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General principle


  • ▪ The EEG is unable to distinguish between different etiologies. The major usage of the EEG is to determine the severity of encephalopathy, prognosis, and response of treatment.

  • ▪ Common etiology:

    • ▸ Metabolic, toxic, inflammation, anoxic, and degenerative diseases

  • ▪ Few EEG patterns associated with more specific etiologies for the encephalopathy:

    • ▸ Periodic pattern:

      • Anoxic encephalopathy

      • Certain encephalitis

    • ▸ Triphasic waves (TWs) or 14- and 6-Hz positive spike bursts:

      • Metabolic encephalopathy Lithium and ifosphamide toxicity

    • ▸ High-voltage beta activity:

      • Benzodiazepine or barbiturate intoxication

    • ▸ Low-voltage fast patterns:

      • Alcohol withdrawal

    • ▸ Bursts of high-voltage delta activity interspersed with mixed frequencies:

      • PCP (angel dust) intoxication

  • ▪ Prognosis in most EEG patterns is usually correlated with underlying diseases and reactivity of EEG to external stimuli.

    • ▸ Ischemic strokes and anoxic ischemia after cardiorespiratory arrest are almost completely irreversible.

    • ▸ Brain injury produced by head trauma, subdural hemorrhages, and some intracranial hemorrhages, in the absence of raised intracranial pressure, may be partially, moderately, or occasionally wholly reversible.

    • ▸ Electrical disturbances with seizures and status epilepticus (SE), metabolic, and some toxic encephalopathies may be completely reversible.

  • ▪ Some particular patterns have been identified that may have some prognostic significance:

    • ▸ Poor prognosis

      • Triphasic waves (TWs).

      • Alpha coma (AC) patterns in patients with anoxic encephalopathy nonreactive to noxious stimuli.

      • Continuously diffuse polymorphic delta activity (unless due to a toxic/metabolic disturbance) typically bodes poorly for the patient, when these patterns are low voltage.

      • Marked bilateral suppression coma.

      • Burst-suppression (B-S) patterns.

    • ▸ Better prognosis:

      • Spindle coma (SC) patterns

      • Beta coma

  • ▪ Severity:

    • ▸ Milder encephalopathy:

      • Spontaneous variability

      • Evidence of EEG reactivity to painful stimulation

        • ◊ Reduction of amplitude, increase in frequency, and reduction in the slow activity

        • Paradoxical activation, which is a period of more severe delta slowing following painful stimuli

    • ▸ Severe encephalopathy:

      • Invariant EEG—no spontaneous variability or reactivity to external stimuli

  • ▪ Combination of diffuse and focal EEG abnormalities:

    • ▸ Associated focal process such as old infarction or tumor

    • ▸ Nonketotic hyperosmolar coma

    • ▸ Focal seizure

    • ▸ Herpes simplex encephalitis and Creutzfeldt-Jakob disease (CJD)


Selected specific conditions


Drug intoxication


  • ▪ Generalized theta-delta activity with superimposed beta frequency activity is highly characteristic of sedative drug intoxication.

  • ▪ With more severe intoxication, the fast activity shows a slower frequency (10–13 Hz), widespread distribution, but anterior predominance.

  • ▪ In the absence of prominent slow activity, the anterior-dominant generalized fast activity caused by sedative drug intoxication produces an alpha and SC pattern in the EEG that is indistinguishable from that seen with severe anoxic encephalopathy.

  • ▪ Phencyclidine (PCP) or ketamine is associated with a distinctive EEG pattern similar to that of subacute sclerosing panencephalitis (SSPE).


Anoxic encephalopathy


  • ▪ EEG should be done at least 5–6 hours after resuscitation.

  • ▪ B-S pattern or electrocerebral silence (ECS) does not carry as ominous prognosis as when they occur in the setting ...

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