An Experimental Study for Effect of Controlled Hypotension on Acute Ischemic Brain Lesion

Controlled hypotension and temporary clip of feeding artery are used to reduce bleeding and to facilitate the neurosurgical operations, especially in intracranial aneurysm surgery, but the microvasculature of acute ischemic brain from impaired blood flow is quite susceptible to decrease in blood pressure and blood volume. The reversibility of brain damage following an ischemic brain lesion depends on the amount of regional cerebral flow as well as the severity of ischemia. The present study was designed to elucidate the effect of controlled hypotension on cerebral blood flow, cerebrovascular resistance, and pathological changes in acute ischemic brain lesion. Cerebral ischemia was induced in cats by middle cerebral artery occlusion for 6 hours through the transorbital approach. Forty-nine cats were divided into 3 groups, namely control group with mean blood pressure maintained at normal after right middle cerebral artery occlusion, hemorrhagic hypotension group with mean blood pressure decreased to 80, 60, and 40mmHg by with drawing of blood after right middle cerebral artery occlusion and drug-induced hypotension group with mean blood pressure decreased to 80, 60, and 40mmHg with arfonad infusion after right middle cerebral artery occlusion. Regional cerebral blood flow was measured by the hydrogen clearance method following middle cerebral artery clipping and gradual decreasing mean blood pressure. Cerebrovascular resistance was calculated after regional cerebral blood flow was measured and size of infarct were examined in each groups after the experiment was completed. Results were as follows : 1) In control group, regional cerebral blood flow and cerebrovascular resistance of the right parietal area with mean blood pressure maintained at normal after right middle cerebral artery occlusion were 19.4+/-2.1ml/2.1ml/100g/min and 5.5+/-0.4mmHg/ml/100g/min. The size of cerebral infarct was minimal in 71% of the control group. 2) In hemorrhagic hypotension group, regional cerebral blood flow of the right parietal area with mean blood pressure decreased to 80, 60, and 40mmHg was 17.6+/-1.5, 15.4+/-3.8, 7.8+/-2.9ml/100g/min respectively, thus 6, 25, and 57% lower than the control group. Cerebrovascular resistance of the right parietal area with mean blood pressure. With mean blood pressure reduced to 40mmHg, the cerebrovascular resistance drastically increased to 5.1+/-0.5mmHg/ml/100g/min. When mean blood pressure was reduced to 60 and 40mmHg, the size of infarct was marked in 57 and 85% of the hemorrhagic hypotension group. 3) In drug-induced hypotension group, regional cerebral blood flow of the right parietal area with mean blood pressure reduced to 80, 60, and 40mmHg was 19.1+/-2.3, 17.8+/-3.1, and 7.4+/-2.7ml/100g/min respectively, thus 2, 10, and 38% lower than the control group. the regional cerebral blood flow of the right parietal area in the drug-induced hypotension group was slightly higher than the hemorrhagic hypotension group when mean blood pressure was reduced to 80 or 60mmHg, while there was no significant difference of regional cerebral blood flow in the both groups when mean blood pressure was reduced to 40mmHg. Cerebrovascular resistance of the right parietal area with mean blood pressure at 80 and 60mmHg was 4.1+/-0.3 and 3.1+/-0.2mmHg/ml/100g/min respectively, thus showing a gradual decrease in relation to decreasing mean blood pressure. With mean blood pressure reduced to 40mmHg, the cerebrovascular resistance was 5.6+/-0.9mmHg/ml/100g/min, thus higher than the hemorrhagic hypotension group. When mean blood pressure was decreased to 60 and 40mmHg, the size of infarct was marked in 42 and 85% of the drug-induced hypotension group. The extent of cerebral infarct was more extensive in the hemorrhagic hypotension group than in the drug-induced hypotension group. 4) In the contralateral hemisphere of the infarct, there was no change in regional cerebral blood flow when the mean blood pressure was decreased to 80 and 60mmHg but when the mean blood pressure decreased to 40mmHg, the regional cerebral blood flow was markedly reduced in all groups. When the mean blood pressure decreased to 60mmHg there was no change in cerebrovascular resistance, however when the mean blood pressure was at 40mmHg, there was a drastic increase in cerebrovascular resistance in all groups. Due to to loss of autoregulation in the ischemic brain lesion, the regional cerebral blood flow depends on the brain perfusion and accordingly when there is ischemic brain lesion, the hemorrhagic hypotension produces serious brain infarction and edema than drug-induced hypotension.

Gas-Forming Brain Abscess due to Peptostreptococcus

A gas forming brain abscess that was resistant to treatment with antibiotics, blycerol, and steroids is reported. A CT scan showed a frontal epidural gas shadow which progressed in 3 weeks to massive frontal cerebritis with gas within the abscess, ventricle, and basal cisterns. An anaerobic culture of CSF revealed peptostreptococus, which was been increasing recently as a causative organism in brain abscess. We feel that the primary management of brain abscess should be surgical excision followed by appropriate antibiotic therapy.

Giant Global Intracranial Aneurysm in an Infant: Case Report

No abstract available.

A Case of Sparganosis in the Intradural Space of the Thoracolumbar Spine

The authors experienced a case of sparganosis involving the intradural space of the thoracolumbar spine, in which unusual pathologic findings such as caseous necrosis without any inflammatory cells were noted. We confirmed the sparganosis by microscopic findings of the worm and immunologic studies of serum and cerebrospinal fluid. Epidemiology, pathogenesis and particularly diagnostic methods in association with CNS sparganosis are discussed.

A Case of Sparganosis in the Intradural Space of the Thoracolumbar Spine

The authors experienced a case of sparganosis involving the intradural space of the thoracolumbar spine, in which unusual pathologic findings such as caseous necrosis without any inflammatory cells were noted. We confirmed the sparganosis by microscopic findings of the worm and immunologic studies of serum and cerebrospinal fluid. Epidemiology, pathogenesis and particularly diagnostic methods in association with CNS sparganosis are discussed.

Auditory Brainstem Evoked Potential Responses in Focal Brain Lesions

Brainstem auditory response abnormalities directly reflect disturbance of neural function rather than the underlying anatomic cause of that disturbance. The test has advantage in detecting lesions that alter electrophysiology but do not produce detectable alterations of radiodensity, displace surrounding structures or change vascular supply and permeability. A sequence of seven low-amplitude potentials that occur in the initial 10 msec following click signals can be recorded from scalp electrodes in 44 patient with focal brain lesions using computer averaging techniques. The potentials, termed auditory brainstem responses, are thought to be the far-field reflection of electrical events originating in the auditory pathway during its course through the brainstem. We have studied auditory brainstem evoked potential responses in a variety of focal brain lesions and found them to be of assistance in evaluating the localization of pontomedullary, pons, midbrain, thalamus, subcortical and functional recovery. 1) Distortion of early components (type I) was occured in the brainstem lesions. 2) Distortion of late components (type II) was developed in the diencephalon or subcortical lesions. 3) Distortion of all components (type III) was developed in the brainstem and diffuse brain contusions. 4) Serial recordings provided information about the evolution of brain stem lesions and good functional recovery marker.

Auditory Brainstem Evoked Potential Responses in Focal Brain Lesions

Brainstem auditory response abnormalities directly reflect disturbance of neural function rather than the underlying anatomic cause of that disturbance. The test has advantage in detecting lesions that alter electrophysiology but do not produce detectable alterations of radiodensity, displace surrounding structures or change vascular supply and permeability. A sequence of seven low-amplitude potentials that occur in the initial 10 msec following click signals can be recorded from scalp electrodes in 44 patient with focal brain lesions using computer averaging techniques. The potentials, termed auditory brainstem responses, are thought to be the far-field reflection of electrical events originating in the auditory pathway during its course through the brainstem. We have studied auditory brainstem evoked potential responses in a variety of focal brain lesions and found them to be of assistance in evaluating the localization of pontomedullary, pons, midbrain, thalamus, subcortical and functional recovery. 1) Distortion of early components (type I) was occured in the brainstem lesions. 2) Distortion of late components (type II) was developed in the diencephalon or subcortical lesions. 3) Distortion of all components (type III) was developed in the brainstem and diffuse brain contusions. 4) Serial recordings provided information about the evolution of brain stem lesions and good functional recovery marker.

The Changes of Somatosensory Evoked Potentials in Experimental Cerebral Missile Injury and the Effect of Mannitol

Since every component of the evoked response is considered to relate with topographically specific neural structure, it is possible that the location and severity of brain dysfunction could be defined by careful analysis of evoked responses. The purpose of this investigation was to study the change in cardiopulmonary functions, somatosensory evoked potential(SEP) following a right occipitofrontal missile injury in cats and to evaluate the effects of mannitol on them. Forty adult cats weighing 2.7 to 4.2 Kg were divided into operated control(n=20) group and mannitol treated group(n=20). In each group cardiopulmonary functions and SEP were checked on 1 min, 10 min, 30 min, 1 hour and 6 hours after missile injury. 1) After injury with a pellet at 90m/sec, there was rapid rise in intracranial pressure, bradycardia, changes in blood pressure and marked alteration in respiration. 2) The somatosensory evoked potential was detected shortly after injury and markedly altered in shape. The early components(N0, N1) of the SEP were suppressed first, followed by the late component(N2) of the SEP in the control group. This suggests that the specific somatosensory pathways are most vulnerable to high kinetic missile-injury. The late component of SEP(N2) was easily and severely suppressed possibly used due to functionally interrupted brainstem multisynaptic pathway and nearly not recovered. At an intracranial pressure(ICP) of 29 cmH2O, the early components(N0, N1) of SEP were significantly suppressed to 80% of the normal control. At the ICP higher than 40 cmH2O, not only N0, N1 appeared flat, but also the N2 was suppressedzz.

Effect of Phentolamine on the Lung and Hypothalamic Lesions in the Experimental Neurogenic Ulmonary Edema in Cats

This experiment was performed to define the paricipation of a discrete hypothalamic neural structure in the genesis of pulmonary edema and the effect of alpha adrenergic blockade. Fifty adult cats weighing 2.5 to 4.0 Kg, were used in this study. The components of the pathophysiological systemic changes, lung weight, and histopathological changes of lung and hypothalamus were studied in groups of animals when intracranial pressure(ICP) was raised to 200 mmH2O of 300 mmH2O for 2 hours by intraventricular infusion with normal saline. The animals were divided into 5 groups : The normal control group was comprised in 10 normal cats. Control and phentolamine treated animal groups which had an elevated ICP of up 200 mmH2O consisted of 10 cats each. Control and phentolamine treated animal groups which had an elevated ICP of up to 300 mmH2O consisted of 10 cats each. The results obtained were as follows : 1) In the animal groups of elevated ICP to 200 mmH2O or 300 mmH2O, there were hemodynamic systemic changes which were neurogenically mediated and caused an immediate elevation in blood pressure of 30 mmHg to 60 mmHg. The hemodynamic data of the animals that had an elevated ICP of up to 300 mmH2O were significantly more deviated from normal control values than the 200 mmH2O ICP groups. The hemodynamic responses of the phentolamine treated animal with elevated ICP of up to 200 and 300 mmH2O were less deviated from normal control values. 2) The lung weights of the animals with an elevated ICP of up to 200 and 300 mmH2O were significantly heavier than the normal control value(p<0.05) and the lung weights of the animals with an elevated ICP of 300 mmH2O were significantly heavier than those with an ICP of 200 mmH2O(p<0.01). The lung weights of the phentolamine treated animal groups were significantly lighter than the control group but showed little increase in the lung weight when compared to the normal value. 3) By controlling the elevated ICP above 200 mmH2O in the experimental animals we have confirmed gross and microscopic appearances of hemorrhagic pulmonary edema. Histopathological changes of the phentolamine treated animals were significantly less sever than in the control groups. 4) By elevating ICP above 200 mmH2O in the experimental animals, we have confirmed discrete bilateral hemorrhagic spots of the anterior hypothalamus, preoptic region induced by increased intracranial pressure. Histopathological changes of the phentolamine treated animals with the elevated ICP were significantly less severe than of the control groups. 5) This experimental model may define the specific particification of the hypothalamus in the pathophysiological pathogenesis of neurogenic pulmonary edema. These results suggest that the lungs are directly affected by the intense sympathetic discharge evoked by release phenomenon from the sympathoinhibitory influence of the hypothalamus, and pulmonary edema was effectively eliminated by alpha adrenergic blockade.

Hyperosmolar Hyperglycemic Nonketotic Coma in Neurosurgery:Report of Six HHNC

In 1957 Sament and Schwartz reported patient with profound coma and hyperglycemia but without ketonemia or acidosis. This syndrome in usually termed hyperosmolar hyperglycemic nonketotic coma(HHNC). Six critically ill patients while on the neurosurgical service were studied to establish the diagnosis of HHNC. Criteria for the diagnosis of HHNC included. 1) Serum glucose over than 220 mg/dl wigh glucosuria. 2) absence of significant acetonuria. 3) serum Na over than 150 mEq/l. 4) serum osmolarity over than 310 mOsM/kg. 5) neurological dysfunction. The production of the characteristic stupor and diminution of mental acuity appears to result from a decrease in intracellular water content within the brain due to the osmotic effects of those predominately extracellular substances. Factors documented to be significant in it's development include nonspecific stress to primary illness, hyperosmolar tube feeding. Dehydration, and mannitol, dilantin and steroid administration. The treatment of HHNC recommended the division of replacement into two stages: 1) rapid repair of water deficits which was calculated by described formula and correct the Na abnormality. 2) insulin replacement according to the degree of glucosuria. During the replacement therapy of water deficit and insulin, it should be necessary to repeat plasma electrolytes and blood glucose at 4 hour intervals until normal levels are approached. One among the 6 cases of HHNC became good recovery and 5 cases were expired on treatment, Fatal complications of this syndrome, such as acute renal failure, terminal arrhythmias and cardiopulmonary dysfunction, both cerebral and systemic, were common in these cases.