An increase in cerebral blood volume (CBV) due to a decrease in cerebrovascular tonus has been though to be a major factor in the cause of acute brain swelling. It has been reported that the dorsomedial nucleus of the hypothalamus (DM), one of the brain-stem vasomotor centers, regulates cerebrovascular tonus. The DM and other vasomotor centers, such as the midbrain reticular formation (MBRF) and the reticular formation of the medulla oblongata (MORF), are connected through a series of nerve fibers. This experiment was designed to clarify the neurogenic control of the DM, MBRF, and MORF on cerebrovascular tonus. Using fifty-six cats, unilateral and bilateral DM(A 1.2, L2.0, H-10.0), MBRF (A4.0, L4.0, H0), and MORF (P10.0, L2.5, H-9.0) were coagulated stereotaxically with the condition of 15-10 mA for 1 minute. The lesions in the DM and MBRF were enlarged by increasing the current intensity of electrical coagulation. The effects of the increase on a number of simultaneously coagulated lesions were examined. Changes in systemic blood pressure (BP), intracranial pressure (ICP), and CBV were continuously recorded. Temporary increases in ICP (mean increase 16 mmHg, n = 14) and CBV were observed after unilateral coagulation of the DM. These increases were associated with transient systemic hypotension. The changes lasted only for approximately 5 minutes. The changes that occurred in ICP and CBV as a result of unilateral coagulation in the MBRF were almost the same as those that occurred after coagulation of the DM. In the latter case, the duration of the change was approximately 6 minutes with a mean increase of 12 mmHg (n=12).(ABSTRACT TRUNCATED AT 250 WORDS)
This study has been carried out to evaluate the effect of supratentorial mass lesions on the local cerebral blood flow (CBF) of the brain stem. Local CBF of the thalamus, inferior colliculus, and medulla oblongata, and supra- and infratentorial pressure were serially measured in 52 cats with intracranial hypertension produced by supratentorial balloon expansion. The mean control local CBF's in the thalamus, inferior colliculus, and medulla oblongata were 37.5, 42.1, and 30.7 ml/100 gm/min, respectively. At 20 to 30 mm Hg of supratentorial pressure, the local CBF of the thalamus started to decrease, and at 20 mm Hg of infratentorial pressure, the local CBF of the inferior colliculus began to decrease. Finally, at 40 to 60 mm Hg of infratentorial pressure, the local CBF of the medulla oblongata was affected. At the beginning of uncal herniation, indicated by anisocoria, the mean local CBF of the inferior colliculus abruptly decreased from 33.7 to 19.6 ml/100 gm/min in 16 cats. The Cushing response was evoked at a mean supratentorial pressure of 93.4 mm Hg and infratentorial pressure of 49.9 mm Hg in 16 cats. When the systemic arterial pressure was increased to the highest level in 13 cats, the mean local CBF of the medulla oblongata did not show significant change (a decrease from 22.8 to 20.9 ml/100 gm/min). The results suggest that at the beginning of uncal herniation, the local CBF of the upper brain stem markedly decreased. During the Cushing response, the local CBF of the medulla oblongata did not change significantly.
A 50-year-old male presented with a choroid plexus papilloma in the foramen magnum manifesting as dysesthesia in the right hand and severe headache. Magnetic resonance imaging clearly showed that the tumor was located in the cerebellomedullary cistern, without extension into the fourth ventricle. However, differentiation from hemangioblastoma or foramen magnum tumor was difficult by neuroimaging. Intraoperative observation found the tumor was located extraventricularly and attached to the choroid plexus of the foramen of Magendie. The tumor was grossly totally resected. Histological examination proved the tumor was a choroid plexus papilloma without malignancy. His neurological deficits resolved almost completely.
The purpose of the present study is to clarify the effects of destruction and stimulation of the brain-stem on intracranial pressure (ICP) in experimentally induced subarachnoid hemorrhage (SAH). Using 23 cats, blood pressure (BP), ICP and local cerebral blood volume (CBV) were continuously measured. Acute SAH was produced by injection of autogenous blood (3 to 7 ml) into the cisterna magna. The animals were divided into two groups. Group A: those in which hypothalamic dorsomedial nucleus (DM) and reticular formation of the midbrain (MBRF) were coagulated bilaterally one hour after SAH and Group B: in addition to the procedure of Group A, reticular formation of the medulla oblongata (MORF) was electrically stimulated bilaterally. In 19 out of 23 cats of both groups, transient small increases in ICP and CBV were observed during coagulation and/or stimulation of DM, MBRF and MORF respectively in the animals whose ICP remained approximately 20 mmHg or below and progressive increase in ICP was never evoked. In 3 animals of Group A whose ICPs remained high at more than 20 mmHg, sequential destruction of DM and MBRF induced stepwise increase in ICP to 40 to 80 mmHg and consequently resulted in acute brain swelling. In 1 animal of Group B whose ICP fluctuated around 20 to 40 mmHg, biphasic increase in ICP to 100 mmHg was repeatedly evoked by stimulation of MORF. It is concluded that in the condition of increased ICP produced by SAH, lesions in the DM and MBRF and stimulating condition of MBRF may result in acute brain swelling.
The present study was carried out to evaluate the effects of methylprednisolone (MP, 30 mg/kg) on brain edema and subcortical neural activity in anaesthetized cats with the cerebral cortex exposed to the air. MP was administered intravenously immediately after cortical exposure. After treatment with MP, significant reduction of edema was demonstrated in the primary sensorimotor cortex, white matter, and thalamus compared to the control. MP significantly increased local blood flow in the cortex and thalamus, but not in the white matter, and also protected the cortex against the ischemic suppression of the direct cortical response. However, MP did not affect the prolongation of the N1 latency of the somatosensory evoked response. The effect of steroids on cortical neural activity, including their beneficial effect on cortical edema and ischemia, may explain the rapid clinical improvement following administration of steroids.
The present experiment was designed to examine the effect of vasogenic brain edema produced by exposure to air on the electrical activity of the thalamocortical pathway and local cerebral blood flow (1CBF) measured by the hydrogen clearance method. A large area of unilateral cerebral hemisphere of anaesthetized cats was exposed to air for 12 hours, and vasogenic brain edema was produced in the cortical and subcortical structure.Water content of the primary sensorimotor cortex, white matter, and thalamus, which was measured by the specific gravity method, significantly increased by 1.9, 4.1, and 0.7% g water/g tissue, respectively, after 12 hours of exposure to air. After six hours of exposure, the blood flow in the cortex, white matter, and thalamus significantly decreased from control levels of 56.8±12.7, 21.7±5, 2, 44, 1±13.4 ml/100g/min to 46.5±13.2, 16.3±5.0, and 31.3±11.9 ml/100g/min, respectively. These decreases were accompanied by diminution in the amplitude of the direct cortical responses (DCRs) and prolongation of N1 latencies of the somatosensory evoked responses (SERs) recorded at the primary sensorimotor cortex. Both electrical activities were progressively suppressed in proportion to the reduction of 1CBF after six hours of exposure. These results suggest that thalamocortical ischemia is probably responsible for the neural electrical suppression observed in this experimental edema.There was a significant correlation between the amount of edema and the degree of ischemia in the white matter. Accumulation of the edema fluid may induce ischemia affecting sensory conduction through the white matter as suggested by prolongation of the N1 latency of SER.
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