"Embedded in the front
end of the probe is a light source that illuminates the vaginal walls. Light is reflected and diffused through the tissues
of the vaginal wall and reaches a photosensitive cell surface mounted within the body of the probe. Changes in the
resistance of the cell correspond to changes in the amount
of back-scattered light reaching the light-sensitive surface.
It is assumed that a greater back-scattered signal reflects
increased blood volume in the vaginal blood vessels (Levin,
1992). Hoon et al. (1976) introduced an improved model of
the vaginal photometer that substituted an infrared LED
(light-emitting diode) for the incandescent light source
and a phototransistor for the photocell. These innovations
reduced potential artifacts associated with blood oxygenation levels, problems of hysteresis, and light history effects.
The vaginal photometer is designed so that it can be easily placed by the participant. A shield can be placed on
the probe's cable so that depth of insertion and orientation
of the photoreceptive surface is known and held constant
(Geer, 1983; Laan, Everaerd, & Evers, 1995).
The photometer yields two analyzable signals. The first is the DC signal, which is thought to provide an index of the total amount of blood (Hatch, 1979), often abbreviated as VBV (vaginal blood volume). The second is the AC signal, often abbreviated as VPA (vaginal pulse amplitude), which is thought to reflect phasic changes in the vascular walls that result from pressure changes within the vessels (Jen- nings et al., 1980; see Figure 11.2). Although both signals have been found to reflect responses to erotic stimuli (e.g., Geer, Morokoff, & Greenwood, 1974; e.g., Hoon, Wincze, & Hoon, 1976), their exact nature and source is unknown. Heiman et al. (2004) compared, in 12 women, VPA and genital volume changes as measured using MRI, and found no significant correlations between the two. Heiman and Maravilla (2005) suggested it may be possible that at moderate levels of arousal the vaginal probe might detect changes to vaginal tissue that do not correspond with other genital blood volume changes. (Interestingly, however, the same study reported higher correlations with subjective sexual arousal for VPA than for MRI variables.) The interpretation of the relationship between the photometer's output and the underlying vascular mechanisms is hindered by the lack of a sound theoretical framework (Levin, 1992) and of a calibration method allowing transformation of its output in known physiological events. At present, most researchers describe their findings in relative measures, such as mm pen deflection or change in microVolts. Levin (1997) stated that one of the basic assumptions underlying use of the plethysmograph is that changes in VBV and VPA always reflect local vascular events. In his discussion of findings from studies on the effects of exercise and orgasm on VBV and VPA, however, he suggests that the signals are likely to reflect rather complex interactions between sympathetic and parasympathetic regulatory processes and between circulatory and vaginal blood pressure. However, Prause et al. (2004) found that, whereas VPA discriminated between sexual, sexually threatening, and threatening film stimuli, blood pressure (while increased during all three conditions) did not.
The construct validity of VPA is better established than that of VBV. Researchers have reported high correlations between VPA and VBV, particularly with stronger sexual stimuli, but others have found low or no concordance between the two signals (Heiman, 1976; Meston and Gorzalka, 1995). VPA appears to be more sensitive to changes in stimulus intensity than VBV (Geer et al., 1974; Osborn & Pollack, 1977). VPA also corresponds more closely with subjective reports of sexual arousal than VBV (Heiman, 1977). Finally, VBV changes in response to increases in general arousal, indicating that VBV is less specific to sexual arousal than VPA (Laan, Everaerd, & Evers, 1995). Two studies have directly assessed the sensitivity and specificity of VPA (Laan et al., 1995; Prause, Cerny, & Janssen, 2004). Both studies measured responses of sexually functional women to sexual, anxiety inducing, sexually threatening, and neutral film excerpts, and found maximal increases in VPA to the sexual stimulus and moderate increases to the sexually threatening film. (Participants also reported intermediate levels of sexual arousal to the sexual-threat stimulus.) On both studies, VPA did not increase in response to anxiety-inducing stimuli. These results demonstrate response specificity of vaginal vasocongestion to sexual stimuli."