A dragging gait of the lower extremities is a clinical manifestation of corticospinal tract lesions in gait abnormalities. In corticospinal tract lesions, spastic hemiplegic gait is a unilateral lesion. The upper extremity of the diseased side is usually in a flexed, pronated posture with the lumbar region tilted to the healthy side, while the lower extremity is straightened and externally rotated, with outward forward swing compensating for the weakness of the hip, knee flexors and ankle dorsiflexors. How to diagnose lower limb dragging gait? I. Spastic hemiplegic gait is a unilateral lesion. The upper extremity on the sick side is usually flexed and inward, the waist is tilted to the healthy side, the lower extremity is straightened and externally rotated, swinging outward in front (compensating for the dragging gait caused by the weakness of hip, knee flexors and ankle dorsiflexors), and walking in a circle-like gait; mild patients only show the dragging gait of the lower extremity. It is seen in post-stroke sequelae, etc. 1, cerebrospinal fluid examination: in idiopathic pediatric acute hemiplegia generally do not do lumbar puncture, because the cerebrospinal fluid does not have specific changes, unless confirmed meningitis or subarachnoid hemorrhage to check the cerebrospinal fluid. 2. Hematological examination: blood count, blood gas, sedimentation, prothrombin time, fibrinogen, etc., and hemoglobin electrophoresis if necessary. When hypercoagulable state is suspected, check protein C, S, antithrombin III for deficiency. 3.Metabolic disease examination: blood electrolytes, amino acids in blood or urine, lactic acid, urine sugar, organic acids, blood lipids, urea, liver function, etc. can be checked according to the characteristics of each case. 4.Other: when autoimmune disease is suspected, lupus antibody, antiphospholipid antibody, etc. should be measured. Spastic paraplegic gait Bilateral severe spastic hypertonicity, the patient’s lower limbs are tonic and inward, with compensatory trunk movement, walking effort, and scissor-like gait. It is common in children with cerebral palsy, spinal cord trauma, etc. According to the family history, the disease develops in childhood (a few aged 20-30 years) with slowly progressive bilateral lower limb spastic paraplegia, scissor gait, optic nerve atrophy, extrapyramidal symptoms, ataxia, myasthenia gravis, dementia and skin lesions. Laboratory tests: blood, urine, stool and cerebrospinal fluid were normal.