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Pain Brain Images

Pain in the Brain

There are several mechanisms that can create a sensation of pain, which has been described as 'an unpleasent sensory and emotional experience in response to perceived or potential tissue damage'. Hence, pain can be the result of peripheral inflammation, vascular compromise, necrosis, swelling, etc. Importantly, higher centres of the central nervous system not only perceive such sensitization of the peripheral nerve receptors, they can also modulate and control the intensity and tolerability of the perceived sensation. However, the higher centres can create a 'state' of perceived 'threat' to the body through emotions such as fear and anxiety. Rather than the brain acting as a filter of unwanted sensation, in the higher centre induced pain state, rumination and magnification of sensations occur to create a pathological state.  In such instances the pain doesn't represent the sensation of pathology but rather pain has become the pathology. Hence, the brain generates pain in the brain, where the pain is perceived to be some sort of non-existant inflammatory or pathological sensation in the periphery. Furthermore, brain white matter structural properties have been shown to predict transition to chronic pain (Mansour et al 2013, Pain, 154, 10, 2160-2168). Specifically, differential structural connectivity to medial vs lateral prefrontal cortex and connectivity between medial prefrontal cortex and nucleus accumbens in people with persistent low back pain. In this case the back pain becomes the inciting event and given the persons' structural propensity, establishes specific functional coonectivity strength.  The following are a pictorial representation of research depicting normal and pathological pain processing in the brain.

fMRI pain signature Wager 2013

This image created by Tor Wager of the University of Colorado, Boulder shows regions of the "neurologic pain signature," a standard map that can be applied to individual people who may be experiencing pain. The map was developed based on heat pain applied to a group of participants' forearms. Activity in yellow-colored areas is predictive of higher levels of pain, and activity in blue-colored areas is predictive of lower levels of pain. In a provocative new study, scientists reported Wednesday, April 10, 2013 that they were able to “see” pain on brain scans and, for the first time, measure its intensity and tell whether a drug was relieving it. Though the research is in its early stages, it opens the door to a host of possibilities. Scans might be used someday to tell when pain is hurting a baby, someone with dementia or a paralyzed person unable to talk. They might lead to new, less addictive pain medicines. (AP Photo/University of Colorado, Boulder, Tor Wager)


Brain imaging of spatial discrmination versus perceived pain

Brain activation related to spatial discrimination of noxious stimuli is distinct from that related to perceived pain. These images are located at x = 0 mm, x = 30 mm, z = 5 mm, and y = –30 mm in standard stereotaxic space. IPL/SPL, Inferior parietal lobule/superior parietal lobule; GP/PT, globus pallidus/putamen; M1, primary motor cortex; DISCRIM., discrimination. (Oshiro et al The Journal of Neuroscience, March 28, 2007, 27(13):3388-3394)

Spontaneous brain activity in chronic low back pain

Brain activity for spontaneous CBP shows two distinct patterns: one for phases identified as high pain and another for increasing pain phases. A, Random-effects average brain activity in CBP patients for time periods in which spontaneous pain is high. Activity is limited mainly to the mPFC and rACC. B, Fixed-effects analysis yields additional activations bilaterally in posterior thalamus, amygdala, and ventral striatum (VS). C, BOLD response for peak activations in rACC (10, 22, 28) and mPFC (18, 60, 12) for periods when spontaneous pain is high. Across-subject mean and SEMs are shown. D, Random-effects analysis for periods when spontaneous pain is increasing. Brain activity does not overlap with A and is primarily located in right anterior insula, mACC, and supplementary motor area (SMA), left primary somatosensory (S1), and motor (M1) regions, right secondary somatosensory cortex (S2), and cerebellum. Fixed-effect analysis did not reveal additional brain activity (data not shown). E, BOLD response for peak activations in the mACC (0, 3, 46), right insula (54, 16, –4) and right S2 (46, –20, 28) for time period when spontaneous pain is increasing. Across-subject mean and SEMs are shown. A complete list of activations is found in supplemental tables 2 and 3, available at as supplemental material. Activity maps are presented in MNI space, x, y, and z coordinates in millimeters. Baliki et al, The Journal of Neuroscience, November 22, 2006, 26(47):

Spontaneous chronic Low back pain

Spontaneous brain activity in chronic low back pain

(1) the insular region correlated with pain duration is active during increases in pain whereas mPFC (medial prefrontal cortex) region is not, and (2) the mPFC region best correlated to intensity of pain is active during high pain (for a longer duration than the insula) and in this time period the insular activity is transient and precedes the mPFC activity. This analysis indicates that intensity and duration of CBP can be explained by the differential activity for the two phases of spontaneous pain. (Baliki et al 2006)

Brain activity to thermal stimuli in CLBP

A, Average pain ratings for thermal stimulus applied to the back in CBP patients (n = 11) and matched normal controls (n = 11). There is no significant difference in pain ratings between the two groups. Bottom shows temperature profile of the stimulus applied to the  back. B, Random-effects average brain activity for high pain of spontaneous CBP includes mPFC and rostral parts of the anterior cingulate. It is similar to the brain activity pattern observed for spontaneous pain in study 1 (compare Fig. 1A) and does not encompass brain areas activated for noxious heat in CBP (middle) and matched healthy controls (right). C, Similar brain activity patterns are seen for noxious heat applied to the back in CBP (orange) and in healthy normal subjects (blue). It includes the bilateral insular cortex, medial ACC, and supplementary motor areas, in addition to cerebellum and somatosensory regions. Baliki et al The Journal of Neuroscience, November 22, 2006, 26(47)

Nocebo Hyperalgesia

Nocebo hyperalgesia

Kong et al ; J Neurosci. 2008 December 3; 28(49)

Brain regions displaying different frequencies of activation between high- and low-sensitivity subgroups

high and low sensitivity brain imaging

Brain regions displaying different frequencies of activation between high- and low-sensitivity subgroups. Circles are centered on regions where the peak differences between groups were located. Colors in A and C correspond to the number of individuals displaying statistically significant activation at a given voxel (frequency), whereas colors in B and D correspond to the z-score of the subgroup analysis. Slice locations in A and B are - 2 mm from the midline, whereas slice locations in B and C are 32 mm from the midline (in standard stereotaxic space). Structural MRI data (gray) are averaged across all individuals involved in corresponding functional analysis. Coghill R C et al. PNAS 2003;100:8538-8542

Changes in pain-related activity associated with previous hypnotic training by using suggestions for modulating pain sensation (Upper) or pain unpleasantness (Lower)

Hypnosis and pain

Changes in pain-related activity associated with previous hypnotic training by using suggestions for modulating pain sensation (Upper) or pain unpleasantness (Lower). Both images represent data from control scans, in which no hypnotic suggestions were given. Each image represents the subtraction of PET data recorded when the hand was submerged in thermally neutral water (35°C) from data recorded when the hand was submerged in painfully hot water (47°C). PET data were averaged across 10 experimental sessions in the sensory study (Upper) and, in a different group of subjects, 11 experimental sessions in the affective study (Lower). The PET data are illustrated against the average MRI for that subject group. Bushnell M C et al. PNAS 1999;96:7705-7709

Pain and Fear

Pain and Fear Brain imaging

Brain activations in each contrast. Activated brain areas in each contrast: pain – rest, fear – rest, and pain – fear conditions. Pain – rest and pain – fear contrasts revealed activations in the SII region and PPC areas and in the affective components of the pain matrix such as the ACC, anterior insula, and cerebellum while viewing images showing painful events. The fear – rest contrast revealed activations in the left amygdala and ACC. Ogini et al (2006) Cerebral Cortex, 17, 5, 1139-1147

Motor cortical representation and pain

Motor cortical representations have been shown to change in the presence of chronic pain.Trans-cortical stimulation investigations in women with chronic knee pain have shown a reduced volume and location of the quadriceps muscle and especially the VMO (vastus medialis) in the brain. Interestingly, peripheral electrical muscle stimolation can re-establish muscle cortical representation.

The representation of the knee muscles in the brain


The research findings present an interesting dimension in the treatment of musculoskeletal disorders. Whilst the Musculoskeletal and Manipulative Physiotherapist use their hands to treat the biomechanics and neurophysiology of the peripheral nervous system and its pathology, the use of exercise regimes and cognitive strategies inducing central nervous system involvement is always inherently important. Since the brain is use to instigating motor responses, it is plausible that the 'motoric intent' determines the signifance of sensations from the peripheral nervous system, rather than what was commonly believed to be that sensation determined motor responses. However, in some instances, the brain can magnify the pain through increased arousal towards a 'perceived or real threat', with the consequence that the person only ever sees the 'negative', where 'the bucket is only ever 1/2 empty'. Manifestations of 'learned helplessness' may occur, giving rise to severe deconditioning through 'fear-avoidance' behaviour which affects the immune system. It is important for the person to understand the way pain is processed in the brain and how thought processes can turn a 'bad' pain into a 'good' pain, or alternatively, a normal sensation can be turned into a pathological one due to rumination and magnification of innocuous stimuli.

Hence, higher centres need to be engaged in rational cognitive processing. This may be reflected in something as simple as establishing a dialogue with the client, where 'concerns, fears, beliefs and anxieties' can be ascertained, and whereby explanations can be given, misconceptions are nullified, and empathy can be shown towards the person suffering an affliction.  The brain is like a highly tuned orchestra where multiple brain functions are integrated for movement. Client expectations and perceptions will drive the outcome, it is up to the clinician to bring clarity into the management process, by introducing the conductor to the orchestra. Please read the sections about chronic low back pain and the immune system elsewhere on this website.

 Updated : 6 March 2017

ini et al (2006) Cerebral Cortex, 17, 5, 1139-1147


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  • Thu 22 Dec 2016

    Ehlers Danlos Syndrome

    Is your child suffering Ehlers Danlos Syndrome? Hypermobile joints, frequent bruising, recurrent sprains and pains? Although a difficult manifestation to treat, physiotherapy can help. Joint Hypermobility Syndrome (JHS) When joint hypermobility coexists with arthralgias in >4 joints or other signs of connective tissue disorder (CTD), it is termed Joint Hypermobility Syndrome (JHS). This includes conditions such as Marfan's Syndrome and Ehlers-Danlos Syndrome and Osteogenesis imperfecta. These people are thought to have a higher proportion of type III to type I collagen, where type I collagen exhibits highly organised fibres resulting in high tensile strength, whereas type III collagen fibres are much more extensible, disorganised and occurring primarily in organs such as the gut, skin and blood vessels. The predominant presenting complaint is widespread pain lasting from a day to decades. Additional symptoms associated with joints, such as stiffness, 'feeling like a 90 year old', clicking, clunking, popping, subluxations, dislocations, instability, feeling that the joints are vulnerable, as well as symptoms affecting other tissue such as paraesthesia, tiredness, faintness, feeling unwell and suffering flu-like symptoms. Autonomic nervous system dysfunction in the form of 'dysautonomia' frequently occur. Broad paper like scars appear in the skin where wounds have healed. Other extra-articular manifestations include ocular ptosis, varicose veins, Raynauds phenomenon, neuropathies, tarsal and carpal tunnel syndrome, alterations in neuromuscular reflex action, development motor co-ordination delay (DCD), fibromyalgia, low bone density, anxiety and panic states and depression. Age, sex and gender play a role in presentaton as it appears more common in African and Asian females with a prevalence rate of between 5% and 25% . Despite this relatively high prevalence, JHS continues to be under-recognised, poorly understood and inadequately managed (Simmonds & Kerr, Manual Therapy, 2007, 12, 298-309). In my clinical experience, these people tend to move fast, rely on inertia for stability, have long muscles creating large degrees of freedom and potential kinetic energy, resembling ballistic 'floppies', and are either highly co-ordinated or clumsy. Stabilisation strategies consist of fast movements using large muscle groups. They tend to activities such as swimming, yoga, gymnastics, sprinting, strikers at soccer. Treatment has consisted of soft tissue techniques similar to those used in fibromyalgia, including but not limited to, dry needling, myofascial release and trigger point massage, kinesiotape, strapping for stability in sporting endeavours, pressure garment use such as SKINS, BSc, 2XU, venous stockings. Effectiveness of massage has been shown to be usefull in people suffering from chronic fatigue syndrome (Njjs et al 2006, Man Ther, 11, 187-91), a condition displaying several clinical similarities to people suffering from EDS-HT. Specific exercise regimes more attuned to co-ordination and stability (proprioception) than to excessive non-stabilising stretching. A multi-modal approach including muscle energy techniques, dry needling, mobilisations with movement (Mulligans), thoracic ring relocations (especially good with autonomic symptoms), hydrotherapy, herbal supplementaion such as Devils Claw, Cats Claw, Curcumin and Green Tee can all be useful in the management of this condition. Additionally, Arnica cream can also be used for bruising. Encouragment of non-weight bearing endurance activities such as swimming, and cycling to stimulate the endurance red muscle fibres over the ballistic white muscles fibres, since the latter are preferably used in this movement population. End of range movements are either avoided or done with care where stability is emphasized over mobility. People frequently complain of subluxation and dislocating knee caps and shoulders whilst undertaking a spectrum of activities from sleeping to sporting endeavours. A good friend of mine, Brazilian Physiotherapist and Researcher, Dr Abrahao Baptista, has used muscle electrical stimulation on knees and shoulders to retrain the brain to enhance muscular cortical representation which reduce the incidence of subluxations and dislocations. Abrahao wrote : "my daughter has a mild EDS III and used to dislocate her shoulder many times during sleeping.  I tried many alternatives with her, including strenghtening exercises and education to prevent bad postures before sleeping (e.g. positioning her arm over her head).  What we found to really help her was electrostimulation of the supraspinatus and posterior deltoid.  I followed the ideas of some works from Michael Ridding and others (Clinical Neurophysiology, 112, 1461-1469, 2001; Exp Brain Research, 143, 342-349 ,2002), which show that 30Hz electrostim, provoking mild muscle contractions for 45' leads to increased excitability of the muscle representation in the brain (at the primary motor cortex).  Stimulation of the supraspinatus and deltoid is an old technique to hemiplegic painful shoulder, but used with a little different parameters.  Previous studies showed that this type of stimulation increases brain excitability for 3 days, and so we used two times a week, for two weeks.  After that, her discolcations improved a lot.  It is important to note that, during stimulation, you have to clearly see the humerus head going up to the glenoid fossa" Surgery : The effect of surgical intervention has been shown to be favourable in only a limited percentage of patients (33.9% Rombaut et al 2011, Arch Phys Med Rehab, 92, 1106-1112). Three basic problems arise. First, tissues are less robust; Second, blood vessel fragility can cause technical problems in wound closure; Third, healing is often delayed and may remain incomplete.  Voluntary Posterior Shoulder Subluxation : Clinical Presentation A 27 year old male presented with a history of posterior shoulder weakness, characterised by severe fatigue and heaviness when 'working out' at the gym. His usual routine was one which involved sets of 15 repetitions, hence endurance oriented rather than power oriented. He described major problems when trying to execute bench presses and Japanese style push ups. In a comprehensive review of 300 articles on shoulder instability, Heller et al. (Heller, K. D., J. Forst, R. Forst, and B. Cohen. Posterior dislocation of the shoulder: recommendations for a classification. Arch. Orthop. Trauma Surg. 113:228-231, 1994) concluded that posterior dislocation constitutes only 2.1% of all shoulder dislocations. The differential diagnosis in patients with posterior instability of the shoulder includes traumatic posterior instability, atraumatic posterior instability, voluntary posterior instability, and posterior instability associated with multidirectional instability. Laxity testing was performed with a posterior draw sign. The laxity was graded with a modified Hawkins scale : grade I, humeral head displacement that locks out beyond the glenoid rim; grade II, humeral displacement that is over the glenoid rim but is easily reducable; and grade III, humeral head displacement that locks out beyond the glenoid rim. This client had grade III laxity in both shoulders. A sulcus sign test was performed on both shoulders and graded to commonly accepted grading scales: grade I, a depression <1cm: grade 2, between 1.5 and 2cm; and grade 3, a depression > 2cm. The client had a grade 3 sulcus sign bilaterally regardless if the arm was in neutral or external rotation. The client met the criteria of Carter and Wilkinson for generalized liagmentous laxity by exhibiting hyperextension of both elbows > 10o, genu recurvatum of both knees > 19o, and the ability to touch his thumbto his forearm Headaches Jacome (1999, Cephalagia, 19, 791-796) reported that migraine headaches occured in 11/18 patients with EDS. Hakim et al (2004, Rheumatology, 43, 1194-1195) found 40% of 170 patients with EDS-HT/JHS had previously been diagnosed with migraine compared with 20% of the control population. in addition, the frequency of migraine attacks was 1.7 times increased and the headache related disability was 3.0 times greater in migraineurs with EDS-HT/JHS as compared to controls with migraine (Bendick et al 2011, Cephalgia, 31, 603-613). People suffering from soft tissue hypermobility, connective tissue disorder, Marfans Syndrome, and Ehler Danlos syndrome may be predisposed to upper cervical spine instability. Dural laxity, vascular irregularities and ligamentous laxity with or without Arnold Chiari Malformations may be accompanied by symptoms of intracranial hypotension, POTS (postural orthostatic tachycardia syndrome), dysautonomia, suboccipital "Coat Hanger" headaches (Martin & Neilson 2014 Headaches, September, 1403-1411). Scoliosis and spondylolisthesis occurs in 63% and 6-15% of patients with Marfans syndrome repsectively (Sponseller et al 1995, JBJS Am, 77, 867-876). These manifestations need to be borne in mind as not all upper cervical spine instabilities are the result of trauma. Clinically, serious neurological complications can arise in the presence of upper cervical spine instability, including a stroke or even death. Additionally, vertebral artery and even carotid artery dissections have been reported during and after chiropractic manipulation. Added caution may be needed after Whiplash type injuries. The clinician needs to be aware of this possibility in the presence of these symptoms, assess upper cervical joint hypermobility with manual therapy techniques and treat appropriately, including exercises to improve the control of musculature around the cervical and thoracic spine. Atlantoaxial instability can be diagnosed by flexion/extension X-rays or MRI's, but is best evaluated by using rotational 3D CT scanning. Surgical intervention is sometimes necessary. Temperomandibular Joint (TMJ) Disorders The prevelence of TMJ disorders have been reported to be as high as 80% in people with JHD (Kavucu et al 2006, Rheum Int., 26, 257-260). Joint clicking of the TMJ was 1.7 times more likely in JHD than in controls (Hirsch et al 2008, Eur J Oral Sci, 116, 525-539). Headaches associated with TMJ disorders tend to be in the temporal/masseter (side of head) region. TMJ issues increase in prevelence in the presence of both migraine and chronic daily headache (Goncalves et al 2011, Clin J Pain, 27, 611-615). I've treated a colleague who spontaneously dislocated her jaw whilst yawning at work one morning. stressful for me and her! Generally, people with JHD have increased jaw opening (>40mm from upper to lower incisors). Updated 18 May 2017  Read More
  • Fri 09 Dec 2016

    Physiotherapy with Sharna Hinchliff

    Physiotherapy with Sharna Hinchliff    Martin is pleased to welcome the very experienced physiotherapist Sharna Hinchliff to Back in Business Physiotherapy for one on one physiotherapy sessions with clients in 2017.  Sharna is a passionate triathelete and mother and has had several years experience working locally and internationally (New York and London) in the field of physiotherapy. Originally from Western Australia, Sharna graduated from the world renowned Masters of Manipulative Physiotherapy at Curtin University. read more Read More
  • Mon 07 Nov 2016

    Pilates – with Brunna Cardoso

    Pilates – with Brunna Cardoso Martin is pleased to welcome the bubbly Brunna Cardoso to Back in Business Physiotherapy for Pilates Classes in February 2017.  Brunno is an experienced pilates instructor and has had several years experience training with pilates instructors in Brazil. Read more Read More

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Updated : 10 May 2014

No responsibility is assumed by Back in Business Physiotherapy for any injury and/or damage to persons or property as a matter of product liability, negligence, or from any use of any methods, products, instruction, or ideas contained in the material in this and it's related websites. Because of rapid advances in the medical sciences, the author recommends that there should be independent verification of diagnoses and exercise prescription. The information provided on Back in Business Physiotherapy is designed to support, not replace, the relationship that exists between a patient/site visitor and their treating health professional.

Copyright Martin Krause 1999 - material is presented as a free educational resource however all intellectual property rights should be acknowledged and respected