forthcoming in The Journal of Philosophy.

Many bodily sensations are connected quite closely with specific actions: itches with scratching, for example, and hunger with eating. Indeed, these connections have the feel of conceptual connections. With the exception of D. M. Armstrong, philosophers have largely neglected this aspect of bodily sensations. In this paper, I propose a theory of bodily sensations that explains these connections. The theory ascribes intentional content to bodily sensations but not, strictly speaking, representational content. Rather, the content of these sensations is an imperative: (...) in the case of itches, 'Scratch!' The view avoids non-intentional qualia and hence accords with what could be called, generalizing Lycan slightly, the 'hegemony of intentionality'. (shrink)

Cognitivism about imperatives is the thesis that sentences in the imperative mood are truth-apt: have truth values and truth conditions. This allows cognitivists to give a simple and powerful account of consequence relations between imperatives. I argue that this account of imperative consequence has counterexamples that cast doubt on cognitivism itself.

In 1986, I argued that pains are essentially not phenomenal states. Using a Wittgen-steinian son of argument, I showed that the same sort of phenomena can be had on different occasions, and on one occasion persons be in pain, while on another occasion persons not be in pain. I also showed that very different phenomena could be experienced and, yet, organisms have the same sort of pain. I supported my arguments with empirical data from both laboratory and clinical studies. There (...) is nothing about this thesis I would now retract. However, there was a further thesis that needs to be reconsidered. I argued that phenomenal states are only accompaniments of pains, that pains are essentially a combination of cognitive, affective and behavioural/motivational states. This thesis I do now zaish to retract. I now argue that phenomenal states are necessary for pains, but still not sufficient. There must also be a cognitive state which involves an evaluation of the phenomenon as something like, 'Harm to the body'. The evaluation is a kind of de re belief, regarding the phenomenon as itself representing harm to the body. Besides admitting that phenomenal states are necessary for pains, I also now claim that other relevant belief states, affective states, and behavioural/motivational states are not necessary for pain, but normal consequences of pain. This revised theory is preferable to the 1986 one because it fits better with empirical facts (including providing better explanations for anomalous cases), fits better with certain powerful common-sense intuitions, and fits better with a larger theory of consciousness I have been developing. Among other things, it turns out that being in pain is a quite peculiar conscious state and considering it as a paradigm for consciousness is a serious mistake. (shrink)

Differential diagnosis of motor symptoms, for example, akinesia, may be difficult in clinical neuropsychiatry. Symptoms may be either of neurologic origin, for example, Parkinson's disease, or of psychiatric origin, for example, catatonia, leading to a so-called “conflict of paradigms.” Despite their different origins, symptoms may appear more or less clinically similar. Possibility of dissociation between origin and clinical appearance may reflect functional brain organisation in general, and cortical-cortical/subcortical relations in particular. It is therefore hypothesized that similarities and differences between Parkinson's (...) disease and catatonia may be accounted for by distinct kinds of modulation between cortico-cortical and cortico-subcortical relations. Catatonia can be characterized by concurrent motor, emotional, and behavioural symptoms. The different symptoms may be accounted for by dysfunction in orbitofrontal-prefrontal/parietal cortical connectivity reflecting “horizontal modulation” of cortico-cortical relation. Furthermore, alteration in “top-down modulation” reflecting “vertical modulation” of caudate and other basal ganglia by GABA-ergic mediated orbitofrontal cortical deficits may account for motor symptoms in catatonia. Parkinson's disease, in contrast, can be characterized by predominant motor symptoms. Motor symptoms may be accounted for by altered “bottom-up modulation” between dopaminergic mediated deficits in striatum and premotor/motor cortex. Clinical similarities between Parkinson's disease and catatonia with respect to akinesia may be related with involvement of the basal ganglia in both disorders. Clinical differences with respect to emotional and behavioural symptoms may be related with involvement of different cortical areas, that is, orbitofrontal/parietal and premotor/motor cortex implying distinct kinds of modulation – “vertical” and “horizontal” modulation, respectively. Key Words: Bottom-up modulation; catatonia; horizontal modulation; Parkinson's disease; top-down modulation; vertical modulation. (shrink)