ABSTRACT
When the diagnosis of “severe stroke,” “brain damaged,” or “brain tumor” is applied to a loved one, we are emotionally crushed. This is because, in contrast to diseases, no “cure” is at hand, and we see the effects persisting endlessly into the future. This despair is most marked when we believe the damage to be in the cerebral hemispheres to which we attribute most higher associative and cognitive functions. But is the future so bleak as is assumed? Oftentimes we in fact do see recovery of some functions. Or, with slow-growing tumors—those that Hughlings Jackson (1873) described as of “low momentum”—behavioral consequences can be very modest. How does recovery occur, or, at least, when can we expect it to occur. Why does slowly developing destruction have lesser effects? Are there prior or postdamage experiences that can modulate the rates of recovery? These important questions are being addressed in retrospective clinical studies with human patients and more directly with a variety of animal models. Each animal model is selected because of some special neuroanatomical, neurophysiological, or functional behavioral advantage or opportunity that it affords. Although the fish brain shares the same gross anatomical divisions as all vertebrates, it has some special features (see Hollis & Overmier, 1978; Laming, 1981), and some work on the problem of sparing and recovery of function is going forward using the teleost or “bony” fish as the model.
