Yasuaki Hosaka

Primary pontine hemorrhage: clinicopathological correlations.

In 18 autopsies from patients with primary pontine hemorrhage we studied the sites of bleeding, the volumes and development of hematomas and clinicopathological correlations. A modular optical electronic planimeter was introduced to measure the size of hematomas. The series of patients can be divided into 2 groups from the viewpoint of bleeding sites, their development and clinical symptomatology. These are 1) the tegmentobasiiar type and 2) the tegmentai type. The precise location of the orgin of hemorrhage, and the approximate volume of hematomas can now be determined with the help of computerized tomography. This information will be of help in understanding clinical symptoms. Two different typical patient reports, selected from the collection, are presented.

Haemodynamic changes during the apnoea test for diagnosis of brain death.

Haemodynamic responses to the apnoea test jor the diagnosis of brain death were investigated in nine patients with severe head injury or cerebrovascular disease. To prove apnoea, the ventilator was disconnected for ten minutes and oxygen was insufflated to avoid hypoxaemia. No respiratory movement was séen in any patient. Ten minutes after disconnecting the ventilator, PaCO2 was increased to 78 ± 3 mmHg and pH was reduced to 7.17 ± 0.02. Adequate oxygenation was maintained in all patients. Cardiac output increased from 4.8 ± 0.7 to 5.7 ± 0.8 L · min− 1 (P < 0.05), and mean pulmonary artery pressure increased from 11 ± I to 17 ± 2 mmHg (P < 0.01). However, mean arterial pressure, heart rate, pulmonary artery wedge pressure and right a trial pressure did not change. Plasma catecholamines were measured in three patients. Plasma norepinephrine concentrations increased in all three patients but the changes in plasma epinephrine were minimal. These circulatory responses to acute hypercapnia were less than those reported in awake volunteers and in patients during general anaesthesia. However, since plasma norepinephrine concentration increased during the test, some sympathoadrenal response, probably of spinal origin, was present, and may have prevented the direct depressant circulatory effects of acute hypercapnia. In conclusion, the apnoea test did not produce haemodynamic disturbances when respiratory acidosis was limited toapH 7.17±0.02 and PaCO2 60–80 mmHg.RésuméLors de l’établissement du diagnostic de mon cérébrale chez neuf patients victimes de traumatisme on de maladie cérébrovasculaire, nous avans mesuré la réponse hémodynamique an test d’apnée. Le ventilateur était débranché pendant dix minutes alors qu’on insujflait de l’oxygène afin d’éviter l’ hypoxémie. Aucun patient tie fit de mouvement respiratoire el an bout de dix minutes la PaCO2 était de 78 ± 3 mmHg alors que le pH était de 7,17 ± 0,02 el que chez tons, l’oxygénation était adéquate. Le débit cardiaque passa de 4,8 ± 0,7 à 5,7 ± 0,8 L-min− 1 (P < 0,05) et la pression moyenne de l’artére pulmonaire de 11 ± 1 à 17 ± 2 mmHg (P < 0,01). La tension artérielle systémique, le pouls, la pression pulmonaire capillaire bloquée el la pression de l’oreillette droite resterént les mêmes. Nous avons mesuré les niveaia de cathécolamines plasmatiques chez trois patients et avons identifié une petite augmentation de la noradrenaline chez tous trois lors du test (NS) alors que l’adrénaline, elle, variait tiés pen. L’amplitude de la réponse hémodynamique à une hypercarbie aigué mesurée dans notre étude est beaucoup moindre que celle notée chez des volontaires conscients on chez des patients sous anesthésie générale. L’augmentation, limitée certes, de la noradrenaline plasmatique indique toutefois qu’il persistait une certaine réponse sympathoadrénergique, probablemenl d’origine spinale, pouvant contrecarrer l’effet dépresseur direct de l’hypercarbie aiguë sur la circulation. Bref, le test d’apnée n’entraîne pas de perturbations hemodynamiques lorsque l’acidose respiratoire se limite à un pH de 7,17 ± 0,02 et à une PaCO2 entre 60 et 80 mmHg.

How to Determine a Cryptic AN. Malformations. Clinico-Pathological Study of 16 Cases

The frequency of determination of cryptic AVM largely depends on the method of search during surgery. We introduced our method here together with a discussion of the microscopic and electron microscopic views. Generally, cryptic AVM is rarely found by angiography, and the key to its discovery is a skillful and thorough search for it during surgery rubbing all under a surgical microscope, the wall of the hematoma cavity is rubbed all over with a piece of cotton soaked with physiological saline solution, and a histological specimen is obtained from the easily-bleeding portion. We have performed patho-histological examinations on these specimens. In the last six years, we had 16 cases of histologically confirmed cryptic AVM, among them 12 cases were in the subcortex, and four in the brain stem. We suspected cryptic AVM in 15 cases having no histories of hypertension or blood diseases. Among these we found small nidi and achieved histological confirmations in 12. Of these 12, only seven had been found to have cryptic AVM by pre-operative angiography. They were found most frequently in the frontal lobe (8 cases), followed by the temporal lobe. In almost all, onset of cryptic AVM was relatively slow in spite of the presence of hematoma. Consciousness was clear and the outcome was generally good. Most of them were found in younger age groups, but we did find a few in older groups. In the four cases of cryptic AVM in the brain stem, there had been no particular indications of it before the operation. We are of the opinion that conventional histological classification of cryptic AVM is not adequate in view of the actual status.

Clinico-pathological Study of Ruptured Intracranial Aneurysm in Acute Stage

During the past three years, we admitted 326 cases of cerebro-vascular disease which included 109 cases of intracranial hematoma and 67 cases of ruptured intracranial aneurysm. Of those aneurysm cases, 36 cases were admitted in acute stage or within 24 hours after the attack. On admission, 27 cases of them showed severe disturbance of consciousness with the grade of 4 or 5. 12 cases died in acute stage and 11 cases of them were autopsied. On postmortem examination all of them showed severe primary cerebral damage and massive subarachnoid or intracerebral hemorrhage. The extension of subarachnoid and intracerebral hematoma depended upon the location of the aneurysm and the direction of its dome. Among 11 autopsy cases 8 cases had massive subarachnoid hematoma and 8 cases had intracerebral hematoma. 6 cases of them had associated ventricular perforation. Though it was difficult to clarify the mechanism of the acute death, the following conditions seemed to be contributing; massive subarachnoid hematoma in basal cistern surrounded the brain stem and constricted it. The basal artery was streched and separated from the brain stem. Ventricular perforation often caused early tentorial herniation and developed secondary midbrain hemorrhage. There would be still considerable cases in which if they were admitted in the early stage after the attack and had the hematoma removed, they could be rescued with satisfactory function. In our series of acute cases, one third of them was succeeded to return to the social life.

Clinicopathological study in cases of fulminant hemorrhage in the basal ganglia or thalamus

過去6年来脳卒中の早期診療に努め, 外側型脳出血に対しては超早期手術を推進してきたが, この様な大脳基底核部出血中には約10%前後の割合で発症後2～3時間以内に脳幹症状を呈して不可逆状態に陥いる激症型と呼ぶべき脳出血症例がある.短時間で死亡するため剖検の承諾を得るのは非常に困難であるが, この様な激症経過をとった大脳基底核部13例について剖検を得, 興味ある結果を得た. (1) 外側型 (被殻外包) 出血では短時間で大血腫を形成し, 血腫そのものにより脳ヘルニアを生じ, また中脳, 橋上部に続発性出血を起こしていたs全例に中脳の圧排, 挫滅, 変形, 出血のいずれかが認められた. (2) 激症経過をとった視床出血では血腫は下方に進展し, 直接に視床下部, 中脳を破壊していた. (3)「混合型」出血の多くは視床出血の進展型と考えられた. (4) いずれの例にも延髄, 下部橋には肉眼的所見を認めず上記の様な中脳の破壊が死亡の主因をなすと考えられた.