Approach to the EEG
· Uses at least 2 electrodes: reference and active and measures potential difference b/n two
· Waveform amplitudes are attenuated by CSF, meninges, skull and scalp (skin electrodes)
· Scalp recorded potential represent extracellular current flow driven by summated EPSP and IPSP not action potentials.
SENSITIVITY AND SPECIFICITY OF EEG IN EPILEPSY:
· specificity of EEG in the diagnosis of epilepsy (with the clinical history): 90%
· Niedermeyer (1999)- healthy military populations: discharges in 0.3-9%. Generalized spike-wave complexes: 0-2.7% of patients . Focal discharges were found in 0-6.4%.
· sensitivity of a single EEG: 50% (10% -77%). After one or more repeat EEG (incl Sleep deprived), sensitivity rises to 80-90%. Even after several days of continuous recording, small minorities of patients with intractable epilepsy, 2-3%, do not have IEDs detectable on surface recording. This percentage may be higher among patients whose epilepsy is controlled.
· IEDs are most likely to appear in the recordings of children, within hours or days of a seizure, and in association with idiopathic or symptomatic generalized epilepsies
Activation techniques and prolonged recording
· Sleep recordings increase the sensitivity of EEG (?beyond its effect on promoting sleep).
· hyperventilation (HV) and intermittent photic stimulation (IPS), occasionally elicit IEDs that do not appear at other times.
· HV and IPS are more effective in inducing generalized epileptiform IEDs than focal IEDs.
· delaying or missing medications is not recommended, does not increase diagnostic benefit.
· Increasing the time of recording makes detection of IEDs more likely
UTILITY OF EEG
The EEG may be used for the following:
· To exclude nonconvulsive status epilepticus
· To identify focal interictal epileptiform activity or confirm clinical suspicion that seizures may contribute to the condition
· to record functional disturbance in individuals whose brain MRI is "normal" but brain dysfunction is evident clinically (eg, metabolic encephalopathies)
· to record disease-specific patterns in the proper clinical setting, such as progressive myoclonic epilepsies, CJD, SSPE
· To help a psychiatrist with the multitude of complex disorders masking as potential epilepsy or encephalopathy
· To identify focal or lateralized changes that suggest a structural cause to the encephalopathy
EEG is nonspecific and cannot diagnose etiology or localization well (eg, the cause of coma). However, the question from the clinician is whether the brain is involved and the extent of brain damage, if any. To answer these questions, presently no clinical tool is more useful than the EEG.
· Alpha waves - 8-13 Hz Beta waves (smallest amplitude)- > 13 Hz
· Theta waves - 3.5-7.5 Hz Delta waves - <3 Hz
· Normal waves are >7.5Hz in awake adults, <7 Hz is abnormal if awake
· seen in all age groups (most common in adults)
· occur rhythmically on both sides of the head (often slightly higher in amplitude on the nondominant side)
· present posteriorly more than anteriorly and are especially prominent with closed eyes and with relaxation.
· Alpha activity disappears normally with attention (eg, mental arithmetic, stress, opening eyes).
· Beta waves are observed in all age groups and represent intense mental activity
· They tend to be small in amplitude and usually are symmetric and more evident anteriorly.
· Many drugs, such as barbiturates and benzodiazepines, augment beta waves.
· Theta waves normally are seen in sleep at any age.
· In awake adults, these waves are abnormal if they occur in excess.
· Theta and delta waves are known collectively as slow wave
· They normally are seen in deep sleep in adults as well as in infants and children.
· Delta waves are abnormal in the awake adult.
· the largest amplitude of all waves.
· Delta waves can be focal (local pathology) or diffuse (generalized dysfunction).
Disappearance of alpha and appearance of low amplitude theta and mild increased beta
· Stage 1: < 50% alpha; Vx waves appear; increasing proportion of beta and theta frequency
· Stage 2: increasing beta, sleep spindles, Vertex complexes
· Stage ¾ slow wave activity with increased proportion delta (stage 3 20-50%; stage 4 >50%)
· REM: mixed frequency, low voltage and increasing proportion of alpha
· The interictal marker of a seizure focus is the spike or sharp wave. The distinction between these 2 patterns has no etiologic significance (only morphological)
· Spike: < 70 milliseconds in duration,
· Sharp wave: duration of 70-200 milliseconds.
· may arise from any region most commonly in the anterior temporal, frontal, or centrotemporal regions.
· anterior temporal spike or sharp wave” the likelihood of the occurrence of a clinical seizures is > 90%.
· Frontal spikes and sharp waves. the likelihood of the occurrence of a clinical seizures is 70-80%
· Frontal spikes or sharp waves are more likely to be associated with mass lesions such as neoplasms, traumatic lesions, or congenital cerebral malformations.
· Centrotemporal or rolandic sharp waves are often a marker for a particular epilepsy syndrome of childhood known as benign rolandic epilepsy or benign focal epilepsy of childhood with centrotemporal spikes. This is a disorder in which a child, typically aged 4-12 years, develops focal seizures with sensory or motor seizures in the mouth or face region. These children also may have generalized seizures; typically, these seizures are nocturnal. The EEG pattern is unusual in that a simultaneous negative waveform often occurs in the centrotemporal region and a positive one in the frontal region. This pattern of EEG polarity is virtually diagnostic of benign rolandic epilepsy.
· Epileptiform EEG patterns are seen less commonly in the occipital, central, or parietal regions. Occipital spikes typically are seen in young children and may or may not be associated with clinical seizures. Discharges in any of these regions may indicate the presence of partial epilepsy
· TWs invariably are associated with an impaired consciousness (mild confusion to deep coma)
· Appears when there has been diffuse slowing of background rhythms
· 3 most common causes of TWE are hepatic encephalopathy, renal failure, and anoxic injury
· DDx: infx; toxic, stroke, thyroid,
· Clinical and EEG improvement occur simultaneously
· Large amplitude 1.5-3 Hz
· TWs have not been reported in children.
· Generally, the TW pattern carries a poor prognosis with a high mortality rate if it occurs in association with rapid neurological and clinical deterioration
PLEDS (periodic lateralizing epileptiform discharges)
· Signify presence of large destructive lesion in 1 hemisphere
· DDx: tumor, abscess, hematoma, HSV encephalitis
· #1 etiology: acute cerebral infarction (2nd to HSV encephalitis with necrosis)
· consisting of repetitive spike or sharp wave discharges, which are focal or lateralized over one hemisphere, recur at intervals of 0.5-5 seconds, and continue through most of the duration of the EEG study
CREUTZFELDT-JAKOB DISEASE: biphasic or triphasic discharges that are initially sporadic and may even be asymmetric. As the disease advances, the pattern becomes generalized and synchronous with continuous periodic stereotypic 200- to 400-millisecond sharp waves occurring at intervals of 0.5-1.0 seconds. Myoclonic jerks often occur in association with the sharp waveforms, but the relationship is not constant. Late in the illness and during sleep, myoclonic jerks disappear, despite the persistence of the periodic EEG. The sharp waves typically react to external stimuli. Early in the disease, alerting the patient may elicit the periodic pattern; later, when the periodic pattern is readily apparent, rhythmic photic or other stimuli can "drive" the periodic frequency. Benzodiazepines or barbiturates can temporarily eliminate both myoclonic jerks and periodic patterns.
Hypoxia causes diffuse slowing in the EEG. The acute and prolonged anoxia of cardiac arrest exhibits no changes initially. In 7-10 seconds, slow waves appear. This is followed by rhythmic, high-voltage delta activity; subsequently, attenuation and EEG flattening occurs. As a rule, irreversible brain damage results in 4-8 minutes. Certain patterns carry a poor outcome: flat EEG and burst-suppression pattern nearly always carry a poor prognosis. Postanoxic EEGs may exhibit a variety of abnormal patterns: triphasic activity, alpha coma pattern, repetitive complexes, and bilateral PLEDs.
The EEG resembles changes described with hypoxia; hyperventilation response is exaggerated and FIRDA may be observed. If prolonged coma ensues, the EEG changes persist and may become permanent. In most cases of hypoglycemia, a generalized disorganization of record occurs; in patients with long-term diabetes, the EEG is usually mildly to moderately diffusely disorganized and slow.
In cases of
clinical dementia, a normal EEG with preserved alpha might help establish the
diagnosis of Pick disease, while a slowed and shifted alpha frequency is seen
in AD and PSP. Low-voltage, flat EEG and the appropriate clinical presentation
may raise the suspicion of
1. Polymorphic delta activity:
· arrhythmic slow waves that vary in frequency, amplitude, and morphology.
· focal or generalized distribution.
· Continuous PDA: abnormalities involving subcortical white matter ie structural lesion
· PDA of a structural lesion is referable not to the lesion itself but to the surrounding brain tissue. Because of this limitation, the area of a lesion is indicated not by the maximal amplitude of PDA but rather by a region of relatively low-amplitude slowing.
· Acutely the infarct may show focal slowing but eventually a large proportion will be normal
· DDx: infarct, tumor…
2. Intermittent delta
· Intermittent rhythmic delta activity (IRDA) usually occurs at frequencies of 2-2.5 Hz with relatively sinusoidal, stereotypic, bilaterally synchronous waveforms appearing in short bursts.
· peak amplitude frontally in older individuals (FIRDA) and occipitally in children (OIRDA).
· attenuate with alerting or eye opening.
· Eye closure, drowsiness, and hyperventilation accentuate IRDA.
· Intermittent rhythmic delta activity is associated with structural lesions, most commonly diencephalic, infratentorial, or intraventricular tumors, or with diffuse encephalopathies. Even when IRDA occurs unilaterally in association with a focal cerebral lesion, the lateralization of IRDA may be ipsilateral or contralateral to the lesion.
· primarily with diffuse gray matter disease.
· The degree of encephalopathy manifested appears to correspond to the proportion of IRDA Rhythmic delta activity:
· Generalized continuous theta and delta patterns occur in comatose and encephalopathic states of multiple potential etiologies.
· Patterns that fail to respond, either in amplitude or frequency, to noxious, auditory, or visual stimuli carry a poor prognosis for meaningful neurologic recovery.
· Similar patterns with preserved reproducible reactivity imply potential for some recovery and should be compared to recordings repeated several days later.
· These patterns must be distinguished from those of normal drowsiness and sleep.
Genralized epilepsy: 3 Hz spike and wave
· Increased slow wave activity
· Reactivity is a favorable sign
· Unremitting 8- to 13-Hz EEG activity that is unresponsive to eye opening or other stimulation
· differs in appearance from alpha rhythm: lack of reactivity and its spatial distribution.
· monorhythmic, diffuse, or may have anterior accentuation.
· Only minor fluctuations in amplitude occur, and no reactivity to external stimulation can be elicited.
· Alpha coma can be found in comatose patients with brainstem lesions and in severe posttraumatic and anoxic encephalopathies.
· indicates a poor prognosis, but instances of recovery have been reported occasionally.
· High-voltage bursts of slow, sharp, and spiking activity alternating with a suppressed background
· Myoclonic jerking can occur concomitantly with the bursts and may be ictal. Chemical paralysis in the intubated ventilated patient is required to determine if the patterns of ictal potential persist after elimination of motion artifact.
· Differentiate from Rx-induced (eg, with etomidate, barbiturates, Bz).
· encountered in deep coma and is the final pattern in deterioration of generalized status epilepticus
· prognosis ~ to electrical silence (brain death)
· presence of SEVERE and DIFFUSE disturbance
EEGs are performed occasionally to provide supportive evidence of brain death. Electrocerebral inactivity (ECI), or electrocerebral silence (ECS), is defined as no cerebral activity over 2 mV. No EEG reactivity to strong and thorough tactile, auditory, or visual stimulation
IED with spike and wave (upper tracing) PLEDS
· K complex waves are large-amplitude delta frequency waves, sometimes with a sharp apex.
· occur throughout the brain and usually higher in amplitude and more prominent in bifrontal regions.
· Usually symmetric, they occur each time the patient is aroused partially from sleep.
· V waves are sharp waves that occur during sleep.
· largest and most evident at the vertex bilaterally and usually symmetrically.
· V waves tend to occur especially during stage 2 sleep and may be multiple.
· Often, they occur after sleep disturbances (eg, brief sounds) and, like K complexes, may occur during brief semiarousals.
· Lambda waves occur in the occipital regions bilaterally as positive (upgoing) waves.
· They are triangular in shape and generally symmetric.
· Recorded with awake eyes open during saccades (visual scanning) ie reading, watching TV
Positive occipital sharp transients of sleep
Mu waves - Wicket rhythm or rhythm en arceau
Benign epileptic transients of sleep
Thanks to Dr. Verity J. John for this page.