The future of aphasia treatment.

Although the efficacy of aphasia therapy has been demonstrated, the very fact that this demonstration continues to have detractors shows that the treatment of aphasia, despite its effectiveness, remains unsatisfactory. Why is this the case? We postulate four contributing reasons: (1) The pathophysiology of the late stages of stroke is poorly understood; (2) the therapeutic options for subacute and chronic stroke are too limited; (3) the goals of such therapy are far too modest; and (4) the inherent complexity of language and of the brain’s mechanisms for using it makes aphasia therapy a particularly difficult challenge. Very little is known about the pathophysiology of the postacute stages of stroke. For example, while the manifestations of aphasia change in certain ways over the course of recovery, based on the original manifestations, the age of the patient, mode of therapy, and other factors (Holland, Greenhouse, Fromm, & Swindell, 1989), it is completely unknown what is happening to the brain during this time. Are new synapses forming? Where? Are there neurotransmitter changes occurring? Are areas of the left perisylvian cortex connecting up with their counterparts on the right? In what ways are the therapeutic options for aphasia limited? The main limitation is the constraint that therapy not be directed at the damaged structure itself, but rather at the external manifestations of this structure. Thus, if a patient has a Broca aphasia and has damage to the left frontal lobe, we try to teach him to make full sentences (education) rather than trying to fix the left frontal lobe (biology).