The voluminous literature reporting the effects of cortical lesions has shown contradictory and diverse findings from the earliest studies to the present (Franz, 1907; Klebanoff, 1945; Klebanoff, Singer and Wilensky, 1954; Meyer, 1957). Some investigators found no losses in intellectual function regardless of the locus of the lesion; others, a temporary loss followed by recovery of original capacity. Still others have reported significant losses following brain damage in the forebrain or other portions of the central nervous system. But for investigators in all three categories, what did “brain damage” consist of? The neurologists Brain and Strauss have observed “The study of psychological problems without an adequate knowledge of the physiology and pathology of the central nervous system can be likened to the exploration of the uncharted seas without the aid of a compass; and yet there are many psychologists who undertake the rash venture” (1955, p. vi). And what of the criteria on which the conclusions were based? An additional source of ambiguity is indicated by the fact that the overwhelming majority of conclusions on “mental” changes by psychiatrists and neurologists have generally been based on clinical or subjective estimates.Measurement, a crucial factor in any study, is of special importance in studies of brain damage and brain function, although despite a multiplicity of tests, there are few measures designed with attention to their unique problems. Tests employed in many psychological studies of brain damage were originally oriented toward quite different problems and had been carefully developed and standardized on non-brain damaged populations.
Urokinase-type plasminogen activator is a modulator of synaptic plasticity in the central nervous system: implications for neurorepair in the ischemic brain