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Summary 3.3 Pain (all problems complete)
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- 3.3 Pain
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- Erasmus Universiteit Rotterdam (EUR)
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Representation of Pain in the brain – Apkarian, Bushnell, Schweinhardt (2013)Summary
Nociceptive information is transmitted from the spinal cord to the brain via several different pathways.
Consequently multiple regions of the brain are activated during the complex experience of pain. Cortical
regions activated during pain include limbic, paralimbic and sensory areas, anterior cingulate cortex (ACC),
insular cortex (IC), prefrontal cortex (PFC) and primary and secondary somatosensory cortices (S1 and S2).
Dopamine play a role in play modulation. Modulation of pain derived from psychological factors, such as
attentional, emotional state or expectation is manifested by changes in pain-evoked activity in the cerebral
cortex involves intrinsic descending modulatory circuits.
Clinical pain states often activate similar brain regions as do acute experimental pain conditions, but differences
also exist that probably underlie disruptions in pain modulatory systems, as well as alterations in the
psychological state related to chronic pain states.
It could be that chronic pain is associated with structural brain alterations that might contribute to the
maintenance of pain, as well as to some of the sequelae of living with pain, such as emotional disturbances.
Historical perspective
The role of the brain in pain processing: Cortex has a minimal role in pain perception, and the complex
nature of the pain experiences encompasses sensory features, emotional and motivational
components.
Some suggests that the conscious appreciation of pain must include activation and interaction of
multiple brain regions. It is thus not surprising that specific lesions or focal stimulation of the cortex
did not produce the experience of pain
Some patients with epileptic foci involving the primary or secondary somatosensory cortices (S1 and
S2) had been observed to experience painful seizures. Lesions involving S1 & S2 has been shown to
reduce pain perception.
Neurosurgeons had observed that lesions involving the anterior cingulate cortex (ACC) reduced the
distress associated with chronic intractable pain. Scarcity of both animal and human evidence of
involvement of the cerebral cortex in pain perception led to the continued view in medical textbooks
that pain was a subcortical phenomenon.
Human brain imaging: The advent of modern human brain imaging hemodynamic correlates of pain
which provided that during pain there is an increase of blood flow to the frontal lobes
The first three human brain imaging studies of pain were published, who used positron emission
tomography. They indicated that multiple cortical and subcortical brain areas are activated during
short-duration pain induced by heat.
Defining a pain network in the brain
Human brain activity can be imaged with: PET, SPECT, functional magnetic resonance imaging (fMRI),
electroencephalographic (EEG), and magnetoencephaloigraphic (MEG). Each of these techniques has
advantages and disadvantages in spatial and temporal resolution, sensitivity and cost.
Although there are differences in activation patterns across studies, a consistent cortical and
subcortical network has emerged that includes: sensory, limbic, associative and motor area.
The regions most commonly activated are the S1,S2, ACC, insular cortex (IC), prefrontal cortex (PFC),
thalamus and cerebellum. Pain evoked activity in these areas is frequently observed with either PET
or FMRI techniques and the activation in these regions is consistent with anatomical studies that show
nociceptive connectivity to these regions.
,*Figure: Regions activated by pain in imaging studies receive either
direct or indirect nociceptive input.
The cingulate cortex receives input from medial thalamic nuclei that
contain nociceptive neurons, including the nucleus parafascicularis and
ventrocaudal part of nucleus medialis dorsalis, as well as from lateral
thalamic regions including the ventrocaudal part of the nucleus
medialis dorsalis, as wel as from lateral thalamic regions, including
ventral aspect of the ventroposterior nucleus and the ventroposterior
inferior nucleus.
Nociceptive input to the ACC is further suggested by the observations
that painful stimuli evoke potentials over the human anterior cingulate
gyrus and that single nociceptive neurons are present in the ACC of
humans, monkeys and rabbits specific role for parts of ACC in pain
processing is distinct from the role of ACC in cognitive processes.
Nociceptive activity has been recorded from the human IC.
The cingulate regions observed in human pain brain imaging
studies provide a direct route for controlling motor responses
to painful stimuli
The prefrontal cortical regions are activated in a number of imaging studies of acute pain.
The most common subcortical pain related activation takes place in the thalamus and cerebellum.
Thalamus receive nociceptive input from dorsal horn and cerebellum also has connectivity with the
spinal cord.
The striatum is active in human pain. A specific population of spinal cord lamina 5 neuros project
directly to the basal ganglia
Some human pain imaging studies also indicate activity in the nucleus accumbens and amygdala and
this activity is a reflection of nociceptive transmission through spino-parabrachial- amygdala
projections.
PAG is also observed to be active of somatic and visceral pain. There is evidence that multiple
ascending nociceptive pathways are engaged in signaling the information integrated at cortical level,
in addition to spinothalamic pathways.
Brain Processing of Multidimensionality of Pain
There is now evidence from brain imaging, lesion and electrophysiological studies that different cortical regions
might be involved in different aspects of the complex experience of pain
Somatosensory cortices: most important for the perception od sensory features (location and duration of pain)
S1 & S2: contain neurons that code the spatial, temporal and intensive aspects of innocuous and
noxious somatosensory stimuli. It is relevant for sensory-driscriminative dimension of pain
processing.
Lesions: show deficits in pain sensations (can’t localize or describe the nature of painful stimulus,
they have pain affect without sensory-discriminative component of pain sensation)
ACC and IC (limbic/ emotional areas): important for emotional and motivational aspects of pain
Lesion IC: higher rates of acute thermal pain and increased S1 activity in absence of IC activity.
Disruption of nociceptive input to the IC may be compensated by increased transmittion of NC
information to S1 ( * NC = nociceptive).
ACC and IC are potential candidates for processing the affective-motivational dimension of pain.
Cingulotomy patients showed attenuated emotional responses to pain.
,ACC:
There is selective modulation of ACC pain-evoked activity after hypnotic treatment. There are changes
in pain unpleasantness and correlation between ACC and ratings of pain unpleasantness Therefore,
ACC is involved in the affective dimension of the pain experience
Activation of ACC during conditioning, produces aversive learning, whereas inhibiting ACC activity
seems to block aversive learning (in rodents involvement of ACC in aversive learned behavior).
IC: has been implicated in visceral sensory and motor integration, emotional responses and memory functions
and is also consistently activated by painful stimuli. There is a systematic relationship of intensity of painful
heat stimuli and IC activation as well as cold stimuli. Therefore, IC is involved in coding of noxious and
innocuous temperature. IC activity is also important for pain affect.
IC Lesions: are characterized by pain asymbolia (pain dissociation) in which pain sensations appear
to be normal but behavioral and physiological responses to the noxious stimulus are inappropriate
(pain is experienced without unpleasantness). Unilateral IC may enhance pain perception, but focal
posterior IC lesions seem to lead to central pain and specific deficits in acute pain perceptions
IC seems to be the most specific portion of the cortex in pain perception with subjective experience
of pain
Stimulation of the human IC has been shown to provoke extremely unpleasant painful sensations
which are topographically organized and seem to be evoked by electrical stimulation of the IC
IC in autonomic control: pain has a specific emotion that reflects the homeostatic behavioral drive
and suggests that IC pain-evoked activity is central to this drive
Anterior IC: encodes subjective pain
Prefrontal Cortex (PFC): Prefrontal pain-evoked activity exhibits the highest activity when a stimulus just
becomes painful with lower activation being associated with higher levels of pain. It is more activated in
response to a painful cutaneous stimulus than a visceral stimulus (despite this one is perceived as more
unpleasant)
PFC pain-evoked activity is related to the cognitive aspects of pain perception rather than directly to pain
sensation or affect.
PFC plays a role in pain modulation, specially in mediating pain modulatory effects of psychological states.
Increased PFC activation reflects increased engagement of pain facilitatory or inhibits circuits depending on the
area
Orbital frontal- accubens thalamus: engaged in affective perception of pain and dFC works as a “top down”
(subjective)-driven controller that modulates pain and limits the extent of suffering.
Cerebellum: It’s implicated in the control of various functions, including motor, sensory and cognitive as well as
nociceptive activities. Cerebellum plays a role in the modulation of visceral and somatic nociceptive
responses. Pain-evoked cerebellar activation is present in anesthetized humans, who are not consciously
aware of the pain. Such activity may be more important in the regulation of afferent nociceptive activity than
perception of pain
How do we distinguish Location and Quality of pain?
Despite differences in sensation, emotion and behavioral responses provoked by these different types of pain,
individuals can easily identify each as being painful
Despite pain similarities I experiences and neural activation patterns each pain is unique. Subjects can usually
differentiate noxious heat from noxious cold from noxious pressure
The convergence and similarities in brain regions activated by different types of pain are consistent with
phenomena such as “referred pain” but cannot explain either the ability to identify the origin of the pain or
the contrasting behavioral reactions to cutaneous and visceral pain (withdrawal or quiescence)
, There is evidence that S1 could underlie identification of the locus of cutaneous pain. S1 nociceptive neurons
have discrete receptive fields such that different neurons respond to painful stimulation in different skin areas.
There is a topographic organization of nociceptive responses in the S1 cortex that is similar to tactile responses.
Laterality of Pain representation
Many nociceptive pathways are bilateral, but spinothalamic pathway is contralateral.
Brain imaging studies of pain show bilateral activity in S1 and IC
There is contralateral activity in S1 and ACC
For low-intensity stimuli, activity that is dependent on stimulus intensity is mainly contralateral
Activity that is not correlated with stimulus intensity is mainly right brain dominant.
Although IC activity is almost always bilateral, stimulation within IC evokes pain mostly contralateral
for body and trunk sensations and more bilateral for facial sensations.
It therefore seems that the IC and maybe the S1 cortex are the best candidates for detecting the
laterality of painful stimulus since they show laterality activity for emotion sensations, have
somatotopic organization and are thought to be important in untangling sensory-discriminative
aspects of pain.
Distinct Brain Responses to Nociception and to subjective perceived pain
Discrimination between stimulus localization and stimulus intensity to subdivide the brain areas
related to acute pain were examined. Similarly to vision and audition, it may also consist of a ventral
(intensity coding), stream terminating in the IC and dorsal, spatial localization stream.
The brain should reflect perception A study differentiated between perceived pain and stimulus
representation for thermal painful stimuli and demonstrated that the part of the IC in contiguity with
more dorsal cortex best related to the perceived subjective magnitude of acute pain
Thus although IC reflects subjective pain best, it is a multimodal area that might distill magnitude
information for various sensory modalities
IC responses could be divided into two regions: nociceptive and pain perceptive regions
Temporal sequence of cortical activity during pain perception
Most information about the temporal sequence of pain-evoked brain activation is from EEG or MEG
studies.
The dual pain sensation elicited by a single brief painful stimulus is that due to the different
conduction times in nociceptive A and C fibers (about 1 second difference) is reflected in two
sequential brain activations on EEG and MEG from S1 S2 and ACC
The earliest pain induced brain activity originates in the area of S2. In contrast, tactile stimuli activate
this region only after processing in S2.
The S2 region and adjacent IC are primary receiving areas for nociceptive input to the brain.
Another study suggests that brief painful stimuli evoke sustained cortical activity corresponding to
sustained pain perception. First the pain was particularly related to activation of S1 whereas the
second pain was closely related to ACC (both sensations were associated with S2 activation).
These results are interpreted in the view of different bio functions of the first and second pain
The first pain signals threat and provides precise sensory info for immediate w/drawal whereas the
second pain attracts longer-lasting attention and motivates behavioral responses to limit injury and
optimize recovery.
An MEG study Cold perception resulted in activity on posterior IC. Noxious cold stimulation initially activated
IC in the same latency ranges as innocuous cold stimuli. Neither cold or painful cold produced detectable
activation of S1. The results suggests different processing of cold, painful cold and touch in human brain.
Temporal differences in brain activity for pain have also been study by blood flow techniques. The brain activity
pattern for a repetitive thermal painful stimulus is different depending on the past story It got more
intensive and unpleasant with ongoing pain rather than at it onset
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