Brain Pain Pathways - Introduction

Tutorial 19: Brain Pain Pathways

Part 1: Image-Mapped Tutorial
Part 2: Matching Self-Test
Part 3: Multiple-Choice Self-Test

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The sense of touch is dependent on six different skin receptors that are sensitive to pressure, warmth, cold, and pain. Regions of the nervous system that respond to these so-called somatosensory receptors are organized according to receptive fields; groups of neurons that respond selectively to the sensations occurring in particular segments of skin. Somatosensory neurons project upward through the spinal cord. These neurons synapse in the thalamus before arriving at the somatosensory cortex of parietal lobe. Similar to visual receptive fields, the receptive fields for touch are typically organized in a center-surround fashion, with one being excitatory and the other inhibitory. This arrangement aids in the localization of sensations on the skin. Although the entire body is mapped in somatosensory cortex, the most sensitive regions of skin (such those of the hands, lips, and tongue) are represented by larger areas of cortex.

Pain is essential to our survival, serving as a warning system that something has gone awry. Receptors for the sensation of pain are primarily free nerve endings in the skin. Messages from these receptors are routed to the brain via one of two pathways destined for different areas of the thalamus. The fast pathway records sharp, localized pain (such as that caused by cutting your skin) and transmits this information to the cortex in less than a second. The slow pathway travels through the limbic system, a detour that delays arrival at the cortex by seconds. The slower signals encode temperature as well as the burning, aching pain that often follows the sharper, early onset pain conveyed by the fast pathway.

The transmission of pain signals following tissue damage does not always result in the experience of pain. The perception of pain may be influenced greatly by one's mood, personality, and level of anticipation and attention. Health care workers often take advantage of this feature by asking you a question, to engage your higher thought processes, just as they prepare to administer that injection you are lamenting. Pain is experienced with varied intensity across cultures depending upon the interpretation of pain and its tolerance.

In the 1960's, Ronald Melzack and Patrick Wall made their mark on the scientific community by proposing a theory to explain how higher brain centers block incoming pain signals. Their gate-control theory of pain holds that ascending pain signals may be blocked within the spinal cord (referred to as the gate). When either ascending or descending signals close the gate, the pain transmission is blocked from reaching the higher centers necessary for perception of pain. The descending block signal is characterized by a pattern of neural activity that inhibits neuronal transmission. This theory has profoundly influenced the study of pain. Recent research has upheld the basic tenet of signal blocking, but has revealed a neural mechanism that is somewhat different than the one proposed by Melzack and Wall. These recent findings suggest that a pathway descending from the midbrain, mediates the suppression of pain. A class of neurotransmitters, called the endorphins, which mimic the action of opiate painkillers, likely powers the circuit.

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Recent psychological and neurological data have cast much doubt on the concept of a single pain sensory pathway. Already mentioned is the individual variation of pain experience following tissue damage. The intensity of pain is not simply a graded response to amount of tissue damage, but rather is influenced by attention, anxiety, and prior experience. Neurosurgical techniques designed to cut the co-called pain pathway have yielded mixed results. In particular for patients affected by chronic pain, the experience of pain returns and sometimes, new pains will appear. The variable response of this perceptual system has shifted attention to the modifiability of events in the central nervous system.

Beyond the suggestion that pain impulses are subjected to the modulating effects of a gate in the dorsal horn of the spinal cord, Malzack and Wall's gate control theory of pain proposed specific roles for the fast and slow pathways in this process. The theory suggested that the large fiber inputs stimulated by gentle rubbing tended to close the gates, whereas the small fiber inputs stimulated by hard pinching generally opened the gates. This may be why gentle rubbing at the edge of an inflamed and painful injury seems to reduce the sharp painful experience. The center-surround arrangement of somatosensory receptors may also play a role in this effect. It is also proposed that sensory input is modulated at multiple synapses along the projection pathway leading to the brain. The experience of pain occurs when the number of nerve impulse reaching each area exceeds a critical level.

The sensation of pain has distinct sensory qualities, described as throbbing, unpleasant, or sharp and emotional qualities expressed as punishing, wrenching, exhausting, or overwhelming. Melzack and Casey have proposed three psychological dimensions for the pain experience: sensory-discriminative, motivational-affective, and cognitive-evaluative. Evidence from psychophysiological studies support the possibility that each dimension is mediated by distinct systems in the brain that interact to result in the complex experience of pain. In particular, recent positron emission tomography data indicates that the anterior cingulate gyrus of the limbic system is involved in the motivational-affective dimension of pain. Somatosensory cortex is responsible for the sensory-discriminative dimension, and other, perhaps diffuse, cortical regions likely contribute to the cognitive-evaluative dimension.

One very interesting form of pain occurs after amputation of a limb. After a limb is removed, approximately 70% of amputees experience sensation as though it is generated in the missing limb. Approximately 50% of amputees experience pain in a missing limb. This so-called "phantom limb" phenomenon results in the perception of limb characteristics such as pain, warmth, pressure, itchiness, and moisture. These sensations are convincingly real. Many with this condition have bolted out of bed, certain that their missing limb would support such movement. A common perception of people with amputated hands is that of pain resulting from fingernails digging into the palm of a tightly clenched phantom hand.

An early explanation for the phantom limb phenomenon is that the sensation originates from irritated nerves remaining in the stump. Efforts to treat phantom pain using this line of reasoning have focused on the destruction of the pathways transmitting this information to somatosensory cortex and of structures along the pathway such as the thalamic relay nuclei. The ineffectiveness of the surgical procedures over time has led to a different explanation. It is more recently speculated that cells in parietal lobe, representing the somatosensory activity of the limb, continue to transmit impulses that are interpreted as sensations in the missing limb. Although the connection between the severed limb and cortical neurons is cut, the neurons continue to discharge resulting in a central image of the limb. Input to cortical neurons is, therefore, nonessential to the formation of a central image. Input to somatosensory cortical neurons is necessary, however, for knowledge of the location of a limb and for monitoring movement of the limb. This is demonstrated by the behavior of individuals with an anesthetized normal limb. In this state, the sensation of a phantom limb occurs when the anesthetized limb is out of sight. In addition, these individuals are rarely able to accurately describe the location of the limb.

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Tutorial 19: Brain Pain Pathways

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