Agnosia can result from
strokes,
dementia, or other
neurological disorders. It may also be trauma-induced by a head injury, brain infection, or hereditary. Additionally, some forms of agnosia may be the result of developmental disorders. Damage causing agnosia usually occurs in either the occipital or parietal lobes of the brain. Although one modality may be affected, cognitive abilities in other areas are preserved. Patients who experience dramatic
recovery from blindness experience significant to total agnosia.{{cite magazine | title = The New Yorker: From the Archives: Content The effect of damage to the
superior temporal sulcus is consistent with several types of neurolinguistic deficiencies, and some contend that agnosia is one of them. The superior temporal sulcus is vital for speech comprehension because the region is highly involved with the lexical interface. According to the 1985 TRACE II Model, the lexical interface associates sound waves (phonemes) with morphological features to produce meaningful words. This association process is accomplished by lateral inhibition/excitement of certain words within an individual's lexicon (vocabulary). For instance, if an experimenter were to say DOG aloud, the utterance would activate and inhibit various words within the subjects lexical interface: • DOG activates 3, and inhibits 0 letters in
DOG. – +3 • DOG activates 2, and inhibits 1 letters in F
OG. – +2 • DOG activates 1, and inhibits 2 letters in
DAN. – +1 The consistency of this model to agnosia is shown by evidence that bilateral lesions to the superior temporal sulcus produces 'pure word deafness' (Kussmaul, 1877), or as it is understood today, speech agnosia. Patients with pure word deafness demonstrate the inability to recognize and process speech sounds with normal auditory processing for non-speech sounds below the level of the cortex. ==Diagnosis==