Adrenoleukodystrophy ALD is an accumulation of very-long-chain fatty acids (VLCFA) in tissues due to an inborn defect in the oxidative process of intracellular peroxidase in vivo, mainly involving the white matter of the brain and adrenal glands. This causes extensive neuromyelin formation in the white matter of the brain and atrophy and dysplasia of the adrenal cortex. In recent years, due to advances in medical molecular biology, the causative gene has been identified to be located on chromosome Xq28. Jianmin Zhong, Department of Neurology, Jiangxi Children’s Hospital ALD usually starts at the age of 3 to 14 years, with 5 to 6 years being the most common, or it can start as early as infancy or as late as adulthood. In children, the brain type is the most common. The clinical manifestations are varied and are mainly manifestations of neurological damage and hyperalgesia. For example, progressive mental retardation, behavioral abnormalities, hearing loss, difficulty with diction and swallowing, increased muscle strength, unsteady gait, and recurrent tics. In older children, there is memory loss and a positive cone bundle sign on examination, while hyperalgesia is manifested by hyperpigmentation and salt loss. In this paper, case 1 had hyperpigmentation, and the age of onset was earlier than that reported in the literature in both cases. experimental examination of ALD had hypoadrenocorticism, such as decreased blood cortisol, urinary 17-hydroxy and 17-ketone, and increased VLCFA in blood. MRI changes in this disease are mainly around the posterior horn of both ventricles, parietal and occipital white matter areas with symmetrical butterfly wing-like long T1 and T2 signals, and the corpus callosum is involved in the pressure part, so that the left and right sides of the lesion are connected, and the lesion involves the posterior and temporal parts of the internal capsule bilaterally in the forward direction, and may involve the brainstem in the downward direction, and in the T2 enhancement image, the brain white matter hyperintense signal area is obvious at the occipital, parietal and temporal intersections, while the frontal lobe is mostly unaffected [1]. In this paper, case 2 was a case of central respiratory failure due to extensive brain involvement, especially in the brainstem. Recently, it was observed that the lesion could be roughly divided into three regions from the periphery to the center, namely the peripheral, intermediate, and central regions. The abnormal contrast enhancement shown by MRI is between the peripheral and intermediate regions, suggesting that the lesion is in the active phase with blood-brain barrier disruption, i.e., enhancement of the lesion edge with Gd-DTPA venous enhancement reflects the active phase of the lesion with local inflammation and blood-brain barrier disruption; the advanced lesion The lesion shows long T1 and long T2 signal without enhancement. It is easy to misdiagnose the disease, but if there is also adrenal cortical and neurological involvement, the clinical diagnosis can be made. If only one type of manifestation is present, the diagnosis is difficult and adrenocortical function tests should be performed. In children with undetected VLCFA, MRI imaging data should be carefully analyzed and followed up, and attention should be paid to differentiate them from other demyelinating diseases such as heterogeneous cerebral leukodystrophy, Pelizaeus-Merzbacher disease, multiple sclerosis, etc. The lesions of ALD progress from posterior to anterior, i.e., they involve the occipital, parietal, temporal, and frontal lobes one by one, and another characteristic manifestation is Another characteristic feature of ALD is that Wallerian degeneration occurs in the cortical tracts of the spinal cord. In order to fully characterize ALD, CT scan can be performed at the same time. Most of the ALD can be seen as calcifications in the white matter of the brain around the lateral ventricular triangle. Family lineage investigation can be helpful in diagnosis. From the eugenic point of view, if the mother of a sick child is pregnant again, prenatal diagnosis should be performed in the fourth to fifth month of pregnancy, mainly to detect the sex of the fetus and the VLCFA of the amniotic fluid cells, and to induce labor in time if the baby is male.