Clinical data shows that treatments such as IVIg and plasma exchange which block or remove circulating antibodies reduce pain in patients suggesting a causal role which in some cases has been confirmed with the use of passive transfer models. For example, autoantibodies directed against CASPR2 (a component of the voltage-gated potassium channel complex) cause pain in patients by binding to primary sensory neurons, disrupting ion channel function and increasing neuronal hyperexcitability and thus pain sensitivity. These findings strongly support the idea that autoantibodies are a mechanism to cause pain and a key first step in this process is their binding to sensory neurons. This suggests that binding of patient-IgG to sensory neurons can be used to determine a pathogenic role of autoantibodies in pain conditions. Data will be presented assessing the binding of human IgG to both mouse primary and human IPSC derived sensory neurons using patient sera from several pain conditions (CRPS, FMS, diabetic neuropathy, small fibre neuropathy and sciatica), as well as the functional impact of these antibodies on sensory neuron physiology.