The validity of surgical proceizures in the treatment of intracerebral hematoma was evaluated by a clinical study of 441 cases with intracerbral hematoma admitted to the Department of Neurosurgery, Tokyo Women's Medical College from 1980 to 1987.
The author recognized that the degree of severity of pathological features influencing the prognosis varies with the individual case. From a biological point of view, the conventional clinical classification of patients with intracerebral hematoma is unreasonable and not available for the exact evaluation of therapy. However the evaluation of therapy is used to be done by estimating the prognosis of patients divided into several groups according to a classification formula. Such method of evaluation could not be justified, because of the classification of patients being artificial, and not biological.
The conclusion is as follows. The removal of intracerebral hematoma by craniotomy, CT guided stereotactic aspiration of hematoma or ventricular drainage is an effective procedure at the therapy of intracerebral hematoma in the case of adequate operative indication and procedure by a skillful neurosurgeon.

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It has been known that hypertension is a major risk factor for cerebral infarction. Its relation has been discussed mainly on a static or morphological aspect, based on the epidemiological and clinicopathological studies, but rarely from a hemodynamic standpoint. In this paper, mechanism of development of cerebral ischemia in hypertension is discussed on cerebral hemodynamic aspect.
Regional cerebral blood flows in the cortex and deep structures are reduced in hypertensive humans (measured by PET) as well as animals (measured by H₂ technique), its reduction being related with the severity and duration of hypertension. In similar to normotensives, however, cerebral autoregulation is preserved in hypertensives, although its upper and lower limits are shifted to higher levels in hypertension. The lower limit shift is more rapid and great during development of hypertension in spontaneously hypertensive rats (SHR), followed by a gradual but progressive upward shift even in the established state of hypertension. Therefore, in aged and long-lasting hypertensives the autoregulatory range from blood pressure at rest to the lower limit level becomes narrower, indicating that cerebral blood flow easily reduces when blood pressure falls.
Observing the blood pressure changes in patients who newly or recurrently develop non-embolic cerebral infarction during hospitalization, a greater reduction of blood pressure prior to attacks by antihypertensive treatment seems to play some role in the occurrance of cerebral infarction. In such cases, infarct is relatively large and sited mainly in the watershed area or in the cortical artery territory.
These experimental and clinical data strongly suggest that a blood pressure lowering by treatment of hypertension beyond the lower limit of autoregulation, which significantly shifts upwards, appears to cause cerebral ischemia or infarction. Careful treatment, namely a more slow and less extensive reduction of blood pressure is recommended, and also choice of antihypertensive agents is important, vasodilating drugs being less harmful.

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I. To understand the current status of CEA in Japan, a questionnaire was distributed to each of the 623 board-certified hospitals in which 336 (54%) were returned. This survey shows that a) in 40% of these neurosurgical institutes, CEA has never been experienced. b) Estimated total number of CEA performed in 1987 may be around 500. This represents an annual rate for the population of the Japan of less than 1% of that in the rate for the U.S. c) About 52% of respondents express their hesitation to performing the prophylactic CEA.
II. The author attempted to present a part of the clinical and experimental results conducted mainly by the former Associate Professor Dr. Hirohisa Ono of our department, regarding to the operative technique, reparative process, re-stenosis and so on. Real incidence of re-stenosis resulting from a myointimal hyperplasia is very low (3%). This may partly be due to severe necrobiosis of vascular wall which was ascertained in both an autopsied case and in electron microscopic findings for sequential specimens obtained from CEA experiments in cat.
Anatomical and pathological differences of Japanese carotid plaques from American were distinct. Establishment of rational guidelines of CEA for Japanese patients is strongly indicated.

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Cerebral stroke is an extremely common disease which strikes suddenly and leaves its victims in a seriously disabled state; its prevention remains a medical problem of the highest priority. Though the techniques for neurosurgical treatment following onset were already considered at the beginning of this century when the first surgical attempts were made, there is still room for significant developments in this area.
Computed tomography and microsurgical techniques have become major weapons in the surgeon's armory and notable advances have been made in the surgical therapy of cerebral infarction and hypertensive intracerebral hemorrhage. However, the surgical treatment of cerebral stroke-whether due to aneurysm, AVM, or other mechanisms-has been limited to therapy during the chronic stage following onset; even today, surgical therapy for stroke is not universally accepted as appropriate.
Nonetheless, toward the possibility of acute-stage treatment of cerebral stroke, further progress has been made possible by the emergence of magnetic resonance imaging, positron-emission tomography, and digital subtraction angiography, as well as advances in intravascular neurosurgery and the development of brain-protective agents. It has now become possible to save the lives of stroke victims in the acute stage following onset and to obtain favorable functional recovery.

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