J Manipulative Physiol Ther. 2010 (Mar); 33 (3): 178188 ~ FULL TEXT
Heidi Haavik Taylor, PhD, BSc, Bernadette Murphy, PhD, DC
Director of Research,
New Zealand College of Chiropractic,
Auckland, New Zealand.
OBJECTIVE: The aim of the current study was to investigate changes in the intrinsic inhibitory interactions within the somatosensory system subsequent to a session of spinal manipulation of dysfunctional cervical joints.
METHOD: Dual peripheral nerve stimulation somatosensory evoked potential (SEP) ratio technique was used in 13 subjects with a history of reoccurring neck stiffness and/or neck pain but no acute symptoms at the time of the study. Somatosensory evoked potentials were recorded after median and ulnar nerve stimulation at the wrist (1 millisecond square wave pulse, 2.47 Hz, 1 x motor threshold). The SEP ratios were calculated for the N9, N11, N13, P14-18, N20-P25, and P22-N30 peak complexes from SEP amplitudes obtained from simultaneous median and ulnar (MU) stimulation divided by the arithmetic sum of SEPs obtained from individual stimulation of the median (M) and ulnar (U) nerves.
RESULTS: There was a significant decrease in the MU/M + U ratio for the cortical P22-N30 SEP component after chiropractic manipulation of the cervical spine. The P22-N30 cortical ratio change appears to be due to an increased ability to suppress the dual input as there was also a significant decrease in the amplitude of the MU recordings for the same cortical SEP peak (P22-N30) after the manipulations. No changes were observed after a control intervention.
CONCLUSION: This study suggests that cervical spine manipulation may alter cortical integration of dual somatosensory input. These findings may help to elucidate the mechanisms responsible for the effective relief of pain and restoration of functional ability documented after spinal manipulation treatment.
Key Indexing Terms: Somatosensory Evoked Potentials, Neuronal Plasticity, Spinal Manipulation, Sensory Filtering, Sensorimotor Integration, Chiropractic
From the FULL TEXT Article:
The effectiveness of spinal manipulation for improving spinal function and relieving acute and chronic low back and neck pain has been well established by outcome-based research.  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 neurophysiologic effects of spinal manipulation.
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 that spinal dysfunction may lead to altered afferent input to the central nervous system (CNS).  It is well documented in the literature that altered afferent input to the CNS leads to plastic changes in the way that it responds to any subsequent input ; thus, it is possible that the presence of spinal dysfunction also leads to central neural plastic changes. Several recent studies indicate that spinal manipulation of dysfunctional cervical joints leads to alterations in central processing and sensorimotor integration.  One of these studies demonstrated that spinal manipulation of dysfunctional cervical joints alters cortical processing and sensorimotor integration for at least 20 to 30 minutes after the manipulations,  as reflected by altered N20 and N30 somatosensory evoked potential (SEP) peak amplitudes. The N20 SEP peak reflects processing of peripheral information at the level of the primary somatosensory cortex.  The N30 SEP peak reflects central sensorimotor integration processing involving primary sensory cortex, primary motor cortex, premotor cortex, and deeper brain structures such as the basal ganglia. 
One possible mechanism responsible for altering the amplitude of the cortical N20 and N30 SEP components after spinal manipulation is altered reciprocal sensory inhibition, that is, the filtering of afferent information by the somatosensory system. Reciprocal sensory inhibition enhances the contrast between stimuli, so that information from adjacent body parts is perceived and processed separately. One method, first used in the early 1980s,  to investigate reciprocal sensory inhibition is to stimulate 2 peripheral nerves simultaneously while recording SEPs. By comparing the amplitudes of SEP peaks obtained by stimulating 2 nerves simultaneously, for example, the median and ulnar nerves (MU), with the amplitude obtained from the arithmetic sum of the SEPs elicited by stimulating the same 2 nerves separately (M + U), the resulting ratio (MU/M + U) can be used as a measure of the central interaction between afferent inputs from these 2 peripheral nerves before and after an intervention, such as a 20minute repetitive muscle contraction task. 
This study sought to investigate whether spinal manipulation alters the intrinsic inhibitory interactions within the somatosensory system by comparing the amplitudes of SEP peaks obtained by stimulating 2 nerves simultaneously with the amplitude obtained from the arithmetic sum of the SEPs elicited by stimulating the same 2 nerves separately.
The major finding in this study was that a single session of spinal manipulation of dysfunctional cervical joints resulted in improved suppression of SEPs, evoked by dual upper limb nerve stimulation, at the cortical level of the lemniscal pathway. More specifically, the improved suppression of dual input was evident for the frontal P22-N30 SEP component. This study extends previous work that has demonstrated attenuated parietal N20 and frontal N30 SEP components, reflecting altered cortical processing, for 20 to 30 minutes postmanipulation. 
Evidence for Cortical Neural Plastic Changes After Spinal Manipulation
The current study findings suggest that the initial changes that occur after spinal manipulation occur at the cortical level. This is in agreement with previous research.  The peripheral N9 peak, representing the afferent volley in the brachial plexus,  was maintained stable in this experiment. The changes observed in this study therefore most likely reflect central changes.
However, although the P14 and N18 SEP components, known to originate at the level of the brainstem, [23, 55, 5760] did not show any changes in this study, the design of the study limits the ability to rule out the possibility that subcortical changes did occur. It is generally agreed that although 500 sweeps (and the current study averaged 800 sweeps per trial) are sufficient to record reliable peripheral Erbs and cortical SEP potentials, far-field potentials such as subcortical P14-N18 do generally require a higher number of averaged sweeps. [24, 25] The possibility for subcortical SEP changes after spinal manipulation does therefore need further investigation.
The Frontal P22-N30 SEP Peak Changes
The changes observed in the current study only occurred for the frontal N30 component of the SEP peaks. Although some authors suggest this peak is generated in the postcentral cortical regions (ie, S1),  most evidence suggests that this peak is related to a complex cortical and subcortical loop linking the basal ganglia, thalamus, premotor areas, and primary motor cortex.  The frontal N30 peak is therefore thought to reflect sensorimotor integration.  The decreased frontal N30 SEP peak ratio observed in the current study therefore suggests that there may be an increase in surround inhibition or filtering of sensory information from the upper limb occurring somewhere in these cortical and subcortical loops linking the basal ganglia, thalamus, premotor areas, and primary motor cortex for at least 20 minutes immediately after spinal manipulation. Impaired surround inhibition before spinal manipulation may account for this finding. The SEP ratio changes appear to be due to an increased inhibition of the dual peripheral input, as the MU data significantly decreased for this SEP component after the manipulation intervention.
The passive head movement SEP experiment demonstrated that no significant changes occurred after a simple movement of the subject's head. The results after manipulation are therefore not simply due to altered input from vestibular, muscle, or cutaneous afferents as a result of the doctor of chiropractic's touch or due to the actual movement of the subjects head. This therefore strengthens the argument that the results in this study are more likely specific to the delivery of the high-velocity, low-amplitude thrust to the dysfunctional joints. The passive head movement experiment was to control for the potential neural changes due to the afferent traffic resulting from touch and head movement alone. It was not intended to be a sham manipulation.
The individual median nerve (M) frontal P22-N30 SEP peak amplitude also decreased significantly after spinal manipulation in the current study. This is in agreement with previous research.  The individual M changes observed for this peak after spinal manipulation appears to be more robust than the changes observed previously for the parietal N20-P25 SEP component, known to originate in the primary somatosensory cortex,  as no change to this peak was observed in the current study compared to what has been shown previously. 
The Parietal N20 SEP Peak
No changes were observed for the parietal N20-P25 SEP peak component after spinal manipulation in the current study. Previous research has shown that cervical spine manipulation attenuates both frontal N30 and parietal N20 SEP peak amplitudes after median nerve stimulation at the wrist.  It was therefore surprising to find no changes to the parietal N20 SEP component. It is possible that some of the subjects in the previous study may have experienced some discomfort after the spinal manipulations, as the presence of pain alone is known to induce a significant reduction of the postcentral N20-P25 complex.  Although none of the subjects reported any discomfort after the manipulations, this could be a possible explanation for the significant reduction of the parietal N20-P25 in the previous experiment  because this was not observed in the present study. However, it is also possible that cervical spine manipulation(s) alters the afferent information originating from the cervical spine (eg, from joints and muscles), which in turn can alter the way that the 3b pyramidal cells in the primary somatosensory cortex (S1) respond to any subsequent afferent input such as the median nerve stimulation. It would be reasonable to expect different degrees of such changes in different people, which could also account for altered parietal N20-P25 SEP peak amplitudes in some subjects and not in others.
The current study findings do suggest that the reduced parietal N20 changes observed previously  are not due to enhanced sensory surround inhibition in S1, as no change in the parietal N20-P25 SEP peak ratio were observed in the current study. However, this possibility cannot be ruled out, as this may occur only when observable changes are seen in the individual median nerve SEP peak amplitudes.
Implications for Investigations of Neural Plasticity and Spinal Manipulation
Episodes of acute pain, such as after an injury, may initially induce plastic changes in the sensorimotor system (for a review of this topic please see reference 61. These changes could include dysfunctional motor control of spinal joint segments, that is, the manipulable lesion that chiropractic physicians and other manipulative therapists treat. Pain alone, without deafferentation, has been shown to induce increased SEP peak amplitudes [62, 63] and increased somatosensory evoked magnetic fields.  Sensorimotor disturbances are known to persist beyond acute episode of pain, [65, 66] and these disturbances are thought to play a defining role in the clinical picture and chronicity of different chronic neck pain conditions.  Therefore, the reduced frontal N30 SEP peak ratio observed in the current study after spinal manipulation may reflect an improvement of plastic changes induced by previous injury and may reflect one mechanism for the improvement of functional ability reported after spinal manipulation. This requires further investigation.
Abnormal central integration of a dual somatosensory input has previously been demonstrated at the cortical level after as little as 20 minutes of repetitive thumb abductions  and throughout the somatosensory system in patients with dystonia.  Tinazzi et al  argued that the increased central dual SEP peak ratios represented reduced surround inhibition in the patients with dystonia and that their findings suggest that the inhibitory integration of mainly proprioceptive afferent inputs coming from adjacent body parts is abnormal in patients with dystonia.  Furthermore, they argue that the inefficient integration of dual input was most likely due to altered surround inhibition and could in turn lead to abnormal motor output, contributing to the motor impairment present in dystonia.  Motor impairments are also present in chronic neck pain patients. Impairment of deep cervical neck flexors and significant postural disturbances during walking and standing has been demonstrated in both insidious-onset and trauma-induced chronic neck pain conditions.  Altered sensitivity of proprioceptors within the neck muscles has been suggested to be related to the postural disturbances seen in these patients. [67, 70] It is therefore possible that this leads to altered or inefficient integration of dual input in this patient group also, resulting in the above mentioned motor impairments. There is also evidence to suggest that muscle impairment occurs early in the history of onset of neck pain  and that this muscle impairment does not automatically resolve even when neck pain symptoms improve. [65, 66] Some authors have therefore suggested that the deficits in proprioception and motor control, rather than neck pain itself, may be the main factors defining the clinical picture and chronicity of different chronic neck pain conditions.  These deficits in proprioception and motor control may be partly due to spinal dysfunction causing either inhibition or facilitation of neural input to the muscles surrounding the spine. However, the central sensorimotor plastic changes that occur with spinal dysfunction may also lead to abnormalities in the way the CNS processes incoming information from more distal regions, such as the upper limb. The altered frontal P22-N30 SEP peak ratio after spinal manipulation may reflect an improvement of such maladaptive plastic changes in the current study population, who all had reoccurring neck problems, but were not in acute pain at the time they participated in this study.
This study assessed 13 subjects under specified conditions. Therefore, findings may possibly be different in other populations and with different inclusion and exclusion criteria. Further studies should be performed using larger groups of subjects with different presentations.
The observations in the present study suggest that spinal manipulation of dysfunctional cervical joints may improve suppression of SEPs evoked by dual upper limb nerve stimulation at the level of the motor cortex, premotor areas, and/or subcortical areas such as basal ganglia and/or thalamus, lasting at least 20 minutes postmanipulation. Further studies are needed to elucidate the role and mechanisms of these cortical changes and their relationship to a patient's clinical presentation and their ability to perform daily tasks.
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