<unk>  can be caused by lesions in various parts of the inferior occipital areas (occipital face area), fusiform gyrus (fusiform face area), and the anterior temporal cortex. Positron emission tomography (PET) and fMRI scans have shown that, in individuals without<unk> , these areas are activated specifically in response to face stimuli. The inferior occipital areas are mainly involved in the early stages of face perception and the anterior temporal structures integrate specific information about the face, voice, and name of a familiar person. Acquired<unk>  can develop as the result of several neurologically damaging causes. Vascular causes of<unk>  include posterior cerebral artery infarcts (PCAIs) and hemorrhages in the infero-medial part of the temporo-occipital area. These can be either bilateral or unilateral, but if they are unilateral, they are almost always in the right hemisphere. Recent studies have confirmed that right hemisphere damage to the specific temporo-occipital areas mentioned above is sufficient to induce<unk> . MRI scans of patients with<unk>  showed lesions isolated to the right hemisphere, while fMRI scans showed that the left hemisphere was functioning normally. Unilateral left temporo-occipital lesions result in object agnosia, but spare face recognition processes, although a few cases have been documented where left unilateral damage resulted in<unk> . It has been suggested that these face recognition impairments caused by left hemisphere damage are due to a semantic defect blocking retrieval processes that are involved in obtaining person-specific semantic information from the visual modality. Other less common etiologies include carbon monoxide poisoning, temporal lobectomy, encephalitis, neoplasm, right temporal lobe atrophy, injury, Parkinson's disease, and Alzheimer's disease.
Prosopagnosia
Apperceptive agnosia
Integrative agnosia
Phonagnosia
Finger agnosia
Visuospatial dysgnosia
Autotopagnosia
Metamorphopsia