I have read with great interest the report by Baliki and colleagues
describing increased prefrontal activity (“decreased deactivation”) during
a cognitive paradigm in patients with chronic low back pain (Baliki et
al., 2008). While the authors suggest their findings indicate that
chronic pain alters brain function, by their own admission, study design
disallows definitive mechanistic explanations. Excitatory prefrontal
afferents preferentially target interneurons that inhibit mesolimbic
projections (Carr & Sesack, 2000), while attenuated dopaminergic
activity within the striatum augments nociceptive behavior (Altier &
Stewart, 1999; Saadé et al, 1997). One would therefore anticipate that a
predisposition towards increased prefrontal activity (i.e.
“hyperfrontality”) would produce a proportional decrease in mesolimbic
activity thereby augmenting nociception and, ostensibly, placing one at
increased risk for developing chronic pain. Indeed, relative increases in
prefrontal activity among healthy subjects correlate with increased
subjective pain ratings (Coghill et al., 2003), and clinical pain states
are likewise associated with prefrontal hyperactivity (Apkarian et al,
2001; Cook et al., 2004). Conversely, the inverse relationship between
prefrontal activation and mesolimbic reactivity may underlie the
observation that schizophrenia, which is associated with both
hypofrontality (Andreasen et al., 1997) and mesolimbic hyperactivity
(Bertolino et al., 1999), is also associated with hypoalgesia (Potvin
& Marchand, 2007). Thus, chronic pain might be the result of
increased prefrontal activity rather than its cause.
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