Agnosia

[1] It is usually associated with brain injury or neurological illness, particularly after damage to the occipitotemporal border, which is part of the ventral stream.

[25] 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.

[24] For instance, if an experimenter were to say DOG aloud, the utterance would activate and inhibit various words within the subjects lexical interface: 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.

In order for an individual to be diagnosed with agnosia, they must only be experiencing a sensory deficit in a single modality.

[3] Individuals are usually shown pictures of human faces that may be familiar to them such as famous actors, singers, politicians or family members.

[citation needed] Initially many individuals with a form of agnosia are unaware of the extent to which they have either a perceptual or recognition deficit.

At the National Institute of Neurological Disorders and Stroke (NINDS) they support research for rare diseases like agnosia.

It was introduced by Sigmund Freud in 1891:[27] "For disturbances in the recognition of objects, which Finkelnburg classes as asymbolia, I should like to propose the term 'agnosia'."

Prior to Freud's introduction of the term, some of the first ideas about agnosia came from Carl Wernicke, who created theories about receptive aphasia in 1874.

He noted that individuals with receptive aphasia did not possess the ability to understand speech or repeat words.

He believed that receptive aphasia was due to lesions of the posterior third of the left superior temporal gyrus.

Due to these lesions, Wernicke believed that individuals with receptive aphasia had a limited deafness for certain sounds and frequencies in speech.

[8] After Wernicke, came Kussmaul in 1877 who attempted to explain why auditory verbal agnosia, also known as word deafness, occurs.

Contrary to Wernicke's explanations, Kussmaul believed auditory verbal agnosia was the result of major destruction to the first left temporal gyrus.