Study Guidelines

  • 1.

    Describe the general methodology performed to record sensory evoked potentials, the sensory modalities assessed, and an example of clinical disorders and expected abnormality.

  • 2.

    Contrast the performance of a motor evoked potential versus a motor nerve conduction study.

  • 3.

    Provide an example of how motor evoked potentials can be used to detect physiologic changes in the motor cortex.

  • 4.

    Provide an example of how acupuncture may have its clinical effect.

Sensory Evoked Potentials

The term sensory evoked potentials is used to define the response of the central nervous system (CNS) to specific sensory stimulation. In clinical neurophysiology, the specific stimuli relate to vision, hearing, and cutaneous sensations.

A difficulty with these evoked potentials is that their low amplitudes, of 20 μV or even less, render them undetectable in routine electroencephalogram (EEG) recordings because of the interference from the normal and higher amplitude background EEG.

However, advantage is taken of the regularity of the evoked response to repeated stimuli of the same type. With repetitive stimulation followed by computer averaging, irregular background rhythms cancel each other out and the evoked potentials can be clearly seen.

The three basic kinds of sensory evoked potentials are described as visual , auditory , and somatosensory.

Visual Evoked Potentials

The speed and amplitude of impulse conduction in the visual pathway are tested by a technique known as pattern reversal or pattern shift visual evoked potential (VEP). With one eye covered at a time, the patient stares at a spot in the centre of a screen illuminated in a black-and-white checkerboard pattern (small optic nerve lesions can be detected by the technique of multifocal VEP where separate responses can be obtained from up to 60 different regions of the central visual field). Once or twice per second, the pattern is reversed (to white and black), for a total of 100 repetitions. Averaging is performed on the first 500 ms of data from a bipolar recording at the occipital and parietal midline EEG sites (OZ and PZ).

The wave peak of interest is called P1 (or P100). In healthy subjects it is a positive deflection 100 ms post stimulus ( Fig. 30.1 ). In the clinical example shown, taken from a patient with a presumptive diagnosis of multiple sclerosis (MS), the normal P1 wave from the right-eye test indicated that both optic tracts and both optic radiations were clear. The P1 wave from the left eye was both delayed and of reduced amplitude, suggesting the presence of a defect in optic nerve conduction, anterior to the optic chiasm. This type of abnormality is encountered in demyelinative optic neuropathies such as one caused by myelin degeneration from multiple sclerosis and in this example, involving the left optic nerve. ( Note: On screen and in printouts, it is now customary for these waveforms to be ‘flipped’, with positive responses registering as upward deflections.) Conduction defects caused by demyelination are more often expressed in the form of latency delays of the kind shown than in the form of amplitude abnormalities.

Fig. 30.1, Visual evoked potentials. The patient’s right eye has been tested and is now shielded. The left eye is fixated on the spot in the centre of the checkerboard during pattern reversal episodes. The pattern from the right eye is normal, showing a positive deflection at 100 ms post stimulus. In the recording from the left eye, the P1 is both delayed and reduced in amplitude. The combined results indicate the presence of a lesion in the left eye or left optic nerve. The waveforms are identified with their typical nomenclature ( N1 indicates the first negative waveform, a negative polarity is indicated by a downward trace; P1 the first positive, N2 the second negative) as well as an alternative nomenclature which combines the surface recorded polarity as well as the average time for the signal to appear in a normal control population ( P100 is the waveform of positive polarity that appears on average at 100 ms). Both forms of nomenclature are used clinically.

In the absence of any evidence for MS elsewhere, an abnormal P1 amplitude from one eye may be caused by an ocular disease such as glaucoma or by compression or ischemia of the optic nerve; visual evoked potential abnormalities do not specify aetiology. Bilateral abnormal P1 recordings can indicate pathology in one or both optic radiations.

Brainstem Auditory Evoked Potentials

Remarkably, it is possible to follow the sequence of electrical events in the auditory pathway, step by step, from cochlea to primary auditory cortex. Following placement of temporal scalp recording electrodes, 0.1 ms click sounds are presented at approximately 10 Hz to each ear in turn through conventional audiometric earphones. Click intensity is adjusted to 60 to 65 decibels (60 to 65 dB nHL; decibels relative to the threshold of a control population) above the click hearing threshold for the ear being tested. The contralateral ear is ‘masked’ by white noise. (The number of stimuli necessary to elicit clear waveforms is in the order of several thousand, in part because of their small relative amplitude.)

A sequence of seven averaged-out waves (I to VII) constitutes the brainstem auditory evoked response (BAER). They are accounted for in the caption to Fig. 30.2 .

Fig. 30.2, Brainstem auditory evoked potentials. Sources of evoked potentials: 1 , distal auditory nerve (cochlear hair cells); 2 , cochlear nucleus and distal auditory nerve; 3 , cochlear nucleus and superior olivary complex; 4 , lateral lemniscus; 5 , inferior colliculus (inferior brachium); 6 , medial geniculate nucleus (auditory radiation); 7 , primary auditory cortex.

Pathology anywhere along the auditory pathway results in reduction or abolition of the wave above that level. The technique is a sensitive screening test for acoustic neuroma. A diagnostic feature here is I to III interpeak latency separation. ( Interpeak latency refers to the time interval between the recorded waveforms; s eparation refers to extension of the interval, in this case between waves I and III, which is caused by a conduction delay along the affected cochlear nerve that also causes a characteristically reduced amplitude wave II. While the absolute latency of subsequent waves is delayed, the interpeak latency between wave III and V is normal.)

In about 30% of patients who have MS with no clinical evidence of brainstem lesions, BAER is abnormal. The most frequent abnormalities are reduced amplitude of wave V and overall slowing of conduction indicated by increased interwave intervals.

Another clinical application of the BAER technique is the assessment of cochlear function in infants under suspicion of congenital deafness. Assessment of brainstem auditory evoked potentials is also important in the medicolegal domain, to assess deafness induced by environmental noise in industry.

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