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For years now, doctors in Europe and throughout the world have used musculoskeletal ultrasound to deliver unprecedented pain relief to their patients.
Musculoskeletal ultrasound allows a physician to see into the body, similar to the 100% safe, noninvasive ultrasound performed on a pregnant woman. In 2007, after years of experience and research in rehabilitation and pain management, I became convinced that I would have to invest in musculoskeletal ultrasound technology and training to deliver superior pain relief to my patients. When I started using musculoskeletal ultrasound to treat my patients, even I was surprised at the difference in results! Nociceptor inputs can trigger a prolonged but reversible increase in the excitability and synaptic efficacy of neurons in central nociceptive pathways, the phenomenon of central sensitization. Central sensitization represents an enhancement in the function of neurons and circuits in nociceptive pathways caused by increases in membrane excitability and synaptic efficacy as well as to reduced inhibition and is a manifestation of the remarkable plasticity of the somatosensory nervous system in response to activity, inflammation, and neural injury. In essence we are talking about changes within the central nervous system that underpin the widespread, unpredictable and varied nature of persisting pain. Evidence that central sensitisation is present in patients with shoulder impingement syndrome and influences the outcome after surgery. Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, Nuffield Orthopaedic Centre, Windmill Road, Headington, Oxford OX3 7LD, UK.
Impingement syndrome in the shoulder has generally been considered to be a clinical condition of mechanical origin.
Psychophysical and functional imaging evidence supporting the presence of central sensitization in a cohort of osteoarthritis patients.
The groin pain experienced by patients with hip osteoarthritis (OA) is often accompanied by areas of referred pain and changes in skin sensitivity. Twenty patients with hip OA awaiting joint replacement and displaying signs of referred pain were recruited into the study, together with age-matched controls. Patients were found to have significantly lower threshold perception to punctate stimuli and were hyperalgesic to the noxious punctate stimulus in their areas of referred pain. Using psychophysical (QST) and brain imaging methods (functional MRI), we have identified increased activity with the periaqueductal grey matter associated with stimulation of the skin in referred pain areas of patients with hip OA. The problem of painChronic pain affects 20% of the population and is the largest global health burden.
At Specialist Pain Physio Clinics you will receive treatment, rehabilitation and coaching based upon the latest pain science.


Unfortunately, this technology is still very expensive in the US and very few doctors use it. By doing so, the physician is able to administer a treatment to the exact source of the pain with pin-point accuracy. Recovery times plummeted, post-treatment complications disappeared, and I was seeing patients using less pain medication.
Cant Pick a Physician?Read How my Acurate Diagnoses and Effective Treatments Can Speed Up Your Recovery!" title="Suffering From Pain? Central sensitization manifests as pain hypersensitivity, particularly dynamic tactile allodynia, secondary punctate or pressure hyperalgesia, aftersensations, and enhanced temporal summation. The net effect of central sensitization is to recruit previously subthreshold synaptic inputs to nociceptive neurons, generating an increased or augmented action potential output: a state of facilitation, potentiation, augmentation, or amplification.
However, anomalies exist between the pathology in the subacromial space and the degree of pain experienced.
We aimed to identify the supraspinal influences that underlie these clinical manifestations that we consider indicative of possible central sensitization.
All subjects completed pain psychology questionnaires and underwent quantitative sensory testing (QST) in their area of referred pain. Functional brain imaging illustrated significantly greater activation in the brainstem of OA patients in response to punctate stimulation of their referred pain areas compared with healthy controls, and the magnitude of this activation positively correlated with the extent of neuropathic-like elements to the patient’s pain, as indicated by the PainDETECT score. This offers a central target for analgesia aimed at improving the treatment of this largely peripheral disease.
By using state of the art imaging technology, I am able to provide treatment that is extremely accurate, drastically minimizing recovery times, complications and need for pain medication. This eliminates any possible treatment mistakes and allows the doctor to deliver ultra-precise pain care that does not harm other parts of the body.
It can be readily and rapidly elicited in human volunteers by diverse experimental noxious conditioning stimuli to skin, muscles or viscera, and in addition to producing pain hypersensitivity, results in secondary changes in brain activity that can be detected by electrophysiological or imaging techniques. Central sensitization is responsible for many of the temporal, spatial, and threshold changes in pain sensibility in acute and chronic clinical pain settings and exemplifies the fundamental contribution of the central nervous system to the generation of pain hypersensitivity. I really need to know what it is that is prolonging this protection and is it really worthwhile for the individual.
These may be explained by variations in the processing of nociceptive inputs between different patients.


Twelve of 20 patients and their age- and sex-matched controls underwent functional magnetic resonance imaging (MRI) while the areas of referred pain were stimulated using cold stimuli (12 degrees C) and punctate stimuli (256 mN). A leading pain care practitioner, she works at 2 hospitals and is a leading voice in pain relief. Studies in clinical cohorts reveal changes in pain sensitivity that have been interpreted as revealing an important contribution of central sensitization to the pain phenotype in patients with fibromyalgia, osteoarthritis, musculoskeletal disorders with generalized pain hypersensitivity, headache, temporomandibular joint disorders, dental pain, neuropathic pain, visceral pain hypersensitivity disorders and post-surgical pain.
Because central sensitization results from changes in the properties of neurons in the central nervous system, the pain is no longer coupled, as acute nociceptive pain is, to the presence, intensity, or duration of noxious peripheral stimuli.
We investigated the evidence for augmented pain transmission (central sensitisation) in patients with impingement, and the relationship between pre-operative central sensitisation and the outcomes following arthroscopic subacromial decompression. The comorbidity of those pain hypersensitivity syndromes that present in the absence of inflammation or a neural lesion, their similar pattern of clinical presentation and response to centrally acting analgesics, may reflect a commonality of central sensitization to their pathophysiology. Instead, central sensitization produces pain hypersensitivity by changing the sensory response elicited by normal inputs, including those that usually evoke innocuous sensations.
We recruited 17 patients with unilateral impingement of the shoulder and 17 age- and gender-matched controls, all of whom underwent quantitative sensory testing to detect thresholds for mechanical stimuli, distinctions between sharp and blunt punctate stimuli, and heat pain. An important question that still needs to be determined is whether there are individuals with a higher inherited propensity for developing central sensitization than others, and if so, whether this conveys an increased risk in both developing conditions with pain hypersensitivity, and their chronification. PERSPECTIVE: In this article, we review the major triggers that initiate and maintain central sensitization in healthy individuals in response to nociceptor input and in patients with inflammatory and neuropathic pain, emphasizing the fundamental contribution and multiple mechanisms of synaptic plasticity caused by changes in the density, nature, and properties of ionotropic and metabotropic glutamate receptors. Diagnostic criteria to establish the presence of central sensitization in patients will greatly assist the phenotyping of patients for choosing treatments that produce analgesia by normalizing hyperexcitable central neural activity.
We have certainly come a long way since the first discovery of activity-dependent synaptic plasticity in the spinal cord and the revelation that it occurs and produces pain hypersensitivity in patients. Nevertheless, discovering the genetic and environmental contributors to and objective biomarkers of central sensitization will be highly beneficial, as will additional treatment options to prevent or reduce this prevalent and promiscuous form of pain plasticity. These are felt to represent peripheral manifestations of augmented central pain processing (central sensitisation). These observations confirm the presence of central sensitisation in a proportion of patients with shoulder pain associated with impingement.



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