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