Lesions of posterior parietal cortex (PPC) in humans result in a constellation of symptoms often referred to as the “Parietal syndrome”

Since its original description the core of the PS consisted of optic ataxia (OA), psychic paralysis of gaze, and impaired spatial attention, now referred to as hemineglect (HN).

In subsequent years, a number of action disorders, such as constructional apraxia have also been described after parietal damage, calling for an interpretation of the consequences of parietal lesions in terms of a general impairment of spatial cognition. A century of intensive neuropsychological study today offers a picture of the PS which is more refined than that provided by earlier studies, in at least three main respects, i.e., the analysis of the behaviour of parietal patients, the anatomical localization of the lesions responsible for the different symptoms, as well as the conceptual frame/s adopted to understand them. Yet, the physiological mechanisms whose collapse results in the deficits typical of damage of the PPC remain elusive.

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