Research On The Functional Reorganization Of The Primary Somatosensory Cortex

The concept of plasticity comes frommedical field. When it was introduced into cognitive neuroscience, its contents are expanded. Plasticity mainly describes the changes of the external environment and their own conditionstransform the brain. Factors affecting changes can be learning, experience, injury, etc. Brain plasticity lasts throughout life. It mainly reflected in alterations of brain structure and function. Structural plasticity can occur in the cerebral cortex and the neuron loop,such as the cortical thickness, cortical area, the dendritic length, density of dendritic spines, and number of neurons, etc. Functional reorganization may show for changes in the level of neuron synaptic connections, functional reorganization of cerebral cortex and neural network level across the channel to connect different feeling. Some researches indicate that causes of diseases are closely related to brain plasticity, just as the primary somatosensory cortex and clinical pain. Meanwhile, the development of fMRI and EEG provides more rapid and correct method to observe the change of this relationship. Neural plasticity had been an important topic incognitive neuroscience.“Phantom limb sensation" is a kind of complications often happened after the amputation of part of the body. It is a global feeling that the missing limb is still present. Phantom limb pain is characterized by pain in the amputated limb as well as burning, spasm, etc. It is important to note that this kind of feeling is not a delusion, but an illusion. In some cortical reorganization cases, if we touch somebody surface, it may induce phantom limb sensation. These areas are called "trigger" area. Touch, temperature, acupuncture, flowing all can induce phantom limb. Yet the mechanisms of phantom limb pain are unclear. Cortical reorganization is one of the mechanisms widely accepted. Many studies have shown that functional reorganization of primary somatosensory cortex may be the causes of phantom limb pain. The higher functional reorganization of SI, the higher of phantom limb pain. So patients with phantom limb pain are ideal objects to study neural plasticity of SI. At first the study of plasticity focused on physical damages. It is also existed in normal brain actually which is mainly affected by learning and training. Its occurrence area can be the primary somatosensory cortex, the primary motor cortex, the auditory cortex, the visual cortex and so on. We chose healthy peoples as subjects for the same fMRI experiments to identify if there is a stable relationship between phantom limb pain and functional reorganization of S1. Whether the function of some cortical areas(e.g., S1 of the amputated limb) could be enhanced in terms of sensitivity to pain-related context in response to the long-lasting pain experience.In pain research, the laser evoked EEG(Electroencephalography) response, also known as laser evoked potentials(LEPs), is a widely accepted electrophysiological way to measure pain in recent years. EEG has several advantages: no traumatic, low-cost, high temporal resolution. The laser stimuli is brief, well-positioned, controllable, and it can selectively activate Aδ fiber and C fiber. EEG response evoked by low-intensity somatosensory stimuli, such as transcutaneous electrical nerve stimulation, also known as the somatosensory evoked potential(SEPs), can activate the larger Aβfiber, and then pass through a complex pathway to the brain cortex. Aβfiber, Aδ fiber and C fiber have differences in the conduction velocity, diameter and their function. Aβis big fiber myelination, diameter of 6~12 um, the conduction velocity of 35 ~ 75 m/s. It is mainly responsible for non-damaging afferent nerve conduction, but also participation in the regulation of pain; Aδ fiber is a kind of small fiber myelination, diameter of 1~5 um, the conduction velocity of 5 ~ 30 m/s, It has very big effect to locate noxious stimulus and noxious reflection; Finally, C fiber is small fiber without myelination, diameter of 0.2 ~ 1.5 um, conduction velocity of 0.5 ~ 2 m/s. Because of low conduction velocity, their main function is to protect painful area from further injury. Compared with normal LEPs and SEPs, abnormal LEPs and SEPs have different amplitude and latency. We assessed the functional integrity of the nociceptive and non-nociceptive somatosensory pathways using laser-evoked potentials(LEPs) and tactile-evoked potentials(TEPs) respectively.Functional Magnetic resonance imaging(fMRI) has a high spatial resolution, so it can be a complementary technology to EEG in pain research. In this experiment, the stimulations are the laser stimuli and pain empathy images(i.e., the observation of video clips showing painful or non-painful stimulation of left or right hand). Researchers have found that important brain areas involved in pain perception are primary somatosensory cortex(S1), secondary somatosensory cortex(S2), the anterior cingulate cortex(ACC), anterior insula(AI) and brain lateral fissure. Laser stimuli can accurately locates brain regions associated with pain. Pain empathy is a kind of ability to feel others’ pain. It also can activate pain related brain regions such as ACC, AI, S1, etc. We expect the function to process the pain related information did not change in normal brain under the same pain empathy tasks. Due to the long-lasting pain experience, the function of some cortical areas(e.g., S1 of the amputated limb) could be enhanced in terms of sensitivity to pain-related context.The studies are includes two experiments. The first experiment uses EEG and fMRI technology in a patient with 21-year phantom limb pain. Experimental stimuliare laser stimuli and empathy images. EEG experiment showed that both laser-evoked potentials(LEPs) and tactile-evoked potentials(TEPs) were clearly presented only when radiant-heat laser pulses and electrical pulses were delivered on the shoulder of the healthy limb, but not of the amputated limb. This observation suggested the functional deficit of somatosensory pathways at the amputated side. fMRI experiment showed that when laser stimuli pulses were delivered on the surface of right hand, the ipsilateral S1 and the cerebellumwas obviously activated. Significant larger brain activations to painful than to non-painful stimuli in video clips were observed not only at visual-related brain areas and anterior/mid-cingulate cortex, but also at S1 contralateral to the amputated limb. Further ROI analysis showed signal changes(%) of BOLD responses in left S1 were not significantly modulated by stimulated hand, stimulation modality, and their interaction. In contrast, signal changes ofBOLD responses in right S1 were significantly modulated by stimulation modality, but not bystimulated hand, and their interaction. Specifically, signal changes of BOLD responses inright S1 was significantly larger to “left pain” video clips than to “left touch” video clips, butnot significantly different between “right pain” and “right touch” video clips. This observation suggested the increased sensitivity of S1 of the amputated limb to pain-related context. In addition, such increase of sensitivity was significantly larger if the context was associated with the amputated limb of the patient.In the second stage, 16 normal adults were tested with same fMRI experiment, aged from 39-61 years(M=48.8, S.D.=5.8).The results showed when laser pulses were delivered on the surface of right hand, the contralateral S1 and insular was obviously activated. S1,occipital lobe and MCC were obviously activated in both painful and non-painful stimulus stimuli in video clips. No any differences to painful than to non-painful stimuli in video clipswere observed.The observation of S1,occipital lobe and MCC showed that participants can accept the pain and visual information normally. Further ROI analysis showed signal changes(%) of BOLD responses in left S1 were not significantly modulated by stimulated hand, stimulation modality, and their interaction, so did right S1. These results indicate that plasticity of normal brain was existed, mainly associated with learning and experience, but the function to process the pain of normal brain will not therefore change. Which proved that the increased sensitivity of S1 of the amputated limb is not because of the experiment material. Phantom limb pain and functional reorganization of S1 is closely related. It further demonstrated persistent pain was almost the important cause for the functional reorganization of S1.If this is a kind of abnormal neural signal characteristics of persistent pain, then we can measure persistent pain more accurate by neural physiological means. Consideringthat neuroplasticity could be observed rapidly after the bodily injury, we speculated ourobservation i.e., the enhanced sensitivity of the primary somatosensory cortex topain-related and amputated-limb-related context, could be observed for patients withphantom limb pain lasting shorter than 21 years, especially for the younger patients. Indeed,the reliability and validity of our observation should be tested using neurophysiological datafrom more phantom limb pain patients. Maybe our strategy could be used to assess the levelof neuroplasticity of phantom limb pain patients in the future.