To the best of our knowledge, this is the first study to compare SSEPs and giant SEPs. The current study showed that N20o–N20 and N20–P25 amplitudes were significantly different between the SSEPs and giant SEPs conditions. This is most likely due to the fact that Fz, the reference electrode on the SSEPs condition, is influenced by cortical SEPs [12, 13]. In addition, a previous report described that the amplitude of the middle latency cortical component after N20 decreases with use of a high bandpass filter and high stimulus rate [11, 14].
In this study, the N20–P25 amplitude on SSEPs was equivalent to 78% of that on giant SEPs. The initial prototype of recording condition of giant SEPs was described in 1977, which used a logarithmic scale and considered deviation beyond 2.38SD from the mean value of the normal control group as abnormal . Based on the data, the same group determined an SEP as ‘giant’ when N20–P25 amplitude was larger than 8.6 µV or P25–N33 amplitude was larger than 8.4 µV [2, 3]. In 1990’s, the upper normal limit was set at the mean + 3SD of the logarithmic values recorded from normal subjects, i.e., N20–P25 amplitude larger than 6.3 µV and P25–N35 amplitude larger than 9.8 µV [5, 6](Ikeda et al., 1995; Terada et al., 1997). More recently, the mean + 3 SD of amplitudes obtained from the control subjects without logarithmic transformation are employed; N20–P25 >10.0 µV or P25–N35 >8.1 µV for the younger subgroup and N20–P25 >20.0 µV or P25–N35 >14.8 µV for the older subgroup . In general, it is currently accepted that an amplitude more than 10 µV have high diagnostic significance in cortical myoclonus and epilepsy . Our findings suggest that N20–P25 amplitude larger than 8 µV in the SSEP condition could be considered as giant SEPs. In the posterior tibial nerve stimulation, the upper limit was set at the mean + 2SD  or +3SD  of normal subjects. We previously evaluated a diagnostic validity of giant evoked potentials using different upper limits, i.e., the mean + 2SD or the mean +3SD, in familial myoclonic epilepsy . Cumulative data would enable us to determine the optimum reference range in accordance with the purpose of evaluation and the tentative diagnosis.
The increased amplitude of SEPs can be seen in patients with other central nervous system disorders, such as cerebrovascular disease, demyelinating disease, spinal cord disease, and hydrocephalus . Thus, it can be useful in patients with suspected central nervous system pathologies. In patients with amyotrophic lateral sclerosis, a report showed that an SEP amplitude of more than 8 µV on SSEPs is a predictive factor for poor prognosis . The amplitude corresponds to 10 µV for the giant SEPs, as shown in our study. Abnormal enhancement of cortical excitability can be associated with worsening of neurodegeneration, and evoked potential amplitude can be a surrogate marker for disease progression. A recent study of conventional SEPs recording which set the upper limit at the mean + 2.5 SD, giant SEPs were found in 6.6% of patients evaluated in neurology department . It should be emphasized that a tentative diagnosis of functional disorders would need to be reconsidered if amplitude of SEPs were enlarged.
The most important limitation of this study is small sample size. However, in previous studies control data were determined from approximately 20 normal subjects [2, 5, 8]. Large studies across a wide range of age groups would be useful to confirm the correlation between the two conditions.
In conclusion, our study showed that the amplitude in SSEPs condition was equivalent to approximately 80% of that in the giant SEPs condition. Further studies, including various neurological disorders, are warranted to evaluate the diagnostic significance and the predictive value for prognosis.