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Disorders Related to Damage in the Inferior Temporal Gyrus

Prosopagnosia

Prosopagnosia, also called face blindness, is a disorder that results in the inability to recognize or discriminate between faces. It can often be associated with other forms of recognition impairment, such as place, car, or emotional recognition.^[1] A study conducted by Gross et all in 1969 found that certain cells were selective for the shape of a monkey hand, and they observed that as the stimulus they provided began to further resemble a monkey hand, those cells became more active. A few years later, in 1972, Gross et al discovered that certain IT cells were selective for faces. Although it is not conclusive, ‘face-selective’ IT cortex cells are assumed to play a large role in facial recognition in monkeys.^[2] After the extensive research into the result of damage to the IT cortex in monkeys, it is theorized that lesions in the IT gyrus in humans result in prosopagnosia. Rubens and Benson’s 1971 study of a subject in life with prosopagnosia reveals that the patient is able to name common objects on visual presentation flawlessly, however she cannot recognize faces. Upon necropsy conducted by Benson et al, it was apparent that a discrete lesion in the right fusiform gyrus, a part of the inferior temporal gyrus, was one of the main causes of the subject’s symptoms.^[3]

A more in depth observation can be seen with the example of patient L.H. in the study conducted by N.L. Etcoff and colleagues in 1991. This 40 year-old man was involved in an automobile accident when he was 18, which resulted in severe brain injury. Upon recovery, L.H. was unable to recognize or discriminate between faces, or even recognize faces that were familiar to him before the accident. L.H. and other patients with prosopagnosia are often able to live relatively normal and productive lives despite their deficit. L.H. was still able to recognize common objects, subtle differences in shapes, and even age, sex, and “likeability” of faces. However, they use non-facial cues, such as height, hair color, and voice to differentiate between people. Non-invasive brain imaging revealed that L.H.’s prosopagnosia was a result of damage to the right temporal lobe, which contains the inferior temporal gyrus.^[4]

Deficits in Semantic Memory

Certain disorders, such as Alzheimer’s disease and semantic dementia, are characterized by a patient’s inability to integrate semantic memories, which results in patients being unable to form new memories, lacking awareness of time period, as well as lacking other important cognitive processes. Chan et al 2001 conducted a study that used volumetric magnetic resonance imaging to quantify the global and temporal lobe atrophy in semantic dementia and Alzheimer’s disease. The subjects were selected and confirmed to be in the middle of the spectrum of their respective disorders clinically, and then further confirmation came from a series of neuropsychological tests given to the subjects. The study treated the inferior temporal cortex and the middle temporal cortex as one in the same, because of the, often indistinct, border between the gyri.^[5]

The study concluded that in Alzheimer’s disease, deficits in inferior temporal structures were not the main source of the disease. Rather, atrophy in the entorhinal cortex, amygdala, and hippocampus was prominent in the Alzheimer’s inflicted subjects of the study. With respect to semantic dementia, the study concluded that “the middle and inferior temporal gyri [cortices] may play a key role” in semantic memory, and as a result, unfortunately, when these anterior temporal lobe structures are injured, the subject is left with semantic dementia. This information shows how, despite often being grouped in the same category, Alzheimer’s disease and semantic dementia are very different diseases, and are characterized by marked differences in the subcortical structures they are associated with.^[5]

Cerebral Achromatopsia

Cerebral achromatopsia is a medical disorder characterized by the inability to perceive color and to achieve satisfactory visual acuity in high light levels. Congenital achromatopsia is characterized the same way, however it is genetic, which Cerebral Achromatopsia occurs as a result of damage to certain parts of the brain. One part of the brain that is particularly integral to color discrimination is the inferior temporal cortex. A 1995 study conducted by Heywood et al was meant to highlight the parts of the brain that are important in achromatopsia in monkeys, however, it obviously sheds light on the areas of the brain related to achromatopsia in humans. In the study, one group of monkeys (group AT) received lesions in the temporal lobe anterior to V4 and the other group (group MOT) received lesions to the occiptio-temporal area that corresponds in cranial location to the lesion that produces cerebral achromatopsia in humans. The study concluded that group MOT had no impairment of their color vision while the subjects in group AT all had severe impairments to their color vision, consistent with humans diagnosed with cerebral achromatopsia.^[6] This study shows that temporal lobe areas anterior to V4, which includes the inferior temporal gyrus, play a large role in patients with Cerebral Achromatopsia.

References