Naming

see INTRODUCTION TO SYSTEMS: Naming

Naming DS Race and AB Hillis, Johns Hopkins University School of Medicine, Baltimore, MD, USA ã 2015 Elsevier Inc. All rights reserved.

Glossary Anomia Deficit naming an item, although comprehension of the name is intact. Aphasia Deficit in the production (e.g., oral and written) or comprehension of language (e.g., reading and performing to commands). Brodmann regions (BA) Brain regions divided by differences in neuron type and architecture.

Introduction Naming is the ability to produce a word (e.g., spoken, written, and sign language), given a concept. For example, a person is likely to produce the word ‘chair’ given the concept of ‘an object with four legs and a back that is used for sitting.’ The fundamental role that naming plays in language is apparent considering that, in general, words across grammatical categories are associated with a conceptual representation (e.g., pronoun/verb/preposition/determiner/adjective for ‘She sat in the large chair.’). Although the process of naming generally goes unnoticed, everyone has occasional difficulty (e.g., retrieving the name of a relative, the name of a hotel, or an object in the basement). The relative ease of naming is somewhat deceptive, as research indicates that it is a complex process that can be disrupted at multiple points along the path from concept to word. Naming declines with normal aging. In addition, naming difficulty is the most common language impairment caused by left hemisphere stroke or neurodegenerative disease and is the most common residual deficit after recovery from most types of aphasia. This current article explores how naming is accomplished by the brain. While many aspects remain unclear or controversial, there is broad consensus that naming requires a number of cognitive processes that involve different regions of the brain, mostly in the left hemisphere, to different degrees. Damage to any one of these regions will cause a naming deficit, but the nature of the deficit will depend on the region affected.

Cognitive Model of Naming Cognitive models of naming generally agree that naming takes place across two main stages – conceptual and word form processing. The conceptual stage encompasses computation of the semantic representation of the item. We assume that all representations are ‘distributed representations’ composed

Brain Mapping: An Encyclopedic Reference

Modality-dependent Processing that is associated with a particular mode of input (e.g., vision, sound, and tactile) or output (e.g., oral and written). Modality-independent (amodal) Processing at a level of representation that encompasses all modes of representation.

of features that overlap with related representations (Dell, 1986; Dell & O’Seaghdha, 1992; Lambon, McClelland, Patterson, Galton, & Hodges, 2001; Plaut, 2002). For example, the semantic representation of ‘chair’ might have features of , , , etc., while the semantic representation of ‘stool’ might have features of , , etc., but not . Computing a semantic representation can begin with the recognition of a stimulus to be named, processed in a relevant input modality (e.g., visual and auditory), with computation of increasingly abstract representations until the representation becomes amodal. Alternatively, computation of a semantic representation can begin with an amodal concept to be expressed (e.g., something on which I can sit and lean back on), which is instantiated in a more specific semantic representation (e.g., chair). Word form processing encompasses (at least) access to a phonological or orthographic representation and the motor movements for either oral or written output. In many models, there is an intervening representation, the lemma level, which is a modality-independent lexical representation (Levelt, Roelofs, & Meyer, 1999). One of the main sources of evidence for the lemma level comes from the ‘tip-of-the-tongue’ phenomena (anomia), in which speakers have a clear concept that they want to express, but cannot retrieve either the spoken or the written word form associated with that message (Brown, 1991; Brown & McNeill, 1966; Burke, MacKay, Worthley, & Wade, 1991; Kohn et al., 1987; Shwartz, 2002). Speakers can usually give a description of the word indicating that their semantic representation is intact and that the problem is likely due to a later stage of processing (i.e., word form). The lemma level is not modality-specific, because when a person is anomic, they can neither say nor write the word. There remains controversy regarding whether the ‘lemma’ or modalityindependent lexical level is a representation with content, as proposed by some authors (Levelt et al., 1999), or a means of accessing other representations (e.g., node in a network; DeLeon et al., 2007) or even unnecessary (Caramazza, 1997). However, it is clearly necessary to compute modality-specific

http://dx.doi.org/10.1016/B978-0-12-397025-1.00267-0

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INTRODUCTION TO COGNITIVE NEUROSCIENCE | Naming

lexical representations (phonological representations for speaking and orthographic representations for writing) that serve to guide the motor plans for producing the word. Evidence that processing at these modality-specific levels of representations is independent from earlier stages comes from brain-damaged patients who are selectively impaired in naming in only one output modality, despite intact motor speech and motor writing skills. For example, one patient, who spoke fluently with clear articulation, was very poor in oral naming of objects although written naming of those objects was relatively intact, while another patient showed the opposite pattern: very poor written naming of the same objects despite relatively spared oral naming (Caramazza & Hillis, 1990). In some cases, the modality-specific impairment in naming is even specific to a single grammatical category, such as nouns or verbs (Caramazza & Hillis, 1991; Hillis & Caramazza, 1995b). Throughout the naming process, difficulty arises due to overlap between the target word and competitors. As the target is activated, competitor items that share features with the target are also activated. For example, at the conceptual stage, the concept of ‘something on which I can sit and lean back on’ may activate ‘stool’ to some degree as well as ‘chair’ because of shared features of and . It is easy to understand that individuals who have impairment at the semantic level of representation may make errors that are semantically related to the target. That is, if ‘chair’ is not available, ‘stool’ (which is partially activated) would be selected instead. However, in addition, individuals with focal injury who are not impaired at the semantic level also produce semantically related word errors in naming. These errors likely arise because the individual features in the semantic representation serve to activate the lexical representations to which they correspond. For example, activates ‘stool,’ ‘chair,’ ‘table,’ etc.; activates , , , , etc., and activates , , etc. Normally, only the lexical (or lemma) representation that corresponds to all of the features will receive maximum activation and therefore will be selected for output. However, if the target is not available (due to brain damage), a semantically related representation that is partially activated might be selected, leading to a semantic error. In this case, the individual would likely be aware of the error, but unable to correct it. Alternatively, at word form stage, might activate not only ‘chair’ but also ‘hair’ and ‘care’ and ‘chain’ and ‘change’ to some degree because of shared phonology. As the amount of overlap increases, so too does the difficulty in selecting the target over a competitor.

Neural Regions That Support the Cognitive Processes That Underlie Naming Conceptual Processing

associated with regions known for relatively modality-specific processing such as the visual, auditory, and somatosensory cortices. Damage to these regions generally results in agnosia, in which recognition of an item is impaired although basic sensory perception is intact. Importantly, with agnosia, the semantic and word form representations are intact, so that a speaker would be able to name an item if presented in the unaffected modalities. Visual agnosia is generally divided between two subtypes, apperceptive and associative. Apperceptive agnosia is thought to stem from a deficit in the perception of items. Patients generally recognize the basic features of items, such as size and color, but have difficulty using that knowledge to access a semantic representation (Grossman, Galetta, & D’Esposito, 1997). They are often unable to even copy a simple drawing. Apperceptive agnosia is associated with bilateral lesions to the occipital and occipital–temporal regions (Brodmann areas (BAs) 17, 18, and 19). With associative agnosia, patients are able to combine the perceptual features of objects as they can draw copies of objects and know whether or not two pictures are the identical. However, patients are unable to compute a semantic representation from vision, as they cannot name visual objects or point to named objects (Farah, 2004; McCarthy & Warrington, 1986). Associative agnosia is associated with bilateral lesions in the juncture of the posterior inferior temporal lobe and the occipital lobe (BAs 18, 19, and 37) or the combination of lesions in the left occipital lobe and splenium of the corpus callosum. Associative agnosia is sometimes known as optic aphasia (Farah, 2004; Hillis & Caramazza, 1995a). Auditory agnosia is characterized by deficits in processing verbal or environmental sounds (Buchtel & Stewart, 1989; Goldstein, 1974; Lewis et al., 2004; Saygin, Dick, Wilson, Dronkers, & Bates, 2003; Saygin, Leech, & Dick, 2010). Patients with verbal auditory agnosia tend to have difficulty comprehending speech although reading, writing, and speech production are relatively intact. In contrast, patients with environmental auditory agnosia have difficulty matching an environmental sound to its source. For example, a patient responded ‘cow,’ ‘baby,’ and ‘gunfire’ to the sound of a sheep, a crow, and a helicopter, respectively (Saygin et al., 2010). Auditory agnosia is associated with bilateral lesions to the middle and posterior superior temporal cortex (BAs 22, 41, and 42). Tactile agnosia is characterized by deficits in understanding what an object is when the only source of input is touch (Bohlhalter, Fretz, & Weder, 2002; Ho¨mke et al., 2009; Reed, Caselli, & Farah, 1996). However, patients are able to perceive features of objects, such as size, weight, and texture and use that knowledge to discern the difference between objects. Tactile agnosia is associated with lesions of the somatosensory cortex (BAs 1, 2, 3, and 4) and the parietal cortex (BAs 7, 39, and 40).

Modal processing Modal processing encompasses the representation of the to be named object for a particular mode of input (e.g., visual, auditory, tactile, and olfactory). Although it is not generally considered as a core aspect of semantic processing, it is often crucial for computing a multimodal semantic representation in the conceptual stage. Unsurprisingly, modal processing is

Amodal semantics Amodal semantic processing is what we think of when we think of core semantic processing. Deficits in amodal processing result in naming errors across input and output modalities. Crucially, amodal processing goes beyond language processing as deficits also affect interaction with objects.

INTRODUCTION TO COGNITIVE NEUROSCIENCE | Naming

Impairment in amodal processing is generally related to damage in the temporal lobes. More specifically, it seems that damage must be bilateral to incur significant deficits (Lambon Ralph, Cipolotti, Manes, & Patterson, 2010; Tsapkini, Frangakis, & Hillis, 2011). In particular, most of the data suggest that damage to the anterior temporal lobes affects amodal processing. Most of this evidence comes from patients with semantic variant primary progressive aphasia (svPPA, formally known as semantic dementia) or herpes encephalitis, both of which affect the anterior and inferior temporal lobes, often asymmetrically but bilaterally. svPPA is characterized by both linguistic and nonlinguistic semantic deficits in contrast to relatively normal abilities in other aspects of cognition (Snowden, Goulding, & Neary, 1989). Both naming and comprehension are affected across all input and output modalities (Lambon, Graham, Ellis, & Hodges, 1998; Lambon et al., 2001). Furthermore, patients have difficulty with nonlinguistic tasks such as matching an object to its auditory, olfactory, or tactile properties (Bozeat, Lambon Ralph, Patterson, Garrard, & Hodges, 2000; Lambon, Graham, Patterson, & Hodges, 1999). They even begin to exhibit difficulties in using items in everyday life because of trouble appreciating their meaning and what distinguishes the item from related items. For example, a person with svPPA tried to brush her teeth with shaving cream. Patients with herpes encephalitis have a similar language profile, although the course is relatively acute onset, and now recover rapidly if treated quickly with appropriate antiviral medication. Before antiviral treatment was available, patients often had a chronic semantic impairment due to permanent damage to the anterior and mesial temporal cortex. Often, the naming impairment was relatively specific to living things (animals, vegetables, and fruits).

Lexical semantics Lexical semantics refers to the computation of the representation of the meaning of a word. Impairment in lexical semantics leads to semantic errors in both production (across all input and output modalities) and comprehension of words (Hillis, Rapp, Romani, & Caramazza, 1990). Note that in contrast to amodal semantic deficits, a patient with a lexical-semantic deficit would still be able to perform nonlinguistic tasks with the conceptual representation. For example, they would know that a chair or stool, rather than a table, was for sitting, although they might name a picture of a chair as ‘table’ or match the word ‘chair’ to a picture of a table. Lexical semantic deficits are most commonly seen after focal lesions in the posterior superior temporal gyrus (BA 22), the angular gyrus (BA 39), and posterior middle temporal gyrus (BA 21), restricted to the left hemisphere (Leff et al., 2002; Hillis, Barker, et al., 2001; Hillis, Wityk, et al., 2001). Both acute and chronic lesions of left BA 22 often result in the clinical syndrome of Wernicke’s aphasia, which is characterized by occasions of fluent but meaningless speech, repetition, and writing along with impaired comprehension in conversation and reading. In the acute setting, the severity of hypoperfusion in left BA 22 correlates with the error rate in word comprehension (Hillis, Wityk, et al., 2001), and the restoration of blood flow in left BA 22 improves both comprehension and naming (Hillis & Heidler, 2002; Hillis, Barker, et al., 2001). Lesions adjacent to BA 22 (i.e., BAs 21, 39, and 40) can result

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in the clinical syndrome of transcortical sensory aphasia, which differs from Wernicke’s aphasia in that repetition is intact, but lexical semantics is also impaired (Jefferies & Lambon Ralph, 2006; Servan, Verstichel, Catala, Yakovleff, & Rancurel, 1995). In contrast to patients with svPPA or herpes encephalitis (who have bilateral temporal damage), patients with impaired lexical semantics (who have focal left temporal or inferior parietal damage) have no trouble with the meaning of objects themselves, but only the meaning of words. They use objects appropriately, and comprehension is often facilitated by pictures or gestures. Patients commit a mixture of semantic and phonological errors, as well as extended English jargon. Functional imaging data also indicate that left BA 22 is highly involved in word comprehension and production (Fridriksson & Morrow, 2005; Fridriksson, Richardson, Filmore, & Cai, 2012) as well as phonological processing. PET and FMRI studies reveal activation in the left BAs 21, 22, and 39 during a variety of lexical-semantic tasks, including picture naming and comprehension (Farias, Harrington, Broomand, & Seyal, 2005; Saur et al., 2006; Sebastian & Kiran, 2011), although posterior BA 22 is the area where activation is most reliably correlated with both naming and comprehension (Wise et al., 1991).

Lexical Access Modality-independent lexical access Lexical access involves linking the lexical-semantic representation with its phonological representation for spoken naming or orthographic representation for written naming. A problem with lexical access across all output modalities, or anomia, is characterized by oral and written naming difficulty, while comprehension and nonlinguistic knowledge remain intact. Anomia is most commonly seen in isolation after lesion in the left posterior inferior temporal gyrus (within BA 37). Lesions to this region tend to result in semantic errors for both written and spoken outputs (DeLeon et al., 2007; Raymer et al., 1997). Errors arise in picture naming, naming the source of a sound, and naming from tactile input (Tranel, Grabowski, Lyon, & Damasio, 2005). Reperfusion of left BA 37 after stroke, in the acute setting, is associated with improvement in naming but not comprehension (Hillis et al., 2006). Functional imaging studies indicate that left BA 37 is activated during oral and written naming (Emerton, Gansler, Sandberg, & Jerram, in press; Rapcsak & Beeson, 2004) and during oral reading (Cohen et al., 2000, 2002; McCandliss, Cohen, & Dehaene, 2003). However, the more medial part of BA 37, in left fusiform cortex, may be more important for early written word recognition, while the lateral part of left BA 37, in inferior temporal cortex, may be important for modalityindependent lexical access (Cohen, Jobert, Bihan, & Dehaene, 2004; Sebastian et al., 2014 for review of this evidence).

Phonological representation or spoken word form Computation of a spoken word form or phonological representation can be impaired independently of computation of a written word form. However, patients with this selective deficit are relatively rare and tend to have large lesions (Caramazza & Hillis, 1990; Ellis, Miller, & Sin, 1983; Rapp & Caramazza,

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INTRODUCTION TO COGNITIVE NEUROSCIENCE | Naming

2002). Therefore, the areas of the brain essential for spoken word form processing are not entirely clear. Acute lesions or atrophy in posterior frontal areas sometimes causes modalityindependent output deficits in oral naming or written naming of actions, even when the patients are able to speak or write names of objects (showing that it is not a motor deficit that limits their output) (Hillis, Wityk, Barker, & Caramazza, 2003; Hillis, Chang, & Breese, 2004; Hillis, Oh, & Ken, 2004). Functional imaging studies show a number of areas that are engaged during word form processing (e.g., oral naming and oral reading compared to saying ‘1, 2, 3’; Parker Jones et al., 2012), including the left middle and superior temporal gyrus, inferior frontal gyrus, and premotor cortex (BAs 21, 22, 37, 44, 45, and 6; see also Kemeny et al., 2006). However, just because an area is engaged during a task does not mean that it is necessary for the task. Lesions in these areas variably cause deficits in word form processing (Hillis, Tuffiash, Wityk, & Barker, 2002).

imaging and lesion studies will be essential in refining our models of the neural architecture underlying naming. Another important area of continuing research concerns the individual variability of brains and the impact of this variability on naming breakdown and recovery. We know from both lesion studies and functional imaging studies that there is some individual variability in the brain regions that are engaged in, or necessary for, this task. There is also variability in how well people recover from naming impairment and how much naming declines with atrophy in a critical area. This variability in part might reflect individual variability in structure–function relationships in the brain. It may also reflect fluctuations in the process within individuals. These fluctuations and individual variability are not accounted for in the model described earlier and are among its limitations.

Motor Output

This work was supported in part by grant from the National Institutes of Health, NIDCD RO1 DC 05375.

Phonetic processing involves motor planning and execution of the muscles used for speech (i.e., the articulators). Phonetic processing is most closely associated with the inferior frontal gyrus (notably Broca’s area), portions of the insular gyrus, the supplementary cortex, and the premotor cortex. Damage to these regions is associated with deficits in speech praxis or orchestration of motor plans of the lips, tongue, jaw, palate, vocal folds, and muscles of respiration to articulate speech (Ash et al., 2009; Davis et al., 2008; Trupe et al., 2013). Note that problems with speech praxis are separate from impairment in strength, tone, rate, range, or coordination of the articulatory muscles, known as dysarthria.

Discussion We have discussed evidence that the apparently simple task of naming involves a number of relatively distinct cognitive processes that depend on a number of regions in the left hemisphere. Given these results, it is crucial to point out that there is no one-to-one correspondence between a cognitive process and a particular region of the brain. While one region may be closely associated with a particular cognitive function, there are almost always multiple regions that support effective processing. One of the most important areas of continuing research is to understand how these regions work in conjunction during naming. Carefully designed functional imaging studies have demonstrated that left hemisphere perisylvian areas – such as posterior inferior frontal cortex and superior temporal cortex – are active throughout overt naming and interact with visual and heteromodal areas during early lexical access and then interact with motor and primary auditory areas during overt speech articulation (Kemeny et al., 2006). Lesion studies reveal that distinct distributions of damage across regions or nodes in this complex network underlying naming produce different types of errors and patterns of errors across tasks of oral and written naming and comprehension of various stimuli (DeLeon et al., 2007). Integration of results from functional

Acknowledgment

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