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40 Cards in this Set
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Normalities: Normal Pediatric EEG
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Normal Pediatric EEG activity has more variation than adult EEG.
Focalities are not always abnormal. EEG varies greatly by age, therefore interpretation needs to be age specific for the Conceptual Age. For a complete EEG, all states (Awake, Drowsy, and Sleep) should be recorded. Lack of state change is abnormal in infants. Dysmaturity is an non-specific abnormality; "baby encephalopathic slowing". |
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Age catagories to consider for Pediatric EEG Interpretation:
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Pre-term: Below 38 weeks GA
Neonatal: Less than 1 month CA (38 to 44 weeks GA) Infants: Age 1- 12 months Age 1 to 3 years Age 3 to 6 years Age 6 to 12 years Age 13 to 19 |
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The ideal EEG should contain
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Awake
Drowsiness Transitions Sleep Arousal Activation Hyperventilation: when able to cooperate and if not medically contraindicated (HgbSS, Congenital heart disease, CF or active asthma) Photic Stimulation: if greater than 6 months of age |
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Age 1 month to 12 months: Awake EEG
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Poorly defined "fast" 20 mV background while awake in the first 1-3 months.
at 3 months: posterior dominant rhythm established at 3-4 Hz at 6 months: average posterior dominant posterior rhythm is 5 Hz, should be at least 4 Hz at 12 months: posterior dominant rhythm is 6 to 7 Hz. |
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Age 1 month to 12 months: Drowsy EEG
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EEG background may slow by 1-2 Hz from the waking frequency
Transition may be gradual over several minutes evidenced by reduction in artifact multiple partial and full alertings common After 6 months a prominent mono-rhythmic theta may develop Fronto-central dominant and may reach 200mV |
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Age 1 month to 12 months: Sleep EEG
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Spindles may develop in 2nd month
Spindles are 12 to 15 Hz and may last up to 10 seconds Spindles are asymmetrical at onset below 6-9 months Spindles frequently alternate from side of the head to the other below 6 months Spindles may be asymmetrical by 1 to 5 seconds at onset from 6 to 12 months then Spindles become increasingly symmetrical as sleep progresses Vertex sharp waves and K-complexes develop at 5 months Background is 0.75 to 3 Hz in sleep |
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Age 1 month to 12 months: Activation:
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Hyperventilation can not be performed. Crying in older infants often produces a HV response with slowing of the EEG background which should not be called abnormal.
Photic Stimulation: Not done less than 6 months of age because of concern over retinal over-stimulation. PS Response over 6 months of age at slow flash frequencies (1-3 Hz) is a VEP. Response can be asymmetrical because of uneven stimulation of the visual fields. Exaggerated response (very high voltage) with: infantile neuronal ceroid lipofusinosis, Gaucher's disease and biopterin deficiency. |
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1-3 years: Awake EEG
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Posterior Dominant Rhythm at Age 1 is 6-7 Hz and gradually increases by Age 3 to 6-8 Hz
Underlying diffuse 2 - 5 Hz activity Mu develops age 1 to 2 years Beta frequently occurs at 18 to 25 Hz |
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1-3 years: Drowsy EEG
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Semi-rhythmic 4 to 6 Hz background
Hypnagogic Hypersynchrony most prominent in the central and parietal areas Hypnagogic Hypersynchrony often occurs in burst and may resemble spike-and-wave activity (Phantom spike-wave |
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1-3 years: Sleep EEG
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1 to 6 Hz background
Bilaterally symmetrical spindles at 12 to 14 Hz Vertex often resemble high voltage frontal sharp waves |
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1-3 years: Activation EEG
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Limited HV because of cooperation
HV response with crying possible, especially at beginning of the recording if upset from electrode application Variable PS driving |
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3 to 6 Years: Awake EEG
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Often 8 Hz by age 3, usually mixed theta and alpha
Amount of alpha increases with age, often all 8-9 Hz by age 5-6 Awake voltage frequently 100 mV range and above Posterior Slow waves of youth: 2.5 to 4.5 Hz slowing Anterior 6 to 7 Hz theta Rolandic Mu is frequent |
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3 to 6 Years: Drowsiness EEG
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Alpha attenuation with background theta
Hypnagogic Hypersynchrony present until age 11 14 and 6 Hz positive spikes begin but are uncommon |
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3 to 6 Years: Sleep EEG
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Uniform sleep background unless reach slow wave sleep
Very clear sleep spindles, V-waves (may be sequential) and K-complexes |
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3 to 6 Years: Activation EEG
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HV: high amplitude slowing, often asymmetrical at onset
Rapid return to baseline unless hypoglycemic (classical reports, but drowsiness can develop with rapid entry into sleep without return to baseline) PS: Prominent driving at slow flash frequencies |
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6 to 12 Years: Awake EEG
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8 to 9 Hz by 7 years, 9 to 10 Hz by 9 or 10
If not 8 Hz by 8 years then clearly abnormal allowing for slowing of drowsiness Posterior slowing remains prominent but is arrhythmic, attenuates with eye-opening Beta is normal in 25% of EEGs Rolandic Mu present Occipital lambda begins Burst of Anterior Rhythmic theta at 6 to 7 Hz begins |
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6 to 12 Years: Drowsiness EEG`
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Alpha is reduced and replaced by theta and some delta
Hypnagogic hypersynchrony is less frequent with age Paroxysmal Hypnagogic hypersynchrony burst between ages 4 and 9 years |
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6 to 12 Years: Sleep EEG
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Sleep spindles and vertex wave in stage 2
POSTS (Positive Occipital Sharp Transients of Sleep) begin to appear 14 and 6 positive spikes may be present |
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6 to 12 Years: Activation EEG
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HV: high voltage slow activity is common
PS: maximal response at 6-16 Hz (medium flash rates) |
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13 to 19 years: Awake EEG
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Well defined alpha 9-11 Hz (occasionally into 12-13 Hz Beta)
Posterior consistently decreases with age Rolandic Mu common Lambda common Burst of Anterior Rhythmic theta at 6-7 Hz maximal at 13 to 15 years of age |
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13 to 19 years: Drowsy EEG
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Low voltage Alpha with intermixed moderate to high voltage theta
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13 to 19 years: Sleep EEG
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Stage 2: spindles, vertex
POSTS 14 and 6 positive sharp waves Deep sleep: delta and theta frequencies |
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13 to 20 years: Activation EEG
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HV: moderate intermittent slowing
PS: symmetrical driving |
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Posterior Slow Activity (Waves) of Youth:
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Waking, sinusoidal 2.5 to 4.5 Hz slow wave that interrupts the background alpha with voltage similar to the alpha voltage
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Mu Rhythm
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Waking, central 9Hz (7-11 Hz) comb shaped that is blocked by movement (thought of movement) of the contra-lateral extremity
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Lambda Waves:
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Waking, positive sharp waves over the occipital region from looking at a complex visual target. Usually 20 to 50 m V with a duration of 200 to 300 ms. Bilaterally synchronous with moderate voltage asymetries. Disappear with eye closure
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Vertex
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wider projection in children, usually fronto-central not just frontal as in adults. Often very high in voltage in early childhood, maximal ages 2-4. May appear on one side initially then be symmetrical once stage 2 sleep is well established. Repetitive or sequential at onset may look like fronto-central spikes
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POSTS (Positive Occipital Sharp Transients of Sleep)
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Surface positive, occipital waves during stage 1 and 2 sleep, typically bilaterally synchronous (may have voltage asymmetries), that occur in runs of 4 to 5 Hz. Onset as young as 4 years, maximal at 15-35 years
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14 and 6 Positive Spikes
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Onset at 3 or 4 years, peaks at 13-14 years, minimal by 17-18 years. Rhythmic trains of spikes followed by a smooth rounded component lasting 0.5 to 1 s. Occur most often in the posterior temporal regions and may be asynchronous or appear independently on the two sides. (COMMENT: I haven't seen in age of digital EEG! I'm not sure if the digital, referrential amplifiers fail to pick up the activity or if the CRT displays of the EEG machine alter the presentation of "14 and 6" so it is not recognizable
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Psychomotor Variant
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is rhythmic theta (monomorphic and monorhythmic) burst often notched at 5 to 7 Hz. Psychomotor Variant occurs bilaterally and independently and may shift from side to side. Psychomotor Variant begins in late adolescence and continues into adulthood.
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Photic stimulation
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is a very useful and important activation procedure in Pediatric EEG because of the activation of Generalized Spike-Wave activity. This is a common finding in children wiht Primary Generalized Epilepsy. Of note, children investigated after seizures caused by Pokemon TV episode in Japan were found to have partial (focal onset) seizures induced by photic stimulation
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The Photoparoxysmal Response
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is bilaterally synchronous, generalized spike-and-slow-wave and can have multiple spike and slow wave complexes to repetitive flash stimulation (Chatrian et al., 1983), poly-spike waves are the most significant abnormality. Reilly and Peters (1973) report Prolonged PPR (spike-wave discharges outlasts the flash stimulus) associated with seizures in a significantly higher incidence than Self-Limited PPR (spike wave ceases when the flash stops).Jayakar and Chiappa (1990) found no difference in clinical seizures for individuals with prolonged PPS and self-limited PPS on EEG
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Generalized 3-Hz spike-and wave complex
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s always abnormal. 3-Hz s-w activity may need to last 6 to 10 seconds before clinical absence seizure activity occurs. The generalized spikes may become poly-spikes in sleep and have a more variable frequency (especially in stage 3 and 4 sleep). During sustained burst of the "3-Hz" the frequency may begin closer to 3.5 to 4-Hz and slow to 2.5 to 3-Hz. Hyperventilation(HV) for 3 to 4 minutes usually will produce 3-Hz spike and wave activity if present. If 3-Hz activity is highly suspected based on history but does not occur than a second attempt at HV for 5 minutes should be performed. HV is as likely to record 3-Hz spike wave as 24 hours of continuous EEG. Onset of 3 Hz spike and wave with Absence seizures is commonly reported as most likely at 5-6 years of age. Often children have been having absence seizures for at least 6 months before diagnosis and occasionally have been having events consitently for year. Onset can occur before age 2. EEG in child of 23 months with 3-hz spike-wave and "pauses" in activity.
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Hypsarrhythmia
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is a term to describe an EEG with 0.5 to 3 Hz chaotic, asynchronous slow waves with voltages greater than 300 mV. Voltages of 1000 to 2000 mV can occur. Multifocal spikes and sharp and slow waves are also present. Intervals of attenuation can occur with and without clinical myoclonic activity or flexor spasms. Hypsarrhythmia can begin at 3 to 4 months of age and may persist into the 2nd year of life. Hypsarrhythmia is present in about 2/3 of infants with infantile spasms.
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Infantile Spasms
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is a clinical syndrome of clusters of axial myoclonic seizures that occur in infants from 2 to 18 months of age
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Slow Spike and Wave
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occurs at 1 o 2.5 Hz and may be widely distributed and synchronous over both hemispheres or may be asymmetric and present in only one hemisphere. Slow Spike and Wave is often seen for several seconds without any clinical change. There are usually other background abnormalities such as slowing and mutifocal spikes. Slow Spike and Wave usually appears between 2 and 6 years of age and activates with drowsiness and sleep. Slow spike and wave is not activated by HV and will block with eye opening. Slow spike and wave is one of 3 features of the Lennox-Gastaut Syndrome. The other 2 are refractory seizures and mental retardation
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Multifocal Spike and Wave
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is defined as "spikes in 3 non-contiguous electrode positions with at least one focus in each hemisphere" (Blume 1982). Multifocal Spike and Wave activity is frequently seen in children with multiple seizure types and retardation
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Rolandic Spikes
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occur exclusively in children with peak age of 6 to 10 years but may be present at age 2 or 3 years until age 12 to 15 years. Spikes are most commonly highest in voltage in the C3-C4 electrodes spreading into the T3-T4 electrodes. A horizontal dipole may be present with a surface positive field in the frontal-polar electrode. During drowsiness and sleep the Rolandic spikes increase in numbers and often cluster in trains of 3 to 6 over 1-2 second intervals. Rolandic spikes may be unilateral, bilateral synchronous or bilateral independent. Rolandic spikes frequently seen as an incidental finding and have only a 50% correlation with underlying seizure disorder. Begin Rolandic Epilepsy (BRE) is a syndrome where simple partial seizures occur early in sleep or on awakening. Many children may have just one such event. Occasionally secondary generalization and rarely prolonged seizures occur. Rolandic spikes are also present in children with other generalized epileptiform activity
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SSPE
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Subacute sclerosing panencephalitis produces double and triple sine waves at about 1 Hz that may occur in long runs superimposed on normal background. Early in the illness, short burst of slow sharp waves may be produced by noise. SSPE is a delayed onset, progressive measles encephalitis
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Slowing
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may be present post-ictally or with underlying structural abnormality which usally has to be large in size and involves the white matter
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