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Balance impairments and neuromuscular changes in breast cancer patients with chemotherapy-induced peripheral neuropathy.
Clinical Neurophysiology : Official Journal of the International Federation of Clinical Neurophysiology 2016 Februrary
OBJECTIVE: Chemotherapy-induced peripheral neuropathy (CIPN) is a common side effect of cancer treatment. Resulting sensory and motor dysfunctions often lead to functional impairments like gait or balance disorders. As the underlying neuromuscular mechanisms are not fully understood, we compared balance performance of CIPN patients with healthy controls (CON) to specify differences responsible for postural instability.
METHODS: 20 breast cancer patients with CIPN (PAT) and 16 matched CONs were monitored regarding centre of pressure displacement (COP) and electromyographic activity of M. soleus, gastrocnemius, tibialis anterior, rectus femoris and biceps femoris. We calculated antagonistic co-contraction indices (CCI) and elicited soleus H-reflexes to evaluate changes in the elicitability and sensitivity of spinal reflex circuitry.
RESULTS: PAT's COP displacement was greater than CON's (p=.013) and correlated significantly with the level of CCIs and self-reported CIPN symptoms. PAT revealed prolonged H-wave latency (p=.021), decreased H-reflex elicitability (p=.001), and increased H-reflex sensitivity from bi- to monopedal stance (p=.004).
CONCLUSIONS: We summarise that CIPN causes balance impairments and leads to changes in elicitability and sensitivity of spinal reflex circuitry associated with postural instability. We assume that increased simultaneous antagonistic muscle activation may be used as a safety strategy for joint stiffness to compensate for neuromuscular degradation.
SIGNIFICANCE: Sensorimotor training has the potential to influence neuromuscular mechanisms in order to improve balance performance. Therefore, this training modality should be evaluated as a possible treatment strategy for CIPN.
METHODS: 20 breast cancer patients with CIPN (PAT) and 16 matched CONs were monitored regarding centre of pressure displacement (COP) and electromyographic activity of M. soleus, gastrocnemius, tibialis anterior, rectus femoris and biceps femoris. We calculated antagonistic co-contraction indices (CCI) and elicited soleus H-reflexes to evaluate changes in the elicitability and sensitivity of spinal reflex circuitry.
RESULTS: PAT's COP displacement was greater than CON's (p=.013) and correlated significantly with the level of CCIs and self-reported CIPN symptoms. PAT revealed prolonged H-wave latency (p=.021), decreased H-reflex elicitability (p=.001), and increased H-reflex sensitivity from bi- to monopedal stance (p=.004).
CONCLUSIONS: We summarise that CIPN causes balance impairments and leads to changes in elicitability and sensitivity of spinal reflex circuitry associated with postural instability. We assume that increased simultaneous antagonistic muscle activation may be used as a safety strategy for joint stiffness to compensate for neuromuscular degradation.
SIGNIFICANCE: Sensorimotor training has the potential to influence neuromuscular mechanisms in order to improve balance performance. Therefore, this training modality should be evaluated as a possible treatment strategy for CIPN.
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