Semantic cognition refers to our ability to use, manipulate and generalize knowledge that is acquired over the lifespan to support innumerable verbal and non-verbal behaviours. This Review summarizes key findings and issues arising from a decade of research into the neurocognitive and neurocomputational underpinnings of this ability, leading to a new framework that we term controlled semantic cognition (CSC). CSC offers solutions to long-standing queries in philosophy and cognitive science, and yields a convergent framework for understanding the neural and computational bases of healthy semantic cognition and its dysfunction in brain disorders.

Different neuropsychological populations implicate diverse cortical regions in semantic memory: semantic dementia (SD) is characterized by atrophy of the anterior temporal lobes whilst poor comprehension in stroke aphasia is associated with prefrontal or temporal-parietal infarcts. This study employed a case-series design to compare SD and comprehension-impaired stroke aphasic patients directly on the same battery of semantic tests. Although the two groups obtained broadly equivalent scores, they showed qualitatively different semantic deficits. The SD group showed strong correlations between different semantic tasks--regardless of input/output modality--and substantial consistency when a set of items was assessed several times. They were also highly sensitive to frequency/familiarity and made coordinate and superordinate semantic errors in picture naming. These findings support the notion that amodal semantic representations degrade in SD. The stroke aphasia group also showed multimodal deficits and consistency across different input modalities, but inconsistent performance on tasks requiring different types of semantic processing. They were insensitive to familiarity/frequency--instead, tests of semantic association were influenced by the ease with which relevant semantic relationships could be identified and distractors rejected. In addition, the aphasic patients made associative semantic errors in picture naming that SD patients did not make. The aphasic patients' picture naming performance improved considerably with phonemic cues suggesting that these patients retained knowledge that could not be accessed without contextual support. We propose that semantic cognition is supported by two interacting principal components: (i) a set of amodal representations (which progressively degrade in SD) and (ii) executive processes that help to direct and control semantic activation in a task-appropriate fashion (which are dysfunctional in comprehension-impaired stroke aphasic patients).

Wernicke (1900, as cited in G. H. Eggert, 1977) suggested that semantic knowledge arises from the interaction of perceptual representations of objects and words. The authors present a parallel distributed processing implementation of this theory, in which semantic representations emerge from mechanisms that acquire the mappings between visual representations of objects and their verbal descriptions. To test the theory, they trained the model to associate names, verbal descriptions, and visual representations of objects. When its inputs and outputs are constructed to capture aspects of structure apparent in attribute-norming experiments, the model provides an intuitive account of semantic task performance. The authors then used the model to understand the structure of impaired performance in patients with selective and progressive impairments of conceptual knowledge. Data from 4 well-known semantic tasks revealed consistent patterns that find a ready explanation in the model. The relationship between the model and related theories of semantic representation is discussed.

The clinical presentation of patients with semantic dementia is dominated by anomia and poor verbal comprehension. Although a number of researchers have argued that these patients have impaired comprehension of non-verbal as well as verbal stimuli, the evidence for semantic deterioration is mainly derived from tasks that include some form of verbal input or output. Few studies have investigated semantic impairment using entirely non-verbal assessments and the few exceptions have been based on results from single cases ([3]: Breedin SD, Saffran EM, Coslett HB. Reversal of the concreteness effect in a patient with semantic dementia. Cognitive Neuropsychology 1994;11:617-660, [12]: Graham KS, Becker JT, Patterson K, Hodges JR. Lost for words: a case of primary progressive aphasia? In: Parkin A, editor. Case studies in the neuropsychology of memory, East Sussex: Lawrence Erlbaum, 1997. pp. 83-110, [21]: Lambon Ralph MA, Howard D. Gogi aphasia or semantic dementia? Simulating and assessing poor verbal comprehension in a case of progressive fluent aphasia. Cognitive Neuropsychology, (in-press). This study employed sound recognition and semantic association tasks to investigate the nature of the verbal and non-verbal comprehension deficit in 10 patients with semantic dementia. The patients were impaired on both verbal and non-verbal conditions of the assessments, and their accuracy on these tasks was directly related to their scores on a range of other tests requiring access to semantic memory. Further analyses revealed that performance was graded by concept and sound familiarity and, in addition, identified significant item consistency across the different conditions of the tasks. These results support the notion that the patients' deficits across all modalities were due to degradation within a single, central network of conceptual knowledge. There were also reliable differences between conditions. The sound-picture matching task proved to be more sensitive to semantic impairment than the word-picture matching equivalent, and the patients performed significantly better on the picture than word version of a semantic association test. We propose that these differences arise directly from the nature of the mapping between input modality and semantic memory. Words and sounds have an arbitrary relationship with meaning while pictures benefit from a degree of systematicity with conceptual knowledge about the object.

Objectives-To investigate the prevalence of changes in mood, personality, and behaviour in frontotemporal dementia (FTD) and Alzheimer's disease (AD) and hence, which features reliably distinguish between them. To establish whether the frontal and temporal variants of FTD are characterised by diVerent behavioural changes. Methods-A questionnaire was designed to assess a wide range of neuropsychiatric changes; it incorporated features reported in previous studies of FTD and components of the neuropsychiatric inventory. Results-Factor analysis showed four robust and meaningful symptom clusters: factor 1-stereotypic and eating behaviour; factor 2-executive dysfunction and self care; factor 3-mood changes; factor 4-loss of social awareness. Only stereotypic and altered eating behaviour and loss of social awareness reliably diVerentiated AD from FTD with no eVect of disease severity. By contrast, executive dysfunction, poor self care, and restlessness showed a significant eVect of disease severity only, with the more impaired patients scoring more highly. Changes in mood were found to be equally prevalent in the three patient groups. Analysis of individual symptoms showed increased rates of mental rigidity and depression in the patients with semantic dementia compared with those with fv FTD. Conversely, the latter group showed greater disinhibition. Discriminant function analysis correctly classified 71.4% overall and 86.5% of the patients with AD. Conclusions-This questionnaire disclosed striking diVerences between patients with FTD and AD, but only stereotypic behaviour, changes in eating preference, disinhibition, and features of poor social awareness reliably separated the groups. The patients with fv FTD and semantic dementia were behaviourally very similar, reflecting the involvement of a common network, the ventral frontal lobe, temporal pole, and amygdala. Dysexecutive symptoms and poor self care were found to be aVected by the severity of the disease, reflecting perhaps spread to dorsolateral prefrontal areas relatively late in the course of both FTD and AD. This questionnaire may be of value in the diagnosis and the monitoring of therapies.