>*"do we just have a neurological* ***damage*** *that can't be fixed?"* According to research ([1](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8802677/)): **Neurogenic stuttering**: The underlying pathophysiological mechanism of **neurogenic stuttering** is not yet fully understood. Contributing to this is the fact that neurogenic stuttering may be associated with multiple pathologies and with different **lesion** sites. Brain **lesions** are areas of **damaged** brain tissue. This kind of **damage** happens because of brain injuries or medical conditions. A stroke, for example, is a type of brain lesion. **Persistent developmental stuttering (PDS)**: this usually isn't associated with brain lesions, neuropathology, or impairment in other areas of cognition. Compared to neurogenic stuttering, PDS has a high recovery rate. A subset of persistent stutterers recover unassisted in adulthood (see [this](https://drive.google.com/file/d/15SrKiiAz-GWB_CUB-x8AQQ6_vnXrHl7S/view?usp=sharing) research). In the general population of people who stutter, the vast majority of cases are considered to be developmental in nature. It's estimated that around 80-85% of all cases of stuttering fall into the developmental category. This leaves a smaller percentage, around 15-20%, that could be attributed to neurogenic causes. Gray matter volume can also change with motor training. A major challenge in stuttering research is determining what sorts of anomalies indicate plasticity and which are more likely to reflect congenital disorganization or disconnection. The possibility that some of the structural differences observed (particularly the unilateral ones) are a consequence of maladaptive functional reorganization cannot be ruled out.