What is the role of (N/P13) deflection in somatosensory evoked potential (SEP) testing?

Updated: Oct 25, 2019
  • Author: Andrew B Evans, MD; Chief Editor: Selim R Benbadis, MD  more...
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Answer

Most human clinicopathologic correlations suggest that the N/P13 waveform is generated in the lower medulla, probably in the dorsal column nuclei. The negativity recorded in the Fz-Cc derivation (N19) is the difference in negativity between the 2 electrode sites and thus is a “derived” waveform. N19 generally is believed to originate in the primary sensory cortex; however, good human clinicopathologic data are available to suggest that much of N19 is generated in the thalamus.

Chiappa et al and Goldie et al published data on a series of patients with instructive lesions, indicating that much of the negativity after 15 msec was generated in the thalamus. [44, 32] Regli and Despland studied 50 patients who had acute infarctions and found N19 to be preserved in small lesions confined to the postcentral gyrus but absent in large lesions involving the underlying white matter and thalamus. [45] Epileptogenic lesions of the sensory cortex often produce augmentation of P22 but not of N19.

These data suggest that the negative deflection appearing 16-19 msec after stimulation of the median nerve at the wrist is probably generated in the thalamus. The widespread negative activity seen at 25-30 msec with lower-limb stimulation (ie, the posterior tibial nerve at the ankle) is also believed to be generated in the thalamus. The subsequent positive activity (N/P37) is probably generated in the primary sensory cortex.

When lower-limb stimulation is employed, absence of the cauda equina potential (LP) suggests the presence of a lesion at or below that level. Technical considerations (eg, muscle artifact) also may obscure the LP potential.

Clinical interpretation is based on the time interval between wave peaks. Registering a good Erb point or LP potential is important for allowing measurement of central conduction times. Side-to-side comparisons of latencies can be useful in clinical diagnosis. Like BAEPs, SEPs are fairly resistant to changes by widespread influences other than structural pathology in somatosensory tracts. SLSEPs are not significantly altered by barbiturate doses sufficient to render the electroencephalogram (EEG) isoelectric or by general anesthesia.

Yiannikas et al found that both SEPs and electromyography (EMG) were of limited clinical utility in patients with cervical spondylosis who presented with symptoms but without neurologic signs of root compression. [46] In patients with clinical signs of neurologic deficit, EMG and SLSEPs may be helpful or confirmatory.

In patients with clinical evidence of myelopathy, performing SLSEPs from both upper and lower extremities may be informative and may reveal or disprove a conduction block. [46] Patients with syringomyelia often have abnormal central conduction time after upper-limb stimulation. In cervical spondylosis, an abnormal latency difference may be noted between brachial plexus (EP) and lower medullary (N/P13) components after upper limb stimulation.

Le Pera et al documented selective abnormality of the N13 spinal SEP to dermatomal stimulation in patients with cervical monoradiculopathy. [47] Scalp SEPs to dermatomal stimulation have proved to be only partially useful in the diagnosis of monoradiculopathy, mostly in cases without motor impairment.

The aim of the study was to test the sensitivity of the spinal N13 potential in uncovering lesions of single cervical roots. [47] The investigators studied 5 patients suffering from cervical monoradiculopathy by using a technique that allowed specific recording of the genuine N13, which probably is generated by dorsal horn cells.

None of the patients showed signs of muscle impairment, and needle EMG findings were always normal. [47] In 4 patients, the N13 SEP was absent after stimulation of the dermatome corresponding to the damaged root, whereas both the lemniscal P14 and the cortical N20 components were normal. SEP recorded after stimulation of upper-limb nerves showed no abnormality in any of these patients.

Apparently, loss of N13 potential after dermatomal stimulation could be due to deafferentation of dorsal horn neurons; the N13 is particularly sensitive to initial root compression. A montage allowing recording of the genuine N13 SEP, therefore, can improve the sensitivity of dermatomal SEP recording in patients with suspected cervical monoradiculopathies.


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