Bilateral lesions of the transverse gyri of Heschl, while rare, are known to cause a central deafness. Henschen, in his extensive review of 1,337 cases of aphasia that had been reported up to 1922, found 9 in which these parts were destroyed by restricted vascular lesions, with resulting deafness. There are now many more cases of this type in the medical literature; lesions in other parts of the temporal lobes have no effect on hearing. These observations are the basis for the localization of the primary auditory receptive area in the cortex of the transverse gyri (chiefly the first) on the posterosuperior surface of the temporal lobe, deep within the sylvian fissure (areas 41 and 42). Subcortical lesions, which interrupt the fibers from both medial geniculate bodies to the transverse gyri, as in the two cases described by Tanaka and colleagues, have the same effect. With left-sided superotemporal lesions, there is usually an aphasia because of the proximity of the transverse gyri to the superotemporal association cortex. Hécaen has remarked that “cortically deaf” persons may seem to be unaware of their deafness, a state similar to that of blind persons who act as though they could see (the latter, called Anton syndrome, is described further on).
For a long time, unilateral lesions of Heschl gyri were believed to have no effect on hearing; it has been found, however, that subtle deficits can be detected with careful testing. If very brief auditory stimuli are delivered, the threshold of sensation is elevated in the ear opposite the lesion. Also, while unilateral lesions do not diminish the perception of pure tones or clearly spoken words, the ear contralateral to a temporal lesion is less efficient if the conditions of hearing are rendered more difficult (binaural testing). For example, if words are slightly distorted (electronically filtered to alter consonants), they are heard less well in the ear contralateral to the lesion. In addition, the patient has more difficulty in equalizing the volume of sounds that are presented to both ears and in perceiving rapidly spoken numbers or different words presented to the two ears (dichotic listening). Few of these changes are evident by clinical examination.
Lesions of the secondary (unimodal association) zones of the auditory cortex—area 22 and part of area 21—have no effect on the perception of sounds and pure tones. However, the appreciation of complex combinations of sounds is severely impaired. This impairment, or auditory agnosia, takes several forms: inability to recognize sounds, different musical notes (amusia), or words and presumably each has a slightly different anatomic basis.
In agnosia for sounds, auditory sensations cannot be distinguished from one another. Such varied sounds as the tinkling of a bell, the rustling of paper, running water, and a siren all sound alike. The condition is usually associated with word deafness (see “Pure Word Deafness” in Chap. 22 and in the following text) or with amusia. Hécaen observed an agnosia for sounds alone in only two cases; one patient could identify only half of 26 familiar sounds, and the other could recognize no sound other than the ticking of a watch. Yet in both patients, the audiogram was normal, and neither had trouble understanding spoken words. In both, the lesion involved the right temporal lobe and the corpus callosum was intact.