Normal cranial pressure hydrocephalus (NPH) refers to a group of special clinical syndromes with normal intracranial pressure and enlarged ventricles, and memory, mental retardation, unsteady gait and urinary incontinence, which is often mistaken for dementia because of mental decline. I. Etiology: This disease can be divided into two categories: one has subarachnoid hemorrhage, craniocerebral trauma, meningitis, craniotomy and other clear causes; the other category is called idiopathic NPH, often without a clear cause, and the patient manifests as unsteady gait and dementia. Pathophysiology: For NPH cases with clear etiology, the mechanism of hydrocephalus is easy to understand, such as tumors can block the cerebrospinal fluid circulation pathway causing obstructive hydrocephalus. Subarachnoid hemorrhage can cause cerebrospinal fluid reabsorption obstruction causing traffic hydrocephalus. However, the pathogenesis of idiopathic NPH is still unclear. Symon and Dorsch observed that many patients with idiopathic NPH had intermittent increase in intracranial pressure, which could not be detected by lumbar puncture in the first or second time, and Hakin and Adam observed that patients with increased intracranial pressure and enlarged ventricles in the early stage of the disease, and then the pressure returned to the normal level later (Laplace’s law). The enlargement of the ventricles despite normal cranial pressure indicates that the pressure on the ventricular walls is still increased. Recent studies have found abnormalities in the brain parenchyma in NPH, and Sklar et al. found altered brain elasticity in these patients, which may be related to ventricular enlargement. At the same time, it was found that patients with idiopathic NPH had a diffuse decrease in cerebral blood flow, which could be improved after shunt surgery. C. Clinical manifestations: The course of the disease is long, from onset to ventricular enlargement can be experienced for many years. Symptoms can often be progressively aggravated and can develop at different rates. Gait instability is the first symptom, but may also appear simultaneously with cognitive dysfunction, urinary incontinence, etc. Occasionally, it may appear after intellectual decline and urinary incontinence. Gait instability may be manifested as a slight imbalance in walking, and the difference between small, wide steps and the gait of Parkinson’s disease is that there is no change in the rhythm of walking. There is no panic gait, which is present in all cases. There is often a history of falls, which in severe cases manifests as an inability to walk or stand. Mental symptoms are mainly cognitive dysfunction, ranging from mild memory loss (especially near memory) to slowed thinking, and in severe cases the patient becomes abulic, inattentive, or mildly demented. About 2/3 of the patients present with varying degrees of psychiatric symptoms. About half of the patients with urinary incontinence mainly do not know urinate, and therefore wet the bed or pants. Fourth, diagnosis: the diagnosis of NPH mainly relies on clinical manifestations, according to the history and neurological examination, the application of head CT or MR to confirm the diagnosis of clinical impression. (i) CT or MR imaging can measure the size of the ventricles. Table 108-1-1 lists the data of normal ventricle size, according to which the degree of ventricle enlargement can be judged. Sometimes the etiology causing hydrocephalus can be found, and the degree of ventricular shrinkage after cerebrospinal fluid shunt surgery can also be observed, with or without complications.CT and MRI show that ventricular enlargement is obvious, but cerebral cortical atrophy is less obvious, and MRI can be helpful in understanding the etiology of the disease by observing the changes in cerebrospinal fluid dynamics. Low-signal changes in T-weighted images around the ventricles indicate that hydrocephalus is still in the process of progression, and MR coronal scanning often sees cerebrospinal fluid spaces become smaller (obstruction) in the convex surface of the brain, according to which it can be differentiated from cerebral atrophy. (Lumbar puncture: the pressure does not exceed 180mmH2O (24Kpa), and the quantification of glycoprotein is often at normal level. The cell count is normal. In some cases lumbar puncture released 20~30ml cerebrospinal fluid after symptoms have significantly improved, the efficacy can last 12~36 hours. This test is called Tap-test. positive Tap-test is an indication that cerebrospinal fluid shunt surgery is effective, but negative Tap-test is not an indication that cerebrospinal fluid shunt surgery is inevitably ineffective, and this type of patient can be slowly improved after several months of shunt surgery. (C) Intracranial pressure monitoring: routine intracranial pressure measurement is often in the normal range, but 24-hour continuous intracranial pressure monitoring may have scattered high-pressure waves. (d) Other tests: cerebral blood flow, radioisotope polygraphy, cerebral poolography, and electroencephalography can be used as parameters to determine changes after cerebrospinal fluid shunt surgery. Figure 108-1-1 shows the guidelines for the diagnosis and treatment of idiopathic normal cranial pressure hydrocephalus. V. Treatment: Once the diagnosis of NPH is established, ventricular skin shunt surgery should be performed as early as possible. Literature reports that: according to the characteristics of normal cranial pressure hydrocephalus intracranial pressure is at the normal level, therefore, it is appropriate to choose a low-pressure shunt tube of 60-90 mmH2O. The improvement rate after cerebrospinal fluid shunt surgery is 93%. Literature reports: the mortality rate of the operation is 0~9%, and the complications are 5~25%, and the common complications are subdural hematoma (3~23%), epilepsy (0~10%), and shunt device infection (2~5%). Prognosis: NPH with clear etiology has a good prognosis, shorter duration of disease, and age is also related to the prognosis.