Evoked Potentials are electrical events in regions of the brain that can be recorded following natural or electrical stimulation of a sensory nerve.
Changes in the latency of these potentials allows the presence of lesions to be determined, and in some cases also the site of the lesion that gives rise to the abnormal changes.
The Visual Evoked Potential can be recorded from the visual cortex following the sudden presentation of a visual to the eye, and follows that stimulus at a characteristic latency.
The visual evoked potential cannot be easily recorded following a single visual stimulus; instead, a computer is used to reduce the background noise of the EEG and enhance to evoked activity by averaging the responses to many stimuli.
The Auditory evoked potentials can also be averaged following presentaion of sudden sounds, such as clicks, to the ear. The complex waveforms of this evoked potential may allow the location of a lesion to be determined.
Averaging computers can be used to identify somatosensory evoked potentials following electrical stimulation of sensory nerves in the limbs.
Enhancement of evoked potential (EP) by means of averaging technique; a stimulus is applied at time zero. The EEG noise is progressively reduced, and the EP morphology becomes more recognizable as the number of averaged sweeps (N) is increased.
Sensory Evoked Potentials
Electrical signals from sensory receptors converge on the cerebral cortex, and impulses arrive continuously. The temporal and spatial distribution of sensory impulses cannot be clearly defined using electrodes attached to the scalp.
Evoked potential techniques identify the arrival of synchronous impulses in a sensory pathway, and the activity may be recorded a few milliseconds after activating many axons in a sensory pathway.
In the visual system synchronous activation of retinal receptors can be achieved by flashing a light or using a checkerboard that alternates betweeen black and white squares. In the auditory system, a loud click can produce synchronous activation of auditory receptors; and in the somatosensory system, an electrical pulse to a sensory nerve can be used.
The arrival of sensory impulses at the cortex can be recorded as a weak electrical event in the appropriate area of cortex, as shown in the top trace of the diagram opposite; this weak signal is recorded on top of normal EEG activity, and can be difficult to distinguish from the background EEG.
This weak response can be enhanced by repeating the stimuli and using an averaging computer that eliminates random background electrical activity, and enhances signals that arrive synchronously. The averaging process results in a peak of electrical activity that follows the stimulus after a fixed period of time, called the latency. The latency of the peak activity in the cortex can be interpreted as the time taken for impulses to travel along the the length of sensory pathway.
Notice how the randon EEG activity that occurs before the stimulus (at time zero) averages to a flat line, while cortical activity following the stimulus, and synchronised with it, is enhanced.
Image source: tidsskriftet.net
The recordings are from a patient who was suspected of having a history of optic neuritis. There are normal VEP amplitudes with a symmetrical response from the right (RO) and left (LO) lateral occipital region. VEP latency of P100 recorded over the midline occipitally (MO, channel 2) is prolonged from the left eye (118 ms) compared with normal latency on the right side (98 ms). The finding confirmed the clinical suspicion of previous optic neuritis.
The Visual Evoked Potential (VEP)
Because of the spontaneous electrical activity of the cerebral cortex (EEG), the potentials generated from the visual cortex when there are changes in the pattern of light falling on the eye are superimposed on the EEG. Averaging computers are used to filter out the background 'noise' generated by the EEG; the computer can identify cortical waves of electrical activity synchronised with the visual stimulus, and the time taken for conduction of the impulses from the retina to the visual cortex can be calculated.
The latency of the visual evoked potential is increased when there is damage to the myelin in the visual pathway, and these changes in the latency are used to identify some of the effects of multiple sclerosis on the visual system.
The latency of the VEP is longer than might be expected from the short length of the conduction pathway. However much sensory processing takes place in the visual cortex, and the primary sensory area is deep within the occipital lobe, particularly at the anterior end of the calcarine fissure.
The EEG electrodes used to monitor the VEP are located over a number of different visual areas, concerned with different aspects of the visual image, each of which receives it sinput form the primary (and other) visual areas.
Image source: library.med.utah.edu
Visual stimuli directed to the eyes separately can reveal defects in one of the optic nerves. This is shown in the diagram, and the P100 wave is delayed in the lower trace. because of optic neuritis, a common condition in multiple sclerosis, associated with transient loss of sight in one part of the visual field.
Abnormal Visual Evoked Potentials
If one records potentials generated in the occiptial lobe of the brain during repetitive visual stimulation, it is possible to record evoked potential changes which have characteristic latencies in normal people.
The commonest visual stimulus is a checkerboard in which the black squares are exchanged for white ones, and vice versa, while the subject's gaze is fixed on the centre of the board.
There is normally a positive potential at around 100 msec latency (called the P100 wave), and this wave is delayed if part of the visual pathway is affected by demyelination, as in multiple sclerosis (see the recordings below).
One reason for a delay in the peak of the VEP is demyelination of the optic nerve, a condition known as optic neuritis, which is commonly associated iwth multiple sclerosis. In the diagram opposite, the P100 wave is delayed in the lower trace.
Visual stimuli to one eye can produce a normal VEP (top) while similar stimulation of the opposite eye dshows a longer latency, which indicates a defect in one of the optic nerves.
The demyelination in optic neuritis is commonly associated with a defect in visual function that may be transient.
Image source: Neurologic Labs
Schematic of auditory neural pathway. The Auditory Brainstem Response (ABR) is initiated by stimulation of the cochlea with a broadband click stimulus given via an ear insert in the external auditory canal. Neural generators of the ABR peaks are shown.
Brainstem Auditory Evoked Potential
Evoked potentials recorded from scalp electrodes in response to clicks in one ear consist of waves of activity that are associated with each of the many synapses in the auditory pathway.
The auditory pathway uses the VIIIth cranial nerve which can be damaged by some type of fractures of the skull, acoustic neuroma and other pathologies.
The central pathway is bilateral and complex, but the peaks of the auditory evoked potential may provide evidence of the existence of lesions that interrupt the pathway.
Image source: JNNP BMJ
Upper trace: normal brainstem auditory evoked potentials (BSAEPs) following alternating click stimulation. Lower trace: abnormal BSAEPs in a patient with an acoustic neuroma showing poorly formed waveforms with prolonged I–III inter-peak latencies and subsequent I–V inter-peak latency.
Image source: JNNP BMJ
Left side: normal short latency somatosensory evoked potentials (SSEPSs) after stimulation of the median nerve (top picture) and posterior tibial nerve (bottom picture). Right side: top picture shows normal median nerve SSEPSs while the scalp potentials from the posterior tibial nerve (bottom picture) show a dispersed P37 potential with a prolonged latency.
Somato-Sensory Evoked Potentials (SSEP)
Somatosensory evoked potentials can be recorded from the scalp following electrical stimuation of peripheral nerves.
Stimulation of upper and lower limb nerves typically produce evoked activity within 30 ms and 60 ms, respectively, of percutaneous electrical stimulation.
This activity is dependent on transmission of action potentials along the main somatosensory pathways, and delays in transmission indicate lesions of thes pathways.
Similar evoked potentials can also be recorded by placing electrodes over the neck or the lumbar regions, which allow delays arising within the peripheral nerves and spinal cord to be identified (see the diagram).