Neurophysiology
Electroencephalography
I. Origin of the Electroencephalogram (EEG)
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Sum of excitatory postsynaptic potentials and inhibitory postsynaptic potential
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EEG rhythm depends on thalamic pacemaker cells and the reticular activating formation.
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One third of the cortex can be seen by scalp electrodes.
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At least 6 cm2 of cortex must be involved to be detected by surface electrodes.
II. EEG Recording
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Electrical Resistance: 1000 to 5000 ohms
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R >5000 ohms attenuates signal and causes 60-Hz noise.
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R <100 ohms results in a short circuit.
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Filters: Low frequency is 0.5 to 1 Hz; high frequency is 70 Hz. Filters are variable but may alter spike morphology.
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Amplifier sensitivity: variable; typically set at 7 µV/mm
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Paper speed: variable; typically 3 cm/sec
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Montages
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Bipolar
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Localizes potential by direction of pen deflection (phase reversal)
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Distorts wave shape and amplitude.
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Referential
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Localizes potential by amplitude of pen deflection.
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Potentials at the reference electrode may appear in all channels.
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Interelectrode distance alters the amplitude.
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Activation procedures-
Hyperventilation
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Normal: generalized slowing (3 to 5 minutes)
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Abnormal: Prolonged slowing caused by hypoglycemia or anoxia; 75% of absence seizures are elicited.
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Photic stimulation
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Normal: occipital driving at stimulus frequency or no response
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Abnormal:
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Photomyoclonic (photomyogenic) response
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Photoparoxysmal (photoconvulsive) response
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Asymmetric response
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III. Normal Adult EEG
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Alpha 8 to 13 Hz
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Voltage: 15 to 45 µV; decreases with age; higher on right; maximal at occiput
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Attenuates with eye opening and concentration
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Drops out with drowsiness but may persist through drowsiness and into sleep as alpha intrusion
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Mu 7 to 11 Hz
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Arch-shaped alpha variant. Best seen in bipolar montage in the centroparietal areas.
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Attenuates with contralateral hand movement (e.g., fist)
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Enhanced by immobility and hyperventilation
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Beta > 13 Hz
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Voltage < 25 µvV
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Frontocentral attenuates with movement.
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Global does not attenuate with movement.
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Posterior is a fast alpha variant.
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Increases with benzodiazepines, barbiturates, and anxiety
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Found over skull defects (less filtered by skull)
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Lambda
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Occipital positive sharp saw-tooth transients
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Occur with visual scanning (visual evoked potentials)
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Vertex waves
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Negative sharp transients at the vertex
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Normal with sleep
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Kappa
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Temporal bursts of low amplitude alpha or theta. Occur with deep thought.
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Posterior slowing of youth ages 8 to 14 years
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Delta range mixed with alpha
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Duration of each wave equals 4 to 6 alpha waves (a subharmonic of alpha)
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Temporal slowing of older persons
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Medium-to-high amplitude bursts of theta or delta (<1% of the record)
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Six per second spike and wave discharges (phantom spike and wave)
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Posterior low amplitude waves increase with Benadryl.
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Frontal high amplitude waves
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Small Sharp Spikes of Sleep (SSSS) or (BETS)
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Temporal monophasic or biphasic spikes that may have a broad field
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Normal finding in sleep, but may be confused with an epileptic spike
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IV. Sleep
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Components
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POSTS—positive occipital sharp transients of sleep
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Vertex waves
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Sleep spindles 11 to 15 Hz
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Duration >0.5 sec
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Maximal centrally
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K complexes
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Negative sharp wave followed immediately by a slower positive component
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Duration at least 0.5 sec.
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Location: maximal at vertex
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Stages
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Stage W (wakefulness)
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Alpha rhythm with eyes closed but may be absent as a normal variant
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Blinks occur at 5 to 10 Hz (vertical deflections)
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Stage I
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Alpha replaced by slow 2 to 7 Hz activity
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Muscle artifact decreases.
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Vertex waves occur.
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POSTS appear at the end of stage I.
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Stage II
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Vertex waves
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Sleep spindles
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K complexes
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POSTS
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Slow waves at 2 to 7 Hz
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Stage III
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Sleep spindles
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POSTS
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K complexes
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20% to 50% delta activity
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Stage IV
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>50% delta activity
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Rapid eye movement
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Eye movements
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Low voltage
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Decreased muscle activity
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Increased heart rate
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V. Neonatal EEG
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EEG depends on conceptual age.
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Less than 29 weeks of age
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Discontinuous with bursts of moderate-to-high amplitude on a flat background
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Interval between bursts is approximately 6 seconds.
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Interhemispheric synchrony develops at this age.
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Delta brush (0.3 to 1.5 Hz) central and occipital
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29 to 31 weeks of age
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Abundant delta brushes over central temporal and occipital regions
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32 to 34 weeks of age
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EEG becomes more continuous and reactive. Multifocal sharp transients.
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34 to 37 weeks of age
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Decreased multifocal sharp waves. Frontal sharp waves appear.
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37 to 42 weeks of age
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Continuous theta and delta activity
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Less than 44 weeks of age
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Multifocal spikes are normal.
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6 months of age
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Occipital rhythm at 6 Hz
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3 years of age
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Occipital rhythm at 8 Hz
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VI. Abnormal EEG
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Amplitude
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Decreased generalized activity
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Bilateral cortical damage (bilateral infarcts, anoxia)
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Widespread cerebral damage (Huntington disease, Creutzfeldt-Jakob syndrome)
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Widespread disturbance of cortical function (hypothermia, hypothyroidism, postictal)
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Bilateral subdural hematomas
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Decreased alpha rhythm activity
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Mild metabolic disturbances (hepatic, hypothyroidism, hypoparathyroidism)
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Functional subcortical disturbances (anxiety)
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Decreased focal activity (stroke, tumor, subdural hematoma)
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Increased beta rhythm activity (benzodiazepines, hyperthyroidism)
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Frequency
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Generalized asynchronous slow waves (polymorphic delta activity)
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Widespread structural damage of both hemispheres (stroke, anoxia, postictal, degenerative disease)
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Medication effect
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Persistent polymorphic delta activity—seen in white matter lesions, postictal states, or ipsilateral thalamic lesions
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Intermittent rhythmic delta activity—possibly from dysfunction of subcortical centers influencing activation of cortex
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Focal slow waves
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Local structural damage (stroke, tumor, multiple sclerosis, tuberous sclerosis, porencephaly)
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Epileptiform discharges
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Spike, <70 msec duration
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Sharp wave, 70 to 200 msec duration
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VII. Epilepsy
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30-minute EEG in a patient with known epilepsy
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50% abnormal
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Absence—95% abnormal
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Simple partial—75% abnormal
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Complex partial—50% abnormal
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Tonic-clonic—30% abnormal
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2% to 4% of nonepileptic people have interictal epileptiform activity
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Three 30-minute EEGs should diagnose 90% of the cases with epilepsy.
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Maneuvers to increase sensitivity
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Sleep—complex partial
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Sleep deprivation—complex partial, juvenile myoclonic epilepsy
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Hyperventilation-absence
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Extra electrodes
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Sphenoidal—mesial temporal sclerosis
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FT9/FT10—mesial temporal sclerosis
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Longer recording time
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Spike
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Neuronal burst firing
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Possible thalamic recruitment
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Wave
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Neuronal inhibitory response to spike
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Recruitment
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Anticonvulsant effects
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Anticonvulsants suppress the change from interictal to ictal.
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Most antiepileptic medications do not tend to suppress interictal firing (benzodiazepines and barbiturates are exceptions with other antiepileptic drugs resulting in a less significant effect).
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Generalized epileptiform activity
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3-Hz spike and wave
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Absence seizures
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35% of siblings have similar epileptiform abnormalities
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10% of parents have similar epileptiform abnormalities
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Autosomal dominant with age-dependent penetrance
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Polyspike and wave
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Generalized tonic-clonic seizures, atonic seizures, massive myoclonus, akinetic, hypsarrhythmia, infantile spasms
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Spike and wave (>10-Hz fast waves with occasional spike and wave)
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Clonic seizure
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Slow spike and wave (10 Hz with decreasing frequency)
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Tonic seizure
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Spike and wave
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Generalized tonic-clonic seizure
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Generalized paroxysmal fast activity
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Lennox-Gastaut syndrome
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3- to 5-Hz spike and wave and polyspike activity with a normal background
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Juvenile myoclonic epilepsy
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Photoparoxysmal response in 38%
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Specific disorders causing generalized epilepsy
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Unverricht-Lundborg syndrome
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Myoclonic epilepsy
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Lafora inclusion body epilepsy
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Creutzfeldt-Jakob disease
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Ramsay-Hunt syndrome of dyssynergia cerebellaris myoclonica
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Stürge-Weber syndrome
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Riley-Day familial dysautonomia
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Microgyria, agyria, holoprosencephaly
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Metabolic and toxic encephalopathies
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Addison disease
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Hyperglycemia/hypoglycemia, hypocalcemia, hypomagnesemia
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Hyponatremia, acute intermittent porphyria, uremia
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Pyridoxine deficiency
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Toxic agents—alcohol, phenothiazines, tricyclic antidepressants, haloperidol, INH, heavy metals (lead, mercury), barbiturate withdrawal
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Hyperthermia
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Focal epileptiform activity
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Benign childhood epilepsy with centrotemporal spikes
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Centrotemporal with a horizontal dipole
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Short runs of spike and wave at 1.5 to 3 Hz
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Childhood epilepsy with occipital paroxysms
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Interictal spikes at 1 to 3 Hz
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Visual seizures during wakefulness and ictal vomiting may occur.
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Landau-Kleffner syndrome
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Multifocal, temporal, and parieto-occipital spikes
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Continuous spike wave of sleep
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Moderate-to-high amplitude interictal spikes
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Simple/complex partial epilepsy
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Developmental disorders
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Tuberous sclerosis
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Stürge-Weber syndrome
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Porencephaly
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Polymicrogyria, pachygyria, heterotopias,and so forth
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Acute metabolic encephalopathies
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Inborn errors of metabolism
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Acute infarct, ischemia
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Trauma
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Tumors
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Common in slow-growing cortical tumors
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Infection
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Abscess (bacterial, toxoplasmosis, cysticercosis)
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Herpes (temporal lobes with periodic lateralizing epileptiform discharges)
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Venous sinus thrombosis
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Periodic complexes
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Periodic lateralizing epileptiform discharges
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Cause: infarction, tumor, encephalitis
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Duration: 0.06 to 0.5 seconds
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Frequency: 1- to 2-second interval
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Periodic generalized sharp waves
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Creutzfeldt-Jakob disease
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Generalized 0.15- to 0.6-second duration spikes
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Frequency: 0.5- to 2-second interval
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Exaggerated photic response to low flash frequencies in Creutzfeldt-Jakob
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Periodic generalized complexes
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Subacute sclerosing pan encephalitis (PCP overdose may look similar)
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Generalized symmetrical 0.5- to 3-second sharp wave complexes
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Frequency: 3- to 20-second interval
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