Viktig studie som nevner smertedempende effekt av høyfrekvent vibrasjon på huden. Det er A-beta fiber (pacini) som blir stimulert, som er de tettes og tykkest myeliniserte og raske nervefibrene. «homotopic» betyr «på samme sted». Med vibrasjon på samme sted som smerten får man en 40% smerteredusering, sier studien. Nevner også at smertereduksjonen kommer av spinal inhibition (gate control).
Several lines of evidence implicate abnormalities of central pain processing as contributors for chronic pain, including dysfunctional descending pain inhibition. One form of endogenous pain inhibition, diffuse noxious inhibitory controls (DNIC), has been found to be abnormal in some chronic pain patients and evidence exists for deficient spatial summation of pain, specifically in FM. Similar findings have been reported in patients with localized musculoskeletal pain (LMP) disorders, like neck and back pain.
Whereas DNIC reduces pain through activation of nociceptive afferents, vibro-tactile pain inhibition involves innocuous A-beta fiber.
Homotopic vibro-tactile stimulation resulted in 40% heat pain reductions in all subject groups.
Although the pathogenesis of CWP is only incompletely understood (Vierck, Jr. 2006), increasing evidence points toward the important roles of abnormal peripheral (Staud et al., 2009; Staud et al., 2010) and central pain mechanisms (Desmeules et al., 2003; Staud 2009). Biochemical abnormalities in the cerebrospinal fluid (CSF) of some CWP patients, like FM include low levels of serotonin (5HT) and noradrenaline (NA) (Russell et al., 1992), high levels of substance P (Russell et al., 1994; Vaeroy et al., 1988) and of nerve growth factors (Giovengo et al., 1999) providing indirect evidence for abnormal central pain modulation. Abnormal levels of CSF neurotransmitters may also account for some of the symptoms experienced by many CWP patients such as sleep disturbance, fatigue, cognitive abnormalities, and depression. Moreover, reductions of 5HT and NA in the CSF seem to suggest dysfunction of the descending inhibitory systems (Lautenbacher and Rollman 1997) which may, at least in part, be responsible for the widespread pain of these patients.
Inadequate pain inhibition has been detected in FM patients but not in healthy control subjects (NC) during noxious counter-stimulation experiments (Kosek and Hansson 1997; Lautenbacher and Rollman 1997; de Souza et al., 2009). Similar findings have been reported in patients with localized musculoskeletal pain (LMP) disorders like osteoarthritis (OA) (Arendt-Nielsen et al., 2010). Dysfunctional central pain inhibition also appears to be responsible for abnormal spatial summation (Julien et al., 2005) and reduced pain habituation in FM patients (Montoya et al., 2006; Smith et al., 2008).
A mechanism yet to be tested is that of vibro-tactile analgesia which relies on high frequency stimulation of low threshold A-beta mechanoreceptors (e.g., Pacinian corpuscles), segmental dorsal horn mechanisms (Salter and Henry 1990a; Salter and Henry 1990b), and possibly mechanisms within the somatosensory cortex (Peltz et al., 2011) (Tommerdahl et al., 1999a; Tommerdahl et al., 2005).
Vibro-tactile analgesia is mechanistically very different from various forms of counter-stimulation that rely on stimulation of high threshold primary afferent neurons (e.g., DNIC and high intensity- low frequency TENS). Vibro-tactile stimulation of A-beta primary afferents produces potent inhibition of dorsal horn nociceptive neurons (Salter and Henry 1990a; Salter and Henry 1990b) and somatosensory cortical neurons in area 3B (Tommerdahl et al., 1999a).
verage (SD) vibration intensity at detection threshold was .012 (.006) m/s2 for NC, .013 (.004) m/s2 for FM, and .013 (.004) m/s2 for LMP participants.
The results of our study demonstrate robust attenuation of experimental pain by either homotopic or heterotopic vibro-tactile stimulation in NC, FM, and LMP patients. The magnitude of endogenous analgesic effects was large (ca. 40% pain reductions) and not statistically different across all three subject groups.
The analgesic effect of vibro-tactile stimuli was greater during homotopic compared to heterotopic conditioning stimulation (40% vs. 32%) in all groups studied. Considerable neurophysiological evidence supports spinal segmental inhibition as an explanation for this effect (Salter and Henry 1990a; Salter and Henry 1990b). Such an analgesic mechanism had originally been envisioned by Melzack & Wall in 1965 (Melzack and Wall 1965).
Overall, vibro-tactile stimulation appears to reliably activate analgesic mechanisms in chronic musculoskeletal pain patients which can powerfully inhibit experimental pain.
Using optical intrinsic signal imaging, Tommerdahl and Whitsel have shown that cutaneous vibro-tactile stimuli result in frequency-dependent reduction in cortical responsiveness to heat nociceptive input. (Whitsel et al., 1999; Tommerdahl et al., 1999b). In contrast to 25 Hz skin stimulation which does not seem to change S1 activation, vibro-tactile stimulation frequencies, similar to those used in the present study (100 Hz), resulted in potent suppression/inhibition of heat nociceptive responses within S1 (Tommerdahl et al., 1999a; Whitsel et al., 2000).
Recent evidence indicates that patients with idiopathic pain disorders, such as temporo-mandibular disorders, FM, tension headache, migraine and irritable bowel syndrome, demonstrate lower DNIC efficiency compared to NC (Julien et al., 2005; Maixner et al., 1995; Pielsticker et al., 2005). Similarly, less efficient DNIC has been associated with an extended history of pain among healthy subjects (Edwards et al., 2003).
Overall, vibro-tactile stimulation tests appear to be well tolerated by study participants and well suited for characterizing not only pain modulatory capacities of NC but also of individuals with chronic pain.
Given the potent effects observed in the present study, clinical investigations of analgesia using vibro-tactile stimulation in various musculoskeletal pain disorders, including FM and LMP, seem warranted.