Cold aggravates abnormal excitability of motor axons in oxaliplatin‐treated patients

Introduction Cold allodynia is often seen in the acute phase of oxaliplatin treatment, but the underlying pathophysiology remains unclear. Methods Patients scheduled for adjuvant oxaliplatin for colorectal cancer were examined with quantitative sensory testing and nerve excitability tests at baselin...

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Bibliographic Details
Published in:Muscle & nerve 2020-06, Vol.61 (6), p.796-800
Main Authors: Bennedsgaard, Kristine, Ventzel, Lise, Grafe, Peter, Tigerholm, Jenny, Themistocleous, Andreas C., Bennett, David L., Tankisi, Hatice, Finnerup, Nanna B.
Format: Article
Language:English
Subjects:
allodynia
Axons
Channel gating
Clinical Research Short Report
Clinical Research Short Reports
Cold
Colorectal cancer
Colorectal carcinoma
Cooling
Cooling effects
Excitability
Motor neurons
nerve excitability testing
neuropathy
Oxaliplatin
oxaliplatin toxicity
Pain
Pain perception
Peripheral nerves
Potassium
potassium channel dysfunction
Potassium channels
Potassium channels (voltage-gated)
Refractory period
Sensory testing
Skin temperature
sodium channel dysfunction
Sodium channels (voltage-gated)
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Summary:Introduction Cold allodynia is often seen in the acute phase of oxaliplatin treatment, but the underlying pathophysiology remains unclear. Methods Patients scheduled for adjuvant oxaliplatin for colorectal cancer were examined with quantitative sensory testing and nerve excitability tests at baseline and after the second or third oxaliplatin cycle at different skin temperatures. Results Seven patients were eligible for examination. All patients felt evoked pain and tingling when touching something cold after oxaliplatin infusion. Oxaliplatin decreased motor nerve superexcitability (P < .001), increased relative refractory period (P = .011), and caused neuromyotonia‐like after‐activity. Cooling exacerbated these changes and prolonged the accommodation half‐time. Discussion The findings suggest that a combined effect of oxaliplatin and cooling facilitates nerve excitability changes and neuromyotonia‐like after‐activity in peripheral nerve axons. A possible mechanism is the slowing in gating of voltage‐dependent fast sodium and slow potassium channels, which results in symptoms of cold allodynia.
ISSN:0148-639X
1097-4598
DOI:10.1002/mus.26852