general auditory agnosia, this disorder is likely under-diagnosed because patients are often not aware of their disorder, and thus don't seek medical intervention. throughout the 20th century, all reported non-verbal auditory agnosia patients had bilateral or right temporal lobe damage. for this reason, the right hemisphere was traditionally attributed with the perception of environmental sounds. however, tanaka et al reported 8 patients with non-verbal auditory agnosia, 4 with right hemisphere lesions and 4 with left hemisphere lesions. saygin et al also reported a patient with damage to the left auditory cortex. the underlying deficit in non-verbal auditory agnosia appears to be varied. several patients were characterized by impaired discrimination of pitch whereas others reported with impaired discrimination of timbre and rhythm (discrimination of pitch was relatively preserved in one of these cases). in contrast, to patients with pure word deafness and general auditory agnosia, patients with non-verbal auditory agnosia were reported impaired at discriminating long gaps between click sounds, but impaired at short gaps. a possible neuroanatomical structure that relays longer sound duration was suggested by tanaka et al. by comparing the lesions of two cortically deaf patients with the lesion of a word deafness patient, they proposed the existence of two thalamocortical pathways that inter-connect the mgn with the auditory cortex. they suggested that spoken words are relayed via a direct thalamocortical pathway that passes underneath the putamen, and that environmental sounds are relayed via a separate thalamocortical pathway that passes above the putamen near the parietal white matter. amusia auditory agnosia patients are often impaired in the discrimination of all sounds, including music. however, in two such patients music perception was spared and in one patient music perception was enhanced. the medical literature reports of 33 patients diagnosed with an exclusive deficit for the discrimination and recognition of musical segments (i.e., amusia). the damage in all these cases was localized to the right hemisphere or was bilateral. (with the exception of one case.) the damage in these cases tended to focus around the temporal pole. consistently, removal of the anterior temporal lobe was also associated with loss of music perception, and recordings directly from the anterior auditory cortex revealed that in both hemispheres, music is perceived medially to speech. these findings therefore imply that the loss of music perception in auditory agnosia is because of damage to the medial anterior stg. in contrast to the association of amusia specific to recognition of melodies (amelodia) with the temporal pole, posterior stg damage was associated with loss of rhythm perception (arryhthmia). conversely, in two patients rhythm perception was intact, while recognition/discrimination of musical segments was impaired. amusia also dissociates in regard to enjoyment from music. in two reports, amusic patients, who weren't able to distinguish musical instruments, reported that they still enjoy listening to music. on the other hand, a patient with left hemispheric damage in the amygdala was reported to perceive, but not enjoy, music. word meaning deafness / associative auditory agnosia in 1928, kleist suggested that the etiology of word deafness could be due either to impaired perception of the sound (apperceptive auditory agnosia), or to impaired extraction of meaning from a sound (associative auditory agnosia). this hypothesis was first tested by vignolo et al (1969), who examined unilateral stroke patients. they reported that patients with left hemisphere damage were impaired in matching environmental sounds with their corresponding pictures, whereas patients with right hemisphere damage were impaired in the discrimination of meaningless noise segments. the researchers then concluded that left hemispheric damage results in associative auditory agnosia, and right hemisphere damage results in apperceptive auditory agnosia. although the conclusion reached by this study could be considered over-reaching, associative auditory agnosia could correspond with the disorder word meaning deafness. patients with word meaning deafness are characterized by impaired speech recognition but intact repetition of speech and left hemisphere damage. these patients often repeat words in an attempt to extract its meaning (e.g., "jar....jar....what is a jar?"). in the first documented case, bramwell (1897 - translated by ellis, 1984) reported a patient, who in order to comprehend speech wrote what she heard and then read her own handwriting. kohn and friedman, and symonds also reported word meaning deafness patients who are able to write to dictation. in at least 12 cases, patients with symptoms that correspond with word meaning deafness were diagnosed as auditory agnosia. unlike most auditory agnosia patients, word meaning deafness patients are not impaired at discriminating gaps of click sounds. it is yet unclear whether word meaning deafness is also synonymous with the disorder deep dysphasia, in which patients cannot repeat nonsense words and produce semantic paraphasia during repetition of real words. word meaning deafness is also often confused with transcortical sensory aphasia, but such patients differ from the latter by their ability to express themselves appropriately orally or in writing. neurological mechanism auditory agnosia (with the exception of non-verbal auditory agnosia and amusia) is strongly dependent on damage to both hemispheres. the order of hemispheric damage is irrelevant to manifestation of symptoms, and years could take between the damage of the first hemisphere and the second hemisphere (after which the symptoms suddenly emerge). a study that compared lesion locations, reported that in all cases with bilateral hemispheric damage, at least in one side the lesion included heschl's gyrus or its underlying white matter. a rare insight into the etiology of this disorder was reported in a study of an auditory agnosia patient with damage to the brainstem, instead of cortex. fmri scanning of the patient revealed weak activation of the anterior heschl's gyrus (area r) and anterior superior temporal gyrus. these brain areas are part of the auditory 'what' pathway, and are known from both human and monkey research to participate in the recognition of sounds.