陈志刚教授基于“脑气-脑髓-脑神”一体论论治皮质基底节变性

皮质基底节变性是一种罕见、起病隐匿的神经系统变性病,其常见的临床表现为非对称性肌强直及失用。陈志刚教授结合古代医家论述及其临床经验,提出中医脑病“脑气-脑髓-脑神”一体论的核心辨治体系,指出脑气紊乱、毒邪留滞脑髓、脑神失用是本病发生的病理基础。治法以理气、祛毒,益髓充脑为主,具有较好疗效。附1则验案以佐证。

安神补脑胶囊结合针刺对原发性失眠(心神不宁型)的临床研究

目的探究安神补脑胶囊结合针刺对原发性失眠(心神不宁型)的临床研究。方法选取2021年6月—2022年6月收治的124例原发性失眠患者为研究对象。根据治疗方法分为观察组(n=64)与对照组(n=60),对照组采用针刺治疗,观察组在此基础上结合安神补脑胶囊治疗。采用阿森斯量表(Athens Insomnia Scale,AIS)、生活质量评分(the MOS item short from health survey,SF-36)量表、失眠严重指数量表(The insomnia severity index,ISI)记录两组患者治疗前后水平。观察组两组患者治疗前后血清指标肿瘤坏死因子(Tumor necrosis factor,TNF-α)、γ-氨基丁酸(γaminobutyric acid,GABA)、5-羟色胺(5-hydroxy tryptamine,5-HT)、核因子κB(nuclear factor kappa-B,NF-κB)含量水平变化。观察两组患者临床疗效和中医症候积分。结果两组患者治疗前入睡时间、白天情绪、白天身体功能、夜间苏醒、总睡眠时间、总睡眠质量、白天思睡评分、比期望的时间早醒评分无显著差异(P>0.05)。治疗后观察组入睡时间、白天情绪、白天身体功能、夜间苏醒、总睡眠时间、总睡眠质量、白天思睡评分、比期望的时间早醒评分显著低于对照组(P<0.05)。两组患者治疗前生理功能、身体疼痛、角色限制、总体健康、社会功能、活力、精神健康、情感职能无显著差异(P>0.05)。治疗后观察组生理功能、身体疼痛、角色限制、总体健康、社会功能、活力、精神健康、情感职能评分显著高于对照组(P<0.05)。两组患者治疗前ISI、中医症候积分无显著差异(P>0.05)。治疗后观察组ISI、中医症候积分较对照组显著降低(P<0.05)。两组患者治疗前TNF-α、NF-κB、GABA和5-HT水平无显著差异(P>0.05)。治疗后观察组TNF-α、NF-κB水平较对照组显著降低,且GABA和5-HT水平较对照组显著升高(P>0.05)。观察组总有效率为93.75%显著高于对照组81.67%(χ^(2)=4.252,P=0.039)。结论安神补脑胶囊结合针刺能有效改善血清因子水平,提升睡眠质量、提高临床疗效和生活质量。

“心主神明”与“脑主神明”的再认识

首先分析了诸家对“心主神明”与“脑主神明”争论所存在的误区 ;其次阐明了“心主神明”并非《内经》原旨以及“神”、“神明”、“神志”的内涵 ;并揭示了“心神”与“脑神”的关系及其实质 ;最后结论说明“神明”之争是无价值的。心神说和脑神说可在“神经 内分泌 免疫网络”理论中获得完美的结合。

康脑神颗粒治疗急性脑梗死临床研究

目的观察康脑神颗粒治疗急性脑梗死疗效并探讨其作用机理。方法将69例患者随机分为两组,在西医常规治疗基础上,治疗组口服康脑神颗粒,对照组口服益脑复健胶囊,两组疗程均为28d;治疗前后检测血清白介素1β(IL-1β)、白介素8(IL-8)、血清可溶性细胞间粘附分子(sICAM-1)。结果治疗组临床疗效及对神经功能、IL-1β、IL-8、sICAM-1的改善作用均优于对照组。结论抑制炎性细胞因子、粘附分子等的过度产生,可能是康脑神颗粒保护缺血损伤的作用机理之一。

心脑神力口服液对小鼠抗氧化损伤作用的实验研究

目的研究心脑神力口服液对小鼠的抗氧化损伤作用。方法将50只昆明种小鼠随机分为对照组,新药低、中、高剂量组和旧药组,对照组给予蒸馏水,各给药组分别给予不同剂量的心脑神力口服液,给药途径均为灌胃,给药4周后,测定其血清SOD活力和MDA含量。结果与对照组相比,各给药组SOD活力增加;新药中、高剂量组MDA的含量低于对照组,差异有显著性。结论心脑神力口服液对小鼠具有抗氧化损伤作用,能增加SOD活力,降低MDA含量。

回神醒脑汤联合高压氧改善脑梗死患者神经、认知和肢体功能及生活能力的作用分析

目的探究高压氧联合回神醒脑汤改善脑梗死患者神经、认知和肢体功能及生活能力的作用分析。方法选取2018年3月—2019年10月在医院接受治疗的86例脑梗死患者为研究对象,采用随机数字表法分为对照组与观察组,每组43例。对照组采用常规治疗,观察组在此基础之上采用高压氧联合回神醒脑汤治疗,疗程4周。观察两组临床疗效、神经功能、认知功能、肢体运动功能、日常生活能力及血清学指标。结果观察组总有效率高于对照组(P<0.05)。治疗后,两组C反应蛋白(CRP)、D-二聚体(D-Dimer)、血栓调节蛋白(TM)、白介素-6(IL-6)和脑源性神经营养因子(BDNF)较治疗前降低(P<0.05),且观察组低于对照组(P<0.05)。治疗后,两组NIHSS和MMSE评分较治疗前降低(P<0.05),且观察组低于对照组(P<0.05);治疗后,两组FMA和ADL评分较治疗前升高(P<0.05),且观察组高于对照组(P<0.05)。结论高压氧联合回神醒脑汤能够有效改善患者的神经和肢体运动功能障碍,并能显著提高患者的认知功能和日常行为能力,疗效确切。

Isotropic volumetric MRI for displaying cranial perineural spread of cranial nerve in nasopharyngeal carcinoma

Objective To observe the value of isotropic volumetric MRI for displaying perineural spread(PNS)of cranial nerve(CN)in nasopharyngeal carcinoma.Methods Eighty-seven patients with pathologically proven nasopharyngeal carcinoma were prospectively enrolled.MR scanning,including three-dimensional liver acquisition with volume acceleration-flexible(3D LAVA_Flex)image,T2WI with fat suppression(T2WI-FS),T1WI,contrast enhancement(CE)T1WI-FS of nasopharynx and neck region were performed.The displaying rates of CN PNS were evaluated and compared between 3D LAVA_Flex and T2WI-FS,T1WI,CE-T1WI-FS at patient level,CN group level and neural level,respectively.Results The displaying rate of CN PNS in all 87 nasopharyngeal carcinoma patients by 3D LAVA_Flex sequence was 49.43%(43/87),higher than that of conventional MRI(30/87,34.48%,P=0.001).Among 59 patients with advanced nasopharyngeal carcinoma diagnosed with conventional sequences,the displaying rate of CN PNS was 71.19%(42/59)by 3D LAVA-Flex sequence,higher than that of conventional MRI(30/59,50.85%,P=0.001).At both patient level and posterior CN level,significant differences of the displaying rate of CN PNS were found between 3D LAVA-Flex sequence and T2WI-FS,T1WI,CE-T1WI-FS,while at CN level,the displaying rates of mandibular nerve PNS,CNⅨ—ⅪPNS in jugular foramen(P<0.05)and CNⅨ—ⅫPNS in carotid space of 3D LAVA_Flex sequence were all significantly higher than that of T2WI-FS,T1WI and CE-T1WI-FS(all P<0.05),of PNS of CNⅢ—Ⅴin cavernous sinus were higher than that of T2WI-FS(P<0.05),while of PNS of hypoglossal nerve were significantly higher than that of T2WI-FS and T1WI(both P<0.05).Conclusion 3D LAVA_Flex sequence could be used to effectively display CN PNS of nasopharyngeal carcinoma.

Autophagy is activated and might protect neurons from degeneration after traumatic brain injury

Objective To investigate changes of autophagy after traumatic brain injury （TBI） and its possible role. Methods Rat TBI model was established by controlled cortical injury system. Autophagic double membrane structure was detected by transmission electronic microscope. Microtubule-associated protein 1 light chain 3 （LC3） and Beclin 1 were also used to investigate the activation of autophagy post-TBI. Double labeling with LC3 and caspase-3, or Beclin 1 and Fluoro-Jade, to show the relationship between autophagy and apoptosis or neuron degeneration after TBI. Results An increase of autophagic double membrane structure was observed in early stage （1 h）, and the increase lasted for at least 32 d post-TBI. LC3 and Beclin 1 proteins also began to elevate at 1 h time point post-TBI in neurons, 3 d later in astrocytes, and peaked at about 8 d post-TBI. In both cell types, LC3 and Beclin l maintained at a high level until 32 d post-TBI. Most LC3 and Beclin 1 positive cells were near the side （including hippocampus）, but not in the core of the injury. In addition, in the periphery of the injury site, not all caspase-3 positive （＋） cells merged with LC3 （＋） cells post-TBI; In hippocampal area, almost all Beclin 1 （＋） neurons did not merge with Fluoro-Jade （＋） neurons from 1 h to 48 h post-TBI. Conclusion Autophagy is activated and might protect neurons from degeneration at early stage post-TBI and play a continuous role afterwards in eliminating aberrant cell components.

Changes of cell proliferation and differentiation in the developing brain of mouse

Objective To investigate the cell proliferation and differentiation in the developing brain of mouse. Methods C57/BL6 mice were divided into 3 groups at random. Bromodeoxyuridine （BrdU） was injected into the brains in different development periods once a day for 7 d. The brains were retrieved 4 weeks after the last BrdU injection. Immunohistochemical and immunofluorescent studies were carried out for detecting cell proliferation （BrdU） and cell differentiation （NeuN, APC, lbal, and S 100β）, respectively. Results The number of BrdU labeled cells decreased significantly with the development of the brain. Cell proliferation was prominent in the cortex and striatum. A small portion of BrdU and NeuN double labeled cells could be detected in the cortex at the early stage of development, and in the striatum and CA of the hippocampus in all groups. The majority of BrdU labeled cells were neuroglia, and the number of neuroglia cells decreased dramatically with brain maturation. Neurogenesis is the major cytogenesis in the dentate gyrus. Conclusion These results demonstrated that cell proliferation, differentiation and survival were age and brain region related.

Beneficial effects of moderate voluntary physical exercise and its biological mechanisms on brain health

This article reviewed the beneficial effects of moderate voluntary physical exercise on brain health according to the studies on humans and animals, which includes improving psychological status and cognitive function, enhancing psychological well-being, decreasing the risks of Alzheimer＇s disease （AD） and dementia, and promoting the effects of antidepressant and anxiolytic. The possible underlying neurobiological mechanisms are involved up-active and down-active pathways. The up-active pathway is associated with enhancements of several neurotransmitters systems afferent to hippocampus, including norepinephrine （NE）, serotonin （5-Hydroxytryptamine, 5-HT）, acetylcholine （ACh） and γ-aminobutyric acid （GABA）. The down-active pathway is mainly concerned with up-regulation of the brain-derived neurotrophic factor （BDNF） and neurogenesis. It is suggested that NE activation via β-adrenergic receptors may be essential for exercise-induced BDNF up-regulation. The possible intracellular signaling pathways of NE-mediated BDNF up-expression may be involved in GPCR-MAPK-PI-3K crosstalk and positive feedback.

Therapeutic Effects of Stereotactic Radiotherapy on 389 Cases of Brain Glioma

Objective： To investigate the treatment effectiveness and side effects of stereotactic radiotherapy for brain glioma. Methods： From Jun. 1995 to Dec. 1998, 389 cases of brain gliomas were treated by stereotactic radiotherapy, among which 151 cases were treated by stereotactic radiosurgery （SRS） and the other 238 cases, by fractionated stereotactic radiotherapy （FSRT）. In the SRS group, the marginal tumor dose was 20 to 30 Gy （median, 2.6 Gy）. One to 6 isocenters （median, 2.48） and 5 to 21 irradiation arcs （median, 8.45） were applied. In the FSRT group, the per-fraction marginal tumor dose was 8 to 12 Gy with 1 to 6 isocenters （median, 2.53）, 6 to 20 irradiation arcs （median, 8.25） and 2-5 fractions delivered everyday or every other day. Results： Three months after treatment, the complete and partial response rates were 13.9% and 45.7% in SRS group respectively. The stable disease rate was 17.2%. The total effective rate was 76.8%. In FSRT group, the complete and partial remission rates were 19.7% and 47.9% respectively. The stable disease rate was 20.6%. The total effective rate was 88.2%. The total effective rate of FSRT group was higher than that in SRS group （X^2=9.874, P=0.020）. The 1-year, 3-year and 5-year survival rate of all patients was 54.3%, 29.3%, 16.5% respectively. The 1-year, 3-year and 5-year survival rate in SRS group and FSRT group was 52.3% vs 26.5%, 11.9% vs 55.5%, and 31.1 vs 19.3% respectively. There was no significant difference between the two groups （X^2=2.16, P=0.1417）. The brain edema caused by the main radiation was more severe in the SRS group than in FSRT group （X^2=4.916, P=0.027）. Conclusion： It is effective for brain glioma to be treated by stereotactic radiotherapy. Compared with SRS, the FSRT has the advantage of good effect and less side response.

Effects of Oestrogen on Ischemia-induced Neurogenesis in the Dentate Gyrus of Rats

To study the effects of oestrogcn on ischemia-induced neurogenesis in the hippocampal dentate gyms, thirty-two adult male rats were randomly divided into four groups： the control surgery group with eestrogen administration （SE）, the control surgery group with normal saline administration （SN）, the middle cerebral artery occlusion （MCAO） group with oestrogen administration （ME） and the MCAO group with normal saline administration （MN）. The MCAO rats were occluded for 90 rain by an intraluminal filament and then recirculated. After 1, 3, 12, 24 and 28 h of MCAO, the rats of the four groups were killed to investigate the infarct volume, apoptosis and neurogenesis. The cerebral infarct volume in the ME group was significantly smaller than that of the MN group （P 〈 0.05）. No significant cell loss was seen in the dentate gyms. Cerebral ischemia led to increased neurogenosis, which is independent of cell death in the ipsilateral dentate gyrus（P 〈 0.05）. BrdU-pesitive cells in the ipsilateral dentate gyms of the ME group were significantly increased when compared with those of the MN group（P 〈 0.05）. In the SE group, BrdU-positive cells in both the ipsilateral and contralateral dentate gyms, were increased when compared with those of the SN group （ P 〈 0.05 ）. We concluded that ocstregen plays an important role in neurogenesis, which is independent of ischemia-induced by MCAO in the hippocampal dentate gyms of rats.

Effects of Pravastatin on neuroprotection and neurogenesis after cerebral ischemia in rats

Objective Statins inhibit hydroxymethylglutaryl coenzyme A （HMG-CoA） reductase activity and lower total serum cholesterol levels. We investigated the effects of Pravastatin on neuroprotection and neurogenesis in the dentate gyrus （DG）, subventricular zone （SVZ） and striatum after cerebral ischemia in rats. Methods The filament method was used for temporary middle cerebral artery occlusion （tMCAO）. Pravastatin or saline post-ischemically were administered at subsequent time points： 6 h after tMCAO, and then on every subsequent day up to day 14 after tMCAO. Neurological outcome was investigated by using a neuroscore, the beam balance test and the rotarod test. Cholesterol and triglycerides levels were determined by blood sample analysis prior to sacrifice. Infarct area was calculated by microtubule-associated protein 2 （MAP2） staining. Neurogenesis was evaluated by triple staining with bromodeoxyuridine （BrdU）, doublecortin （DCX）, and neuronal nuclei （NeuN）. Results Compared with the control groups, Pravastatin treated animals were significantly improved in neurological outcome in rotarod test, with smaller infarct size. Pravastatin increased BrdU- positive cells number in the DG （P = 0.0029） and the SVZ （P = 0.0280） but not in the striatum （P = 0.3929）. Furthermore, Pravastatin increased BrdU-labeled DCX positive cells number in the DG （P = 0.0031）, SVZ （P = 0.0316） and striatum （P = 0.0073）. We also observed a DCX-positive cells stream from the SVZ to the striatum, suggesting a migration route of those immature neurons. No significant differences of total serum cholesterol and triglycerides were observed between groups. Conclusion The Pravastatin administration strategy is safe and could promote neurological recovery in ischemic stroke. Pravastatin induces neurogenesis in the DG and SVZ, and increases the number of migration cells in the striatum. These effects are independent of the cholesterol-lowering property of Pravastatin.

Effects of spinal cord stimulation on cerebrovascular flow: role of sym-pathetic and parasympathetic innervations

Objective Cervical spinal cord stimulation （SCS） has been found to augment cerebral blood flow （CBF） in a number of animal models. However, the effective use of SCS is hampered by a lack of understanding of its mechanism（s） of action. In this paper, we focus on the sympathetic and parasympathetic effects of SCS on CBF. Method SpragueDawley rats were selected for the experimental series. The animals were divided into 5 groups to underwent SCS and laser Doppler flowmeter （LDF） recordings. Control group, the animal underwent SCS and LDF recordings without any surgery of the nerve fibers and ganglia. V 1 group, the animal underwent bilateral resection of the nasociliary and post-ganglionic parasympathetic nerve fibbers. SCG group, the animal underwent bilateral resection of supper cervical ganglion. V 1 ＋ SCG group, the animal underwent both surgeries as V1- and SCG-group animals did. Sham group, the animal underwent the carotid manipulation with blunt-tipped forceps as well as the dissection of nasociliary and post-ganglionic parasympathetic nerve fibers around the ethmoidal foramen, but without cutting any nerves. Results During the SCS, the LDF was no statistical difference between the V 1 or SCG group and the control group. Yet, the effects of SCS on CBF are completely abolished in V1＋ SCG group. Conclusions Surgical interruption of both the parasympathetic and sympathetic pathways has the contradict effect on SCS-induced CBF augmentation.

Regulation of axonal regeneration following the central nervous system injury in adult mammalian

It has been well established that the recovery ability of central nervous system （CNS） is very poor in adult mammals. As a result, CNS trauma generally leads to severe and persistent functional deficits. Thus, the investigation in this field becomes a ＂hot spot＂. Up to date, accumulating evidence supports the hypothesis that the failure of CNS neurons to regenerate is not due to their intrinsic inability to grow new axons, but due to their growth state and due to lack of a permissive growth environment. Therefore, any successful approaches to facilitate the regeneration of injured CNS axons will likely include multiple steps： keeping neurons alive in a certain growth-state, preventing the formation of a glial scar, overcoming inhibitory molecules present in the myelin debris, and giving direction to the growing axons. This brief review focused on the recent progress in the neuron regeneration of CNS in adult mammals.

颐神养脑胶囊对血管性痴呆大鼠认知功能的影响及其机制研究

目的:探讨颐神养脑胶囊对血管性痴呆大鼠(VD)的认知功能的影响及其作用机制。方法:采用双侧颈动脉永久性结扎(间隔7天分2次结扎)复制血管性痴呆模型,以Morris水迷宫法进行学习记忆能力测试;并测定脑组织乙酰胆碱酯酶(AchE)、乙酰胆碱转移酶(CHAT)、五羟色胺(5-HT)、超氧化物歧化酶(SOD)和丙二醛(MDA)含量;免疫组化染色法观察海马区Caspase-3、bax蛋白的阳性表达。结果:480mg/kg的颐神养脑胶囊能够显著提高血管性痴呆大鼠学习记忆能力,显著降低血管性痴呆大鼠脑组织AchE和MDA含量,升高脑组织CHAT、5-HT及SOD含量,显著减少血管性痴呆大鼠海马区Bax蛋白和Caspase-3蛋白阳性表达,减少海马区神经细胞凋亡。结论:颐神养脑胶囊能够显著改善VD大鼠的学习记忆功能,其作用机制可能与其增加脑内Ach和5-HT含量、减轻脑组织脂质过氧化损伤、抑制神经细胞凋亡有关。

Efficacy of Spinal Pia Mater Incision and Laminoplasty Combined with Internal Fixation for Old Spinal Cord Injury

Objective To evaluate the clinical efficacy of incising spinal pia mater to relieve pressure and unilateral open-door laminoplasty with internal screw fixation for treatment of the dated spinal cord injury. Methods From March, 2009 to July, 2010, 16 cases with chronic cervical cord injury underwent spinal dura mater incision and unilateral open-door laminoplasty with internal screw fixation. Nerve functions of preand postoperation were evaluated by Frankel classification and the Japanese Orthopaedic Association (JOA) scale. The improvement rate of JOA score at the indicated time was recorded. Results Postoperative Frankel classification rating of 16 patients improved obviously. JOA scores at the 1st month, 3rd month, 6th month, and 12th month after surgery were 7.9±2.3, 8.5±1.6, 8.9±2.1, and 12.4±2.5, respectively, and significantly increased compared with that prior to surgery (5.5±0.6). At the end of follow-up period, JOA score was significantly higher than that of pre-treatment (P<0.05). The recovery was relatively rapid during the first 3 months following the surgery, then entered a platform period. Conclusion It is effective for patients with dated spinal cord injury to undergo spinal decompression and laminoplasty.

Repair of glutamate-induced excitotoxic neuronal damage mediated by intracerebroventricular transplantation of neural stem cells in adult mice

Objective To investigate a possibility of repairing damaged brain by intracerebroventricular transplantation of neural stem cells （NSCs） in the adult mice subjected to glutamate-induced excitotoxic injury. Methods Mouse NSCs were isolated from the brains of embryos at 15-day postcoitum （dpc）. The expression of nestin, a special antigen for NSC, was detected by immunocytochemistry. Immunofluorescence staining was carried out to observe the survival and location of transplanted NSCs. The animals in the MSG＋NSCs group received intracerebroventricular transplantation of NSCs （approximately 1.0×10^5 cells） separately on day 1 and day 10 after 10-d MSG exposure （4.0 g/kg per day）. The mice in control and MSG groups received intracerebroventricular injection of Dulbecco＇s minimum essential medium （DMEM） instead of NSCs. On day 11 after the last NSC transplantation, the test of Y-maze discrimination learning was performed, and then the histopathology of the animal brains was studied to analyze the MSG-induced functional and morphological changes of brain and the effects of intracerebroventricular transplantation of NSCs on the brain repair. Results The isolated cells were Nestin-positive. The grafted NSCs in the host brain were region-specifically survived at 10-d post-transplantation. Intracerebroventricular transplantation of NSCs obviously facilitated the brain recovery from glutamate-induced behavioral disturbances and histopathological impairs in adult mice. Conclusion Intracerebroventricular transplantation of NSCs may be feasible in repairing diseased or damaged brain tissue.

Maternal zinc deficiency impairs brain nestin expression in prenatal and postnatal mice

Effects of maternal dietary zinc deficiency on prenatal and postnatal brain development were investigated in ICR strain mice. From d 1 of pregnancy (E0) until postnatal d 20 (P20), maternal mice were fed experimental diets that contained 1 mg Zn/kg/day (severe zinc deficient, SZD), 5 mg Zn/kg/day (marginal zinc deficient, MZD), 30 mg Zn/kg/day (zinc adequately supplied, ZA) or 100 mg Zn/kg/day (zinc supplemented, ZS and pair-fed, PF). Brains of offspring from these dietary groups were examined at various developmental stages for expression of nestin, an intermediate filament protein found in neural stem cells and young neurons. Immunocytochemistry showed nestin expression in neural tube 10.5 d post citrus (dpc) as well as in the cerebral cortex and neural tube from 10.5 dpc to postnatal d 10 (P10). Nestin immunoreactivities in both brain and neural tube of those zinc-supplemented control groups (ZA, ZS, PF) were stronger than those in zinc-deficient groups (SZD and MZD). Western blot analysis confirmed that nestin levels in pooled brain extracts from each of the zinc-supplemented groups (ZA, ZS, PF) were much higher than those from the zinc-deficient groups (SZD and MZD) from 10.5 dpc to P10. Immunostaining and Western blots showed no detectable nestin in any of the experimental and control group brains after P20. These observations of an association between maternal zinc deficiency and decreased nestin protein levels in brains of offspring suggest that zinc deficiency suppresses development of neural stem cells, an effect which may lead to neuroanatomical and behavioral abnormalities in adults.

New technologies to investigate the brain-gut axis

Functional gastrointestinal disorders are commonly encountered in clinical practice, and pain is their commonest presenting symptom. In addition, patients with these disorders often demonstrate a heightened sensitivity to experimental visceral stimulation, termed visceral pain hypersensitivity that is likely to be important in their pathophysiology. Knowledge of how the brain processes sensory information from visceral structures is still in its infancy. However, our understanding has been propelled by technological imaging advances such as functional Magnetic Resonance Imaging, Positron Emission Tomography, Magnetoencephalography, and Electroencephalography （EEG）. Numerous human studies have non-invasively demonstrated the complexity involved in functional pain processing, and highlighted a number of subcortical and cortical regions involved. This review will focus on the neurophysiological pathways （primary afferents, spinal and supraspinal transmission）, brainimaging techniques and the influence of endogenous and psychological processes in healthy controls and patients suffering from functional gastrointestinal disorders. Special attention will be paid to the newer EEG source analysis techniques. Understanding the phenotypic differences that determine an individual＇s response to injurious stimuli could be the key to understanding why some patients develop pain and hyperalgesia in response to inflammation/injury while others do not. For future studies, an integrated approach is required incorporating an individual＇s psychological, autonomic, neuroendocrine, neurophysiological, and genetic profile to define phenotypic traits that may be at greater risk of developing sensitised states in response to gut inflammation or injury.