| |
With this background
in mind, studies of the "normal warning" response to
brief pain may be less relevant than is often assumed to research
on persistent pain. Researchers should understand the strong evidence
supporting a differential information processing of sensory vs.
affective information pain. Neuro-anatomical data suggest such
differential processing occurs via distinct thalamic and suprathalamic
brain structures which allow for several dimensions of the pain
experience (Price,
2000). Experimental evidence linking frontal lobe limbic activity
with pain affect in humans comes from a study using positron emission
tomography (PET). Unlike the primary somatosensory cortex, significant
changes in pain-evoked activity within the anterior cingulate
cortex are observed during hypnotic suggestions that alter selectively
the unpleasantness of noxious stimuli without changing their perceived
intensity (Rainville,
Duncan et al., 1997).
Patients' perception
of brief pain is typically captured by sensory descriptors (e.g.
aching, throbbing, radiating). In contrast, prolonged and sustained
pain stimuli induce significant pain affect, which in itself constitutes
an integral and meaningful part of the experience of pain in a
clinical context (Stohler
and Kowalski, 1999). Pain affect is expressed by descriptors,
such as tiring, exhausting, frightening, and fearful (Melzack,
1975).
| Table
5.1: Duration of Pain and Pain Affect
|
|---|
| Temporal
| Pain
Affect
|
|---|
| Brief
or initial experimental pain | Minimal |
| Sustained
experimental pain > 10 min | Significant |
| Persistent
clinical pain | Significant |
| Note:
Brief refers to pain of short duration, initial refers
to the early part of pain that will proceed to sustained
pain |
|
|