There is no uniform performance among patients with<unk> ; therefore it is not possible to attribute specific phonetic or phonological deficits to the syndrome. In order to diagnose AVA, two intact abilities need to be established: * Words that are heard must have undergone adequate acoustic analysis as evidenced by correct repetition; * The semantic representation of the word must be intact as evidenced by immediate comprehension of the word when presented in written form. If both of these criteria are met and lack of<unk><unk>  comprehension is apparent, a diagnosis of AVA may follow. In at least one instance, the Boston Diagnostic Aphasia Examination has been used to profile AVA. This method was able to show that the patient experienced marked difficulty in speech perception with minor to no minor deficits in production, reading, and writing, fitting the profile of AVA. While this provides a well-known example, other<unk> -audio test batteries can and have also been used to diagnose pure speech deafness. Cognitive deficits<unk>  is the inability to distinguish phonemes. In some patients with unilateral<unk> , there is evidence that the ability to acoustically process speech signals is affected at the prephonemic level, preventing the conversion of these signals into phonemes. There are two predominate hypotheses that address what happens within the language center of the brain in people that have AVA. One of the hypotheses is that an early stage of<unk>  analysis is impaired. The fact that AVA patients have the ability to read shows that both the semantic system and the speech output lexicon are intact. The second hypotheses suggests that there is either a complete or partial disconnection of the<unk>  input lexicon from the semantic system. This would suggest that entries in the lexicon can still be activated but they cannot go on to cause subsequent semantic activation. In relation to these two different hypotheses, researchers in one study differentiated between two different types of AVA. According to this study, one form of AVA is a deficit at the prephonemic level and is related to the inability to comprehend rapid changes in sound. This form of AVA is associated with bilateral temporal lobe lesions. Speech perception in patients with this form of AVA has been shown to improve significantly in understanding when the pace of speech is drastically slowed. The second type of AVA that the study discusses is a deficit in linguistic discrimination that does not adhere to a prephonemic pattern. This form is associated with left unilateral temporal lobe lesions and may even be considered a form of Wernicke's aphasia. Often individuals diagnosed with<unk>  are also incapable of discriminating between non-verbal sounds as well as speech. The underlying problem seems to be temporal in that understanding speech requires the discrimination between specific sounds which are closely spaced in time. Note that this is not unique to speech; studies using non-speech sounds closely spaced in time (dog bark, phone ring, lightning, etc.) have shown that those with<unk>  are unable to discriminate between those sounds in the majority of cases, though a few putative examples of speech-specific impairment have been documented in the literature. Neurological deficits<unk>  is caused by bilateral damage, often in the form of cerebrovascular accidents which form as a result of an embolism, to the posterior superior temporal lobes or disruption of connections between these areas. A unilateral lesion in the left or right superior temporal lobe can also result in pure word deafness, this being much more common in the left hemisphere than the right. It is often associated with lesions to the left posterior superior temporal lobe, but no such unilateral case has yet been documented without damage to the white matter tract connecting superior temporal lobes bilaterally or bilateral damage to the superior temporal lobe. In cases where unilateral damage to the left superior temporal lobe has been documented, patients exhibited problems processing both speech and non-speech sounds (in other words, not typical of<unk> . These facts, in combination with the existence of cases of damage to these white matter tracts without detectable cortical damage, in combination with cases of pure word deafness resulting enlargement of the third ventricle alone suggest that the disorder results from damage to the left-right superior temporal circuit rather than the superior temporal area on one hemisphere or the other. Many of the bilateral cases share one essential feature: after the first (unilateral) lesion, speech perception was typically intact after an initial period of disturbance. Only after the second lesion (in the other hemisphere) were permanent speech perception problems the consistent outcome. The fact that most of these patients only manifested<unk>  subsequent to the second lesion supports the hypothesis that both sides of the superior temporal gyrus are necessary.<unk>  is rarely diagnosed in its pure form.<unk>  can present as the result of acute damage or chronic, progressive degeneration over time. Cases have been documented that result from severe acute head trauma resulting in bilateral temporal lobe damage. In contrast,<unk>  has also been documented to present progressively over several years. In one such case, the patient exhibited progressive word deafness over a 9-year period but did not exhibit any other cognitive of mental deterioration. This patient was found, using MRIs, to have cortical atrophy in the left superior temporal lobe region.
Auditory verbal agnosia
Visuospatial dysgnosia
Apperceptive agnosia
Integrative agnosia
Hemispatial neglect
Phonagnosia
Associative visual agnosia
Social-emotional agnosia