How pain preempts cognition - and about itching

I found these two articles on pain and itching interesting, particularly since I've been going through an orgy of both after exposing myself to poison oak or ivy while working in the yard. Bingel et al. show some brain correlates of why I found it difficult to focus on normal cognitive activities during this period:

It is well known that pain attracts attention and interferes with cognition. Given that the mechanisms behind this phenomenon are largely unknown, we used functional magnetic resonance imaging and presented visual objects with or without concomitant pain stimuli. To test for the specificity of pain, we compared this modulatory effect with a previously established modulatory effect of working memory on visual object processing. Our data showed a comparable behavioral effect of both types of modulation and identified the lateral occipital complex (LOC) as the site of modulation in the ventral visual stream, for both pain and working memory. However, the sources of these modulatory effects differed for the two processes. Whereas the source of modulation for working memory could be attributed to the parietal cortex, the modulatory effect of pain was observed in the rostral anterior cingulate cortex (rACC), an area ideally suited to link pain perception and attentional control.
A) fMRI effects of the interaction of background visibility with working memory load were observed in bilateral LOC, reflecting a phasic modulation of LOC activity.
(B) Corresponding activation and parameter estimates related to the interaction of Pain × Visibility.

Now, on to itching (also central to my poison oak story, still going on....). Johanek et al. note a curious distinction between histamine induced itching and itching caused by cutaneous application of spicules from the cowhage plant. They show a different class of afferent C-fiber afferents signaling non-histamine induced itching:

The neuronal pathways for itch have been characterized mainly based on responses to histamine. Intracutaneous application of histamine produces intense itch and a large area of axon-reflexive vasodilation ("flare") around the application site. Both phenomena are thought to be mediated through neuronal activity in itch-specific, mechanoinsensitive C-fiber afferents (CMi). However, mechanical and electrical stimuli that do not activate CMi fibers can cause the sensation of itch, and itch may occur without flare, suggesting that other neuronal itch pathways exist. Because cutaneous application of spicules from the plant Mucuna pruriens (cowhage) has been anecdotally reported to produce itch without flare, we performed psychophysical experiments to investigate whether the mechanisms underlying cowhage- and histamine-induced itch differ. Although histamine and cowhage produced itch of similar magnitude, the itch to cowhage was not correlated with the itch to histamine; some subjects had intense itch to cowhage and little itch to histamine and visa versa. Laser Doppler measurements of blood flow revealed that histamine led to a large area of vasodilation, whereas cowhage produced vasodilation restricted to the application site. Pretreatment of the skin with an antihistamine blocked the itch produced by histamine but did not prevent cowhage-induced itch. Desensitization of the skin with topical capsaicin abolished cowhage-induced itch but did not significantly alter histamine-induced itch. These findings indicate that cowhage itch is signaled through a population of capsaicin-sensitive afferent nerve fibers that is distinct from CMi fibers mediating histamine-induced itch. Cowhage may be useful to investigate the neural pathway mediating nonhistaminergic itch.