Hi,

I am going to post a few article abstracts to illustrate your point that your brain for sure can rewire itself in pain situations.......

[Psychosomatics, psychotherapy and neuronal plasticity--how words change our mind]

[Article in German]


Rüegg JC.
Institut für Physiologie und Pathophysiologie der Universität Heidelberg, Heidelberg, Deutschland. Caspar.Rueegg@gmx.de
Certain psychosomatic disorders such as chronic psychosomatic pain, phobias and other anxiety disorders as well as depression are often stress-related but may also be acquired by learning associated with traumatic experience. As learning is based on changes in neuronal networks, the brain will be altered in these diseases. In turn, brain structure and function may also be influenced and even changed by effective psychotherapy as well as by other (behavioural) cognitive interventions--words and thoughts--when leading to cognitive restructuring. Due to their neuronal plasticity our brains are capable of constantly rewiring themselves so that we can--in Andreasen's words--"literally change our mind".


1: Brain. 2008 Aug 30. [Epub ahead of print] Links
Abnormal pain processing in chronic tension-type headache: a high-density EEG brain mapping study.

Buchgreitz L, Egsgaard LL, Jensen R, Arendt-Nielsen L, Bendtsen L.
Danish Headache Center, Department of Neurology, Glostrup Hospital, University of Copenhagen, DK-2600 Glostrup and Center for Sensory-Motor Interaction (SMI), Department of Health Sciences and Technology, Aalborg University, DK-9220 Aalborg E, Denmark.
Central sensitization caused by prolonged nociceptive input from muscles is considered to play an important role for chronification of tension-type headache. In the present study we used a new high-density EEG brain mapping technique to investigate spatiotemporal aspects of brain activity in response to muscle pain in 19 patients with chronic tension-type headache (CTTH) and 19 healthy, age- and sex-matched controls. Intramuscular electrical stimuli (single and train of five pulses delivered at 2 Hz) were applied to the trapezius muscle and somatosensory evoked potentials were recorded with 128-channel EEG both in- and outside a condition with induced tonic neck/shoulder muscle pain (glutamate injection into the trapezius muscle). Significant reduction in magnitude during and after induced tonic muscle pain was found in controls at the P200 dipole in response to both the first (baseline versus tonic muscle pain: P = 0.001; baseline versus post-tonic muscle pain: P = 0.002) and fifth (baseline versus tonic muscle pain: P = 0.04; baseline versus post-tonic muscle pain: P = 0.04) stimulus in the train. In contrast, there were no differences between the conditions in patients. No consistent difference was found in localization or peak latency of the dipoles. The reduction in magnitude during and after induced tonic muscle pain in controls but not in patients with CTTH may be explained by impaired inhibition of the nociceptive input in these patients. This may be the first evidence that the supraspinal response to muscle pain is abnormal in patients with CTTH.

Curr Opin Support Palliat Care. 2007 Aug;1(2):109-16.Links
Neuroimaging of pain mechanisms.

Tracey I.
Centre for Functional Magnetic Resonance Imaging of the Brain, Departments of Clinical Neurology and Nuffield Department of Anaesthetics, Oxford University, Oxford, UK. irene@fmrib.ox.ac.uk
PURPOSE OF REVIEW: Functional neuroimaging has made a huge impact scientifically, not least within the field of pain research. The noninvasive identification of pain mechanisms that underpin chronicity, such as central sensitization and other amplification processes related to the cognitive or emotional state of the patient, is of considerable interest to the clinical pain community and pharmaceutical industry. Relating data to a person's specific pain report or measure of pain relief provide a clearer understanding of the mechanisms driving and maintaining this complex experience. It is timely, therefore, to review the advances in neuroimaging applications to pain. RECENT FINDINGS: New data have emerged to further support the descending modulatory system's critical role in chronic pain. The neural correlates that underpin tonic, ongoing and spontaneous pain in patients are being identified. Additionally, the prefrontal cortex is emerging as a critical brain region for pain processing, especially in patients. Finally, data from structural and molecular imaging studies are highlighting the extent of damage the brain sustains when patients live with their chronicity unrelieved. SUMMARY: Neuroimaging tools have advanced our understanding of central pain mechanisms in normals and patients, forcing us to reconsider issues related to diagnosis and provision of treatment.
hope some of this helps you
love and hugs,
Victoria