in Figure 4-3) Alpha rhythm and posterior slow waves of youth are activated by eye closure.

Slow Alpha Variant. EEG of a 9-year-old boy with recurrent vertigo showing rhythmic notched theta or delta activities that have a harmonic relationship with the alpha rhythm (one-third or half the frequency). Slow alpha variants are rare benign EEG variants (less than 1% of normal adult), have a harmonic relationship with the alpha rhythm, and show similar distribution and reactivity as a normal alpha rhythm.⁴ It should not be misinterpreted as occipital intermittent rhythmic delta or theta activity activities, pathologic findings seen in children and adults.

Slow Alpha Variant. EEG of an 11-year-old girl with recurrent staring episodes showing slow alpha variants that are activated by eye closure.

Slow Alpha Variants. EEG of a 10-year-old boy with behavioral disturbance and headache showing slow alpha variants (subharmonic of the alpha rhythm) with notched appearance. They are intermingled with normal alpha rhythms and activated by eye closure.

Asymmetric Alpha Rhythm; Dyke-Davidoff-Mason Syndrome Due to Intrauterine Stroke. A 9-year-old-left-handed girl with right hemiparesis and hemiatrophy due to intrauterine stroke of who developed a new-onset right-sided focal motor seizure with secondarily generalized tonic-clonic seizure. Cranial MRI shows encephalomalacia in the left frontal-temporal region, left cerebral hemiatrophy, and thickening of the clavarium. These findings are compatible with Dyke-Davidoff-Mason syndrome. EEG shows consistent suppression of alpha rhythm and intermixture of theta and delta activities in the left occipital region.

Focal lesions in the thalamocortical circuit including occipital cortex and anteroventral thalamus can cause changes in alpha rhythm including (1) slowing of frequency (1 Hz or more differences between both sides), (2) loss of reactivity and modulation, (3) voltage attenuation, (4) Bancuad’s phenomenon (failure of reactivity of alpha rhythm to eye opening), (5) intermixed theta or delta activity (must be differentiated from posterior slow waves of youth), and (6) epileptiform activity.⁵

Dyke-Davidoff-Mason syndrome is first reported in 1934 by Dyke.⁶ The syndrome includes contralateral hemiatrophy and hemiparesis and seizure accompanied by cerebral hemiatrophy and compensatory bone alterations in the clavarium, such as thickening, hyperpneumatization of the paranasal sinuses and mastoid cells, and elevation of the petrous pyramid and the upper edge of the orbita.^6–9

Alpha Rhythm Changes Affected by Right Occipital Tumor. A 20-year-old boy with intractable epilepsy caused by low-grade tumor in the right occipital region. His seizures are described as simple visual hallucination (colors and shapes) with or without versive seizure (head and eyes deviating to the left) and GTCS. MRIs show a well-defined tumor in subcortical area of the right occipital region without mass effect. EEG shows asymmetry of alpha rhythm, which is normal on the left but significantly attenuated (>30%), poorly regulated on the right, and failure of the alpha rhythm to attenuate with eye opening (*). There is focal theta and polymorphic delta activity intermingled with the alpha rhythm.

Focal lesions in the occipital cortex and anteroventral thalamus can cause changes in alpha rhythm including (1) slowing of frequency (1 Hz or more differences between both sides), (2) loss of reactivity and modulation, (3) voltage attenuation, (4) Bancuad’s phenomenon (failure of reactivity of alpha rhythm to eye opening), (5) intermixed theta or delta activity (must be differentiated from posterior slow waves of youth), and (6) epileptiform activity.⁵

Bancaud’s Phenomenon; Dyke-Davidoff-Mason Syndrome. (Same patient as in Figure 4-8) EEG demonstrates failure of alpha rhythm to attenuate with bilateral eye opening in the left occipital region (open arrow). This is so-called “Bancaud’s phenomenon.” In 1995, Bancaud described unilateral failure of alpha blocking with eye opening.^7,8 The patients had focal structural lesions in the temporal, parietal, and occipital regions. The side on which alpha activity failed to attenuate with eye opening was ipsilateral to the side of the lesion.

In the study of 120 patients with defective alpha activity by mental arithmetic at Mayo Clinic, 32 patients had Bancaud phenomenon. Associated focal slowing and/or epileptiform abnormalities were present over the temporal region in 60 patients, the parietal region in 33, posterior head regions in 14, and the frontal region in 6.⁹

Symptomatic Focal Epilepsy; Congenital Hydrocephalus with Ventriculoperitoneal Shunt. An 11-year-old boy with congenital hydrocephalus and ventriculoperitoneal shunt insertion who developed recurrent staring spells accompanied by “gulping sound.” CT shows dilatation of temporal horn of the right lateral ventricle, multiple hypodensity areas of the right occipital lobe, and VP shunt catheters. EEG demonstrates marked attenuation of alpha rhythm in the right occipital region and polymorphic delta activity and spikes in the right temporal region.

VP shunt insertion can cause injury to the cortex or interfere with postnatal neuronal migration or in combination. These can lead to focal seizures.

Epilepsy is an important predictor of poor intellectual outcome in the children with hydrocephalus with shunts. Epilepsy was significantly affected by the causes of hydrocephalus, shunt complications, increased ICP caused by hydrocephalus or shunt malfunction, and the presence of a shunt by itself.¹⁰

Ipsilateral Attenuation of Alpha Rhythm & Polymorphic Delta Activity (PDA); Focal Cortical Dysplasia, Left Occipital Lobe. EEG of a 6-year-old girl with intractable occipital lobe epilepsy due to focal cortical dysplasia in the left occipital region. There is consistent slowing and decreased voltage (less than 50% of the right side) of physiologic alpha rhythm and intermingled theta and polymorphic delta activity (PDA) in the left occipital region.

Consistent focal slowing of physiological rhythms by 1 Hz or more on one side is a reliable sign of focal abnormality of the side of slower frequency whether the amplitude of the rhythm is increased or decreased.¹¹ In this patient, the EEG also shows focal PDA and alpha asymmetric (decreased voltage by more than 50%, compared to the right side).

Intermittent Polymorphic Delta Activity & Attenuation of Alpha Rhythm; Systemic Lupus Erythrematosus (SLE). A 17-year-old boy with a history of SLE and epilepsy. EEG shows asymmetric alpha rhythm with suppression in the left occipital region, intermittent polymorphic delta activity in the left temporal region, and left temporal sharp transients.

EEG was abnormal in 87.1% of the patient with SLE who had a history of seizures. Left hemisphere abnormalities were identified in 79.6% and right hemisphere abnormalities in 7.4%. Abnormalities included theta, delta slowing, and sharp wave. In 74.4% of the patients with left hemisphere abnormalities, the abnormalities were localized to the left temporal leads. These findings suggest selective damage to the left temporal limbic region in patients with SLE.¹²

Asymmetric Reactivity of Alpha Rhythm; Hemorrhagic Stroke Caused by Streptococcal Infection. A 6-year-old girl with a new-onset seizure described as fall followed by generalized tonic-clonic seizure associated with streptococcal infection. Her MRI/MRA is compatible with the diagnosis of hemorrhagic infarction in the left temporal-occipital region. CT angiogram was normal. EEG shows depression of reactivity to eye closure (open arrow), decreased amplitude, and frequency of alpha rhythm in the left occipital region.

Simultaneous EEG and fMRI study revealed the correlation between increased alpha power and decreased MRI signal in multiple regions of occipital, superior temporal, inferior frontal, and cingulate cortex, and with increased signal in the thalamus and insula.¹³ Using simultaneous EEG and PET scan, a correlation between alpha power and metabolism of the bilateral thalamus and the occipital and adjacent parietal cortex was found.¹⁴ These results support the role of thalamus as, in part, a generator of alpha rhythm. Therefore, involvement of thalamocortical circuit can cause suppression of alpha rhythm.

Unilateral Attenuation of Alpha Rhythm; Right Thalamic Heterotopia. A 6-year-old boy with intractable symptomatic absence epilepsy caused by right thalamic heterotopia (arrow). EEG showed secondary bilateral synchrony with lateralized epileptic focus in the right hemisphere. In addition, background activity shows attenuation of alpha rhythm in the right hemisphere.

Not only the lesions in the occipital lobes but also the lesions in the anteroventral thalamus or thalamocortical circuit can cause unilateral attenuation of alpha rhythm.¹⁵ The studies using combined EEG/fMRI indicated the alpha rhythm may be generated, in part, by the thalamus.^13,16 The studies using combined EEG/PET showed a correlation of alpha rhythm in the pons, anterior midbrain, hypothalamus, medial thalamus, amygdala, the basal prefrontal cortex, insula, and the right dorsal premotor.^14,17,18 It is therefore possible that the mesencephalic-medial thalamic network is correlated with occipital EEG alpha rhythm.

Attenuation of Alpha Rhythm & Focal Polymorphic Delta Activity; Acute Focal Axonal Injury. A 5 1/2-year-old boy with a new-onset generalized tonic-clonic seizure followed by right-sided Todd paralysis caused by traumatic brain injury. Axial T2-weighted image shows small hemorrhage in the left mesial temporal area (open arrow). EEG performed 2 hours after the seizure shows polymorphic delta activity (PDA) in the left temporal region and slowing of frequency of alpha rhythm in the left occipital region.

Focal PDA and slowing of alpha frequency are supportive of focal structural abnormality in the left temporal-occipital region consistent with the MRI finding. PDA mixed with substantial amount of theta or alpha activity usually indicates reversible cause such as mild TBI, migraine, postictal, or mild viral encephalitis.

Ipsilateral Attenuation of Alpha Rhythm; Focal Cortical Dysplasia, Left SSMA. (Same EEG recording as in Figure 4-31 to 4-36) A 7-year-old-left-handed girl with multiple types of seizures including focal myoclonic seizure, drop attack, and secondarily generalized tonic-clonic seizure. (A) MRI with FLAIR sequence shows focal cortical dysplasia (FCD) in the left SSMA (arrow). (B) Interictal PET demonstrates diffuse hypometabolism in the left hemisphere but maximal in the left lateral frontal (open arrow) and SSMA (double arrows) regions, corresponding to the lesion seen in the MRI in A. EEG shows suppression of amplitude and reactivity of the alpha rhythm as well as diffuse theta activity in the left hemisphere. These findings are consistent with involvement of the thalamocortical circuit in the left hemisphere.

Ipsilateral Attenuation of Photic Response; Hemispheric Malformation of Cortical Development (MCD). (Same patient as in Figure 6-16 to 6-18) EEG during photic stimulation with different stimulus frequencies constantly shows asymmetric photic response with lower amplitude and less reactivity in the left compared to the right hemispheres.

Although mild and inconsistent asymmetry of photic response is frequently seen in normal individuals, consistently lateralized voltage and reactivity on one side with all photic stimulus frequencies raises the possibility of structural abnormality in the hemisphere of lower voltage.¹⁹

Ipsilateral Attenuation of Photic Response; Focal Cortical Dysplasia, Left Temporo-Occipital. EEG of a 12-year-old girl with intractable occipital lobe epilepsy due to focal cortical dysplasia. There is depression of photic response in the left occipital region caused by focal cortical dysplasia. Axial FLAIR sequence and coronal

T2-weighted MRIs show thickened cortex, decreased gyral pattern, increased signal intensity, and blurring of gray-white matter junction in the left temporal-occipital region.

Asymmetric Photic Response (Ipsilateral Suppression); Left Temporo-Occipital Tumor. A 4-year-old girl with medically intractable epilepsy caused by tumor. Her seizures were described as pupillary dilatation, right facial distortion, and eyes deviating to the left side, followed by left arm stiffening and shaking. (A) Axial FLAIR shows high signal abnormality over the right temporo-occipital region. (B) Sagittal view demonstrates hypointense lesion in the left temporo-occipital region. EEG shows consistent asymmetry of photic driving response during all flash frequencies over the left occipital region that is concordant with the location of the tumor in the left temporo-occipital region.

A mild and inconsistent asymmetry of photic driving response is frequently seen in normal individuals. An asymmetry in photic driving response may result from a lesion on the side of lower voltage, but an asymmetry in voltage only, although consistently lateralized, in the absence of other EEG changes can be seen in some normal individuals and should not be viewed as abnormal.¹⁹

Asymmetric Photic Response; Left Thalamic Atrophy and Calcification. (Same patient as in Figure 4-26 and 4-27) EEG shows attenuation of photic response in the left hemisphere. MRI and CT show bilateral thalamic calcification, greater expressed on the left with left thalamic atrophy (arrows). Lesions in thalamocortical circuit can cause ipsilateral attenuation of alpha rhythm and photic response.

Alpha Asymmetry with Decreased Photic Response; Hemorrhagic Infarction. A 6-year-old girl with a new-onset seizure described as fall followed by generalized tonic-clonic seizure associated with streptococcal infection. Her MRI/MRA is compatible with the diagnosis of hemorrhagic infarction in the left temporal-occipital region. EEG shows consistent slower frequency and less reactivity of alpha rhythm (open arrow) and attenuation of photic response in the left occipital at all stimulus frequencies (double arrows). Also note left posterior temporal sharp waves (*).

Focal lesions in the occipital cortex and anteroventral thalamus can cause changes in alpha rhythm including (1) slowing of frequency (1 Hz or more differences between both sides), (2) loss of reactivity and modulation, (3) voltage attenuation, (4) Bancuad’s phenomenon (failure of reactivity of alpha rhythm to eye opening), (5) intermixed theta or delta activity (must be differentiated from posterior slow waves of youth), and (6) epileptiform activity. Although mild and inconsistent asymmetry of photic driving response (amplitude and reactivity) is frequently seen in normal individuals, constant asymmetry of photic driving response may result from a lesion on the side of lower voltage or less reactivity. Asymmetry in voltage only, although consistently lateralized, in the absence of other EEG changes can be seen in some normal individuals and should not be viewed as abnormal. Consistent focal slowing of alpha rhythm by 1 Hz or more on one side reliably identifies the side of focal abnormality whether the voltage of the rhythm is increased or decreased.^5,19

Enhancement of Ipsilateral Alpha Rhythm; Unilateral Polymicrogyria (PMG). EEG of a 4-year-old boy with developmental delay and well-controlled focal epilepsy shows alpha asymmetry with voltage higher in the right occipital region. MRIs demonstrate polymicrogyria in the right perisylvian and occipital regions.

Voltage asymmetry alone, unless extreme, constant, or in combination with other abnormalities (slowing of frequency, decreased reactivity or modulation of alpha rhythm and focal PDA) is the least reliable finding and of little clinical significance. Although increased voltage of alpha rhythm may rarely be observed on the side of abnormality, it is usually less reactive and poorly modulated.⁵

Enhancement of Ipsilateral Photic Response; Unilateral Polymicrogyria (PMG). (Same patient as in Figure 4-23) Excessive photic response is noted in the ipsilateral cerebral hemisphere (open arrows).

Alpha Asymmetry; Focal Cortical Dysplasia. A 7-year-old boy with recurrent seizures described as loss of the right visual field followed shortly by eyes rolling and tongue biting. He was confused and disoriented for 45–90 sec. MRI shows a focal cortical dysplasia in the left occipital region (open arrow). EEG demonstrates consistent asymmetry of alpha rhythm with higher amplitude, slowing of alpha frequency and intermixed theta activity in the left occipital region (arrows).

Consistent focal slowing of alpha rhythm by 1 Hz or more on one side reliably identifies the side of focal abnormality whether the voltage of the rhythm is increased or decreased.^5,20

Suppression of Vertex Sharp Waves and Spindles; Congenital Infection; Remote Stroke, Multiple Calcifications and Schizencephaly. A 7-year-old-left-handed girl with microcephaly, spastic right hemiparesis, and mental retardation due to unknown congenital infection and new-onset right focal clonic seizures. MRI and CT show encephalomalacia and open-lip schizencephaly in the left frontal-parietal region (open arrows) and multiple parenchymal calcifications (arrows). EEG during stage 2 sleep demonstrates persistent asymmetry of vertex waves (asterisk) and sleep spindles with voltage lower in the left hemisphere.

Vertex waves and sleep spindles can be affected by cerebral structural abnormalities with abnormality on the side of lower voltage. Lesions in parietal lobe or thalamus can attenuate sleep spindles.^5,21,22

Lateralized Polymorphic Delta Activity in the Left Hemisphere; During Arousal. (Same patient as in Figure 4-26) EEG shows attenuation of photic response in the left hemisphere. MRI and CT show bilateral thalamic calcification, greater expressed on the left with left thalamic atrophy (arrows).

Lesions in thalamocortical circuit can cause ipsilateral attenuation of alpha rhythm and photic response.

Asymmetric Lambda Waves; Status Post Resection of Epileptogenic Zone, Left Parietal. Twenty-four-hour video-EEG of a 5-year-old boy with a history of two-step epilepsy surgery for intractable epilepsy caused by a focal cortical dysplasia in the left frontal-parietal region. There are constant depression of lambda waves (*), alpha rhythm, and photic response (not shown) in the left occipital region associated with polymorphic delta activity in the left parietal-occipital region throughout the waking record. These findings are compatible with breach rhythm occurring at the posterior margin of the previous craniectomy.

Asymmetry of lambda waves is common and should not be interpreted as being abnormal unless there are associated abnormalities such as polymorphic delta activity and persistence of lambda asymmetry.

Anterior Beta Asymmetry; Remote Left Middle Cerebral Artery Stroke. (Same patient as in Figure 4-8 and 4-10) EEG shows attenuation of beta activity (arrows) in the left frontal-temporal region without definite polymorphic delta slowing.

Persistent voltage difference of beta activity of 35% or more between homologous areas of both hemispheres is considered a reliable sign of focal cerebral abnormality or extra-axial blood or cerebrospinal fluid.⁵

Suppression of anterior beta activity is usually more sensitive than focal polymorphic delta activity in determining structural abnormality.

Background Asymmetry and Polymorphic Delta Activity (PDA); Embolic Stroke Secondary to Pneumococcal Septicemia. A 15-year-old boy with metastatic medulloblastoma who developed a sudden-onset high fever, mental status change, right hemiparesis, and focal seizures described as head and eyes deviating to the right side followed by GTCS. Blood culture was positive for streptococcal pneumoniae. Cranial MRI reveals multiple infarctions caused by septic emboli, maximal in the right parietal region. EEG during sleep demonstrates continuously diffuse polymorphic delta activity (PDA), maximally expressed in the left hemisphere with suppression of beta activity, spindles, and vertex waves in the left hemisphere.

Sleep spindles are generated in the reticular nucleus of the thalamus, and through thalamocortical neurons the cortex is triggered to generate spindle bursts.²¹ Extended cortical areas in the centroparietal regions (pyramidal neurons), most likely the whole parietal cortex and the posterior part of the frontal cortex, are involved in the generation of sleep spindles as recorded using the MEG.²² Lesions in the thalamocortical circuit, especially thalamus and parietal lobe, can attenuate the sleep spindles.^5,23,24

Asymmetric Beta, Sleep Spindles and Vertex Waves; Encephalomalacia Caused by Acute Viral Meningoencephalitis in Newborn. A 12-year-old with mild cognitive impairment, left hemiparesis, and intractable epilepsy due to extensive involvement of the right frontal-parietal-temporal, insula, and thalamic regions caused by acute viral encephalitis at the age of 2 weeks. EEG during sleep shows marked suppression of spindles over the right hemisphere.

Sleep spindles are generated in the reticular nucleus of the thalamus, and through thalamocortical neurons the cortex is triggered to generate spindle bursts.²¹ Extended cortical areas in the centroparietal regions (pyramidal neurons), most likely the whole parietal cortex and the posterior part of the frontal cortex, are involved in the generation of sleep spindles as recorded using the MEG.²² Lesions in the thalamocortical circuit, especially thalamus and parietal lobe, can attenuate the sleep spindles.^5,23,24

Focal Cortical Dysplasia; Attenuation of Background Activity During Drowsiness. (Same patient as in Figures 4-104 and 9-106) A 4-week-old boy with very frequent seizures described as epileptic nystagmus and versive seizures. MRI demonstrates extensive focal cortical dysplasia over the left parieto-temporo-occipital regions (arrow). Suppression of premature hypnagogic hypersynchrony over the left hemisphere during drowsiness.

Suppression of Hypnagogic Hypersynchrony; Focal Cortical Dysplasia (FCD). A 2-year-old girl with a history of frequent seizures due to FCD. Her seizures were stereotypic and described as asymmetric tonic seizure with head and eyes deviating to the right side. (A) CT shows mixed hyperdense and hypodense areas in the left mesial frontal region (arrow). (B, C, D) Axial, coronal, and sagittal MR images demonstrate mixed density lesion in the mesial frontal region without enhancement (arrows). These findings are consistent with balloon cell-type focal cortical dysplasia. EEG during drowsiness shows persistently asymmetric hypnagogic hypersynchrony with lower amplitude on the left side. Although asymmetric hypnagogic hypersynchrony with shifting predominance is common, persistent asymmetric hypnagogic hypersynchrony is indicative of structural abnormality in the side of lower amplitude.

Suppression of Hypnagogic Hypersynchrony; Focal Cortical Dysplasia. (Same patient as in Figure 9-41) A 13-month-old-right-handed boy with medically intractable epilepsy due to focal cortical dysplasia (FCD) in the right parietal region. His typical seizure was described as a sudden onset of irritability, left facial twitching, left arm stiffening, and eyes deviating to the left side. EEG shows persistent suppression of hypnagogic hypersynchrony on the right side throughout the recording during drowsiness. The lesion in the parietal lobe can suppress sleep architectures such as hypnagogic hypersynchrony, vertex waves, and sleep spindles.

Unilateral Attenuation of Hypnagogic Hypersynchrony; Subcortical Focal Cortical Dysplasia (FCD). (Same patient as in Figures 4-87 and 4-88)

A 4-year-old girl with medically intractable epilepsy due to focal cortical dysplasia. Her seizure was described as stiffening and clonic jerking of her left arm and leg. Cranial MRI reveals a large focal cortical dysplasia in the right temporal region causing dilatation of a temporal horn of left lateral ventricle. EEG during drowsiness shows attenuation of hypnagogic hypersynchrony (arrow) in the right hemisphere corresponding to the focal cortical dysplasia.

Hypnagogic hypersynchrony is seen in drowsiness in children aged 3 months to 13 years but is rarely seen after age 9 years. This is described as paroxysmal bursts of high-voltage, rhythmic 3–5 Hz activity, maximally expressed in the frontocentral regions. Normal sleep patterns can be affected by cerebral lesions. Lesions of the parietal lobe or thalamus can attenuate sleep spindles.^21,22

Insular Epilepsy with Nocturnal Hypermotor Seizures; Focal Cortical Dysplasia. A 7-year-old-left-handed girl with nocturnal hypermotor seizures and mild mental retardation. She also had frequent episodes of simple partial seizures described as “buzzing in her right ear.” Axial T2-weighted and sagittal T1-weighted MRIs show thickened cortex intermixed with a small abnormal signal intensity (increased in T1 and decreased in T2) in the left insula area (arrow). Interictal EEG shows a run of spikes in the left centrotemporal region (dot) with suppression of physiologic vertex sharp waves (X) in the left hemisphere. The patient underwent resection of epileptogenic zone after extraoperative subdural/depth electrode EEG-video monitoring without any complication. Pathology showed focal cortical dysplasia without balloon cell and microcalcifications (FCD type 2A). The patient has been free of seizures for over 2 years since the surgery.

The anterosuperior portion of the insula and temporal lobe plays a major role in generating nocturnal hypermotor seizures.^25,26 Although it is well known that auditory cortex is located in the superior temporal gyrus, there were case studies supporting for a major role of human insula cortex in auditory processing.²⁵

Late Post-Traumatic Epilepsy; Encephalomalacia Due to Cerebral Contusion (Contrecoup). A 7-year-old girl with a history of head trauma at 13 months of age. She fell down and hit the left side of her forehead on the concrete floor. She was lethargic and vomited without seizures. (A) CT performed immediately after the injury shows multiple small intraparenchymal hemorrhages in the right parietal region. This finding is compatible with countercoup injury. She had had recurrent episodes of very brief imbalance, left leg tingling, “left ear popping,” dizziness and unable to focus without loss of consciousness for over 3 years prior to this EEG recording. (B and C) MRI performed 1 day prior to this recording shows linear area of gliosis with decreased volume of the gray matter and increased T2 signal intensity in the area of calcification seen in the CT. EEG during sleep demonstrates spike in the right centroparietal region corresponding to the lesion seen in both MRI and CT. The seizures disappeared completely after the treatment with carbamazepine.

Late posttraumatic epilepsy usually occurs within the first 2 years after the injury. Seizures are believed to originate from a cerebromeningeal scar.²⁶ The 5-year and 30-year cumulative incidence after severe head injury was 10% and 16.7%, respectively.²⁷ The likelihood of late posttraumatic epilepsy is increased by the presence of any of 3 factors: an acute hemorrhage, a depressed skull fracture, and early epilepsy.^28–31 Annegers and colleagues found that the presence of early posttraumatic epilepsy did not predict late posttraumatic epilepsy.³²

Sturge-Weber Syndrome; Suppression of Sleep Spindles, Vertex Waves, and Beta Activity. A 5-year-old right-handed girl with right-sided facial hemangioma presenting with a new-onset seizure described as eye fluttering and clonic jerking of the left upper and lower extremities lasting for approximately 45 minutes. (A) CT shows calcification in the right parietal region. (B) MRI with FLAIR sequence shows right cerebral atrophy with decreased signal intensity in the white matter. (C) Axial T1-weighted image with GAD shows contrast enhancement over the right hemisphere. EEG demonstrates persistent depression of sleep spindles, vertex waves, and beta activity over the right hemisphere throughout the sleep recording. These findings support the diagnosis of Sturge-Weber syndrome (SWS).

EEG in vertex waves and spindles can be affected by cerebral structural abnormalities with abnormality on the side of lower voltage. Lesion in parietal lobe or thalamus can attenuate sleep spindles.^5,23,24

The typical EEG in SWS is asymmetric, with local voltage depression and background slowing ipsilateral to the affected hemisphere. This asymmetry may be seen from the first months of life, but becomes more evident as atrophy of the hemisphere progresses. Decreased diazepam-enhanced β activity in the EEG is a sensitive criterion of functional abnormality. In patients with subtle structural abnormalities diazepam-enhanced EEG may have added value in diagnosing functional involvement and in monitoring disease progression in patients.^33,34

Ipsilateral Attenuation of Vertex Waves and Spindles; Open-Lip Schizencephaly. A 3-year-old boy with global developmental delay, mild left hemiparesis, and intermittent simple partial seizures described as funny sensation in her left arm with or without left arm stiffening. (A) Axial FLAIR image shows the right narrow open-lip schizencephaly with surrounding irregular gray matter (double arrows). A dimple in the ventricular wall shows the opening of the cleft into the ventricle (open arrow). (B and C) Coronal and sagittal images showed polymicrogyria lining around the cleft (arrows). EEG reveals depression of vertex and sleep spindles in the right frontal-central region (F4-C4). EEG also shows (not shown) sharp waves in the right frontal-temporal region. Suppression of sleep architecture indicates that there is a functional involvement of the thalamocortical circuit over the right hemisphere. The abnormal cortex lining of the schizencephalic cleft, not the cleft itself, which is epileptogenic. Background activity is more altered in the unilateral than in the bilateral form. The background EEG activity can be normal in some patients. In addition to slow waves over the cleft location, contralateral spikes were sporadically seen. There is a causal relation between schizencephaly and epilepsy; the seizure symptoms and EEG interictal and ictal abnormalities were consistent with the cleft location. Epileptiform abnormalities are seen in all patients with seizures and EEG focal abnormalities were on the same side as the cleft location in 60% of cases. EEGs in some patients show focal or bilateral synchronous ESES.^37–39

Suppression of Sleep Architecture; Intrauterine Stroke. A 6-month-old boy with intrauterine stroke. Cranial CT shows encephalomalacia in the right parietal region. EEG demonstrates consistent suppression of sleep spindles and vertex waves in the right hemisphere throughout the recording. Note prolonged sleep spindles in the Cz and C3 that is a physiological finding at 3–6 months of age. Lesion in the parietal lobe or thalamus can attenuate sleep spindles.^5,23,24 A more recent study demonstrates that sleep spindles are generated in the reticular nucleus of the thalamus, and through thalamocortical neurons the cortex is triggered to generate spindle bursts.²¹ A study using magnetoencephalogram (MEG) suggests involvement of the pre- and post-central areas in the generation of MEG sleep spindles.²²

Suppression of Sleep Spindles and Focal Polymorphic Delta Activity (PDA); Left Middle Cerebral Artery Stroke. A 2 1/2-month-old girl who developed left MCA stroke after cardiac catheteralization. T2-weighted axial MRI (A) and DWI (B) show infarction in the left parietal region. EEG demonstrates depression of spindles as well as diffuse polymorphic delta activity in the left hemisphere.

Sleep spindles are generated in the reticular nucleus of the thalamus, and through thalamocortical neurons the cortex is triggered to generate spindle bursts.²¹ Equivalent dipoles of MEG spindles were distributed over the centroparietal region that suggests involvement of the pre- and post-central areas in the generation of MEG sleep spindles.²²

Unilateral Slowing of Spindle Frequency. A 7-month-old right-handed boy born at 28 weeks GA due to abruptio placenta and PROM. He had a normal development until 5 months of age when he started having seizures described as head and eyes deviating to the left and clonic jerking of the left arm and left side of the face. He had developmental regression and preferred to use his right hand more after the onset of his very first seizures. A: Axial T2-weighted image shows heterogeneous signal abnormality (double arrows) extending inward from the abnormal gyri to the surface of the frontal horn of the right lateral ventricle (arrow). B: Sagittal T1-weighted image shows heterogeneous signal abnormality (black arrow) over the surface of the right lateral ventricle. Interictal EEG demonstrates suppression of sleep spindles over the right central region and PLEDs (open arrow) in the right fronto-parietal region.

Focal transmantle dysplasia is a malformation of cortical development that extends through the entire cerebral mantle, from the ventricular surface to the cerebral cortex. The presence of balloon cells suggests that these malformations are associated with maldifferentiation of the stem cells generated in the germinal zone. A focal cerebral lesion is often associated with voltage asymmetry of sleep spindles, usually with depressed voltage on the side of the lesion, and was reported to cause frequency asymmetry in addition to a voltage asymmetry of sleep spindles with the slower frequency spindles occurring on the side of the lesion.

Subtle Delta and Theta Slowing; Focal Cortical Dysplasia, Right Mesial Temporal. EEG of a 14-year-old boy with well-controlled focal epilepsy caused by focal cortical dysplasia in the right mesial temporal region. There is subtle low-voltage smooth polymorphic delta activity (open arrow) and theta activity (double arrows) noted at the F8 and T6 electrodes, respectively. Chronic lesions can cause very little, if any, slow activity over the involved hemisphere, especially deep-seated lesions such as in the mesial temporal region.

Posterior Reversible Leukoencephalopathy; Right Posterior Temporal Theta Slowing. A 7-year-old boy with severe asthma who was admitted to the PICU for status asthmaticus. He received a treatment with high-dose corticosteroid and developed. He became lethargic and developed a new-onset seizure described as headache, vomiting, blindness followed by head and eyes deviating to the left side, left arm clonic jerking and then GTCS after a shooting of blood pressure to 170/110 mmHg. Axial FLAIR-sequence MRI shows multiple hyperintensity lesions in the white matter of the right occipital region (open arrow), the gray matter of the left occipital (double arrows) and periventricular white matter in the left occipital region (arrow). These are consistent with posterior reversible encephalopathy syndrome (PRES) caused by hypertension due to steroid treatment. The patient recovered within 1 week after hypertension was controlled. EEG after the seizure shows rhythmic theta activity intermixed with small spikes in the right parietal-posterior temporal region.

Hypertensive encephalopathy is the cause of this syndrome caused by suddenly increased systemic blood pressure exceeding the autoregulatory capability of the brain vasculature. Regions of vasodilatation and vasoconstriction develop, especially in arterial boundary zones, and there is breakdown of the blood–brain barrier with focal transudation of fluid and petechial hemorrhages. Functional vascular changes and edema, rather than infarction, play a major role. The patients usually have a rapid resolution of clinical and imaging abnormalities when blood pressure is lowered. The hyperintense signal seen mainly in the hemisphere where the seizures predominated. FLAIR is the sensitive sequence to the characteristic cortical and subcortical edema of PRES. The FLAIR sequence shows involvement of gray matter to be a much greater part of this syndrome than previously thought; the vasogenic edema may even originate in the cortex.^35,36

Ipsilateral Beta Attenuation & Monorhythmic Theta Activity; Focal Cortical Dysplasia, Right Parietal. EEG of a 13-year-old girl with intractable epilepsy and mental retardation. Her seizures include a negative myoclonus of her left arm, drop attack, and secondarily GTCS. Axial FLAIR image shows a focal cortical dysplasia in the right parietal (open arrow). Interictal PET scan is concordant and demonstrates hypometabolism in the same area (open arrow). EEG shows depression of anterior beta and persistent monorhythmic theta activity in the right hemisphere, maximal in the parasagittal region throughout the entire recording.

Frontocentral region has fastest-frequency of beta activity and highest level of cerebral blood flow.³⁷ Depression of beta activity is the most sensitive and earliest finding in focal cortical dysfunction. Constant reduction in voltage more than 50% (normal voltage < 20 μV) is strongly suggestive of gray matter abnormality in the hemisphere with lower voltage. Persistent rhythmic theta is also indicative of severe focal cerebral dysfunction.

Pulse Artifact. Pulse artifact can simulate polymorphic delta activity. It can be confirmed by EKG lead that shows the signal time-locked to the slow wave. It is seen only in one electrode (T3 in this patient) and caused by a loosely-applied EEG electrode placing on the artery.

Polymorphic Delta Activity and Sharp Wave; Left Temporal-Occipital Tumor. (Same patient as in Figure 4-20) A 4-year-old girl with medically intractable epilepsy caused by a low-grade tumor. Her seizures were described as pupillary dilatation, right facial distortion, and eyes deviating to the left side, followed by left arm stiffening and shaking. A: Axial FLAIR image shows high signal abnormality over the left temporo-occipital region. B: Sagittal T1-weighted image demonstrates hypointense lesion in the left temporo-occipital region. EEG during a Laplacian montage shows a sharp wave and polymorphic delta activity in the left temporal-occipital with some spreading to the homologous area in the right hemisphere. Asymmetric photic driving response (previous page), in combination with lateralized polymorphic delta activity and sharp wave, supports the diagnosis of focal epilepsy caused by structural abnormality in left temporal-occipital area.

The homologous area in the contralateral hemisphere, especially in the frontal and occipital regions, may be associated with similar slow waves and sharp waves, usually of lower amplitude. These findings may be caused by compression, edema, ischemia in the opposite hemisphere, transmission through commissural fibers, or volume conduction.

Polymorphic Delta Activity (PDA) and Right Temporal Sharp Waves; Focal Cortical Dysplasia (FCD). A 17-year-old boy with intractable epilepsy and mild mental retardation. He developed his first seizure at 2 years of age after severe head trauma. His typical seizure types are generalized tonic-clonic seizure and complex partial seizure described as shouting and crying, taking off his clothes, running away, and confusion. This EEG was performed 1 hour after his last GTCS that was followed by Todd paralysis. MRI was unremarkable except diffuse cerebral atrophy, greater on the right side, especially in the sylvian area (open arrow). Ictal SPECT shows hyyperperfusion in the right lateral temporal area. EEG shows continuously diffuse polymorphic delta activity (PDA) over the right hemisphere, maximally expressed in the midtemporal region (T4). Note sharp waves at the T4 electrode. He has been seizure free after the two-step epilepsy surgery of the right temporal lobe. Pathology revealed focal cortical dysplasia (FCD 2A) with mesial temporal sclerosis.

EEG performed within 24 hours after the seizure has a high yield. The presence of continuously focal PDA and sharp waves are indicative of epileptic focus caused by structural abnormality. Seizures caused by FCD can be precipitated by head trauma. The closer of the epileptic focus to the hippocampus, the higher the risk of secondary hippocampal sclerosis.

Prolonged Complex Febrile Convulsion; Large Hippocampal Volume and Hyperintensity. A 2-year-old girl with mildly global developmental delay and complex febrile seizures described as prolonged right hemiconvulsion. (A and B) Axial T2-weighted image and DWI shows left amygdala hyperintensity. (C) Coronal T2-weighted image shows mild enlargement and hyperintensity of the left hippocampus. EEG demonstrates constant polymorphic delta activity (PDA) with intermixed spikes in the left anterior temporal region.

There was a positive correlation between hippocampal volume and seizure duration. DWI showed hyperintensity in unilateral hippocampus in 3/12 patients with intractable seizures, ipsilateral thalamus in 2/12, and cingulate in 1/12. EEG showed abnormalities in temporal areas ipsilateral to the DWI abnormalities in these patients. Large hippocampal volume and hyperintensity on DWI were seen in patients with prolonged febrile convulsion. Prolonged febrile convulsion lasting for 60 minutes or longer may cause permanent structural changes in limbic structures that could promote later epileptogenesis.³⁸