Chronic subdural hæmorrhage of traumatic origin, and its relation to pachymeningitis hæmorrhagica interna

Abstract

To a considcrablc extent the work of the neurologist is concerned more with the determination of the locality of lesions than with the differentiation of the various grades and types of disturbance of function produced by them. In such neurological work, however, as is usually regarded as being more or less exclusively the province of the surgeon-the care of cases of head injuryit is characteristic of the conditions which have to be dealt with that the actual degree and kind of disturbance of function is no less variable and no less important than the situation of it. The surgery of head injuries furnishes in fact many instances of lesions closely similar in distribution, producing totally different clinical manifestations. Such cases make it clear that there must be some fnctor determining the effects of a given lesion other than its size, shape, and situation. This factor is to be found in the rate a t which the lesion develops.It is a principle of wide application in cerebral pathology, that the great majority of progressive lesions produce their effects on the brain through interference with its circulation rather than by destruction of its substance. This is clearly shown by the possibility of complete disappearance of symptoms after decompressive operations for tumoiir and after the evacuation of abscesses or hzmntomas, though well-defined paralytic focal symptoms may have been present bcforc the operation. The principle applies even more generally to the pathology of head injuries. Here actual destruction of the brain tissue plays a w r y small part in the causation of symptoms, while interferences with the circulation are all-important. Hzmorrhagc and edema are almost exclusively the causes of the cerebral disturbance in such cases, and they produce their cffect by pressing upon the neighbouring blood-vessels and limiting the circulation in the part affected.It is because the effects of the lesion are produced through the agency of the circulation that the rate of development of the lesion exerciscs so remarkable an influence upon the disturbance of function which results.Subdural hmnorrhage is of all pathological conditions the one which most perfectly illustrates the variety of clinical manifestations which arc produced by lesions developing a t different rates. It is well known that a large subdural hzmatonia may, and perhaps usually does, produce the profoilridest and least mistakable evidences of widespread compression of the brain. On thc other hand, a hscmatoma equally large .or even largcr may produce such slight and, according to currcnt teaching, atypical manifestations as not even to be suspected during Iifc. Such variability is somcwliat confusing a t first sight,

The influence of preoperative anticoagulation on outcome and quality of life after surgical treatment of chronic subdural hematoma

“…7 Half a century later, in 1914, Trotter considered the bleeding to be of traumatic and venous origin. 8 His theory became increasingly accepted, even for patients with inapparent trauma, and it remains the accepted cause for most patients. A history of head injury can be identified in 50% to 80% of the patients suffering from CSDH.…”

Evolving management of symptomatic chronic subdural hematoma: experience of a single institution and review of the literature

“…Cat and dog models suggest that once the dura and arachnoid separate, fibrin, from either serum or exudates, can induce proliferation of granulation tissue on the inner dural surface 20 . Wilfred Trotter originally hypothesized in 1914 that this proliferation of dural border cells results in production of a neomembrane, and subsequent growth of new vessels directly within the subdural space 21 . Subsequent studies show that chronic SDH can result from bleeding from these vessels by repeated microhaemorrhage from the neomembrane 22 .…”

Spinal cerebrospinal fluid leak as the cause of chronic subdural hematomas in nongeriatric patients

“…The most commonly accepted pathophysiological explanation of CSDH is that mild head trauma leads to tearing of bridging veins with subsequent bleeding between the inner layer of the dura mater and the arachnoid, or between the outer and inner layers of the dura, thus creating the hematoma. 5,14,28,29 Further and chronic enlargement of the subdural hematoma is believed to be due to microbleedings from fragile walls of sprouting vessels, accumulation of fluid in this newly created space following an osmotic gradient created by blood degradation products, or a combination of these events. 5,10 In older patients, mechanical forces related to brain atrophy enable formation and growth of CSDH.…”