Acute intracranial hypertension produced by extradural ballooning and the circulatory disturbance of the brain were investigated with the technique of colloidal carbon injection in 99 cats.
Ballo ons were placed and inflated in the frontal convexity, frontal tip, frontal base and infratentorial area respectively. The distribution of the cerebral circulatory disturbances and physiological phenomena were observed in sequence to time. The recovery of the cerebral circulation after deflation of balloon was also investigated in relation to time.
At first, the circulatory disturbance of the brain associated with intracranial ballooning began with local area of the brain and then extended diffusely in the whole brain in sequence to time. These patterns of extension and its mechanism were verified and discussed. The relationship between the location of the balloon and the neurological signs and phenomena were also clarified.
In the cases of the balloo ning in frontal tip and frontal base, the signs and phenomena of intracranial hypertension had tendency to appear more rapidly and the distribution of the cerebral circulatory disturbance inclined to be less in extent in comparison with ballooning in other areas. This fact suggests that the cerebral circulatory disturbance and cerebral function are not necessarily parallel.
As the caudal displacement and distortion of the brain stem were noted in almost all experiments, which was proved by the midline sagittal section of the brain frozen by liquid nitrogen, a part of vital signs, especially respiratory arrest, might have been caused by the above mechanical changes. Then, photic evoked potentials in visual cortex, upper brain stem, medulla and peripheral facial nerve were recorded in 14 cats to clarify physiologically the cerebral function concomitant with the circulatory disturbance of intracranial hypertension, and the recovery of evoked potentials after decompression were also recorded.
It is inter esting to note that evoked potentials in the brain stem were affected earlier than those in visual cortex. Thus, it can be concluded that cerebral dysfunction begins with caudal displacement or distortion of the brain stem in early stage and then the circulatory disturbance of the brain produces deterioration of the cerebral function.
The cerebral circulatory disturbances were improved considerably after d ecompression. However, microcirculatory disturbances still remained for a while, especially in the brain stem, where circulatory disturbances had been remarkably observed before decompression. The recovery of evoked potentials in the brain stem after decompression tended to be later than those in visual cortex.
These physiological results we ll correlate the results of morphological observation. Therefore, the remaining circulatory disturbances in the brain stem would concerned with vital prognosis after decompression. Whenever evoked potentials in the brain stem did not recover, the vital prognosis of an animal was extremely poor.
Thus, it is rational to conclude that the evoked response of th e brain stem is one of good indicators to evaluate the function of the brain stem and vital prognosis of an animal.
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