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Variations in intraocular pressure (IOP) may be important in glaucoma pathogenesis, but our understanding of the mechanisms for IOP variation is limited. Circadian variations are particularly interesting since nocturnal IOP is minimally changed at night when measured in the same position as during the day. This occurs despite a decrease in aqueous humor flow of approximately 50% that occurs at night, originally demonstrated by Brubaker and colleagues,1 and consistently replicated by other researchers. If all other factors remained the same, we would expect a significant drop in IOP at night, and not the pattern that is observed.
Liu et al. (138) investigated the changes in aqueous humor dynamics that occur from day to night in healthy mature subjects. They measured aqueous humor flow rate using fluorophotometry, outflow facility using tonography and fluorophotometry, episcleral venous pressure (EVP) using venomanometry, and calculated uveoscleral flow using the modified Goldmann equation. They found that aqueous humor flow decreased by 49% at night, consistent with previous studies, while outflow facility decreased 17% by tonography and 45% by fluorophotometry. Uveoscleral flow decreased significantly at night when calculated with tonographic outflow facility but not with fluorophotometric outflow facility.
Uveoscleral flow decreased significantly at night when calculated with tonographic outflow facility but not with fluorophotometric outflow facility
These findings help to elucidate the changes that may explain the aqueous humor dynamics changes that occur at night to produce the circadian pattern of IOP. In particular, a decrease in tonographic outflow facility and uveoscleral outflow appear to compensate for the reduction in aqueous humor production at night.
However, some limitations in the study are evident. In particular, the calculation of uveoscleral outflow is uncertain due to the limitations associated with the measurement of EVP using venomanometry, which involves estimated the pressure required to partially collapse an episcleral vein. Our recent work to develop an objective measurement of EVP illustrates the limitations of using subjective endpoints for the assessment of venous compression.2 We found that the difference in EVP measurement at the earliest stage of venous collapse was 6.3 mmHg, but increased to 9.6 mmHg at a 50% compression level. This level of variability would have significant implications for the calculation of uveoscleral outflow. Another limitation is that some measurements at night are necessarily performed with the subject awake, including tonometry and tonography, and may not reflect true sleeping values. Further work is required to fully understand the changes in aqueous humor dynamics at night.