On the other hand, despite this level of theoretical sophistication, attempts to delineate the anatomy of speech and language disorders by means of conventional brain imaging techniques in aphasic patients have been somewhat disappointing. In early studies using CT, LeCours and Lhermitte were unable to establish a consistent correspondence between the type of aphasia and the location of the demonstrable lesion. Similarly, Willmes and Poeck, in a retrospective study of 221 aphasic patients, failed to find an unequivocal association between the type of aphasia and the CT localization of the lesion. These poor correlations are in part related to the timing and the crudity of CT. MRI performed soon after a stroke show somewhat more consistent correlations between the type of language disturbance and the location of lesions in the perisylvian cortex, but lesions in identical locations may produce functionally different language disorders. Functional magnetic resonance imaging (fMRI), while subjects are engaged in language production and comprehension, provides an additional perspective for understanding the language process, but so far only the broadest rules of localization can be confirmed. Studies of blood flow and topographic physiology during the acts of reading and speaking, while generally affirming nineteenth-century models of language, have shown widespread activation of Wernicke and Broca areas, as well as of the supplementary motor area and areas of the opposite hemisphere (see Price).
Although localization of the lesion that produces aphasia is in most instances roughly predictable from the clinical deficit, there are wide variations. The inconsistency has several explanations, one being that the net effect of any lesion depends not only on its locus and extent but also on the degree of cerebral dominance, that is, on the degree to which the nondominant hemisphere assumes language function after damage to the dominant one. According to this view, a left-sided lesion has less effect on language function if cerebral dominance is poorly established than if dominance is strong. In all likelihood, the variability between patients in lesion location and the characteristics of aphasia has to do with subtle differences in the organization of the language cortices. Another explanation invokes the poorly understood concept that individuals differ in the ways in which they acquire language as children. This is believed to play a role in making available alternative means for accomplishing language tasks when the method initially learned has been impaired through brain disease. The extent to which improvement of aphasia represents “recovery” of function or generation of new modes of response has not been settled.
The functional supremacy of one cerebral hemisphere is fundamental to language function. There are many ways of determining that the left side of the brain is dominant: (1) by the loss of speech that occurs with disease in parts of the left hemisphere and its preservation with lesions involving corresponding parts of the right hemisphere; (2) by preference for and greater facility in the use of the right hand, foot, and eye in most persons; (3) by the arrest of speech with a focal seizure or with electrical or magnetic stimulation of the anterior (left) language area; (4) by the injection of sodium amytal or an equivalent drug into the left internal carotid artery (the Wada test—a procedure that produces mutism for a minute or two, followed by misnaming, including perseveration and substitution; misreading; and paraphasic speech); (5) by dichotic listening, in which different words or phonemes are presented simultaneously to the two ears (yielding a right ear–left hemisphere advantage); (6) by observing increases in cerebral blood flow during language processing; and (7) by lateralization of speech and language functions following commissurotomy.