Altered Central Integration of Dual Somatosensory
Input After Cervical Spine Manipulation

This section is compiled by Frank M. Painter, D.C.
Send all comments or additions to:

FROM:   J Manipulative Physiol Ther. 2010 (Mar);   33 (3):   178–188 ~ 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. [1-7] 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). [8-12] 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 [13-19]; 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. [20-22] 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, [22] 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. [23-25] 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. [26-33]

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, [34-38] 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 20-minute repetitive muscle contraction task. [39]

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. [22]

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. [22] The peripheral N9 peak, representing the afferent volley in the brachial plexus, [54-56] 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, 57-60] 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), [26-28] 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. [29-33] The frontal N30 peak is therefore thought to reflect sensorimotor integration. [41] 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. [22] 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, [23-25] as no change to this peak was observed in the current study compared to what has been shown previously. [22]

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. [22] 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. [41] 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 [22] 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 [22] 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. [64] 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. [67] 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 [39] and throughout the somatosensory system in patients with dystonia. [53] Tinazzi et al [53] 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. [53] 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. [53] 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. [67-73] 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 [65] 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. [67] 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.


  1. Aker, PD, Gross, AR, Goldsmith, CH, and Peloso, P.
    Conservative management of mechanical neck pain: systematic overview and meta-analysis.
    Br Med J. 1996; 313: 1291–1296

  2. Assendelft, WJ, Bouter, LM, and Kessels, AG.
    Effectiveness of chiropractic and physiotherapy in the treatment of low back pain: a critical discussion of the British randomized clinical trial.
    J Manipulative Physiol Ther. 1991; 14: 281–286

  3. Giles, LG and Muller, R.
    Chronic Spinal Pain Syndromes: A Clinical Pilot Trial Comparing Acupuncture,
    A Nonsteroidal Anti-inflammatory Drug, and Spinal Manipulation

    J Manipulative Physiol Ther 1999 (Jul); 22 (6): 376–381

  4. Hurwitz, EL, Aker, PD, Adams, AH, Meeker, WC, and Shekelle, PG.
    Manipulation and Mobilization of the Cervical Spine: A Systematic Review of the Literature
    SPINE (Phila Pa 1976) 1996 (Aug 1); 21 (15): 1746–1760

  5. Manga, P, Angus, D, Papadopoulos, C, and Swan, W.
    A Study to Examine the Effectiveness and Cost-Effectiveness of
    Chiropractic Management of Low-Back Pain

    Pran Manga & Associates Inc, Ottawa; 1993

  6. Meade, TW, Dyer, S, Browne, W, Townsend, J, and Frank, AO.
    Low Back Pain of Mechanical Origin: Randomised Comparison of
    Chiropractic and Hospital Outpatient Treatment

    British Medical Journal 1990 (Jun 2); 300 (6737): 1431–1437

  7. Vernon, LF.
    Spinal manipulation as a valid treatment for low back pain.
    Del Med J. 1996; 68: 175–178

  8. Bolton, PS and Holland, CT.
    Afferent signaling of vertebral displacement in the neck of the cat.
    Soc Neurosci Abstr. 1996; 22: 1802

  9. Bolton, PS and Holland, CT.
    An in vivo method for studying afferent fibre activity from cervical paravertebral tissue during vertebral motion in anaesthetised cats.
    J Neurosci Methods. 1998; 85: 211–218

  10. Murphy, BA, Dawson, NJ, and Slack, JR.
    Sacroiliac joint manipulation decreases the h-reflex.
    Electromyogr Clin Neurophysiol. 1995; 35: 87–94

  11. Zhu, Y, Haldeman, S, Starr, A, Seffinger, MA, and Su, SH.
    Paraspinal muscle evoked cerebral potentials in patients with unilateral low back pain.
    Spine. 1993; 18: 1096–1102

  12. Zhu, Y, Haldeman, S, Hsieh, CY, Wu, P, and Starr, A.
    Do cerebral potentials to magnetic stimulation of paraspinal muscles reflect changes in palpable muscle spasm, low back pain, and activity scores?.
    J Manipulative Physiol Ther. 2000; 23: 458–464

  13. Brasil-Neto, JP, Valls-Sole, J, Pascual-Leone, A et al.
    Rapid modulation of human cortical motor outputs following ischaemic nerve block.
    Brain. 1993; 116: 511–525

  14. Byl, NN, Merzenich, MM, Cheung, S, Bedenbaugh, P, Nagarajan, SS, and Jenkins, WM.
    A primate model for studying focal dystonia and repetitive strain injury: Effects on the primary somatosensory cortex.
    Phys Ther. 1997; 77: 269–284

  15. Hallett, M, Chen, R, Ziemann, U, and Cohen, LG.
    Reorganization in motor cortex in amputees and in normal volunteers after ischemic limb deafferentation.
    Electroencephalogr Clin Neurophysiol-Suppl. 1999; 51: 183–187

  16. Pascual-Leone, A and Torres, F.
    Plasticity of the sensorimotor cortex representation of the reading finger in Braille readers.
    Brain. 1993; 116: 39–52

  17. Tinazzi, M, Zanette, G, Polo, A, Volpato, D et al.
    Transient deafferentation in humans induces rapid modulation of primary sensory cortex not associated with subcortical changes: a somatosensory evoked potential study.
    Neurosci Lett. 1997; 223: 21–24

  18. Tinazzi, M, Zanette, G, Volpato, D et al.
    Neurophysiological evidence of neuroplasticity at multiple levels of the somatosensory system in patients with carpal tunnel syndrome.
    Brain. 1998; 121: 1785–1794

  19. Ziemann, U, Hallett, M, and Cohen, LG.
    Mechanisms of deafferentation-induced plasticity in human motor cortex.
    J Neurosci. 1998; 18: 7000–7007

  20. Haavik Taylor, H and Murphy, B.
    World federation of chiropractic's 9th biennial congress award winning paper (3rd prize): altered sensorimotor integration with cervical spine manipulation.
    J Manipulative Physiol Ther. 2008; 31: 115–126

  21. Haavik-Taylor, H and Murphy, B.
    Transient modulation of intracortical inhibition following spinal manipulation.
    Chiropr J Aust. 2007; 37: 106–116

  22. Haavik-Taylor, H and Murphy, B.
    Cervical spine manipulation alters sensorimotor integration: a somatosensory evoked potential study.
    Clin Neurophysiol. 2007; 118: 391–402

  23. Desmedt, JE and Cheron, G.
    Central somatosensory conduction in man: neural generators and interpeak latencies of the far-field components recorded from neck and right or left scalp and earlobes.
    Electroencephalogr Clin Neurophysiol. 1980; 50: 382–403

  24. Mauguiere, F.
    Somatosensory evoked potentials: normal responses, abnormal waveforms and clinical applications in neurological diseases.
    In: E. Niedermeyer (Ed.) Electroencephalography: Basic principles, clinical applications, and related fields.
    Williams and Wilkins, Baltimore; 1999

  25. Nuwer, MR, Aminoff, M, Desmedt, J et al.
    IFCN recommended standards for short latency somatosensory evoked potentials. Report of an IFCN committee. International federation of clinical neurophysiology.
    Electroencephalogr Clin Neurophysiol. 1994; 91: 6–11

  26. Allison, T, McCarthy, G, Wood, CC, Williamson, PD, and Spencer, DD.
    Human cortical potentials evoked by stimulation of the median nerve. II. Cytoarchitectonic areas generating long-latency activity.
    J Neurophysiol. 1989; 62: 711–722

  27. Allison, T, McCarthy, G, Wood, CC, Darcey, TM, Spencer, DD, and Williamson, PD.
    Human cortical potentials evoked by stimulation of the median nerve. II. Cytoarchitectonic areas generating short-latency activity.
    J Neurophysiol. 1989; 62: 694–710

  28. Allison, T, McCarthy, G, Wood, CC, and Jones, SJ.
    Potentials evoked in human and monkey cerebral cortex by stimulation of the median nerve. A review of scalp and intracranial recordings.
    Brain. 1991; 114: 2465–2503

  29. Kanovskύ, P, Bare, M, and Rektor, I.
    The selective gating of the n30 cortical component of the somatosensory evoked potentials of median nerve is different in the mesial and dorsolateral frontal cortex: evidence from intracerebral recordings.
    Clin Neurophysiol. 2003; 114: 981–991

  30. Mauguiere, F, Desmedt, JE, and Courjon, J.
    Astereognosis and dissociated loss of frontal or parietal components of somatosensory evoked potentials in hemispheric lesions. Detailed correlations with clinical signs and computerized tomographic scanning.
    Brain. 1983; 106: 271–311

  31. Rossini, PM, Gigli, GL, Marciani, MG, Zarola, F, and Caramia, M.
    Non-invasive evaluation of input-output characteristics of sensorimotor cerebral areas in healthy humans.
    Electroencephalogr Clin Neurophysiol. 1987; 68: 88–100

  32. Rossini, PM, Babiloni, F, Bernardi, G, Cecchi, L, Johnson, PB, Malentacca, A et al.
    Abnormalities of short-latency somatosensory evoked potentials in parkinsonian patients.
    Electroencephalogr Clin Neurophysiol. 1989; 74: 277–289

  33. Waberski, TD, Buchner, H, Perkuhn, M, Gobbele, R, Wagner, M, Kucker, W et al.
    N30 and the effect of explorative finger movements: a model of the contribution of the motor cortex to early somatosensory potentials.
    Clin Neurophysiol. 1999; 110: 1589–1600

  34. Burke, D, Gandevia, SC, McKeon, B, and Skuse, NF.
    Interactions between cutaneous and muscle afferent projections to cerebral cortex in man.
    Electroencephalogr Clin Neurophysiol. 1982; 53: 349–360

  35. Gandevia, SC, Burke, D, and McKeon, BB.
    Convergence in the somatosensory pathway between cutaneous afferents from the index and middle fingers in man.
    Exp Brain Res. 1983; 50: 415–425

  36. Hsieh, CL, Shima, F, Tobimatsu, S, Sun, SJ, and Kato, M.
    The interaction of the somatosensory evoked potentials to simultaneous finger stimuli in the human central nervous system. A study using direct recordings.
    Electroencephalogr Clin Neurophysiol. 1995; 96: 135–142

  37. Huttunen, J, Ahlfors, S, and Hari, R.
    Interaction of afferent impulses in the human primary sensorimotor cortex.
    Electroencephalogr Clin Neurophysiol. 1992; 82: 176–181

  38. Okajima, Y, Chino, N, Saitoh, E, and Kimura, A.
    Interactions of somatosensory evoked potentials: simultaneous stimulation of two nerves.
    Electroencephalogr Clin Neurophysiol. 1991; 80: 26–31

  39. Haavik Taylor, H and Murphy, B.
    Altered cortical integration of dual somatosensory input following the cessation of a 20-minute period of repetitive muscle activity.
    Exp Brain Res. 2007; 178: 488–498

  40. Oldfield, RC.
    The assessment and analysis of handedness: the Edinburgh inventory.
    Neurophychologia. 1971; 9: 97–113

  41. Rossi, S, della Volpe, R, Ginanneschi, F, Ulivelli, M, Bartalini, S, Spidalieri, R et al.
    Early somatosensory processing during tonic muscle pain in humans: relation to loss of proprioception and motor “defensive” strategies.
    Clin Neurophysiol. 2003; 114: 1351–1358

  42. Fujii, M, Yamada, T, Aihara, M et al.
    The effects of stimulus rates upon median, ulnar and radial nerve somatosensory evoked potentials.
    Electroencephalogr Clin Neurophysiol. 1994; 92: 518–526

  43. Ulas, UH, Odabasi, Z, Ozdag, F, Eroglu, E, and Vural, O.
    Median nerve somatosensory evoked potentials: recording with cephalic and noncephalic references.
    Electromyogr Clin Neurophysiol. 1999; 39: 473–477

  44. Hubka, MJ and Phelan, SP.
    Interexaminer reliability of palpation for cervical spine tenderness.
    J Manipulative Physiol Ther. 1994; 17: 591–595

  45. Jull, G, Bogduk, N, and Marsland, A.
    The Accuracy of Manual Diagnosis for Cervical Zygapophysial Joint Pain Syndromes
    Med J Aust 1988 (Mar 7); 148 (5): 233–236

  46. Fjellner, A, Bexander, C, Faleij, R, and Strender, LE.
    Interexaminer reliability in physical examination of the cervical spine.
    J Manipulative Physiol Ther. 1999; 22: 511–516

  47. Smedmark, V, Wallin, M, and Arvidsson, I.
    Inter-examiner reliability in assessing passive intervertebral motion of the cervical spine.
    Man Ther. 2000; 5: 97–101

  48. Pickar, JG and Wheeler, JD.
    Response of Muscle Proprioceptors to Spinal Manipulative-like Loads
    in the Anesthetized Cat

    J Manipulative Physiol Ther. 2001 (Jan); 24 (1): 2–11

  49. Cheron, G and Borenstein, S.
    Specific gating of the early somatosensory evoked potentials during active movement.
    Electroencephalogr Clin Neurophysiol. 1987; 67: 537–548

  50. Cheron, G and Borenstein, S.
    Gating of the early components of the frontal and parietal somatosensory evoked potentials in different sensory-motor interference modalities.
    Electroencephalogr Clin Neurophysiol. 1991; 80: 522–530

  51. Rossini, PM, Caramia, D, Bassetti, MA, Pasqualetti, P, Tecchio, F, and Bernardi, G.
    Somatosensory evoked potentials during the ideation and execution of individual finger movements.
    Muscle Nerve. 1996; 19: 191–202

  52. Sonoo, M, Kobayashi, M, Genba-Shimizu, K, Mannen, T, and Shimizu, T.
    Detailed analysis of the latencies of median nerve somatosensory evoked potential components. 1: Selection of the best standard parameters and the establishment of normal values.
    Electroencephalogr Clin Neurophysiol. 1996; 100: 319–331

  53. Tinazzi, M, Priori, A, Bertolasi, L, Frasson, E, Mauguiere, F, and Fiaschi, A.
    Abnormal central integration of a dual somatosensory input in dystonia. Evidence for sensory overflow.
    Brain. 2000; 123: 42–50

  54. Cracco, RQ and Cracco, JB.
    Somatosensory evoked potential in man: far field potentials.
    Electroencephalogr Clin Neurophysiol. 1976; 41: 460–466

  55. Desmedt, JE and Cheron, G.
    Non-cephalic reference recording of early somatosensory potentials to finger stimulation in adult or aging normal man: differentiation of widespread n18 and contralateral n20 from the prerolandic p22 and n30 components.
    Electroencephalogr Clin Neurophysiol. 1981; 52: 553–570

  56. Jones, SJ.
    Short latency potentials recorded from the neck and scalp following median nerve stimulation in man.
    Electroencephalogr Clin Neurophysiol. 1977; 43: 853–863

  57. Urasaki, E, Wada, S, Kadoya, C et al.
    Amplitude abnormalities in the scalp far-field n18 of sseps to median nerve stimulation in patients with midbrain-pontine lesions.
    Electroencephalogr Clin Neurophysiol. 1992; 84: 232–242

  58. Urasaki, E, Wada, S, Kadoya, C, Yokota, A, Matsuoka, S, and Shima, F.
    Origin of scalp far-field n18 of sseps in response to median nerve stimulation.
    Electroencephalogr Clin Neurophysiol. 1990; 77: 39–51

  59. Sonoo, M, Genba, K, Zai, W, Iwata, M, Mannen, T, and Kanazawa, I.
    Origin of the widespread n18 in median nerve sep.
    Electroencephalogr Clin Neurophysiol. 1992; 84: 418–425

  60. Sonoo, M, Sakuta, M, Shimpo, T, Genba, K, and Mannen, T.
    Widespread n18 in median nerve sep is preserved in a pontine lesion.
    Electroencephalogr Clin Neurophysiol. 1991; 80: 238–240

  61. Wall, JT, Xu, J, and Wang, X.
    Human brain plasticity: an emerging view of the multiple substrates and mechanisms that cause cortical changes and related sensory dysfunctions after injuries of sensory inputs from the body.
    Brain Res Rev. 2002; 39: 181–215

  62. Tinazzi, M, Fiaschi, A, Rosso, T, Faccioli, F, Grosslercher, J, and Aglioti, SM.
    Neuroplastic changes related to pain occur at multiple levels of the human somatosensory system: a somatosensory-evoked potentials study in patients with cervical radicular pain.
    J Neurosci. 2000; 20: 9277–9283

  63. Tinazzi, M, Valeriani, M, Moretto, G et al.
    Plastic interactions between hand and face cortical representations in patients with trigeminal neuralgia: a somatosensory-evoked potentials study.
    Neurosci. 2004; 127: 769–776

  64. Soros, P, Knecht, S, Bantel, C et al.
    Functional reorganization of the human primary somatosensory cortex after acute pain demonstrated by magnetoencephalography.
    Neurosci Lett. 2001; 298: 195–198

  65. Sterling, M, Jull, G, Vicenzino, B, Kenardy, J, and Darnell, R.
    Development of Motor System Dysfunction Following Whiplash Injury
    Pain. 2003 (May); 103 (1-2): 65–73

  66. Jull, G, Trott, P, Potter, H et al.
    A Randomized Controlled Trial of Exercise and Manipulative Therapy for Cervicogenic Headache
    SPINE (Phila Pa 1976) 2002 (Sep 1); 27 (17): 1835—1843

  67. Michaelson, P, Michaelson, M, Jaric, S, Latash, ML, Sjolander, P, and Djupsjobacka, M.
    Vertical posture and head stability in patients with chronic neck pain.
    J Rehabil Med. 2003; 35: 229–235

  68. Alund, M, Ledin, T, Odkvist, L, and Larsson, SE.
    Dynamic posturography among patients with common neck disorders.
    J Vestib Res. 1993; 3: 383–389

  69. Karlberg, M, Persson, L, and Magnusson, M.
    Reduced postural control in patients with chronic cervicobrachial pain syndrome.
    Gait Posture. 1995; 3: 241–249

  70. Persson, L, Karlberg, M, and Magnusson, M.
    Effects of different treatments on postural performance in patients with cervical root compression: a randomized prospective study assessing the importance of the neck in postural control.
    J Vestib Res. 1996; 6: 439–453

  71. Jull, G, Kristjansson, E, and Dall'Alba, P.
    Impairment in the Cervical Flexors: A Comparison of Whiplash
    and Insidious Onset Neck Pain Patients

    Manual Therapy 2004 (May); 9 (2): 89–94

  72. Branstrom, H, Malmgren-Olsson, EB, and Barnekow-Bergkvist, M.
    Balance performance in patients with whiplash associated disorders and patients with prolonged musculoskeletal disorders.
    Adv Physiother. 2001; 3: 120–127

  73. Rubin, AM, Woolley, SM, Dailey, VM, and Goebel, JA.
    Postural stability following mild head or whiplash injuries.
    Am J Otol. 1995; 16: 216–221



Since 10-07-2015

         © 1995–2017 ~ The Chiropractic Resource Organization ~ All Rights Reserved