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Background Individuals with deafblindness experience a combination of hearing and vision impairments. The World Health Organization has developed a global framework referred to as the International Classification of Functioning, Disability and Health (ICF) to describe health and functioning. From the full ICF classification, a selection of categories, referred to as ICF Core Sets, provide users with a tool to describe functioning and disability in specific health conditions. There has been no ICF Core Set created for deafblindness. Given that core sets are instrumental in improving clinical practice, research, and service delivery, the aim of this study is to develop an ICF Core Set for deafblindness. Methods As part of the preparatory phase in the ICF Core Set development, there are four studies that will be conducted. This includes the [1] systematic literature review that examines the researcher’s perspective, [2] qualitative study focusing on the individuals with deafblindness experience, [3] experts survey that looks at health professional’s perspective, and [4] empirical study that examines the clinical perspective. The studies will be conducted using the principles outlined by the ICF Research Branch for the development of ICF Core Sets. The systematic literature review protocol was submitted for registration on PROSPERO CRD42021247952. Discussion An ICF Core Set created for deafblindness will benefit individuals living with deafblindness who are often excluded from social participation, policies, and services. An ICF Core Set for deafblindness will have a significant impact on healthcare professionals, policymakers, researchers, service providers and individuals with deafblindness by facilitating communication among all stakeholder to support the functioning of those with deafblindness.

The aim of this study was to examine whether changes in rat motoneuronal calcitonin gene-related peptide (CGRP) can be correlated with axonal growth and plasticity of neuromuscular synapses. Nerve terminal outgrowth was induced by local paralysis with botulinum toxin. Normal adult soleus and tibialis anterior did not show detectable CGRP content at the motor endplates. Following botulinum toxin injection there was a progressive, transient and bimodal increase in CGRP in both motoneuron cell bodies which innervated poisoned muscles and their motor endplates. CGRP content was moderately increased 1 day after paralysis and, after an initial decline, reached a peak 20 days after injection. This was followed by a gradual decrease and a return to normal levels at the 200th day. CGRP changes in intoxicated endplates were less evident in the tibialis anterior than in the soleus muscle. The CGRP content in motoneurons was positively correlated with the degree of intramuscular nerve sprouting found by silver staining. In situ hybridization revealed an increase in CGRP mRNA in spinal cord motoneurons 20 days after toxin administration. We conclude that motoneurons regulate their CGRP in situations in which peripheral synapse remodelling and plasticity occur.