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

• Published in: Cognitive, affective, & behavioral neuroscience affective, & behavioral neuroscience, 2002-09, Vol.2 (3), p.187-213
• Main Authors: GOTTS, Stephen J, PLAUT, David C
• Format: Article
• Language: English
• Subjects: Adult and adolescent clinical studies; Biological and medical sciences; Brain Damage, Chronic - complications; Brain Damage, Chronic - physiopathology; Humans; Language Disorders - classification; Language Disorders - etiology; Language Disorders - physiopathology; Long-Term Synaptic Depression - physiology; Medical sciences; Mental Processes - physiology; Models, Neurological; Nerve Net - physiology; Organic mental disorders. Neuropsychology; Psychology. Psychoanalysis. Psychiatry; Psychopathology. Psychiatry; Refractory Period, Electrophysiological - physiology; Semantics
• ISSN: 1530-7026; 1531-135X
• DOI: 10.3758/CABN.2.3.187

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.