The somatosensory evoked potential (SSEP) is the sequence of voltage changes generated in the brain and the pathway from a peripheral sensory nerve following a transient electrical stimulus to the sensory cortex. Evidence suggests that these signals are related to large afferent fibers and the peripheral nerve, which ascend through the dorsal column pathways of the spinal cord, proceed to the thalamus, and arrive at the somatosensory cortex. These are the same pathways that mediate light touch two-point discrimination, proprioception, and vibration. Sensitive amplification and averaging techniques enable discrimination between the evoked response and other larger and more random physiologic potentials with which the signal is mixed. As a general rule, SSEP studies may be considered whenever the disease process in question can involve the somatosensory system. SSEPs reflect neurophysiologic activity in the posterior column, medial lemniscus pathways. SSEPs do not reflect activity in the anterolateral column of the spinal cord. Thus, SSEPs correlate better with clinical examinations of proprioception and vibration rather than pain or temperature sensation.

Individual components of the SSEP waveform are identified by their latency (ie, the time at which they occur following a peripheral stimulus), their polarity, the position at which they are observed to be maximal, and to a lesser extent by the amplitude and shape of the waveform. Individual components are referred to by a letter and number. The letter (N for negative or P for positive) refers to the polarity of the wave and the number either to the latency in milliseconds of the signal from the time of the stimulus (eg, N20) or alternatively, especially appropriate in pediatric SSEPs, the order in which the component was observed (eg, N1, P2). Examples of median and tibial SSEPs are shown in Figures 6.16A and 6.17A.

With mixed nerve stimulation, recording electrodes are placed over the peripheral nerve more proximally, thoracolumbar or cervical spine, linked mastoids, and scalp. For upper extremity stimulation, the likely generator source for the cervical spine response is the incoming root, as well as postsynaptic excitatory potentials generated at the dorsal root entry zone (139). For the lower extremity, the lumbar spine responses are similarly a reflection of the root or cauda equina activity and the postsynaptic activity of the cord. The linked mastoid response is generated at the brainstem level. The difference in the latency of scalp N1 and the cervical spine response with median nerve stimulation gives a central conduction time. Similarly, the difference in latency between scalp PI for posterior tibial nerve stimulation and the spinal potential generated over T12 or LI gives a central conduction time.

Filter settings vary from a low-frequency filter of 3 to 30 Hz to a high-frequency filter of 1.5 to 3 KHz. The peripheral nerve is typically stimulated with a rate of 3.1 Hz. Our lab utilizes a stimulation intensity of 1.5 times the motor threshold for mixed nerve stimulation and 2.5 times the sensory threshold for dermatomal stimulation. Electrodes are positioned according to a modified international 10 to 20 electrode system.

SEP latencies decrease with age until well into childhood (139-142). The maturation with the growth of SSEPs is mainly associated with cell-growth processes such as myelination and with cell differentiation and synaptic development. CV along the central pathways progressively increases until 3 to 8 years of age, remains constant between 10 and 49 years of age, and slows thereafter. The N1 scalp latency of the median SSEP decreases until 2 to 3 years of age (owing to peripheral myelination) and then increases with body growth until adulthood. The cervical spine latency is relatively stable during the first 2 years (due to concomitant peripheral myelination and body growth), and then increases with age from 2 to 3 years until adulthood. The median SSEP central inter-peak latency between cervical spine latency and scalp N1, which reflects central conduction time, decreases from a mean of 11.6 msec at 4 to 8 months of age to a mean of 7 msec at 6 to 8 years of age, and remains constant between 6.9 and 7.0 msec until adulthood (143,144).

Among infants less than 4 months of age, sleep can affect the cortical components and is best performed on the awake infant. With children greater than 4 months of age, sleep or sedation usually has little effect on the SEP waveform when performing mixed nerve stimulation. Indeed, the author has had no difficulty obtaining median nerve scalp responses in the pediatric ICU in comatose children with head trauma, or those heavily sedated. Dermatomal SSEPs, on the other hand, are state-dependent responses impacted by both sleep and sedation.

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