Download Where is Pain Percieved?

Clinna Macdonald 1
Clinna Macdonald
Biology 1615: Biology Laboratory
Mohamed Jama
Where is Pain Perceived?
Pain is an inescapable sensation that every human being has experienced at least once in
their lifetimes. The sensation of pain has two ways of being graded on its severity. The first is
the objective intensity of pain, and the second is the subjective pain that the subject feels. Pain is
one of the multitudes of senses that compete for neural acknowledgment and representation [1].
When pain is perceived in the brain, it triggers neuronal oscillations, which is rhythmic or
repetitive neural activity in the central nervous system. Neural tissue can generate oscillatory
activity in multiple ways, triggered either by mechanisms localized within individual neurons, or
by interactions between neurons [2].
This study was done to see where the preferential processing for behaviorally relevant
information, such as pain, induced the neural oscillations [1]. Previously to this research, there
was research done showing the cortical representation of relevant sensory information was
related to neuronal oscillations in the gamma frequency band ranging from approximately 40100 Hz. This research was suggested to represent one piece of the selection and preferred
processing of sensory information. “These induced gamma oscillations represent event-related
modulations of neuronal oscillations, are often observed in early sensory cortices and differ from
evoked neuronal responses in a lack of phase locking to the sensory stimulus… The association
between induced gamma oscillations, and the selection and preferred processing of sensory
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stimulus suggests that these responses may not only be related to the physical stimulus attributes,
but also related particularly to the subjectively weighted percept of a sensory event” [1].
When pain is caused by nociceptive stimuli, a threat is sent to the brain, making that signal
behaviorally prioritized, thus creating neuronal oscillations. Gross et al. hypothesized that
noxious stimuli induce gamma oscillations in the somatosensory cortices. Also, that the paininduced gamma oscillations may not only relate to the objective attributes of pain, but also the
subjective experience of pain. To test the hypothesis, they used magnetoencephalography (MEG)
to record the natural response to noxious stimuli in healthy human beings. They did so by using
magnetoencephalography (MEG) on 12 healthy male participants, while each participant is
delivered 40 noxious cutaneous laser stimuli (applied stimulus intensity of 600mJ at random
intervals of 10- 14 seconds) into the dorsum of the right hand, while neural activity was recorded
with a neuromagnetometer. Each participant was then asked to close their eyes, and perceive the
intensity of the stimuli. Stimulus intensity of 600mJ evoked moderately painful sensations.
Scientists then conducted a second experiment on 13 healthy, right-handed men who are
delivered 40 noxious subcutaneous later stimuli with randomly varied strengths of 150, 300, 450,
or 600mJ. Forty stimuli for each intensity. Three seconds after the stimulus is applied, the
participants are then asked to rate the intensity of the pain from 0-100. 0 Being no pain at all, 100
being the worst pain imaginable. This pain does not include warmth/ second burn after initial
stimuli, this pain is strictly first pain.
The researchers aim was first to identify and characterize spatially and temporally paininduced gamma oscillations in human somatosensory cortices [1]. In the first experiment, 12
healthy male participants had 40 noxious laser stimuli applied to the dorsum of their right hand
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(at 600mJ) and were asked to perceive the intensity of the stimuli. The contralateral primary (S1)
and the bilateral secondary (S2) somatosensory cortices were localized by analyzing the known
pain-evoked (phase-locked) responses. Researchers found that pain induces strong and
significant increases at gamma power of frequencies between 60-95 Hz in the contralateral (S1)
cortex. The pain induced gamma oscillations 100-300 ms after initial stimulus application
coinciding with the pain evoked response from S1 [1]. Note: These pain induced gamma
oscillations were observed without doing anything in particular, thus the task having no effect on
the objectivity nor the subjectivity of pain. No pain-induced changes in gamma power were
observed in the bilateral S2 cortices. Analysis of amplitude and phase dynamics confirmed that
gamma oscillations were not phase locked to stimuli, and therefore represent induced, but not
evoked oscillations.
In the second experiment, the relationship between amplitudes of induced gamma
oscillations in S1, stimulus intensity, and perceived pain intensity was tested.13 healthy right
handed men were asked to perceive the pain of 40 noxious cutaneous lasers at random stimuli,
of 150, 300, 450, 600 mJ which produce sensations ranging from barely detectable, to
moderately painful. The contralateral S1 cortex was localized, and evoked responses and induced
gamma oscillations to stimuli of different intensities were analyzed. Mean amplitudes of evoked
responses and gamma oscillations from S1 were calculated during the time window from 100300ms as compared to baseline altitudes. The results show that the amplitudes of induced gamma
oscillations and amplitudes of evoked responses from S1 increase with the intensity of the
stimulus. The increase in response amplitudes was paralleled by an increase in perceived pain
intensity. These observations show that amplitudes of pain-induced gamma oscillations in S1
vary with objective stimulus intensity, and subjective pain intensity [1].
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References
1. Gross J, Schnitzler A, Timmermann L, Ploner M (2007) Gamma Oscillations in Human
Primary Somatosensory Cortex Reflect Pain Perception. PLoS Biol 5(5): e133.
doi:10.1371/journal.pbio.0050133
2. Fries P (2001). "A mechanism for cognitive dynamics: neuronal communication through
neuronal coherence". TICS 9: 474–480.