Introduction
Charcot's symptom is a neurological sign that characterizes the lack of response of cortical neurons to analytical influence, that is, the “deafness” of the cerebral cortex. The symptom got its name from the French therapist Jean Marie Charcot and his colleagues, who described this phenomenon in 1889. The term was first proposed in the work of the German neurologist Theodor Catterer, “A Study of Reflexes,” published in 1757. However, Charcot himself, in his monograph “Study of the Nervous System,” studied this phenomenon in more detail, but mainly from a medical point of view, as a manifestation of “great sensitivity” or diffuse hyperesthesia, in which skin irritants are perceived as sharp and intense.
**History**
Many diseases affect the peripheral nervous system, such as traumatic injuries, infections, metabolic disorders, inflammatory nerve diseases, autoimmune disorders and tumors. In most cases, damage to the peripheral nervous system is irreversible, and restoring the function of the injured nerve may not be possible. However, some types of lesions, such as Lambert-Eaton syndrome and demyelinating optic neuropathies, are reversed through active interactions between the axon and Schwann cells. Axonal shock and the Charcot reflex are two of the best known examples of axon-mediated action, but the two phenomena are quite different from each other.
Intraanodal current (INACT), better known as axonal shock, is the first example of an axon-mediated action. Axonal schwannomas and other peripheral nerve tumors may affect the outer membrane