Abstracts

Rationale: Photo-paroxysmal response (PPR) evaluation is important in epilepsy and EEG investigations. It has been likened physiologically to the EEG equivalent of a cardiology exercise ECG. Change in PPR has been used in proof of principle trials as a "real patient" method of efficacy evaluation in single dose AED studies. Change in EEG PPR is also proposed as a surrogate marker of chronic AED efficacy. However, poor or inconsistent EEG Photic stimulation technique and difficulties with interpretation of changes in the PPR may lead to underutilisation or misunderstanding of the value of data obtained by this method. Improvement in testing technique and standardization of the results as a "SPR" helps us to obtain maximal information from the PPR and enables use of the SPR to guide treatment efficacy decisions. Methods: Photic stimulation was carried out in non fasted, attentive patients, utilising correct lamp size and brightness, at 30cm from the nasion. IPS PPR sensitivity was tested twice at each time point; on eye closure, with eyes already closed, then with eyes open. Five second trains of flashes & 5 seconds rest were given sequentially in each eye state at the flash frequencies of: 1, 2, 8, 10, 15, 18, 20, 25, 30, 40, 50, & 60 Hz. When stimulation was carried out using this protocol, reproducible results were attained. The resulting photosensitive range data was converted to a standardised result; the "SPR" (Standardised Photosensitive Range). The SPR consists of the number of standard frequencies at which photic stimulation triggered a generalised PPR. This "SPR" result is a single digit, which although non-linear, is ordinal and thus quantifiable. This data may then be reliably compared from time to time in individual patients, and from patient to patient. Results: These studies demonstrate use of PPR and SPR in a single dose AED test protocol; which illustrates the ease with which SPR may be used to track changes in the PPR. They also demonstrate successful use of SPR in a chronic dosing protocol, where SPR was shown to track with myoclonic seizure frequency in a JME cohort switched to LTG from VPA. In that group the SPR worsened after switching to LTG and improved as the LTG dose was increased. Simultaneously the myoclonic seizure frequency initially worsened and then improved with LTG dose increases. Thus demonstrating potential utility of change in SPR as a marker of chronic AED efficacy. Conclusions: Proof of concept is demonstrated. Change in SPR correlates with AED concentration in single doses, and correlates with AED efficacy in chronically dosed patients. Increase in the SPR correlated strongly with worsening seizure control in our patients, and reduction in the SPR following LTG dose increase correlated with improved seizure control. Tracking change in SPR provides early evidence of likely efficacy or likely failure of an AED in any given patient.