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Three unusual cases of fatal meningitis secondary to undetected bacterial psoas abscess occurred at this institution over an 11-year period. All three patients had suffered chronic debilitating disorders before the abscess formation. The superimposed variable clinical presentations led to the initial diagnosis of a progressing cerebrovascular accident in one case, herniated nucleus pulposus at the L3-4 level in another, and osteomyelitis of the hip joint in the third. Analysis of these cases revealed that before the meningeal dissemination, all of the patients had shown evidence of intraabdominal pathology with positive psoas signs. Diagnostic and therapeutic guidelines are discussed.

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.

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.

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.