The impact of synaptic depression following brain damage: A connectionist account of "access/refractory" and "degraded-store" semantic impairments

Abstract

Neuropsychological studies of patients with acquired semantic impairments have yielded two distinct and contrasting patterns of performance in a spoken-word/picture-matching task (Warrington & Cipolotti, 1996). Patients labeled access/refractory are strongly influenced by presentation rate, semantic relatedness of distractors, and repetition, yet they seem relatively unaffected by lexical frequency. Degraded-store patients, on the other hand, are strongly affected by lexical frequency but are less affected by presentation rate, semantic relatedness, or repetition. Our account of these patterns of performance is based on the distinction between two different types of neurological damage:(1) damage to neuromodulatory systems that function to amplify neural signals while suppressing normal refractory-like effects and (2) damage to connections between groups of neurons that encode semantic information and are sensitive to frequency/familiarity. We present a connectionist model that learns to map spoken-word input to semantic representations and that incorporates a particular form of neural refractoriness referred to as synaptic depression, as well as a simple form of neuromodulation. We show that the model is capable of accounting for the contrasting patterns of semantic impairment under these two different forms of damage and, furthermore, demonstrate how it is capable of handling several documented cases that are exceptions to the basic patterns of impairment. Several predictions and limitations of the present model are discussed.

Distinct loci of lexical and semantic access deficits in aphasia: Evidence from voxel-based lesion-symptom mapping and diffusion tensor imaging

“…Models of lexical access in language production assume that semantic interference in naming arises when accessing lexical representations from meanings (Damian et al, 2001;Howard et al, 2006;Levelt et al, 1999;Oppenheim et al, 2010;Roelofs, 1992, whereas theories of semantic interference in language comprehension assume that the effect arises when accessing semantic representations of a given word (Campanella & Shallice, 2011;Forde & Humphreys, 1997Gotts & Plaut, 2002;Warrington & Cipolotti, 1996;Warrington & McCarthy, 1983, 1987. Our findings demonstrating separate neural loci of semantic interference in language production and comprehension provide support for this hypothesis.…”

“…We tested subjects with left hemisphere stroke using structural magnetic resonance and diffusion tensor imaging to investigate first, whether semantic interference in language production and comprehension arises at different brain loci as suggested by cognitive models (e.g., Belke, 2013;Damian et al, 2001;Howard et al, 2006;Levelt et al, 1999;Oppenheim et al, 2010;Roelofs, 1992Gotts & Plaut, 2002;Warrington & Cipolotti, 1996) and second, whether interference in both modalities share a common neural mechanism that acts to resolve competition from co-activated same category representations (Badre, Poldrack, Paré-Blagoev, Insler, & Wagner, 2005;Badre & Wagner, 2007;Jefferies & Lambon Ralph, 2006;Novick, Trueswell, &Thompson-Schill, 2005cf. Biegler et al, 2008;Hamilton & Martin, 2005;McCarthy & Kartsounis, 2000;Schnur et al, 2006Schnur et al, , 2009Wilshire & …”

“…cycles reflected impairments due to greater control demands, or would have occurred more generally for both related and unrelated conditions, thus reflecting a generalized refractory impairment characterized by abnormally prolonged activation (or inhibition) of semantic representations which renders them temporarily inaccessible for a brief period of time following their initial activation (Warrington & Cipolotti, 1996;Warrington and McCarthy, 1983; see also Gotts & Plaut, 2002). 9 We suggest then that (cognitive control) selection and refractory impairments reflect functionally distinct disorders.…”

The Differential Contributions of pFC and Temporo-parietal Cortex to Multimodal Semantic Control: Exploring Refractory Effects in Semantic Aphasia

“…Finally, using an implemented model of semantic processing, Gotts and Plaut (2002) demonstrated that refractory effects can result from neuromodulatory deficits, which generate increased synaptic depression, thus reducing the efficiency with which new stimuli can override current processing during the refractory period. Although this theory does not explicitly consider the issue of modality, if extended to an amodal semantic system, it would predict refractory effects for both verbal and nonverbal tasks, with the effect for both arising from the same general neuromodulatory deficit.…”

Persistence and accommodation in short-term priming and other perceptual paradigms: temporal segregation through synaptic depression

“…Also, as mentioned earlier, Laing and Chow (2002) simulated binocular rivalry using synaptic depression mechanisms. Most recently, damage to synaptic depression processes has been proposed as the mechanism underlying an acquired neurophsychological deficit in semantic processing referred to as "access/refractory" (Gotts & Plaut, 2002).…”