What we talk about when we talk about access deficits

Abstract

Semantic impairments have been divided into storage deficits, in which the semantic representations themselves are damaged, and access deficits, in which the representations are intact but access to them is impaired. The behavioural phenomena that have been associated with access deficits include sensitivity to cueing, sensitivity to presentation rate, performance inconsistency, negative serial position effects, sensitivity to number and strength of competitors, semantic blocking effects, disordered selection between strong and weak competitors, correlation between semantic deficits and executive function deficits and reduced word frequency effects. Four general accounts have been proposed for different subsets of these phenomena: abnormal refractoriness, too much activation, impaired competitive selection and deficits of semantic control. A combination of abnormal refractoriness and impaired competitive selection can account for most of the behavioural phenomena, but there remain several open questions. In particular, it remains unclear whether access deficits represent a single syndrome, a syndrome with multiple subtypes or a variable collection of phenomena, whether the underlying deficit is domain-general or domain-specific, whether it is owing to disorders of inhibition, activation or selection, and the nature of the connection (if any) between access phenomena in aphasia and in neurologically intact controls. Computational models offer a promising approach to answering these questions.

Keywords: access deficit; aphasia; computational models; lexical semantics; refractory access.

Figures

Figure 1.

A schematic diagram of the (implicit) framework underlying the storage–access distinction. The typical adult state is shown on the left—there is a collection of words (or concepts) and a mechanism for accessing them. A storage deficit is shown in the middle—some of the words (or concepts) are missing. An access deficit is shown on the right—the words (or concepts) are intact, but the access mechanism is broken.

Figure 2.

(a) A schematic of abnormal refractoriness. Following activation, there is an abnormally large and/or longer lasting refractory suppression. Solid line denotes excessive, whereas dashed line denotes normal. (b) A schematic of excessive residual activation. Following activation, there is an abnormally slow decay of activation. Solid line denotes normal, whereas dashed line denotes slow.

Figure 3.

Effect of selectivity (solid line denotes high, dashed line denotes medium and dotted line denotes low) on the mapping between relative activation and response probability. Lower selectivity approaches a linear relationship such that any incremental increase in relative activation produces an (almost) equivalent increase in response probability. Higher selectivity approaches a threshold relationship such that suprathreshold relative activation will (almost) always produce that response and subthreshold relative activation will (almost) never produce a response.