Hyperresponsiveness to auditory, visual, and tactile stimuli is one of the manifestations of Krabbe’s disease. Krabbedisease was first reported in 1916 by the Danish pediatrician Krabbe, hence the name Krabbe’s disease, and is also known as infantilefamilialdiffusesclerosis, based on its clinical features, and is an autosomal recessive metabolic disorder with a mutation in the 14p gene. The gene is located at 14p. The genetic defect in Krabbe disease, which causes galactosamine-beta;-galactosidase deficiency, is a genetic metabolic disorder that leads to a major involvement of the white matter of the brain. The prognosis of this disease is extremely poor. Infantile forms often die within 1 year of age. Late onset cases may survive until about 10 years of age. The disease is autosomal recessive, with a mutated gene at 14 p. The affected child has a genetic defect and a deficiency of the enzyme galactosamine-beta;-galactosidase, which leads to the deposition of many galactosaminoglycans in the white matter of the brain. There are two clinical types based on the age of onset: infantile and late onset. Infantile Krabbe’s disease is the main type, and the typical clinical manifestations are divided into 3 stages: 1. The infant is normal at birth and develops within a few weeks to a few months after birth (mostly within 3 months, 10% after 1 year of age); the common features are: the child is easily excited, frightened, cries frequently without any cause, general rigidity, fever and vomiting without any reason, progressive intelligence and activity loss, and slow development. 2. 2. Thereafter, the child gradually develops increased muscle tone, crossed legs, lateral twisting of the body, ankle clonus, excessive response to auditory, visual and tactile stimuli, accompanied by convulsions and progressive psychomotor deterioration. 3. Late stage children further develop blindness, deafness and cachexia state with spastic seizures and decortical tonicity, but no response to the surroundings. A small number of children may have hydrocephalus, high fever and signs such as hyperhidrosis and hirsutism. The prognosis is very poor. Death usually occurs within 1 year of age, and survival for more than 2 years is rare. Late onset disease is rare, with convulsions, progressive cerebellar ataxia, and optic atrophy occurring after 5 to 6 years of age. Early dementia and cone bundle signs are positive. Late onset may survive until about 10 years of age. Typical symptoms provide a reference for clinical diagnosis. Detection of galactoencephalose-beta;-galactosidase activity deficiency in the patient’s blood leukocytes and serum cultured fibroblasts is the main basis for diagnostic determination.