Blindsight is the term commonly used to describe visually guided behaviour elicited by a stimulus falling within the scotoma (blind area) caused by a lesion of the striate cortex. Such “vision” is normally held to be unconscious and to be mediated by subcortical pathways involving the superior colliculus. Blindsight is of considerable theoretical importance since it suggests that destriate man is more like destriate monkey than had been previously believed and also because it supports the classical notion of two visual systems. It is also of potential clinical importance, since it has been claimed recently that systematic practice in blindsight can lead to the recovery of normal visual function in patients with cortical lesions. From a review of the literature it is concluded that all of the phenomena of blindsight can be attributed either to light scatter into unimpaired parts of the visual field or to residual vision resulting from spared striate cortex. The possible contribution f other factors is also considered. It is concluded that blindsight studies have generally failed to control for such nonblindsight interpretations partly because of poor methodology and partly because of difficulties in defining the term “blindsight.”

Experiments were carried out to investigate the extent to which subjects can exhibit performance similar to blindsight when they are using scattered light as a cue. This was done both with hemianopic subjects (by manipulating the amount of scattered and direct light coming from a stimulus) and with normal subjects (by presenting targets within their blind spots). Good blindsight performance was observed when only scattered light was available as a cue to the subjects. It is therefore concluded that an adequate case for blindsight has not been made. It is probably impossible to demonstrate the existence of blindsight on purely behavioural grounds. What is required is the establishment of relationships between visual function and independent anatomical evidence.

Awareness of cognitive dysfunction shown by individuals with Mild Cognitive Impairment (MCI), a condition conferring risk for Alzheimer's disease (AD), is variable. Anosognosia, or unawareness of loss of function, is beginning to be recognized as an important clinical symptom of MCI. However, little is known about the brain substrates underlying this symptom. We hypothesized that MCI participants' activation of cortical midline structures (CMS) during self-appraisal would covary with level of insight into cognitive difficulties (indexed by a discrepancy score between patient and informant ratings of cognitive decline in each MCI participant). To address this hypothesis, we first compared 16 MCI participants and 16 age-matched controls, examining brain regions showing conjoint or differential BOLD response during self-appraisal. Second, we used regression to investigate the relationship between awareness of deficit in MCI and BOLD activity during self-appraisal, controlling for extent of memory impairment. Between-group comparisons indicated that MCI participants show subtly attenuated CMS activity during self-appraisal. Regression analysis revealed a highly significant relationship between BOLD response during self-appraisal and self-awareness of deficit in MCI. This finding highlights the level of anosognosia in MCI as an important predictor of response to self-appraisal in cortical midline structures, brain regions vulnerable to changes in early AD. (JINS, 2007, 13, 450–461.)

Verbal auditory agnosia implies the failure to recognize sounds in a patient who is nevertheless not deaf. We present a child referred to the ENT outpatients for suspected hearing loss investigation. At one point she had grommets inserted on the basis of a flat tympanogram but with no effect. All hearing tests, including electrocochleography and distraction tests, revealed normal hearing thresholds. At the age of three years and three months, and on direct questioning of the parents, we discovered that the child responded remarkably well to music. Paediatric neurologists made the diagnosis of verbal auditory agnosia. The condition is very similar to another acquired language disorder called Landau-Kleffner syndrome. It is unusual for such a case to present primarily to an ENT surgeon.