Cervical spine manipulation alters sensorimotor integration: A somatosensory evoked potential study
Introduction
Spinal manipulation is a commonly used conservative treatment for neck, back, and pelvic pain. The effectiveness of spinal manipulation in the treatment of acute and chronic low back and neck pain has been well established by outcome-based research (for review, see Hurwitz et al., 1996, Vernon, 1996). However, the mechanism(s) responsible for the effective relief of pain and restoration of functional ability after spinal manipulation are not well understood, as there is limited evidence to date regarding the neurophysiological effects of spinal manipulation. The evidence to date indicates that spinal manipulation can lead to alterations in reflex excitability (Herzog et al., 1999, Murphy et al., 1995, Symons et al., 2000), altered sensory processing (Zhu et al., 2000, Zhu et al., 1993) and altered motor excitability (Herzog et al., 1999, Dishman et al., 2002, Suter et al., 2000).
Spinal manipulation is used therapeutically by a number of health professionals, including physical medicine specialists, physiotherapists, osteopaths and chiropractors. The different professions have different terminology for the “entity” or “manipulable lesion” that they manipulate. This manipulable lesion may be called “vertebral (spinal) lesion” by physical medical specialists or physiotherapists, “somatic dysfunction” or “spinal lesion” by osteopaths, and “vertebral subluxation” or “spinal fixation” by chiropractors (Leach, 1986). Joint dysfunction as discussed in the literature ranges from experimentally induced joint effusion (Shakespeare et al., 1985), to pathological joint disease such as osteoarthritis (O’Connor et al., 1993), as well as the more subtle functional alterations that are commonly treated by manipulative therapists (Suter et al., 1999, Suter et al., 2000). For the purposes of this paper, the “manipulable lesion” will be referred to as an area of spinal dysfunction.
There is a growing body of evidence suggesting that the presence of spinal dysfunction of various kinds has an effect on central neural processing. For example, several authors have suggested spinal dysfunction may lead to altered afferent input to the CNS (Bolton and Holland, 1996, Bolton and Holland, 1998, Murphy et al., 1995, Zhu et al., 1993, Zhu et al., 2000). Altering afferent input to the CNS is well known to lead to plastic changes in the way that it responds to any subsequent input (Brasil-Neto et al., 1993, Byl et al., 1997, Hallett et al., 1999, Pascual-Leone and Torres, 1993). Neural plastic changes take place both following increased (Byl et al., 1997, Pascual-Leone and Torres, 1993) and decreased (Brasil-Neto et al., 1993, Hallett et al., 1999, Ziemann et al., 1998) afferent input.
Altered afferent input from joints can lead to both inhibition and facilitation of neural input to related muscles. Numerous studies of painful joints have shown arthrogenous muscle inhibition (Hides et al., 1994, McPartland et al., 1997, Stokes and Young, 1984). However, even painless experimentally induced joint dysfunction (joint effusion) has been shown to inhibit surrounding muscles (Shakespeare et al., 1985). This altered motor control was also shown to persist even after aspiration of the joint effusion (Shakespeare et al., 1985). In the early 1980s, Steinmetz et al. demonstrated that relatively short (15–30 min) episodes of moderately intense afferent input to the spinal reflex pathways of rats causes increases in neural excitability that persists for several hours (Steinmetz et al., 1982, Steinmetz et al., 1985). Once these facilitated areas are established, there may be no need for ongoing afferent input to maintain the altered output patterns. Since these early experiments, numerous studies have shown rapid central plastic changes after injuries and altered sensory input from the body (for review, see Wall et al., 2002). This can explain the findings of Shakespeare et al. (1985) of altered motor control persisting even after aspiration of the joint effusion. This process provides a potential explanation for altered neural processing as a result of joint dysfunction, and a rationale for the effects of spinal manipulation on neural processing that have been described in the literature.
Given that spinal dysfunction would alter the balance of afferent input to the CNS we propose that this altered afferent input may over time lead to potential maladaptive neural plastic changes in the CNS. We further propose that spinal manipulation can effect this. By recording SEPs and monitoring the peripheral nerve afferent volley, it is possible to determine where in the somatosensory pathway changes induced by spinal manipulation may be occurring.
Section snippets
Subjects
Twelve subjects (five women and seven men), aged 20–53 (mean age 29.9), participated in the spinal manipulation study. An additional twelve age-matched subjects (4 males and 8 females), aged 21–35 (mean age 27.1 years), participated in the passive head movement control study. The subjects were allocated into either group in a pseudo-randomized order. It was decided in advance that the first 12 volunteers that fit the inclusion/exclusion criteria for the study would become the manipulation group
Subject statistics
Table 1 shows the spinal manipulation subjects’ details, including age, gender, history of cervical pain or tension, and any known neck and/or head trauma. Table 2 shows the spinal segments manipulated for each subject in this study.
Passive head movement intervention
There were no statistically significant differences between the pre-intervention trials prior to the passive head movement intervention. There were no significant changes observed in either latency or amplitude of any of the SEP peaks following passive head movement
Discussion
The major finding in this study was that a single session of spinal manipulation of dysfunctional joints resulted in attenuated cortical (parietal N20 and frontal N30) evoked responses. On average the frontal N30 changes persisted for 20 min post-manipulation before returning to baseline levels. The parietal N20 changes persisted for at least 30 min, i.e. during all three post-manipulation recordings. To our knowledge, no prior study has shown persistent changes in neither somatosensory
Acknowledgements
The head author was initially supported with a fellowship from the Foundation for Chiropractic Education and Research, and later by a Bright Futures Top Achievers Doctoral Scholarship.
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