Online research in philosophy

Our subjective sensory experiences are thought to be heavily shaped by interactions between expectations and incoming sensory information. However, the neural mechanisms supporting these interactions remain poorly understood. By using combined psychophysical and functional MRI techniques, brain activation related to the intensity of expected pain and experienced pain was characterized. As the magnitude of expected pain increased, activation increased in the thalamus, insula, prefrontal cortex, anterior cingulate cortex (ACC) and other brain regions. Pain-intensity-related brain activation was identified in a widely distributed set of brain regions but overlapped partially with expectation-related activation in regions, including the anterior insula and ACC. When expected pain was manipulated, expectations of decreased pain powerfully reduced both the subjective experience of pain and activation of pain-related brain regions, such as the primary somatosensory cortex, insular cortex, and ACC. These results confirm that a mental representation of an impending sensory event can significantly shape neural processes that underlie the formulation of the actual sensory experience and provide insight as to how positive expectations diminish the severity of chronic disease states.

Our concerns fall into three areas: (1) Barsalou fails to make clear what simulators are (vs. what they do); (2) activation of perceptual areas of the brain during thought does not distinguish between the activation's being constitutive of concepts or a mere causal consequence (Barsalou needs the former); and (3) Barsalou's attempt to explain how modal symbols handle abstraction fails.

Libet's experiments, supported by a strict one-to-one identity thesis between brain events and mental events, have prompted the conclusion that physical events precede the mental events to which they correspond. We examine this claim and conclude that it is suspect for several reasons. First, there is a dual assumption that an intention is the kind of thing that causes an action and that can be accurately introspected. Second, there is a real problem with the method of timing the mental events concerned given that Libet himself has found the reports of subjects to be unreliable in this regard. Third, there is a suspect assumption that there are such things as timable and locatable mental and brain events accompanying and causing human behaviour. For all these reasons we reject the claim that physical events are prior to and explain mental events.

Are judgements and wishes reallybrain events (or brain states) which will be affirmedby a completed scientific account of how humanbehavior is caused? Materialists, other thaneliminativists, say Yes. But brain events do notcause muscle contractions, hence bodily movements,directly. They do so, if at all, by triggeringintermediate causes, viz. firings in motor nerves. Soit is crucial, this paper argues, whether they arecharacterized as biological events –performances of naturally-selected-for operations – orinstead as complex microphysical events. ``Acauses B, B causes C, so A causes C'' is defensible forbiological brain events, but fails for microphysical ones.

In order to make an attempt at grouping the various aspects of brain functional imaging (fMRI, MRS, EEG-MEG, ...) within a coherent frame, we implemented a model consisting of a system of differential equations, that includes: (1) sodium membrane transport, (2) Na/K ATPase, (3) neuronal energy metabolism (i.e. glycolysis, buffering effect of phosphocreatine, and mitochondrial respiration), (4) blood-brain barrier exchanges and (5) brain hemodynamics, all the processes which are involved in the activation of brain areas. We assumed that the correlation between brain activation and metabolism could be due to either changes in the concentrations of ATP and ADP following activation of Na/K ATPase that result from the changes in ion concentrations, or the involvement, in different phases of metabolism, of a second messenger such as calcium. In this article, we show how this type of model enables interpretation of MRS and fMRI published data that were obtained during prolonged stimulations.

According to Hurford, PREDICATE (x) is correlated with deictic object variables during event perception. This claim is inconsistent with some core literature on the perception of motion events. We point out that the perception of events involves the activation of the modal properties and amodal properties of underlying event structure, for which Hurford's target article fails to account.

A proximal mechanism is proposed whereby early crying helps maintain ideal levels of brain activation during the first three postnatal months. The proposal is consonant with both animal and human infant literatures, and new data are presented in its support.

The Theory of Event Coding deals with brief events but has implications for longer, complex events, particularly goal-directed activities. Two of the theory's central claims are consistent with or assumed by theories of complex events. However, the claim that event codes arise from the rapid activation and integration of features presents challenges for scaling up to larger events.

Both Solms and Nielsen acknowledge the difficulty of accounting for the similarities between REM and NREM sleep mentation with a two-generator model, and each link dreams, either explicitly (Solms) or implicitly (Nielsen), to brain activation. At present, however, no data indicate that brain activation can be demonstrated whenever vivid dream reports are obtained. [Nielsen; Solms].