Figure 2-7 (Continued) J. Deep coma following cardiac arrest, showing electrocerebral silence. With the highest amplification, electrocardiogram (ECG) and other artifacts may be seen, so that the record is not truly “flat” or isoelectric. However, no cerebral rhythms are visible. Note the ECG (lower channel). K. Grossly disorganized background activity interrupted by repetitive “pseudoperiodic” discharges consisting of large, sharp waves from all leads about once per second. This pattern is characteristic of Creutzfeldt-Jakob disease. L. Advanced hepatic coma. Slow (about 2 per second) waves have replaced the normal activity in all leads. This record demonstrates the triphasic waves often seen in this disorder.
Figure 2-8. Pattern-shift visual evoked responses (PSVERs). Latency measured to first major positive peak (termed P100 because of its latency from the stimulus of approximate 100 ms) and marked by “o.” Upper two tracings: These, from the right and left eyes, are normal. Middle tracings: PSVER from the right eye is normal but the latency of the response from the left eye is prolonged and its duration is increased. Lower tracings: PSVER from both eyes show abnormally prolonged latencies, somewhat greater on the left than on the right. Calibration: 50 ms, 2.5 mV.
Stimulus12345LATENCY, msec678910AMPLITUDE, µVIAuditorynerve2IICochlearnuclei(pons)Hair cellsIIISuperioroliveIVLaterallemniscusV Inferior colliculus   (midbrain)VIMedialgeniculate(?)VIIAuditoryradiations(?)IIIIIIIVVVIVIICochlearnucleiNucleus oflaterallemniscusCochlear nerveOrgan ofCorti10.40.30.20.10
Figure 2-9. Short-latency brainstem auditory evoked responses (BAERs). Diagram of the proposed electrophysiologic–anatomic correlations in human subjects. Waves I through V are the ones measured in clinical practice.
Figure 2-10. Short-latency SEPs produced by stimulation of the median nerve at the wrist. The set of responses shown at left is from a normal subject; the set at right is from a patient with multiple sclerosis who had no sensory symptoms or signs. In the patient tracing, note the preservation of the brachial–plexus component (EP), the absence of the cervical cord (N11) and lower-medullary components (N/P13), and the latency of the thalamocortical components (N19 and P22), prolonged above the normal mean +3 SD for the interval from the brachial plexus potential. Unilateral stimulation occurred at a frequency of 5 per second. Recording electrode locations are as follows: FZ, midfrontal; EP, the Erb point (the shoulder); C2, the middle back of the neck over the C2 cervical vertebra; and Cc, the scalp overlying the sensoriparietal cortex contralateral to the stimulated limb. Relative negativity at the second electrode caused an upward trace deflection. Amplitude calibration marks denote 2 mV. (Reproduced by permission from Chiappa and Ropper.)
AA˜B˜C˜Ref.11˜2˜2BC