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Fibrin and fibrinogen degradation products in the cerebrospinal fluid (CSF-FDP) were first studied in a group of 29 patients observed during the first and the second week after subarachnoid hemorrhage (SAH), then in a second group of 26 patients for a total of 55 patients. In the latter group only the first FDP value obtained as soon as possible after SAH was taken in consideration. In the whole series of 55 patients several noteworthy factors were found: 1) FDP determination should be performed as soon as possible after SAH; 2) CSF-FDP at or above 40, 80 micrograms/ml was found both in the patients with severe neurological deficits and in those with cerebral ischemia (statistically significant); 3) the significance of CSF-FDP in patients who rebled was also evaluated. In conclusion CSF-FDP could be considered useful in predicting cerebral ischemia.

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Using selectively immunological methods, it was possible, through FSP determination, for plasmin activities and plasminogen concentrations to be occasionally and exclusively detected in inflammatorily altered liquores and in bloody liquores, respectively. Thus, bloody cerebrospinal fluid, in contrast with inflammatorily altered liquor, usually shows free fibrinolytic activity, so that antifibrinolytic therapy of intracranial aneurysmal hemorrhage is pathophysiologically justifiable.

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From the present review it seems clear that the physiopathogenesis of the chronic subdural hematoma is far from being completely understood. However, an analysis of the known data can be summarized as follows: The development of subdural hematomas most likely occurs following minimal trauma in those patients with predisposing factors. Experimental data substantiates the fact that an accumulation of clotted blood in the subdural or subcutaneous space induced the formation of the fibroplastic neomembrane. The hypothesis that blood must come in contact with cerebrospinal fluid in order for the growth to occur, is still controversial. It has been virtually disproven that osmosis, referring to the electrolyte gradient as measured by freezing point depression, has any significance as a growth inducing factor. The protein oncotic gradient theory, having been the most widely accepted explanation as to the progressive enlargement of the subdural hematoma sac, has little experimental data supporting it. A larger body of clinical evidence exists supporting the concept that plasma and/or erythrocytes continuously penetrate into the subdural cavity, where enhanced fibrinolytic activity is present. However, this chronic rebleeding cannot fully explain the observed growth, because the composition of the hematoma fluid is smoewhat different from serum or plasma, and the protein content is also progressively diluted by fluid arising from an unknown source. There is some clinical and experimental evidence to suggest that a production-reabsorption balance may be a significant growth variable. No work has been done to define the role, if any, of local inflammatory mechanisms in the chronic subdural hematoma. Sound clinical evidence has shown that after the initial formation of the subdural clot, growth follows, than a slow, complete reabsorption usually occurs. Aside from the plausible production-reabsorption balance concept, it is not known why the evolution proceeds in this manner.

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Forty-one patients suffering from group A meningococcal meningitis in an area within the epidemic meningococcal belt of tropical West Africa were studied. The serum of only two of these patients contained fibrin degradation products (FDPs). The cerebrospinal fluid of 21 of these cases was also examined for FDPs, which were present in 13. Their presence in the cerebrospinal fluid was associated with a poor prognosis.

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Paired cerebrospinal fluid (CSF) and serum samples collected from 81 of 241 patients admitted to a district psychiatric hospital during a six month period were assayed for fibrin/fibrinogen degradation products (FDP) using a haemagglutination inhibition technique. FDP were found in all serum samples. Fifteen patients (18·5%) had FDP in the CSF (range 0·7-3·75 µg/ml.) and of these 13 (87%) had associated CSF protein abnormalities and 9 (60%) were hypertensive. Mean serum FDP values were the same (4·4 µg/ml.) in patients with and without FDP in the CSF. Three patients had raised serum FDP concentrations but no FDP in the CSF. The evidence suggests that the presence of FDP in CSF indicates recent central nervous system damage. In this series the most common cause was vascular disease.

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