The Effects of Spinal Manipulation on Central Integration
of Dual Somatosensory Input Observed After
Motor Training: A Crossover Study

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

FROM:   J Manipulative Physiol Ther. 2010 (May);   33 (4):   261–272 ~ FULL TEXT

Heidi Haavik Taylor, PhD, BSc, Bernadette Murphy, PhD, DC

New Zealand College of Chiropractic,
Auckland, New Zealand.

OBJECTIVE:   This study sought to investigate the influence of spinal dysfunction and spinal manipulation on the response of the central nervous system to a motor training task.

METHODS:   The dual peripheral nerve stimulation somatosensory evoked potential (SEP) ratio technique was used in 11 subjects before and after a 20-minute typing task and again when the typing task was preceded with cervical spine manipulation. Somatosensory evoked potentials were recorded after median and ulnar nerve stimulation at the wrist (1 millisecond square wave pulse, 2.47 Hz, 1x 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 increase in the MU/M+U ratio for both cortical (ie, N20-P25 and P22-N30) SEP components after the 20-minute repetitive contraction task. This did not occur when the motor training task was preceded with spinal manipulation. Instead, there was a significant decrease in the MU/M+U ratio for the cortical P22-N30 SEP component. The ratio changes appear to be due to changes in the ability to suppress the dual input as concurrent changes in the MU amplitudes were observed.

DISCUSSION:   This study suggests that cervical spine manipulation not only alters cortical integration of dual somatosensory input but also alters the way the central nervous system responds to subsequent motor training tasks.

CONCLUSION:   These findings may help to clarify the mechanisms responsible for the effective relief of pain and restoration of functional ability documented after spinal manipulation and the mechanism involved in the initiation of overuse injuries.

Key Indexing Terms:   Somatosensory Evoked Potentials, Neuronal Plasticity, Spinal Manipulation, Sensory Filtering, Sensorimotor Integration, Chiropractic

From the FULL TEXT Article:


A growing body of evidence suggests that the presence of spinal dysfunction of various kinds has an effect on central neural processing, and it has been suggested that spinal dysfunction could lead to maladaptive central plastic changes. [1, 2] Such plastic changes could result in abnormal responses to any subsequent input to the central nervous system (CNS). The reversal of such changes may be a mechanism by which spinal manipulation improves functional ability. Cervical manipulation to dysfunctional segments in a group of patients with recurrent neck pain and/or stiffness has been shown to alter cortical processing and sensorimotor integration, measured via somatosensory evoked potential (SEP) amplitude changes, for at least 20-30 minutes. [2, 3]

A somatosensory evoked potential is an electrical potential elicited by either physiologic4 or electrical5 stimulation of somatosensory receptors or their axons. These electrical potentials can be recorded at various sites along the pathway of the relevant peripheral nerve, or at its central projections, recorded over the spinal cord or via scalp recording electrodes. The SEP peaks are named based on the approximate latency in milliseconds (ms) from the time of peripheral nerve stimulation, and the different early peaks reflect somatosensory processing at various cortical and subcortical areas. For example, the N20 SEP peak reflects processing of afferent information at the level of the primary somatosensory cortex. [6-8] The N30 SEP peak appears to represent processing and central sensorimotor integration in areas that include the primary sensory cortex, primary motor cortex, premotor cortex, and deeper brain structures such as the basal ganglia. [9-16] The validity of the assignment of the neural generators of most of the early SEP peaks (occurring within 100 ms of nerve stimulation) has been determined by intracortical direct recording during surgery [17] or using dipole source localization and magnetoencephalography. [7] Interpeak, peak, and interside differences (mean ± SD) have good overall reproducibility. [18]

Somatosensory evoked potentials have been used to show altered cortical processing in clinical conditions. Tinazzi et al [19] recorded ulnar nerve SEPs in patients who had had carpal tunnel syndrome compressing the median nerve at baseline and after 4 weeks. They found significant increases in both cortical and brainstem SEP amplitudes after stimulation of the unaffected ulnar nerve, indicative of adaptive plasticity in the noncompressed ulnar nerve. This work indicates that conditions that change afferent input from one part of the body can affect processing in another. Changes in SEP peaks may reflect the perceptual changes seen in an early study where Murphy and Dawson [20] have demonstrated that patients with trigger points in their forearm muscles had an impaired ability to discriminate nonpainful intramuscular sensation delivered to those same muscles and that this could be improved by treating the trigger points.

One mechanism that would explain changes in processing from nearby body parts is changes in surround inhibition. Surround inhibition is a mechanism by which the CNS increases excitability to one area by increasing inhibition to adjacent areas to enhance neural processing. Changes in surround inhibition have been shown to be responsible for therapy-induced cortical reorganization in chronic stroke patients. [21] Abnormally low somatosensory surround inhibition has been demonstrated in subjects with dystonia, a movement disorder that causes twisting and abnormal postures during repetitive movements. [22] Decreasing surround inhibition in the short-term may be one mechanism that leads to motor learning but in certain individuals may also be the trigger for maladaptive plasticity. The dual SEP technique, which measures the ability of the CNS to appropriately suppress the response to simultaneous input from 2 peripheral nerves, as compared to the arithmetic sum of either nerve individually, has demonstrated that the CNS is less able to suppress dual somatosensory input after as little as 20 minutes of repetitive motor training. [23] However, it is unknown whether this reflects a natural process during skill acquisition or a maladaptive process that could over time lead to a degradation of the highly segregated sensorimotor cortical maps, such as has been demonstrated in primates after many weeks of highly articulated hand squeezing movements. [24] The presence of spinal dysfunction may represent one factor that could induce maladaptive central plastic changes as opposed to the adaptive plasticity of skill acquisition. It has been demonstrated that spinal manipulation of dysfunctional cervical joints can improve somatosensory “surround-inhibition-like” filtering of somatosensory information at the cortical level. [3]

This study used the dual SEP techniques to investigate the effect of manipulation, delivered to dysfunctional regions of the spine in a group of participants with recurrent neck pain and/or stiffness, on the CNS response to motor training. It was hypothesized that manipulation would change the way in which the CNS responded to the typing task.


Key Findings

The major finding in this study was that when a 20-minute session of thumb abductions is preceded by spinal manipulation of dysfunctional cervical joints, this altered the way in which the CNS responded to the motor training task. Motor training performed by subjects with reoccurring neck pain, but no acute symptoms at the time of the study, resulted in reduced suppression of the dual input at the cortical level for at least 20 minutes after the cessation of the typing task. This is in accordance with previous research [23] and may reflect the process responsible for use-dependent plastic changes in the sensorimotor cortex. However, when cervical spine manipulation of dysfunctional segments was performed before the same motor training task, there was a significantly increased suppression of the dual input at the cortical level (as reflected by a reduced frontal P22-N30 MU/M+U SEP peak ratio). This finding is similar to what has been shown after spinal manipulation alone [3] and suggests that spinal manipulation leads to an improved ability to integrate dual input from the upper limb. That this was also observed after the combined manipulation and motor training task in the current study suggests that the spinal manipulation not only results in altered sensorimotor integration but also alters the way the CNS responds to a functional task, such as a 20-minute repetitive thumb abduction task.

Implications of the Changes in Different SEP Peaks and Comparison to Other Work

Frontal P22-N30 SEP Changes

The changes observed in the current study after the combined intervention mainly occurred for the frontal N30 component of the SEP peaks. 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. [12-16] The frontal N30 peak is therefore thought to reflect sensorimotor integration. [26] The decreased frontal N30 SEP peak ratio observed after the combined manipulation and motor training intervention in the current study therefore suggests that there may be an increase in “surround-like inhibition” or filtering of afferent information from the upper limb occurring somewhere in these cortical and subcortical loops linking the basal ganglia, thalamus, premotor areas, and primary motor cortex after spinal manipulation, as previously demonstrated, [3] and that this ability is maintained even after a 20-minute motor training task. Impaired surround-like 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 + motor training intervention, and no significant changes in the M+U data was observed.

Parietal N20 SEP Changes

No significant changes were observed for the parietal N20-P25 SEP peak component after the motor task when it was preceded with spinal manipulation in the current study. The motor training intervention, before the manipulation, led to a significant increase in both the frontal P22-N30 and the central N20-P25 SEP peak MU/M+U ratios. The central N20 SEP component is generated in the primary somatosensory cortex (S1). [6-8] This suggests that S1 filtering of the dual input is reduced after motor training in subjects with chronic neck dysfunction and reoccurring pain. This finding may therefore reflect the initiation of a process that over time may result in the desegregation of the normally sharply defined somatosensory maps in S1, as observed by Byl et al [24] in the primate cortex after 20 weeks of repetitive contraction training. No significant changes occurred for the central N20-P25 SEP peak MU/M+U ratio after the motor training task when it was repeated on a different day after manipulation of the subjects' cervical spines. This further suggests that spinal dysfunction may represent one factor that promotes maladaptive plastic changes.

Clinical and Research Implications

The Effects of Spinal Manipulation on Sensorimotor Integration and Neural Plasticity

Somatosensory information is very important for motor control. It can be integrated at multiple levels of the CNS, from simple spinal or cortical reflex loops to highly complex networks involving cortical and subcortical circuits. [32-38] These various sensorimotor processing circuits that make up the sensorimotor integration system continuously monitor and respond to all peripheral input by appropriately altering connectivity and the strength of synaptic connections. The retention of such alterations is thought to underpin sensorimotor skill acquisition. However, these alterations may also in some circumstances, such as after an injury or the sustained performance of repetitive muscular activity, become maladaptive plastic changes that are thought to be responsible for initiating and perpetuating certain movement disorders and chronic pain syndromes. [24,39-51] Furthermore, joint dysfunction originating from an injury may be a cause of ongoing pain and loss of function due to maladaptive sensorimotor integration from a hyperafferentiation of the CNS from the dysfunctional joints and associated structures. [52-58]

Does Repetitive Muscular Activity and Joint Dysfunction Lead to Maladaptive Plasticity?

A previous study has shown that a 20-minute repetitive thumb abduction task leads to altered central integration of dual input, as measured by changes in cortical SEP ratios. [23] Reduced cortical somatosensory filtering was demonstrated for both primary somatosensory cortex (N20) and areas linked to sensorimotor integration (N30). [23] It is possible that the N20 (S1) changes reflect the mechanism responsible for altering the boundaries of cortical sensory maps, thus, altering the way the CNS perceives and processes information from adjacent body parts. It may also reflect the initiation of a process that over time leads to a degradation of the fine somatosensory maps in S1, which has been observed in animals for 20 weeks of behavioral training. [24] Furthermore, it is possible that the N30 changes observed in this study are related to the intracortical inhibitory changes shown previously with both single and paired pulse TMS. [59, 60] This could be reflecting a natural part of motor skill acquisition. However, if these changes are not gained appropriately, they could also reflect the mechanisms by which maladaptive plastic changes develop, resulting in inappropriate motor control similar to that seen in movement disorders such as dystonia.

The key question, therefore, is what circumstances or preexisting patient characteristics need to be present for the process of natural skill acquisition to go wrong and lead to maladaptive plastic changes instead. One possible characteristic is the presence of abnormally functioning spinal segments. As joint dysfunction can lead to altered afferent input to the CNS, [52-58] the presence of joint dysfunction would therefore alter the background milieu into which subsequent sensory input is received and processed. The current study indirectly investigated whether sensory filtering of information is adversely affected when joint dysfunction is present, by determining if manipulation of dysfunctional cervical joints would improve sensory filtering in the CNS. If the reduced sensory filtering after motor training represents a process that could lead to maladaptive plastic changes in the CNS and spinal dysfunction is a component that enables this dysfunction to develop, then this process may be avoided when joint dysfunction is addressed by appropriate manual treatment. The results of this study suggests that this is possible, as an improved ability to filter somatosensory information in sensorimotor integration circuits was observed after the same 20-minute motor training task, when this was preceded with spinal manipulation of the subjects' dysfunctional cervical joints. This finding was similar to what has been previously observed after spinal manipulation alone [3] and indicates that spinal manipulation improves gating or filtering of sensory information, an ability the CNS retains even after the motor training intervention.

It is, however, important that further research is carried out to ensure that manipulation does not simply interfere with the process of skill acquisition. This is unlikely, as no such reports exist in the literature. On the contrary, some evidence suggests that upper cervical manipulation leads to improvement in a complex reaction-time task, [61] suggesting improved cognitive function and skill acquisition after manipulation. Overall, this research has significant implications for understanding the role of altered afferent input from joints and muscles on the ability to appropriately integrate somatosensory input.


Although the sample size was small (11 subjects), this is common in experimental human neurophysiologic studies. As such strongly significant changes were seen in certain SEP peaks with such a small sample size this suggests that these effects are very robust, as it is nearly impossible to make a type I error with a small sample size because the variance is usually very high.


These observations 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, as previously shown,3 and that this improved somatosensory filtering is maintained after a 20-minute repetitive motor training task. 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.

Funding Sources and Potential Conflicts of Interest

The head author was supported with a Bright Futures Top Achievers Doctoral Scholarship awarded by the New Zealand Government. No conflicts of interest were reported for this study.


  1. George, SZ, Bishop, MD, Bialosky, JE,
    Zeppieri, G, and Robinson, ME.
    Immediate effects of spinal manipulation on thermal pain sensitivity: an experimental study.
    BMC Musculoskelet Disord. 2006; 7: 68

  2. Haavik-Taylor, H and Murphy, B.
    Cervical Spine Manipulation Alters Sensorimotor Integration:
    A Somatosensory Evoked Potential Study

    Clin Neurophysiol. 2007 (Feb); 118 (2): 391–402

  3. Haavik Taylor, H and Murphy, B.
    Altered Central Integration of Dual Somatosensory Input
    After Cervical Spine Manipulation

    J Manipulative Physiol Ther. 2010 (Mar); 33 (3): 178–188

  4. Angel, RW, Boylls, CC, and Weinrich, M.
    Cerebral evoked potentials and somatosensory perception.
    Neurology. 1984; 34: 123–126

  5. Cohen, L and Starr, A.
    Vibration and muscle contraction affect somatosensory evoked potentials.
    Neurology. 1985; 35: 691–698

  6. 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

  7. 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

  8. 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

  9. 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

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

  11. 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

  12. 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

  13. 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

  14. 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

  15. Rossini, PM, Babiloni, F, Bernardi, G et al.
    Abnormalities of short-latency somatosensory evoked potentials in parkinsonian patients.
    Electroencephalogr Clin Neurophysiol. 1989; 74: 277–289

  16. Waberski, TD, Buchner, H, Perkuhn, M 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

  17. Wood, C, Spencer, D, Allison, T, Mccarthy,
    G, Williamson, PD, and Goff, WR.
    Localization of human sensorimotor cortex during surgery by cortical surface recording of somatosensory evoked potentials.
    J Neurosurg. 1988; 68: 99–111

  18. Beric, A.
    Stability of lumbosacral somatosensory evoked potentials in a long-term follow-up.
    Muscle Nerve. 1988; 11: 621–626

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

  20. Murphy, BA and Dawson, NJ.
    The assessment of intramuscular discrimination using signal detection theory.
    J Manipulative Physiol Ther. 1995; 18: 572–576

  21. Liepert, J, Haevernick, K, Weiller, C, and Barzel, A.
    The surround inhibition determines therapy-induced cortical reorganization.
    Neuroimage. 2006; 32: 1216–1220

  22. 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

  23. 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

  24. Byl, N, Merzenich, M, Cheung, S, Bedenbaugh, P,
    Nagarajan, S, and Jenkins, W.
    A primate model for studying focal dystonia and repetitive strain injury: effects on the primary somatosensory cortex.
    Phys Ther. 1997; 77: 269–284

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

  26. Rossi, S, Della Volpe, R, Ginanneschi, F 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

  27. 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

  28. Humphreys, BK, Delahaye, M, and Peterson, CK.
    An Investigation into the Validity of Cervical Spine Motion Palpation
    Using Subjects with Congenital Block Vertebrae as a 'Gold Standard'

    BMC Musculoskelet Disord 2004 (Jun 15); 5 (1): 19

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

  30. 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

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

  32. Ciccarelli, O, Toosy, AT, Marsden, JF et al.
    Identifying brain regions for integrative sensorimotor processing with ankle movements.
    Exp Brain Res. 2005; V166: 31–42

  33. Dresel, C, Castrop, F, Haslinger, B,
    Wohlschlaeger, AM, Hennenlotter, A, and Ceballos-Baumann, AO.
    The functional neuroanatomy of coordinated orofacial movements: sparse sampling fMRI of whistling.
    Neuroimage. 2005; 28: 588–597

  34. Nyberg, L, Eriksson, J, Larsson, A, and Marklund, P.
    Learning by doing versus learning by thinking: an fMRI study of motor and mental training.
    Neuropsychologia. 2006; 44: 711–717

  35. Liepert, J, Gorsler, A, Van Eimeren, T,
    Munchau, A, and Weiller, C.
    Motor excitability in a patient with a somatosensory cortex lesion.
    Clin Neurophysiol. 2003; 114: 1003–1008

  36. Fisher, MA. AAEM minimonograph #13:
    H reflexes and F waves: physiology and clinical indications.
    Muscle Nerve. 1992; 15: 1223–1233

  37. Garcia, HA, Fisher, MA, and Gilai, A.
    H reflex analysis of segmental reflex excitability in flexor and extensor muscles.
    Neurology. 1979; 29: 894–991

  38. Bertolasi, L, Priori, A, Tinazzi, M, Bertasi, V, and Rothwell, JC.
    Inhibitory action of forearm flexor muscle afferents on corticospinal outputs to antagonist muscles in humans.
    J Physiol (Lond). 1998; 511: 947–956

  39. Topp, KS and Byl, NN.
    Movement dysfunction following repetitive hand opening and closing: anatomical analysis in owl monkeys.
    Mov Disord. 1999; 14: 295–306

  40. Byl, NN and Melnick, M.
    The neural consequences of repetition: clinical implications of a learning hypothesis.
    J Hand Therapy. 1997; 10: 160–174

  41. Rosenkranz, K, Altenmuller, E, Siggelkow, S, and Dengler, R.
    Alteration of sensorimotor integration in musician's cramp: Impaired focusing of proprioception.
    Clin Neurophysiol. 2000; 111: 2040–2045

  42. Evinger, C.
    Animal models of focal dystonia.
    NeuroRx. 2005; 2: 513–524

  43. Butz, M, Timmermann, L, Gross, J, Pollok, B,
    Dirks, M, Hefter, H et al.
    Oscillatory coupling in writing and writer's cramp.
    J Physiol (Paris). 2006; 99: 14–20

  44. Tamburin, S and Zanette, G.
    Abnormalities of sensory processing and sensorimotor interactions in secondary dystonia: a neurophysiological study in two patients.
    Mov Disord. 2005; 20: 354–360

  45. Kessler, KR, Ruge, D, Ilic, TV, and Ziemann, U.
    Short latency afferent inhibition and facilitation in patients with writer's cramp.
    Mov Disord. 2005; 20: 238–242

  46. Tinazzi, M, Rosso, T, and Fiaschi, A.
    Role of the somatosensory system in primary dystonia.
    Mov Disord. 2003; 18: 605–622

  47. Abbruzzese, G and Berardelli, A.
    Sensorimotor integration in movement disorders.
    Mov Disord. 2003; 18: 231–240

  48. Almeida, QJ, Frank, JS, and Roy, EA.
    An evaluation of sensorimotor integration during locomotion toward a target in Parkinson's disease.
    Neuroscience. 2005; 134: 283–293

  49. Mascia, MM, Valls-Solι, J, Martν, MJ, and Salazar, G.
    Sensorimotor integration in patients with parkinsonian type multisystem atrophy.
    J Neurol. 2005; V252: 473–481

  50. Devos, D, Labyt, E, Cassim, F et al.
    Subthalamic stimulation influences postmovement cortical somatosensory processing in Parkinson's disease.
    Eur J Neurosci. 2003; 18: 1884–1888

  51. 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

  52. Barrack, RL, Skinner, HB, and Buckley, SL.
    Proprioception in the anterior cruciate deficient knee.
    Am J Sports Med. 1989; 17: 1–6

  53. Heikkila, H and Astrom, PG.
    Cervicocephalic kinesthetic sensibility in patients with whiplash injury.
    Scand J Rehabil Med. 1996; 28: 133–138

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

  55. 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

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

  57. 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

  58. 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

  59. Liepert, J, Classen, J, Cohen, LG, and Hallett, M.
    Task-dependent changes of intracortical inhibition.
    Exp Brain Res. 1998; 118: 421–426

  60. Liepert, J, Weiss, T, Meissner, W, Steinrucke, K, and Weiller, C.
    Exercise-induced changes of motor excitability with and without sensory block.
    Brain Res. 2004; 1003: 68–76

  61. Kelly, DD, Murphy, BA, and Backhouse, DP.
    Use of a mental rotation reaction-time paradigm to measure the effects of upper cervical adjustments on cortical processing: a pilot study. J Manipulative Physiol Ther. 2000; 23: 246–251


Since 10-28-2015

         © 1995–2018 ~ The Chiropractic Resource Organization ~ All Rights Reserved