Subclinical recurrent neck pain and its treatment impacts motor training-induced plasticity of the cerebellum and motor cortex

The cerebellum processes pain inputs and is important for motor learning. Yet, how the cerebellum interacts with the motor cortex in individuals with recurrent pain is not clear. Functional connectivity between the cerebellum and motor cortex can be measured by a twin coil transcranial magnetic stimulation technique in which stimulation is applied to the cerebellum prior to stimulation over the motor cortex, which inhibits motor evoked potentials (MEPs) produced by motor cortex stimulation alone, called cerebellar inhibition (CBI). Healthy individuals without pain have been shown to demonstrate reduced CBI following motor acquisition. We hypothesized that CBI would not reduce to the same extent in those with mild-recurrent neck pain following the same motor acquisition task. We further hypothesized that a common treatment for neck pain (spinal manipulation) would restore reduced CBI following motor acquisition. Motor acquisition involved typing an eight-letter sequence of the letters Z,P,D,F with the right index finger. Twenty-seven neck pain participants received spinal manipulation (14 participants, 18-27 years) or sham control (13 participants, 19-24 years). Twelve healthy controls (20-27 years) also participated. Participants had CBI measured; they completed manipulation or sham control followed by motor acquisition; and then had CBI re-measured. Following motor acquisition, neck pain sham controls remained inhibited (58 ± 33% of test MEP) vs. healthy controls who disinhibited (98 ± 49% of test MEP, P<0.001), while the spinal manipulation group facilitated (146 ± 95% of test MEP, P<0.001). Greater inhibition in neck pain sham vs. healthy control groups suggests that neck pain may change cerebellar-motor cortex interaction. The change to facilitation suggests that spinal manipulation may reverse inhibitory effects of neck pain

Interhemispheric interactions between the right angular gyrus and the left motor cortex: a transcranial magnetic stimulation study

This folder contains data for the manuscript: Baarbé, J.K., Vesia, M., Brown, M.J.N., Lizarraga, K.J., Gunraj, C., Jegatheeswaran, G., Drummond, N.M., Rinchon, C., Weissbach, A., Saravanamuttu, J., Chen, R. Interhemispheric interactions between the right posterior parietal cortex and the left motor cortex: a transcranial magnetic stimulation study

Role of Inferior Frontoparietal Structures in Motor Control and Freezing of Gait in Parkinson’s Disease

Freezing of gait (FOG) is a disabling symptom of Parkinson’s disease (PD) in which patients are unable to step forward when desired. Abnormal brain circuits responsible for FOG in PD patients are unclear and experimental paradigms are needed to address this disabling symptom. We hypothesized that motor interruptions of lower limb movements while seated may be related to FOG and may indicate abnormal brain activities. In Study 1, we tested 19 PD patients and 20 healthy controls and showed that motor interruption or cessation of bilateral stepping while sitting correlated with the presence and severity of FOG and this effect persisted in the “on” dopaminergic medication state. In Study 2, we tested how these “lower limb motor blocks” or LLMB are related to changes in 4-30 Hz cortical activities recorded from 64-channel scalp electroencephalography. In 17 PD patients, we found that sporadic LLMB differed from typical steps in the right angular gyrus (RAG, F=154.6, P=0.0185, before and during LLMB>typical steps). LLMB also differed from cued stops in the right inferior frontal gyrus (F=32.0, P=0.0005, before LLMB>cued stops; F=42.0, P=0.0005, during LLMBPh.D

Mean response time and accuracy pre- and post-motor acquisition.

<p>(A) Healthy participants had marginally reduced response time and had no change to accuracy. (B) Neck pain sham control had moderate reduction to response time and dramatically improved accuracy. (C) Neck pain treatment dramatically reduced response time and had only marginal increase to accuracy. (D) All subjects demonstrated overall reduction to response time and accuracy from pre- to post-motor acquisition. Error bars depict 1 SEM. Pre, pre-motor acquisition; Post, post-acquisition. * <i>P</i> = 0.02–0.04; ** <i>P</i> = 0.005; *** <i>P</i> ≤ 0.001.</p

Mean CBI₅₀ responses in each group.

<p>(A) Mean CBI₅₀ response in healthy controls before and after the combined intervention of sham control and motor sequence acquisition. (B) Mean CBI₅₀ response in neck pain control group before and after the combined intervention of sham control and motor sequence learning. (C) Mean CBI response in spinal manipulation group before and after the combined intervention of spinal manipulation and motor sequence learning. Pre motor, prior to spinal manipulation/sham control and motor sequence acquisition; Post motor, following spinal manipulation/sham control and motor sequence acquisition. Error bars depict SEM. *<i>P</i> < 0.001.</p

Raw traces from representative participants from all three groups.

<p>Here, CBI₅₀ is depicted pre- and post-spinal manipulation or sham control and motor training, as relative to raw traces of M1 activation. Pre motor, prior to spinal manipulation/sham control and motor sequence acquisition; Post motor, following spinal manipulation/sham control and motor sequence acquisition.</p

Stimulus-response curves for representative subjects.

<p>(A-C) Stimulus-response curves relative to maximum stimulator output on the x-axis for representative subjects that were (A) healthy, (B) recurrent neck pain sham, and (C) recurrent neck pain manipulation. (D-F) Stimulus-response curves relative to CBI₅₀ as shown on the x-axis for representative subjects that were (D) healthy, (E) recurrent neck pain sham, and (F) recurrent neck pain manipulation. Pre motor, prior to spinal manipulation/sham control and motor sequence acquisition; Post motor, following spinal manipulation/sham control and motor sequence acquisition.</p