The concept of hydrocephalus refers to the excessive accumulation of cerebrospinal fluid in the skull. It is referred to as internal hydrocephalus if the cerebrospinal fluid accumulates in the ventricles, and external hydrocephalus (EH) if the fluid accumulates in the subarachnoid space on the cortical surface. The etiology and pathogenesis of external hydrocephalus (EH) in infants and young children were first proposed by Dandy in 1917 and are not well understood. Encephalitis, meningitis, subdural hematoma, intracerebroventricular and subarachnoid hemorrhage cause mechanical or inflammatory changes in the arachnoid membrane, which can affect its absorption of cerebral fluid and lead to this disease. It is also seen in the recovery period of neonatal hypoxic-ischemic encephalopathy. 2.Diagnostic basis The onset of the disease is before 2 months to 1.5 years old, that is, before the closure of fontanelle. In Maytal’s opinion, an increase in head circumference, especially within a short period of time, is an important basis for the diagnosis of EH. Mcardle et al [3] measured that the normal value of the subarachnoid space is 0 mm to 4 mm, so EH can be diagnosed when the width of the subarachnoid space is >5 mm. External hydrocephalus in infants and children In our daily work, we often encounter parents of infants with trauma or ischemic-hypoxic encephalopathy who come to our department with a CT or MR film of the child’s head from an outside hospital and are diagnosed with subdural effusion, cerebral atrophy or external hydrocephalus because of the symmetrical widening of the subarachnoid space in the frontal lobe or the top of the frontal head. When we asked the child, who often had only minor scalp injury or no symptoms and normal growth and intellectual development, it was easy to make the conclusion that the child was not suffering from subdural effusion, cerebral atrophy or hydrocephalus. Therefore, we explain in detail to the parents of the child about the causes and prognosis of “external hydrocephalus”, and most of the parents of the child express false alarm and then thank us and take the child away happily. The widening of the symmetrical subarachnoid space (extracerebral space) in the frontal or parietal lobes during infancy can be a physiological phenomenon. The normal range of the subarachnoid space is determined by the following criteria: the wide pair of product between the frontoparietal surface of the cerebral cortex and the inner plate of the skull is often 0-4 mm, and the wide pair of product at the anterior part of the longitudinal fissure is often 0-5 mm. Some studies suggest that the wide extracerebral space in infants and neonates evolves in a pattern of small → large → small. In neonates, there is no periaqueductal space and no cerebral sulcus, only a narrow longitudinal fissure can be seen. 2-12 months old infants have a marked widening of the periaqueductal space (subarachnoid space), the most pronounced at 2-6 months of age, and by about 2 years of age most infants have lost their periaqueductal space and cerebral sulcus and have only a narrow longitudinal fissure. Some authors suggest that the apparent widening of the extracerebral space is due to a momentary imbalance in cerebrospinal fluid production and absorption during development and to the fact that cranial development is faster than brain tissue development in the postnatal months. This is a physiological change. This shows that it is wrong to diagnose hydrocephalus as a widening of the subarachnoid space (extracerebral space) in the frontal or parietal lobes of infants and children. External hydrocephalus (E H) is diagnosed when the symmetrical subarachnoid space (extracerebral space) in the frontal or parietal lobes exceeds the normal physiologic range in infants and newborns, and the subarachnoid space is not wide or slightly wide in other areas. The criteria for determining abnormal widening of the subarachnoid space are: the width between the frontoparietal surface of the cerebral cortex and the inner plate of the skull is greater than 5 mm, and the width of the anterior longitudinal fissure is greater than 6 mm. external hydrocephalus is divided into idiopathic and secondary E H. Most scholars believe that E H occurs only in infants with unclosed fontanelles, and that an open cranial suture is necessary for E H to occur. The temporary decrease of cerebrospinal fluid absorption caused by various reasons, together with the increase of cerebrospinal fluid secretion from the choroid plexus, leads to temporary traffic hydrocephalus. The hydrocephalus causes intracranial hypertension, and the infant, because the fontanelle and cranial suture are not yet closed, can buffer the increased pressure by cranial suture opening and fontanelle expansion, so that the symptoms of increased intracranial pressure can be reduced. Secondary E H can be caused by a variety of factors, such as: hypoxic-ischemic encephalopathy, intracranial hemorrhage, septic meningitis, hyperbilirubinemia, premature birth, etc.; those who cannot find the cause are called idiopathic E H . Idiopathic external hydrocephalus generally has a good prognosis, most of the hydrocephalus is reduced after 2-3 months, and can be completely absorbed at the age of 2-3 years, which is a benign self-healing disease. In view of the effect of X-ray radiation on infants, it is advisable not to review CT too frequently, but once or twice every 6-12 months. Secondary EH should vary depending on the etiology and clinical manifestations. In mild cases, the disease will subside and absorb on its own as in idiopathic EH, and asymptomatic or occasional cases may not require treatment. If the damage is serious, cerebral atrophy will occur, and a few infants may develop mild neuropsychiatric disorders such as psychomotor retardation, transient convulsive seizures, behavioral problems, mood disorders, and even cerebral palsy from 2 months to 2 years old, so active treatment is necessary for severe external hydrocephalus. In infants and neonates with a wide frontal or frontoparietal symmetric subarachnoid space (extracerebral space), the main lesions that need to be differentiated on imaging are subdural effusion and cerebral atrophy: 1. Subdural effusion Most subdural effusions have a unilateral onset, but if bilateral, they are asymmetrical, with a “crescent-shaped” medial hypodense area on the cranial plate, with the adjacent brain surface compressed and internally displaced. The adjacent cerebral surface is compressed and flattened, and the cerebral sulcus becomes shallow and flat, with an occupational effect. Because the arachnoid membrane is located in the inner dura, when the subarachnoid space is widened, it is closer to the intracranial plate, and the enhanced dotted vascular shadow (vein) can be seen adjacent to the intracranial plate on the enhanced scan, while the subdural fluid is pushed inward by the arachnoid membrane, and the vascular shadow is far from the intracranial plate. The widening of the subarachnoid space is widespread and not limited to the frontoparietal region, and the widening of the interhemispheric fissure also covers the entire interhemispheric fissure, accompanied by different degrees of ventricular enlargement.C T shows thinning of brain tissue, hypodensity and generalized deepening of the cerebral sulcus, suggesting quantitative and qualitative abnormalities of brain tissue.