Norio NAKAMURA Department of Neurosurgery, University of Tokyo

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1 minutes to 12 hours (average 3 hrs.). Neurological findings, such as hemiparesis, aphasia, diplopia and etc., were proved in 9 cases (820%). Average duration of the free interval were 3 months. In the bridging vein group, transient initial loss of consciousness were observed in 4 cases, and its duration ranged from 1 minute to 30 minutes. Neurological changes were existed in 12 cases (56%). Average duration of lucid interval was 1.9 months. In remained 28 cases we could not find any source of bleeding. In this group, transient initial loss of consciousness was found in 11 cases (3900), and neurological findings were in 17 cases (60%). Average duration of lucid interval was 2.3 months. From the above-mentioned findings it was ascertained that there was some characteristic difference of symptoms between the cortical vessel group and other two groups of the chronic subdural hematomas. In cortical group, not only the loss of consciousness were longer than other groups, but also the lucid interval were also longer than others. These facts means in the cortical vessel group the cerebral damage seemed to be severe but the speed of accumulation of blood in the subdural space be slower than in other groups. S-F-4. The Relationship between Head Injuries and Chronic Subdural Hematoma Norio NAKAMURA Department of Neurosurgery, University of Tokyo During the last 15 years, 135 cases of chronic subdural hematoma in adults, over 15 years of age, were admitted to the neurosurgical department of the University of Tokyo Hospital (Fig. 1). Over 91 %/ of the total had suffered from head injuries in the year prior to the admission (Fig. 2). Therefore, to find the relationship between head injuries and chronic subdural hematoma, clinical investigation was conducted on the histological aspects of subdural hematoma in general. In the case of severe head injuries followed by acute subdural hematoma, some fibroblasts were found to have infiltrated the clots located adjacent to the inner side of the dura mater, sometimes within 9 hours of the injury. On the 11th post-traumatic day, a thin granulation layer, composed of loose connective tissue rich in vessels with thin walls, had already been produced just beneath the dura, which is called the sinusoidal channel

2 Fig. 1. Age distribution of chronic subdural hematoma in comparison with that of head injury. Overwhelmingly greater incidence of chronic subdural hematoma in males than in females. Fig. 2. Chronic subdural hematoma and injury prior to the admission head layer (Fig. 3). On the 20th post-traumatic day, the sinusoidal channel layer extended a sheet of the fibrous tissue over the edge of subdural clot and between: the latter and the brain matter, enveloping the hematoma (Fig. 4).. In chronic cases of subdural hematoma, the appearance of the outer membrane was very similar to the above mentioned sinusoidal channel.:4ayer seen in acute cases. Moreover, the thickness of the fibrous layer inside7the sinusoidal channel layer was found to be directly proportional to the duration of time interval between the head injury and the operation (Fig. 5). In the case of a 10 month-old subdural hematoma, almost all of the outer membrance was composed of the fibrous layer, and vascular channels were found to be poorly developed on the dural side of the outer membrane (Fig. 6). In one of chronic subdural hematomas, instead of total removal, intracapsular drainage and irrigation was done, leaving the membrane intact

3 Subdural granulation layer, called the sinusoidal channel layer Dura mater Fig. 3. Subdural granulation layer on the 11th post-traumatic day. Fig. 4. Subdural grannlation layer on the 20th post-traumatic day.

4 Fig. 5. Outer membrane of chronic su dural hematoma. 3 months duration of time interv between head injury and the operatio Fig. 6. Outer membran of 10-month chronic subdural hematoma.

5 Fig day-old extradural granulation tissue similar to the outer membrane of chronic subdural hematoma. Fig. 8. Reactive membrane developed from the dura mata in man around a sheet of artificial fibrin film (about 1-month duration).

6 The same patient died by accident 6 months later and autopsy revealed that the subdural membrane was found to have calcified already. Similar reaction of the dura mater to blood clot was produced in extradural clot or chronic extradural hematoma (Fig. 7). Futhermore, the same process was found around a sheet of artificial fibrin film, inserted under the dura mater in man (Fig. 8). Apart from these observations, in chronic subdural hematoma, the gross appearance as well as the histological study of the inner membrane revealed Fig. 9. Inner surface of chronic subdural hematoma. The outer membrane overlaps a part of the inner mambrane at its edge.

7 that the outer membrane extended itself over the edge of the hematoma and overlapped a part of the inner membrane at its edge (Fig. 9). Next, the question arises about the origin of subdural bleeding in chronic cases. The author has experienced over 15 cases of ruptured parasagittal bridging veins into the subdural space following mild head injuries. In these cases, accumulation of fresh blood clot took place in the subdural space exactly around the ruptured vein, and clinical manifestations were acute. From these investigations, it is possible to assume the following mechanisms on the production of chronic subdural hematoma: a mild head injury damages a bridging vein, from which blood oozes out into the subdural space, followed by a reactive proliferation from the dura mater which granually covers the blood clot and finally envelopes it (Fig. 10). On the other band, it is well known from clinical observations as well as animal experiments that blood clot in the subdural space can be easily absorbed and resolved commonly and does not produce long-term progressive changes. Futhermore, clinical survey in this department shows that chronic subdural hematoma affects or was encountered predominantly in males and older people (Fig. 1). And 9o/ of the patients did not remember any head injury prior to their admission (Fig. 2). To comprehend the histological survey and the clinical observations simultaneously, the author would like to advocate another supplementary factor "a" in addition to head injury as one of the etiological mechnisms of chronic subdural hematoma. When a subdural blood clot, resulting from an injury of the head, is accompanied by the factor " a ", it may be enveloped by a proliferative reaction from the dura mater in the course of timee and subsequently chronic subdural hematoma ensues. However, neither head injury nor the factor,,a", singly produces chronic subdural hematoma. This factor "a" might be a combination of various dispositions, including intracranial hypotension, cerebrovascular diseases, pachymeningitis interna and so on. The author is planning to undertake an investigation on this factor " a " as the next major problem. _119-

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