The stimulation of sense organs or peripheral nerves evokes an electrical response in the corresponding cortical receptive areas and in a number of subcortical relay stations. However, one cannot place a recording electrode near the nuclear relay stations, nor can one detect tiny potentials of only a few microvolts among the much larger background activity in the EEG. The use of computerized averaging methods, introduced by Dawson in 1954, has provided a means of overcoming these problems. Initially, emphasis was on the study of late waves (over 100 ms after the stimulus) because they are of high amplitude and easy to record. However, there is more clinical utility in recording the much smaller, short-latency waveforms, which are received at each nuclear relay within the main sensory systems. These waveforms are maximized by the computer to a point where their latency and voltage can easily be measured. One of the remarkable properties of evoked potentials is their resistance to anesthesia, sedative drugs, and in states of reduced consciousness such as hypoxic-ischemic encephalopathy. This permits their use for monitoring the integrity of cerebral pathways in situations that limit the value of the EEG.
The interpretation of evoked potentials (visual, auditory, and somatosensory) is based on the prolongation of the latencies of the waveforms after the stimulus, the interwave latencies, and asymmetries in timing. Norms for latencies have been established, but it is advisable to confirm these in each laboratory. Typically 2.5 or 3 standard deviations above the mean latency for any measurement is taken as the definition of abnormality (Table 2-4). The amplitudes of the waves are less informative for clinical work.
For many years it had been known that a light stimulus flashing on the retina evokes a discernible waveform over the occipital lobes. In the EEG, such responses to fast rates of stimulation are referred to as the occipital driving response (Fig. 2-7C). It is also appreciated that a visual evoked response is produced by the sudden change of a viewed checkerboard pattern. These responses, produced by rapidly reversing the pattern of black and white squares, are easier to detect and to measure than are flash responses and are more consistent in waveform from one individual to another. The pattern shift stimulus, applied first to one eye and then to the other, can demonstrate conduction delays in the visual pathways of patients who have had disease of the optic nerve—even when there are no residual signs of reduced visual acuity, visual field abnormalities, alterations of the optic nerve head, or changes in pupillary reflexes. Furthermore, the presence of a normal visual evoked response suggests that blindness is not due to a lesion in the anterior visual pathways and their projections to the occipital cortex, for example, in hysterical blindness. Figure 2-8 illustrates the normal pattern shift visual evoked response (PSVER) and two types of delayed responses. Reductions in the amplitude and duration of PSVER usually accompany prolonged latencies but are difficult to quantify. By presenting the pattern-shift stimulus to one hemifield, it is possible to isolate a lesion to an optic tract or radiation, or one occipital lobe, but with much less precision than that provided by the usual monocular testing.
The expected latency for the positive wave, by convention a downward deflection, is near 100 ms (thus the term P100 has also been used to designate the waveform); an absolute latency from the stimulus longer than 118 ms or a difference in latencies of greater than 9 ms between the two eyes signifies involvement of one optic nerve (see Table 2-4). Bilateral prolongation of latencies, demonstrated by separate stimulation of each eye, can be caused by lesions in both optic nerves, the optic chiasm, or the visual pathways posterior to the chiasm.