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This chapter outlines approaches to top-down cognitive modelling and inferencing, and addresses functionally grounded work on affect. We describe each area and illustrate its potential for addressing questions in clinical discourse analysis. We also review recent work from neuroimaging and lesion studies to suggest some of the relevant neural systems. As usual, we draw on various disciplinary perspectives and theoretical models. Our practical motivation here is to use what works, and has potential for coding corpora in the various linguistic contexts and situations encountered doing clinical discourse analysis.
Cognitive models in general characterize information bundles of various kinds. Perhaps the most familiar are those used to represent words or word-like concepts. Models for words may be more or less detailed depending on the tolerance for elaboration within a particular framework, but morphosyntactic class, inflection and distribution features are typically indicated. How a word is pronounced – its phonological form and regular phonetic variants – will be spelt out in phonological and phonetic representations. Semantic features are often specified only at superordinate levels as in THING/EVENT or merely indexed through the use of the ‘CAPS-for-concept’ convention. Thus, the model for the lexeme ‘cat’ will include the information that it is a common count noun, with the inflectional and distributional features of this class – it can occur as head of a noun phrase and it inflects for plural number /s/. It is pronounced /kæt/.
In this and the following two chapters we present descriptive resources which allow coding of spoken discourse in terms of conversational, grammatical, pragmatic and contextual features. Features that are coded can be counted. This allows both ‘pattern finding’, a replicable way of proceeding inductively to characterizations of discourse (a specialized kind of data mining), and ‘hypothesis checking’ where analyses in terms of the presence, absence, frequency and/or co-occurrence of discourse features are hypothesized to be associated with particular disorders, neurocognitive states, or changes in neurocognitive states.
Our goal is pragmatic: we do not enter into debates or account for the historical development of particular concepts or constructs, but present criteria for description that allow understanding and reliable coding of discourse features. Often this means that we are presenting ‘hybrid’ models, synthesized from works in functional, ethnographic, interactional and formal linguistic traditions. We refer readers to these works but discuss them only when such discussion seems essential for understanding.
The order of presentation, from conversational to contextual analysis, is intended to proceed from the familiar to, perhaps, less familiar ways of describing discourse. However, as is inevitably the case, some terms appear that presuppose knowledge of others presented later. For the most part, we address this by providing examples and/or glosses of terms and references. We use normative examples rather than examples from clinical contexts in presenting the grammar. Normative examples are practical insofar as they do serve to illustrate without the addition of marked features or other distractions.
Discourse represents that aspect of mental activity that most clearly reflects the intimate and over-lapping connections among cognition, language, and communication.
(Ulatowska et al. 1985)
What is clinical discourse analysis?
Clinical discourse analysis is the term we use to describe the analysis of language behaviour observed in clinical contexts. Language behaviour includes well-defined areas of clinical research addressing syntax, vocabulary, phonology, conversation skills and cohesion. It also includes areas less commonly described in clinical research such as argument roles, situational features and functional variation. The focus of clinical discourse analysis is natural language behaviour which requires examination of all these aspects of language use. Even the smallest of texts require analysis that can explore multivariate features.
Consider the following sentence:
(1) I can remember my Mom.
It is extracted from a brief sample of spoken discourse elaborated below. The sentence has an interactional function: it makes a statement which is modalized for capacity (can). It has a predicate that references a cognitive process (remember) and two argument roles, an experiencer (I) and a percept (my mom). It has an unmarked clause order: subject occurs first in English statements unless there is a reason to emphasize some other element of structure. One might also assume that the speaker interprets the situation as an informal one in that she chooses to refer to her mother as Mom rather than mother.
All discourse is produced in context and interpretation depends on contexts of production and interpretation being, in some measure, shared. Early ethnographic work addressed context dependency by positing contexts of culture and context of situation (Malinowski 1923; 1935; Firth 1957). Context of culture accounted for sets of culturally specific beliefs, expectations and practices in terms of which people interpret events around them. Context of situation referred to patterns of behaviour and talk which appear so regularly in association with a particular activity that they are understood as (abstract characterizations of) the function of the situation type. Behaviours which do not reflect some expected pattern can be interpreted as irrelevant, and behaviours which appear totally unrelated to the contexts in which they occur may be judged uninterpretable.
Later work by Halliday, Hasan, Gregory, Martin and others refined and developed ideas of context. Our view is once again a hybrid, informed by Halliday's ethnographic perspective (e.g. 1977; 1978; 1984; 1994), by our awareness that contexts are significantly matters of what speakers know (e.g. van Dijk 1977; 2006; van Dijk and Kintsch 1983; Gregory 1988), and by work in AI, psychology and discourse analysis on top-down cognitive models as to what ‘contextual knowledge’ might be like. The latter approaches (and ours) differ from traditional functionalist and ethnographic approaches in explicitly situating context in neurocognitive domains of semantic and episodic memory (see also van Dijk 2006).
In this chapter, we outline in sequence a grammar for specifying interactional, ideational and organizational features of discourse in English. We use a functional organization for the grammar because we find this perspicuous for discourse analysis. The grammar owes much to Michael Gregory (2009a; 2009b). However, in many cases our approach is once again hybrid; we present a model that draws on social and cognitive perspectives on language, based on our experience of what works. Section 4.1 presents a grammar of interaction. In Section 4.2 we outline the grammar of ideation and Section 4.3 presents the grammar of organization. We presuppose that readers have a basic syntax for English. As much as possible, technical and model-specific terms are limited. Appendix A presents basic grammatical terminology and Appendix B lists the coding options suggested in this chapter.
A grammar of interaction
The interaction relationship has to do, initially, with two types of activity speakers can engage in. The first involves the negotiation of role relationships relative to an addressee and the second involves speakers' expressions of attitude and evaluations. Role relationships are most easily understood in institutional settings with highly generic situation types such as the classroom, court room or clinic, where boundaries may seem relatively fixed: teacher/ student, judge/defendant, doctor/patient, nurse/patient are examples of such role relationships (Goffman 1959; 1961). Less obviously hierarchic and institutionally dependent are peer relationships among colleagues, friends, siblings and partners.
In Chapter 3 we defined the terms Clause and Utterance (pp. 29–32). Here we include brief definitions for convenient reference. The reader is referred to Chapter 3 (pp. 29–32) for broader definitions and examples.
English Clauses can be defined syntactically as consisting of a verb, its arguments and adjuncts as in Cosmo bit Piper yesterday. Independent clauses can also be used alone to ask a question, make a statement or exclamation, or give a command. A simple Clause is also typically spoken as a single tone group.
Meaningful speech phenomena which do not meet the criteria for clause such as incomplete utterances, minimal responses, idiosyncratic vocalizations, and isolated hesitation fillers are labelled as utterances. Utterance refers to any unit which can be assigned a speech function, and/or has a distinct tone group, and/or is a linguistic signal of ideational, interactional, or organizational information about a speaker's message.
MORPHEMES
Morphemes are smallest contrastive units in the grammar. Rabbit, dog, -s, in dogs, -ed in called, -ity in fatality, un- in unhappy, brush in toothbrush are all morphemes. None of these items can be further analysed. For instance, rabbit refers to a small furry long-eared animal that hops, but no part of rabbit is associated with one of these meanings. Morphemes may or may not be words: Whereas rabbit is a word, -s in dogs signifies plural but does not occur as a word.
Words may be simple (e.g. rabbit/dog), compound (toothbrush) or complex (fatality/unhappy).
Intercellular coupling by gap junctions is one of the main features of glial cells, but very little is known about this aspect of satellite glial cells (SGCs) in sympathetic ganglia. We used the dye coupling method to address this question in both a prevertebral ganglion (superior mesenteric) and a paravertebral ganglion (superior cervical) of mice. We found that in control ganglia, the incidence of dye coupling among SGCs that form the envelope around a given neuron was 10–20%, and coupling between SGCs around different envelopes was rare (1.5–3%). The dye injections also provided novel information on the structure of SGCs. Following peripheral inflammation, both types of coupling were increased, but most striking was the augmentation of coupling between SGCs forming envelopes around different neurons, which rose by 8–14.6-fold. This effect appeared to be non-systemic, and was blocked by the gap junction blocker carbenoxolone. These changes in SGCs may affect signal transmission and processing in sympathetic ganglia.
There is a growing body of evidence that cytokines contribute to both induction and maintenance of neuropathic pain derived from changes in dorsal root ganglia (DRG), including the activity of the primary sensory neurons and their satellite glial cells (SGC). We used immunofluorescence and in situ hybridization methods to provide evidence that chronic constriction injury (CCI) of the sciatic nerve induces synthesis of interleukin-6 (IL-6) in SGC, elevation of IL-6 receptor (IL-6R) and activation of signal transducer and activator of transcription 3 (STAT3) signalling. Unilateral CCI of the rat sciatic nerve induced mechanoallodynia and thermal hyperalgesia in ipsilateral hind paws, but contralateral paws exhibited only temporal changes of sensitivity. We demonstrated that IL-6 mRNA and protein, which were expressed at very low levels in naïve DRG, were bilaterally increased not only in L4-L5 DRG neurons but also in SGC activated by unilateral CCI. Besides IL-6, substantial increase of IL-6R and pSTAT3 expression occurred in SGC following CCI, however, IL-6R associated protein, gp130 levels did not change. The results may suggest that unilateral CCI of the sciatic nerve induces bilateral activation of SGC in L4-L5 DRG to transduce IL-6 signalling during neuroinflammation.
Dorsal root ganglia (DRG) respond to peripheral nerve injury by up-regulating nitric oxide (NO) production by neurons and glia in addition to local fibroblasts, endothelium and macrophages. We hypothesise that NO produced from these cells has specific roles. We have shown that when neuronal NO synthase (nNOS) is blocked in axotomised DRG, neurons undergo degenerative changes (Thippeswamy et al., 2001, 2007a). Further, we demonstrated that increased neuronal NO production, in response to axotomy/growth factor-deprivation in vitro, signals glial cells to produce trophic factors to support neuronal survival (Thippeswamy et al., 2005a). Recently, we found that treating satellite glia–neuron co-cultures with nNOS inhibitor, 7-nitroindazole (7NI), decreases the number of nestin+ cells that show neuron-like morphology. Cultured/axotomised DRG also upregulate inducible NOS (iNOS) in non-neuronal cells. Therefore, it is plausible that degenerative changes following nNOS inhibition are also due to iNOS-mediated excessive NO production by non-neuronal cells, which indeed is cytotoxic. NG-nitro-l-arginine methylester (L-NAME), the pan NOS inhibitor did not significantly change nNOS+ neuron number in axotomised DRG compared to 7NI suggesting that iNOS-mediated NO contributes to the degenerative process. In this paper, these findings from our and others' past work on NO-mediated neuron–glia signalling in axotomised DRG are discussed.
The role of adenosine-5′-triphosphate (ATP) and of the ligand-gated P2X3 receptor in neuronal dorsal root ganglia (DRG) pain transmission is relatively well established. Much less is known about the purinergic system in trigeminal ganglia (TG), which are involved in certain types of untreatable neuropathic and inflammatory pain, as well as in migraine. Emerging data suggest that purinergic metabotropic P2Y receptors on both neurons and satellite glial cells (SGCs) may also participate in both physiological and pathological pain development. Here, we provide an updated literature review on the role of purinergic signaling in sensory ganglia, with special emphasis on P2Y receptors on SGCs. We also provide new original data showing a time-dependent downregulation of P2Y2 and P2Y4 receptor expression and function in purified SGCs cultures from TG, in comparison with primary mixed neuron–SGCs cultures. These data highlight the importance of the neuron–glia cross-talk in determining the SGCs phenotype. Finally, we show that, in mixed TG cultures, both adenine and guanosine induce intracellular calcium transients in neurons but not in SGCs, suggesting that also these purinergic-related molecules can participate in pain signaling. These findings may have relevant implications for the development of new therapeutic strategies for chronic pain treatment.
Satellite glial cells (SGCs) undergo phenotypic changes and divide the following injury into a peripheral nerve. Nerve injury, also elicits an immune response and several antigen-presenting cells are found in close proximity to SGCs. Silencing SCG-specific molecules involved in intercellular transport (Connexin 43) or glutamate recycling (glutamine synthase) can dramatically alter nociceptive responses of normal and nerve-injured rats. Transducing SGCs with glutamic acid decarboxylase can produce analgesia in models of trigeminal pain. Taken together these data suggest that SGCs may play a role in the genesis or maintenance of pain and open a range of new possibilities for curing neuropathic pain.
It has been known for some time that the somata of neurons in sensory ganglia respond to electrical or chemical stimulation and release transmitters in a Ca2+-dependent manner. The function of the somatic release has not been well delineated. A unique characteristic of the ganglia is that each neuronal soma is tightly enwrapped by satellite glial cells (SGCs). The somatic membrane of a sensory neuron rarely makes synaptic contact with another neuron. As a result, the influence of somatic release on the activity of adjacent neurons is likely to be indirect and/or slow. Recent studies of neuron–SGC interactions have demonstrated that ATP released from the somata of dorsal root ganglion neurons activates SGCs. They in turn exert complex excitatory and inhibitory modulation of neuronal activity. Thus, SGCs are actively involved in the processing of afferent information. In this review, we summarize our understanding of bidirectional communication between neuronal somata and SGCs in sensory ganglia and its possible role in afferent signaling under normal and injurious conditions. The participation of purinergic receptors is emphasized because of their dominant roles in the communication.