Abstract
The orbicularis oculi muscle contracts in response to photic stimulation as a reflexive action. It is called the photopalpebral reflex and is already present during the newborn period. In adults or animals, the photopalpebral reflex shows the function of the midbrain and cerebrum. It is known that hyperosmolality is a cause of intracranial hemorrhage and the dysfunction of the brain in newborns, but the functional damage is not yet clear. So the dysfunction of the brain induced by hyperosmolality can be examined and was in this study using the photopalpebral reflex, There are two ways of recording the palpebral reflex induced by photic stimulation one way utilizes the changes in the electrical potential between the upper eyelid and the ear, which is known as the photopalpebral reflex (PPR), and the other utilizes acceleration changes of eyelid microvibration, and is known as the photo-evoked eyelid microvibration (MV).The subjects were 9 newborns who had hyperosmolality 4 to 65 hours after birth,107newborns ranging in conceptional age from 25 to 45 weeks, and 5 children (4 to 9 years of age) free of any neurological abnormalities. In both methods, the electrode or pickup was applied to the central part of the upper eyelid with EEG paste and the average of 30 responses was calculated on a digital computer.The reproducibility of MV and PPR in the same individual was fairly good. PPR responses were observed in the following manner; the early component (PPR1,2,3 and PPR4) and the late component (PPRs and PPR5). The latency in the appearance of MV and PPR shortened with growth, but the amplitude of each reaction was not related to growth.In active sleep the latency of MV was prolonged and the amplitude was either markedly suppressed or completely lost. But in other sleep states the amplitude of MV was suppressed to about 30% of the responses in the awake state. While the amplitude of the late PPR component was also suppressed during sleep to about 30% of the amplitude in the awake state, the PPR never disappeared during active sleep. The latency of PPR1,2,3,4 and PPRs was not affected during sleep but the latency of PPR5 was affected. The latency of the late PPR component is the same as the latency of MV, so it is thought that these reactions have the same reaction pathway. And, because the amplitude of late PPR component and MV were suppressed during sleep, the reaction pathway might include the midbrain reticular formation.In the case of the early-infantile epileptic encephalopathy with suppression-burst, the late component of PPR and MV were completely lost, so it is suggested that the late PPR component and MV are related to the brainstem Because the early PPR com ponent alone disappeared upon the extraction of the right eye, it is believed that the early component is the ERG. As MV and the late PPR component were observed in the extracted side, the appearance of these reactions is related to the orbicularis oculi muscle and the movement of the eye scarcely affects these reactions.The latency of MV and PPR s were prolonged and the amplitude of MV and the late PPR component were suppressed with hyperosmolality. But the amplitude of the late PPR component was not directly proportional to the level of plasma osmolality. In newborns, it is believed that the dysfunction of the midbrain reticular formation caused by hyperosmolality can be studied by observing MV.
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