Babinski’s sign is a qualitative aberration of the flexion reflex in the human lower extremity, and its occurrence is closely related to functional and structural disorders of the upper motor neuron (corticospinal) system. The flexion reflex is apparently a fixed response of the purposive theory. When a person steps on a spike or a frog toe is immersed in acid or a lobster foot is crushed by a reef, the limb will retract in a coordinated manner from the injurious stimulus. The main achievement is the analysis of the mammalian flexion reflex. Hindlimb flexion involves coordinated movements of the foot, ankle, knee, and hip joints to move the foot away from the stimulus and flex it toward the trunk. It is important to note that the muscles that cause dorsiflexion of the ankle and toes in this response are anatomically called extensor muscles, such as the extensor digitorum longus. Conversely, flexion of the toes to the face caused by the flexor digitorum longus is part of the extension support reflex to maintain upright posture. In normal conscious, relaxed subjects, the flexion reflex is easily elicited with a moderately injurious stimulus, commonly a pointed object with a pointed head that is drawn distally along the lateral aspect of the foot (the classic Babinski site) or along the lateral aspect of the foot toward the fifth toe (the chaddock site). This reflex is a polysynaptic reflex elicited by two types of nociceptive fibers, unmyelinated and thin and myelinated. The normal threshold response is a contraction of the short toe flexors, perhaps with the aim of facilitating the foot’s avoidance of injurious stimuli. Initially, especially the combined contraction of the anterior tibial and extensor [longus muscles causes the foot to dorsiflex at the ankle; in response to a strong response, contraction of the knee and hip flexors occurs. The normal synergistic effect involves all toe flexion toward the face, mainly due to the activity of the flexor digitorum profundus; although the extensor digitorum longus also contracts at this time, its main effect is to dorsiflex the foot at the ankle joint. In normal subjects, the extensor digitorum longus, the dorsiflexor of the big [toe, is not involved in the response. Since the major active muscles are all anatomically flexors, this normal response pattern of all toes down is referred to as the flexor response in clinical terminology. When the upper motor neuron pathway above the S-1 segment is functionally or structurally impaired, the reflex is hyperactive. This is evidenced by the following phenomena: 1) the stimulus threshold is reduced; 2) the anatomical foci of excitation can be extended beyond the S-1 segment; and 3) any stimulus intensity can elicit a stronger, more widespread motor response. This unique pathological response of practical significance is the result of overexcitation of the efferent signal; the extensor digitorum longus and its anatomical neighbors, as well as the functionally equivalent ankle dorsiflexors, tibialis anterior, and extensor digitorum longus, are recruited into the contraction. The result is [dorsiflexion (extension) of the toe at the joint. Electromyographic and blocking nerve studies demonstrate that this is a mechanical competition: [the downward force of the short toe flexor is overcome by the reverse force of the long extensor [muscle. In terms of reflexes, this dorsiflexion of the big [toe is the only evidence of damage to upper motor neurons, and Kugelberg et al. proposed the concept that the two response patterns of flexion and extension are completely independent in normal subjects, based on experiments in which electrical stimulation was transmitted to many areas throughout the hip and lower extremity. However, they concluded that “pathological reflexes are not new reflexes; they are due to a disruption of the coordinated integration of the extension and flexion components of the normal reflex mechanism. The disruption of supra-segmental regulation impairs the ability of the reflex mechanism to recognize the intensity, pattern, and site of sensory stimuli”. It is controversial whether Babinski’s sign was liberated during the development of the nervous system. Using “a moderate injurious pressure on the thumbnail”, Hogan and Milliken found that 93% of normal neonates had a bilateral flexion response. In contrast, Ross et al. used a particularly strong injurious stimulus and found that 71% of neonates had a bilateral extensor reflex and 21.5% had a unilateral extensor reflex. This shows that most normal newborns have Babinski’s sign. Although detailed quantitative studies of the maturation of this reflex are not available, general experience suggests that most normal children have a flexor reflex by 1 year of age. In conclusion, Babinski’s sign does not differ from the normal nociceptive polysynaptic reflex. More precisely, it is an overactive flexor reflex in which the extensor [longus muscle is involved due to diffusion effects, i.e., synaptic hyperexcitability in the S-l spinal nerve felt. It should be noted that this reflex is commonly referred to as a reflex. The normal response of the big [toe downward is called the flexion reflex (response). The pathologic extension reflex is manifested as [toe dorsiflexion at the toe joint. The name Babinski’s sign (reaction or reflex) is synonymous with the extensor reflex (reaction). The Babinski reflex-word should not be used to indicate the reflex or the site of stimulation; there is no such thing as a Babinski negative.