The general mechanisms of the activation effect of hyperventilation are still poorly understood. The hypoxia theory that suggests that the EEG slowing is due to vasoconstriction and diminution of oxygen and dextrose supply to the cerebral cortex, has many arguments against it: (a) differences exist in the qEEG changes due to HV and hypoxia; and (b) EEG changes are independent of the concentration of inspired oxygen and the reduction of cerebral blood flow.
The hypocapnia theory which implies that low levels of carbon dioxide would lead to the predominance of the nonspecific thalamic projection system over the activating reticular ascending system has also has been questioned by observations that the slow waves on the EEGs of patients and normal individuals appear in a wide range of arterial and expired air CO2 tension. Moreover, indomethacin produces hypoperfusion similar to that caused by hypocapnia without provoking any slowing on the EEG.
Guaranha, Mirian S B, et al. “Hyperventilation revisited: physiological effects and efficacy on focal seizure activation in the era of video-EEG monitoring.” Epilepsia 46.1 (2005):69-75.
Although the ultimate mechanisms implicated in the effects of hyperventilation remain debatable, the observation that hyperventilation precipitates seizures in those with epilepsy was well known long before its introduction in the practice of clinical EEG. This activation method, although classically quoted as typical of idiopathic generalized epilepsies, also can be effective in other types of epilepsies, including focal epilepsies, where positive activation is obtained in 6–9% of the individuals. However, objective data addressing its real contribution as a method of activation of focal seizures are still lacking, even though some epilepsy centers routinely apply it during video-EEG monitoring (video-EEG). In this study we assessed the effectiveness of HV in inducing focal seizures in the setting of video-EEG and in the specific scenario of the presurgical evaluation.