The dorsal subcutaneous injection in rats of 12 ml or more of autologous hemolyzed whole blood clotted in situ induced the formation of sterile, hemispheric lesions, 47% of which showed an initial decrease in volume followed by a progressive enlargement. The behavior, histology, and biochemical characteristics of the liquid contents of these lesions were found to be remarkably similar to those of subdural hematomas in man. To evaluate the role of the various blood components that may have influenced the formation and growth of these lesions, more than 150 clots composed of human platelet-free plasma, autologous hemolyzed blood, or autologous whole blood were implanted subcutaneously in rats by either surgical or injection techniques. The in vitro behavior of the different clots used was also assessed. This systematic approach led to the following conclusions: 1) the composition and volumes of the clots are critical variables; 2) plasma-fibrin provides the matrix shape of the lesions; 3) the breakdown products derived from erythrocytes, hemoglobin, leukocytes, and other solid blood elements induce neomembrane formation and contribute to the lesion's subsequent growth; and 4) inflammation mechanisms appear to be essential, while cerebrospinal fluid plays no discernable role in this process.

Multiple chemical and coagulation determinations were undertaken on the subdural hematoma fluid from the reformed effusions of two patients. It was found that plasma or blood repeatedly reentered the subdural cavity. Coagulation studies compared the in vitro effects of subdural fluid with those of cerebrospinal fluid, serum, and a buffer control. Despite some chemical differences, the subdural fluids from both patients behaved similarly by (1) accelerating the intrinsic clotting system, (2) producing defective clot formation, and (3) accelerating the fibrinolytic system. It is presumed that these continuous hemostatic-fibrinolytic alterations, acting in the subdural sac, may have important implications in the growth and reformation of subdural hematomas, and a hypothesis of the mechanisms involved is presented.

The unusual case of spontaneous hypoliquorrheic headache reported here was clinically identical to that originally described by Schaltenbrand. This is the first case to be studied by radioisotope cisternography, which showed that the cerebrospinal fluid flow was essentially normal. However, the radioactivity counts percent decreased rapidly, with simultaneous appearance of high isotope concentration in the urinary bladder. Scan images did not show cerebrospinal fluid (CSF) leakage at the puncture sites. Our data suggest that this postural headache syndrome is not caused by decreased CSF production, but by a very rapid absorption or unusual CSF leakage.

A previously described experimental hematoma model, achieved by the subcutaneous injection of 12 ml of autologous hemolyzed blood clotted in situ, was made in 33 rats. Sventeen animals served as controls; the other 16 received daily intra-muscular injections of dexamethasone. After an initial decrease in size, 47% of the lesions in the control animals enlarged to a mean weight of 12.1 +/- 2.5 gm, while the lesions in the 16 steroid-treated rats weighted 3.2 +/- 0.70 gm (p less than 0.01). Histologically, lesions from the steroid group showed absence of neomembrane formation. These data offer further support to the theory that the neomembrane development and subsequent enlargement of subdural hematomas is due to inflammatory reactions of tissues in contact with large blood clots.

An elderly man presented with signs of normotensive hydrocephalus. Elevated protein content in the spinal fluid led to the diagnosis of an "asymptomatic" cauda equine neurilemoma and its removal. Within 6 weeks the patient's mental status had dramatically improved. Chronic transudation of plasma proteins including fibrinogen into the subarachnoid space had probably impeded spinal fluid reabsorption. It is suggested that the leakage of fibrinogen into the cerebrospinal fluid may be the cause of hydrocephalus in other clinical settings in which there is an elevation of the spinal fluid protein.