Rotational movements best therapy for Pain

 i found through my practice Rotational movements are the best approach for addressing pain and motion limitation in spine , hip , shoulder, wrists and ankles .

 

 

Cat Stretch & Mobilization for Shoulder

In cases of shoulder joint limited movments in abduction , flextiox such as frozen shoulder and capsulitis i found catch stretch and mobilization movements are of great value for improving range of motion espicially after acute stage after pain subsides .

I ask the patient to take this postion then rock forward , backward and side to side , this will be great if accompanied  by somatics concept of feel , eye closure .

Pain after I fall on my hand

3 days ago , I took my bicycle early morning to work , there were heavey rains  that nigt . I biked litttle fast ,then I had to use the brake on a downroad woden bridge , I fall on my face front supporting on my right hand . The palm  skin  crushed ( not much ) over the scaphoid bone .

I returned back to my apartment , washing my hand using cold water , then I put tap over it .I conutined my day to work , but I could not use my hand , I was really concerned about the scaphoid bone because I had seen many patient with fracture scaphoid bone .

I stopped using my hand on computer and in my work for about 2 hours  . I noted redness of my hand and more pain , I removed the tap and used my hand as normal by 60% , that was very very good , I noted my hand began to return back normal .

Seems looking at the body as normal is of great value , besides to use it as normal but in simple kind way of ordinary daily life activties to keep circular system mobile as possible .Now after 5 days , every thing is nearly normal by 90% .

It was chance to exprience pain . 

Trauma related chronic pain linked to PTSD

GLENVIEW, Ill., July 22 (UPI) — Patients with accident- or trauma-related chronic pain often have post-traumatic stress disorder and depression, University of Michigan researchers said. 

However, what isn’t clearly known, however, is how PTSD relates to mood disorders and pain severity in chronic pain patients.

University of Michigan researchers examined the contribution of PTSD to the pain experience, functional disability and frequency of depressive symptoms. They studied 241 patients referred to the university hospital’s pain rehabilitation program who reported their pain began after a traumatic injury. The subjects completed the McGill Pain Questionnaire and were administered the Pain Disability Index and the Post-traumatic Chronic Pain Test.

The study found PTSD and depression were significantly correlated and both disorders were associated with perceived disability attributed to chronic pain.

The study authors concluded that increased attention to treating PTSD as a primary focus in the rehabilitation of patients with chronic pain and co-morbid depression is important when prior treatment efforts for pain and depression have not been successful

Women feel chronic pain more than men

Women feel chronic pain more than men because their brains are different

By Lucy Cockcroft

Women feel pain more than men because their brains are not “wired” in the same way, scientists believe.

New research suggests that the basic architecture of the brain, and the way it operates, is different in the two sexes.

Previously the different sensitivity to pain between the sexes had been explained by hormones and social pressures.

However, a series of studies have suggested that there “is not just one kind of human brain, but two”, a male version and a female version.

It is well known that women are more likely to seek help for chronic pain than men, and the differences in the brain could explain this.

Men have a pain-suppressing circuit which links their brain to their spinal cord. When the circuit is activated by pain, endorphins are released and help lessen the feeling.

However, new studies have shown that the circuit does not release the analgesic endorphins in women.

Dr Anne Murphy at the University of Georgia in Athens has been examining the anomaly. She said: “This circuit is the Mecca of pain modulation in humans and all vertebrates, yet no one has asked how it is organised in females.

“This pathway is obviously not being used for pain in females.”

In one experiment, scientists chemically blocked the pain receptors found in the brain and spinal cord of a male and female mouse. While this helped control the feeling in the male mice, it had little effect on the females.

Dr Jeff Mogil, who led the research at McGill University in Montreal, Canada, said: “It suggests females have a separate pathway.”

The discovery could have an impact for how pain and illnesses in women are treated. Most of what is currently known about the brain comes from studies of male animals and male human volunteers.

A report, published in the New Scientist today, said: “If even a small proportion of what has been inferred from these studies does not apply to females, it means a huge body of research has been built on shaky foundations.

“Working out exactly how women are different could explain some long-running mysteries, such as why men and women are prone to different mental health problems and why some drugs work well for one sex but have little effect on the other.”

Recent research has suggested that male and female brains are built from markedly different genetic blueprints, which create numerous anatomical differences.

There are also differences in the circuitry that “wires them up” and the chemicals that transmit messages between brain cells, as well as a proportionate size difference in some areas of a male and female brain.

“The mere fact that a structure is different in size suggests a difference in functional organisation,” said neurobiologist Dr Larry Cahill of California University.

Dr Cahill carried out a series of brain-imaging experiments, in which he asked groups of men and women to recall emotionally charged images they had been shown earlier.

He also found that the different sexes used their brains in different ways.

Both men and women consistently recruited the same bundle of neutrons for the task. However, the men enlisted the right side of it, whereas women used the left.

And males recalled the gist of the situation whereas females concentrated on the details

How emotional pain can really hurt

Love really does hurt, just as poets and song lyric writers claim.

New brain scanning technologies are revealing that the part of the brain that processes physical pain also deals with emotional pain.

And in the same way that in some people injury can cause long-lasting chronic pain, science now reveals why some will never get over such heartbreak.

Emotional pain can take many forms; a relationship break-up or social exclusion, for example.

But it does not get any more extreme than losing a loved one, as Scottish broadcaster Mark Stephen did.

In July 1995 he was driving a tractor while hay-making and accidentally hit his young daughter. She died shortly afterwards.

Mark’s grief was overwhelming, he says

“When people talk about a broken heart, that for me was where it was seated, just below your sternum.

“It feels like your heart is leaking and you can’t run away from it because you are the source of that pain.”

Thinking he would go mad with grief, he sought help from David Alexander.

Professor Alexander is director of the Aberdeen Centre for Trauma Research. He led the psychiatric team that first responded to the Piper Alpha oil-rig disaster.

Since then, he has been involved in helping survivors of many disasters including the Asian tsunami, the war in Iraq and, most recently, the earthquake in Pakistan.

He also managed to get Mark Stephen through his darkest days.

‘My guts are aching’

Professor Alexander is not surprised about the link between physical and emotional pain:

“If you listen to people who are damaged emotionally, they will often translate their pain into physical similes: ‘My head is bursting, my guts are aching’ and so on. The parallel is very strong.”

But medical research has tended to concentrate on physical pain.

Neuroscientist Mary Frances O’Connor at the University of California, Los Angeles (UCLA) is one of the scientists who have propelled emotional pain up the research agenda.

“We’re at a very new time when we can use technologies to look at the brain and the heart,” she says.

Naomi Eisenberger at UCLA has shown which parts of the brain are active when we feel emotional pain.

She devised an intriguing computer game in which participants were deliberately made to feel left out.

Simultaneous brain scanning revealed that the pain of being socially rejected was processed in much the same way in the brain as physical pain and in the same area, the anterior cingulate cortex.

‘Complex grief’

Why should physical and emotional pain be linked in this way?

Social relationships are crucial to our survival as a species. In dangerous situations, a lone human is in peril whereas a group may survive.

“The social attachment system is piggy-backed onto the physical pain system to make sure we stay connected to close others,” says Naomi Eisenberger.

“Being wrenched from another or rejected by a group is painful, so we avoid it.”

There is an increased risk of dying in the six months after bereavement Professor Martin Cowie, Brompton Hospital

 

Physical pain warns us not to do something, walk on a broken ankle for instance. And emotional pain too can be a warning – “don’t go near that sort of man again”, “avoid women like her”.

But sometimes physical pain can become chronic, long outlasting its original purpose, and emotional pain is the same.

Mary Frances O’Connor calls it “complex grief” and it occurs in about 10% of people after bereavement.

“They experience a lot of bitterness and anger, that their future is senseless. They don’t adapt with time as others do.”

There is a very strong suspicion that people who are not adapting to bereavement are also those who experience the greatest levels of physical pain.

But can we die from a broken heart?

Martin Cowie is professor of cardiology at the Brompton Hospital. He is very sure of the answer: “Yes, we can.

“There is an increased risk of dying in the six months after bereavement and it’s particularly marked amongst men.”

The bereaved are much more likely to be involved in accidents, which is perhaps understandable, but also to die from heart attacks and stroke. The hormones involved in the stress of bereavement make these events more likely.

This knowledge makes it essential to identify and treat those whose emotional pain is likely to become chronic, causing debilitating depression or even death.

The Pain Of Emotion will be broadcast on Monday, 21 July, 2008 at 2100 BST on BBC Radio 4, and for seven days on BBC iPlaye

Nerves Behind Pain Relief Provided By Stressful Situations

ScienceDaily (Jun. 17, 2008) — The increased beating of the heart that one experiences when in a stressful situation is just one part of the body’s response to stress, something often known as the “fight-or-flight response”.  Another component of the fight-or-flight response is the suppression of pain, also known as stress-induced analgesia (SIA).

Some of the nerves and nerve-produced peptides that are responsible for SIA have been identified, but much remains to be discovered. In a new study, a team of researchers in California, from AfaSci, Inc., Burlingame, and SRI International, Menlo Park, has revealed that nerves producing the peptide N/ORQ and nerves producing the peptide Hcrt are key in regulating SIA in mice.

The research team, which was led by Xinmin Xie and Thomas Kilduff, showed that in the brain of normal mice, Hcrt-producing nerve cells (Hcrt neurons) and N/ORQ-producing nerve cells interacted. N/ORQ affected the electrical current across Hcrt neurons and the release of neurotransmitters by these cells.

Furthermore, administration of N/ORQ blocked SIA in normal mice, but this was overcome by administration of Hcrt at the same time. The authors therefore conclude that N/ORQ likely influences a variety of Hcrt-mediated processes, in addition to SIA, and suggest that these pathways might contribute to medical conditions caused by excessive stress, such as anxiety and post-traumatic stress disorder.

---

Journal reference:

1. Xinmin (Simon) Xie, Thomas Kilduff et al. Hypocretin/orexin and nociceptin/orphanin FQ coordinately regulate analgesia in a mouse model of stress-induced analgesia. Journal of Clinical Investigation, June 12, 2008

Adapted from materials provided by Journal of Clinical Investigation, via EurekAlert!, a service of AAAS.

‘Phantom’ Cell Phone Sensations 

Phantom arms, legs and now cell phone vibrations — you can feel them, you can sense them, but they aren’t really there.Quote:

“If you use your cell phone a lot, it becomes part of you,” says Dr. William Barr, the chief of neuropsychology at the New York University School of Medicine. “You become habituated to it. “It’s like wearing a tight sock all day,” he explains. “When you take it off, you still feel it there on your foot. If your cell phone is not there, you still feel like it is.”

Quote:

Like the phantom limb phenomenon, mysterious cell phone vibrations can also be explained by changing nerve connections in the brain. “Cell phones enter into the neuromatrix of the body — they become appendages,” says Barr. So when you leave your cell phone at home, the brain interprets it as it would a phantom limb — it’s not present, but you feel as though it is. “It’s an interesting technological statement about society that our machines are becoming part of us,” says Barr.Press the Button, Get the MessageKaas says another principle, known as operant conditioning, may also be at play in phantom phone vibrations. In studies of operant conditioning, researchers have found that rats that are rewarded after pressing a lever will learn to press the lever more frequently. The pressing becomes habitual. In the case of cell phones, people are rewarded when they pick up their calls and read their incoming text messages, which causes them to pick up their cell phones more and more frequently.

Quote:

“People are rewarded when they are able to detect low amplitude vibrations so they get better and better at responding,” says Kaas. “It is very rewarding to get the message, so people are able to train their system to detect that signal.” As people repeat this behavior over and over again, connections between nerves in their brain become stronger and new ones are formed, which helps to make the behavior automatic.

Quote:

<H4>Kicking the ‘CrackBerry’ Addiction

Quote:

And just as the brain changes to create phantom sensations, it can also change back to get rid of them. Over time, the phantom limb syndrome goes away as other parts of the brain take over the part that controls the limb. “Sometimes other parts of the brain will move into the real estate occupied by the amputated limb,” says Barr. “Over time, other parts of the brain start to encroach on the part of the brain that represents the phantom limb.” Similarly, experts say that those haunted with BlackBerry vibrations should simply stop using them. “The problem will stop if people stop carrying BlackBerrys,” says Kaas. “It’s not a permanent condition. If people stop carrying their BlackBerrys, the connections between neurons will degrade, and people will be able to retain their neurons to do other things.” However, while phantom sensations arise from similar brain functions, phantom limbs and phantom phone vibrations are in no way similar in how they affect the lives of those experiencing these sensations. Losing a limb and losing a cell phone are not at all comparable, and many experts emphasize that the pain experienced by some amputee victims can be seriously disabling.

Placebo Works in the Brain(Placebo-Neuromodulation)

Researchers Demonstrate How Placebo Effect Works in the Brain  

Columbia University scientists, with colleagues from the University of Michigan, have shown how the neurochemistry of the placebo effect can relieve pain in humans. The scientists found that the placebo effect caused the brains of test volunteers to release more of a natural painkiller.

The placebo effect is an improvement in a medical condition caused by a patient’s belief as opposed to actual treatment. Exactly how the positive expectations created by placebos translate into pain relief had been a mystery until now.Understanding how placebo effects work may give scientists insight into why many drugs have a range of effects on people, how drugs and other treatments work together with psychological states, and how psychology can be effectively used in treatment.The research team was led by Tor Wager, Columbia professor of psychology. “Placebo effects are often observed in clinical practice, but there have been relatively few scientific studies that document the kinds of diseases that can be influenced by placebo treatments and how the treatments work in the brain and body,” Wager said.“Yet, placebo groups are included in virtually every major clinical trial, which is a testament to their importance. Only in the past few years have scientists developed the tools to directly investigate how placebos work in the human brain.”

In the experiment, scientists applied a placebo cream to volunteers’ forearms; volunteers were told it was a pain reliever, though the cream was not. Next, a control cream was applied to a nearby area, and subjects were told it had no effect. Researchers then placed a painfully hot stimulus (similar to a very hot cup of coffee) to both forearm areas and used positron emission tomography (PET) scans to measure and compare brain activity during each application. They found that the placebo treatment caused the brain to release more opioids, a chemical produced by the body and released by the brain, to relieve pain.

The scientists discovered that in the first area treated with a placebo, which volunteers falsely believed to have been treated with a pain reliever, opioid release occurred in brain areas associated with pain relief—in particular, the periadqeductal gray, an area in the brainstem used in neurosurgical interventions to control chronic pain. They also found opioid release in the orbitofrontal cortex and anterior cingulate, parts of the cerebral cortex thought to be related to evaluating and orchestrating responses in the brain and body to deal with a perceived threat—producing, for example, the so-called flight-or-fight response.

“These results extend our knowledge of how beliefs and expectations affect the brain’s neurochemistry and show that one’s mental response to a challenge can affect the brain and body in ways that are relevant to health,” Wager explained. “Understanding these interactions can pave the way for new treatments that are informed by knowledge of mind-body interactions.”

Source: Columbia University

» Next Article in Medicine & Health – Psychology: Prenatal stress keeps infants, toddlers up at night, study says

Neural plasticity after peripheral nerve injury and regeneration

 Prog Neurobiol. 2007 Jun 22; [Epub ahead of print

Navarro X, Vivó M, Valero-Cabré A.

Group of Neuroplasticity and Regeneration, Institute of Neurosciences and Department of Cell Biology, Physiology and Immunology, Universitat Autònoma de Barcelona, E-08193 Bellaterra, Spain; Institut Guttmann, Badalona, Spain.

Injuries to the peripheral nerves result in partial or total loss of motor, sensory and autonomic functions conveyed by the lesioned nerves to the denervated segments of the body, due to the interruption of axons continuity, degeneration of nerve fibers distal to the lesion and eventual death of axotomized neurons. Injuries to the peripheral nervous system may thus result in considerable disability. After axotomy, neuronal phenotype switches from a transmitter to a regenerative state, inducing the down- and up-regulation of numerous cellular components as well as the synthesis de novo of some molecules normally not expressed in adult neurons. These changes in gene expression activate and regulate the pathways responsible for neuronal survival and axonal regeneration. Functional deficits caused by nerve injuries can be compensated by three neural mechanisms: the reinnervation of denervated targets by regeneration of injured axons, the reinnervation by collateral branching of undamaged axons, and the remodeling of nervous system circuitry related to the lost functions. Plasticity of central connections may compensate functionally for the lack of specificity in target reinnervation; plasticity in human has, however, limited effects on disturbed sensory localization or fine motor control after injuries, and may even result in maladaptive changes, such as neuropathic pain, hyperreflexia and dystonia. Recent research has uncovered that peripheral nerve injuries induce a concurrent cascade of events, at the systemic, cellular and molecular levels, initiated by the nerve injury and progressing throughout plastic changes at the spinal cord, brainstem relay nuclei, thalamus and brain cortex. Mechanisms for these changes are ubiquitous in central substrates and include neurochemical changes, functional alterations of excitatory and inhibitory connections, atrophy and degeneration of normal substrates, sprouting of new connections, and reorganization of somatosensory and motor maps. An important direction for ongoing research is the development of therapeutic strategies that enhance axonal regeneration, promote selective target reinnervation, but are also able to modulate central nervous system reorganization, amplifying those positive adaptive changes that help to improve functional recovery but also diminishing undesirable consequences.

PMID: 17643733 [PubMed - as supplied by publisher]

Motor imagery and action observation

Motor imagery and action observation: cognitive tools for rehabilitation.

Mulder T.    J Neural Transm. 2007 Jun 20; [Epub ahead of print

Royal Netherlands Academy of Arts and Sciences, Amsterdam, The Netherlands.

Rehabilitation, for a large part may be seen as a learning process where old skills have to be re-acquired and new ones have to be learned on the basis of practice. Active exercising creates a flow of sensory (afferent) information. It is known that motor recovery and motor learning have many aspects in common. Both are largely based on response-produced sensory information. In the present article it is asked whether active physical exercise is always necessary for creating this sensory flow. Numerous studies have indicated that motor imagery may result in the same plastic changes in the motor system as actual physical practice. Motor imagery is the mental execution of a movement without any overt movement or without any peripheral (muscle) activation. It has been shown that motor imagery leads to the activation of the same brain areas as actual movement. The present article discusses the role that motor imagery may play in neurological rehabilitation. Furthermore, it will be discussed to what extent the observation of a movement performed by another subject may play a similar role in learning. It is concluded that, although the clinical evidence is still meager, the use of motor imagery in neurological rehabilitation may be defended on theoretical grounds and on the basis of the results of experimental studies with healthy subjects.

PMID: 17579805 [PubMed – as supplied by publisher

Lateralization of motor imagery following stroke

Clin Neurophysiol. 2007 Jun 18; [Epub ahead of print]

Stinear CM, Fleming MK, Barber PA, Byblow WD.

Department of Sport & Exercise Science, Movement Neuroscience Laboratory, University of Auckland, Private Bag 92019, Auckland, New Zealand.

OBJECTIVE: Motor imagery may activate the primary motor cortex (M1) and promote functional recovery following stroke. We investigated whether the hemisphere affected by stroke affects performance and M1 activity during motor imagery. METHODS: Twelve stroke patients (6 left, 6 right hemisphere) and eight healthy age-matched adults participated. Experiment 1 assessed the speed and ease of actual and imagined motor performance. Experiment 2 measured corticomotor excitability during imagined movement of each hand separately, and both hands together, using transcranial magnetic stimulation. RESULTS: For control participants, imagined movements were performed more slowly than actual movements, and right-hand MEPs were facilitated when they imagined moving their right hand or both hands together. Patients reported being able to imagine movements with either hand, despite no measurable facilitation of MEPs in the stroke-affected hand. In left hemisphere patients, MEPs were facilitated in the left hand during imagery of the right hand and both hands together. In right hemisphere patients, motor imagery did not facilitate MEPs in either hand. CONCLUSIONS: Motor imagery does not appear to facilitate the ipsilesional M1 following stroke. SIGNIFICANCE: Motor imagery may play a role in rehabilitating movement planning, but its role in directly facilitating corticomotor output appears limited.

PMID: 17581773 [PubMed - as supplied by publisher]

Influence of mirror therapy on human motor cortex.

Int J Neurosci. 2007 Jul;117(7):1039-48.

Fukumura K, Sugawara K, Tanabe S, Ushiba J, Tomita Y. 

Graduate School of Science and Technology, Keio University. Yokohama, Kanagawa. Japan.

This article investigates whether or not mirror therapy alters the neural mechanisms in human motor cortex. Six healthy volunteers participated. The study investigated the effects of three main factors of mirror therapy (observation of hand movements in a mirror, motor imagery of an assumed affected hand, and assistance in exercising the assumed affected hand) on excitability changes in the human motor cortex to clarify the contribution of each factor. The increase in motor-evoked potential (MEP) amplitudes during motor imagery tended to be larger with a mirror than without one. Moreover, MEP amplitudes increased greatly when movements were assisted. Watching the movement of one hand in a mirror makes it easier to move the other hand in the same way. Moreover, the increase in MEP amplitudes is related to the synergic effects of afferent information and motor imagery.

PMID: 17613113 [PubMed - in process]

Motor Imagery & Mirroring-Neuromodulation in Stroke

 J Rehabil Med. 2007 Jan;39(1):5-13

Motor imagery and stroke rehabilitation: a critical discussion.

de Vries S, Mulder T.

Centre for Human Movement Sciences, University Medical Centre Groningen, University of Groningen, the Netherlands. s.j.de.vries@rug.nl

Motor disorders are a frequent consequence of stroke and much effort is invested in the re-acquisition of motor control. Although patients often regain some of their lost function after therapy, most remain chronically disabled. Functional recovery is achieved largely through reorganization processes in the damaged brain. Neural reorganization depends on the information provided by sensorimotor efferent-afferent feedback loops. It has, however, been shown that the motor system can also be activated “offline” by imagining (motor imagery) or observing movements. The discovery of mirror neurones, which fire not only when an action is executed, but also when one observes another person performing the same action, also show that our action system can be used “online” as well as offline. It is an intriguing question as to whether the information provided by motor imagery or motor observation can lead to functional recovery and plastic changes in patients after stroke. This article reviews the evidence for motor imagery or observation as novel methods in stroke rehabilitation.

PMID: 17225031 [PubMed - indexed for MEDLINE]

Mirroring -Neuromodulation 2007

 Neuroimage. 2007;36 Suppl 2:T164-73. Epub 2007 Mar 31.

Action observation has a positive impact on rehabilitation of motor deficits after stroke.

Ertelt D, Small S, Solodkin A, Dettmers C, McNamara A, Binkofski F, Buccino G.

Department of Neurology and Neuroimage Nord, University Hospital Schleswig-Holstein, Campus Lübeck, Ratzeburger Allee 160, 23538 Lübeck, Germany.

Evidence exists that the observation of actions activates the same cortical motor areas that are involved in the performance of the observed actions. The neural substrate for this is the mirror neuron system. We harness this neuronal system and its ability to re-enact stored motor representations as a means for rehabilitating motor control. We combined observation of daily actions with concomitant physical training of the observed actions in a new neurorehabilitative program (action observation therapy). Eight stroke patients with moderate, chronic motor deficit of the upper limb as a consequence of medial artery infarction participated. A significant improvement of motor functions in the course of a 4-week treatment, as compared to the stable pre-treatment baseline, and compared with a control group have been found. The improvement lasted for at least 8 weeks after the end of the intervention. Additionally, the effects of action observation therapy on the reorganization of the motor system were investigated by functional magnetic resonance imaging (fMRI), using an independent sensorimotor task consisting of object manipulation. The direct comparison of neural activations between experimental and control groups after training with those elicited by the same task before training yielded a significant rise in activity in the bilateral ventral premotor cortex, bilateral superior temporal gyrus, the supplementary motor area (SMA) and the contralateral supramarginal gyrus. Our results provide pieces of evidence that action observation has a positive additional impact on recovery of motor functions after stroke by reactivation of motor areas, which contain the action observation/action execution matching system.

PMID: 17499164 [PubMed - in process]

Neuromatrix theory of pain

Evolution of the neuromatrix theory of pain. The prithvi raj lecture: presented at the third world congress of world institute of pain, barcelona 2004

 Pain Pract. 2005 Jun;5(2):85-94      Melzack R.

Department of Psychology, McGill University, Montreal, Quebec, Canada.

The neuromatrix theory of pain proposes that pain is a multidimensional experience produced by characteristic “neurosignature” patterns of nerve impulses generated by a widely distributed neural network-the “body-self neuromatrix”-in the brain. These neurosignature patterns may be triggered by sensory inputs, but they may also be generated independently of them. Acute pains evoked by brief noxious inputs have been meticulously investigated by neuroscientists, and their sensory transmission mechanisms are generally well understood. In contrast, chronic pain syndromes, which are often characterized by severe pain associated with little or no discernable injury or pathology, remain a mystery. Furthermore, chronic psychological or physical stress is often associated with chronic pain, but the relationship is poorly understood. The neuromatrix theory of pain provides a new conceptual framework to examine these problems. It proposes that the output patterns of the body-self neuromatrix activate perceptual, homeostatic, and behavioral programs after injury, pathology, or chronic stress. Pain, then, is produced by the output of a widely distributed neural network in the brain rather than directly by sensory input evoked by injury, inflammation, or other pathology. The neuromatrix, which is genetically determined and modified by sensory experience, is the primary mechanism that generates the neural pattern that produces pain. Its output pattern is determined by multiple influences, of which the somatic sensory input is only a part, that converge on the neuromatrix.

      

Neurobiology of the chronicisation of pain in children: the memory of pain and its painful memory

[Neurobiology of the chronicisation of pain in children: the memory of pain and its painful memory.]

• Cahana A,   Jones D.    Ann Fr Anesth Reanim. 2007 May 22; [Epub ahead of print]

Programme antalgie postoperatoire et interventionnelle, departement d’anesthesiologie, hopitaux universitaires de Geneve, rue Micheli-du-Crest 24, 1211 Geneve 14, Suisse.

Reviewing the development of nociceptive circuits provides the rationale behind the need to modify and reduce premature painful experiences, especially during the “plastic” neonatal phase. Indeed, if physiological mechanisms of the functional nociceptive system follow a harmonious and predetermined development, it is the individual personal experience, intrinsically random, which will shape the final reactivity of this system and the later painful experience. If pain would not have been the organism’s alarm system, we could have simply compared it by analogy to other sensorial systems, which its development depends exclusively on the presence of environmental stimuli. The eyes wait for light, the ears for sound, the skin to be touched, the tongue to taste and the olfactory bulbs to smell. However with pain it is not the quantitative exposure that determines its development, but rather the context-laden aspects of its affliction which in turn create the complex experience and “memory” of pain. Prolonged, but also “unnecessary” exposure to pain transforms it into a futile sensation, which impacts the individual immediately but also resonates into its future. This article reviews recent neurobiological mechanisms (such as neural circuitry, neurotrophins, peripheral and central sensitization, inhibitory pathways) now known to develop during the chronicisation and apprenticing of pain in the growing individual. Its cognizance is vital for a better comprehension of adult pain.

PMID: 17524600 [PubMed - as supplied by publisher]

Complex regional pain syndrome (CRPS)

Hs05 crps – current ideas on management.  ANZ J Surg. 2007 May;77 Suppl 1:A34  

• Shipton EA.

Complex regional pain syndrome (CRPS) is characterised by extreme pain and dysfunction of the sympathetic nervous system in one region of the body, usually an extremity.(1) It involves the somatosensory, sympathetic and the somato-motor systems. It consists of local neurogenic inflammation out of proportion to injury; severe pain in the skin, subcutaneous tissues and joints; and central hyperexcitability that is often compounded with a sympathetic component. It is multifaceted manifesting both central and peripheral neurologic pathophysiology, including a prominent psychosocial component. Mechanisms include trauma related cytokine release, exaggerated neurogenic inflammation, sympathetic afferent coupling, adrenoreceptor pathology, glial cell activation and cortical reorganisation.(2) Diagnostic criteria and tests used will be discussed. Biomedical interventions include the use of primary and secondary analgesics, neural blockade, sympatholysis, ketamine, bisphosphonates, and spinal cord/peripheral nerve stimulation. Psychological and behavioural factors can exacerbate the pain and dysfunction associated with CRPS.(3) Mirror visual feedback was introduced recently for rehabilitation but needs to be evaluated in randomized controlled trials.(4).

PMID: 17490115 [PubMed - in process]

Mirror box therapy added to cognitive behavioural therapy in three CRPS type I

Mirror box therapy added to cognitive behavioural therapy in three chronic complex regional pain syndrome type I patients: a pilot study.

Int J Rehabil Res. 2007 Jun;30(2):181-8

• Vladimir Tichelaar YI,  Geertzen JH, Keizer D, Paul van Wilgen C.

aUniversity Medical Centre Groningen, University of Groningen bCentre for Rehabilitation cNorthern Centre for Health Care Research dDepartment of Anaesthesiology, Pain Centre, University Medical Centre Groningen, University of Groningen, The Netherlands.

Complex regional pain syndrome type I is a disorder of the extremities with disability and pain as the most prominent features. This paper describes the results of cognitive behavioural therapy combined with mirror box therapy in three patients with chronic complex regional pain syndrome type I. Before, during and at follow-up the following measurements were assessed: pain (visual analogue scale, 0-100), range of motion, muscle strength, and the areas of allodynia and of hyperalgesia. Furthermore, patients were asked for their feelings and thoughts about mirror box therapy and about the affected limb. Pain at rest, pain after measuring allodynia/hyperalgesia and pain after measuring strength decreased. Range of motion improved in two patients. Strength improved in one patient. The area of hyperalgesia increased for all three patients, whereas the area of allodynia remained stable in two patients and decreased in one patient. Two patients felt that their affected limb still belonged to them, one did not. Cognitive behavioural therapy combined with mirror box therapy for patients with chronic complex regional pain syndrome type I may facilitate rehabilitation. Measuring whether the affected limb still belongs in the patient’s body scheme could be of prognostic value in the treatment of chronic complex regional pain syndrome type I patients.

PMID: 17473633 [PubMed - in process]

Body perception disturbance in Pain

 Pain. 2007 May 15; [Epub ahead of print

Body perception disturbance: A contribution to pain in complex regional pain syndrome (CRPS).

• Lewis JS, Kersten P, McCabe CS, McPherson KM, Blake DR.

The Royal National Hospital for Rheumatic Diseases NHS Foundation Trust, Bath, UK; The School of Health Professions and Rehabilitation Sciences, University of Southampton, Southampton, UK.

In spite of pain in the CRPS limb, clinical observations show patients pay little attention to, and fail to care for, their affected limb as if it were not part of their body. Literature describes this phenomenon in terms of neurological neglect-like symptoms. This qualitative study sought to explore the nature of the phenomenon with a view to providing insights into central mechanisms and the relationship with pain. Twenty-seven participants who met the IASP CRPS classification were interviewed using qualitative methods to explore feelings and perceptions about their affected body parts. These semi-structured interviews were analysed utilising principles of grounded theory. Participants revealed bizarre perceptions about a part of their body and expressed a desperate desire to amputate this part despite the prospect of further pain and functional loss. A mismatch was experienced between the sensation of the limb and how it looked. Anatomical parts of the CRPS limb were erased in mental representations of the affected area. Pain generated a raised consciousness of the limb yet there was a lack of awareness as to its position. These feelings were about the CRPS limb only as the remaining unaffected body was felt to be normal. Findings suggest that there is a complex interaction between pain, disturbances in body perception and central remapping. Clinically, findings support the use of treatments that target cortical areas, which may reduce body perception disturbance and pain. We propose that body perception disturbance is a more appropriate term than 'neglect-like' symptoms to describe this phenomenon.

PMID: 17509761 [PubMed - as supplied by publisher]