Normal cranial pressure hydrocephalus (NPH) is a specific group of clinical syndromes with normal intracranial pressure and enlarged ventricles, with memory and mental retardation, unsteady gait, and urinary incontinence. I. Etiology: The disease can be divided into two categories: one with subarachnoid hemorrhage, craniocerebral trauma, meningitis, craniotomy and other clear causes. Hakin reported the first case of idiopathic NPH in 1964, in which the patient showed gait instability and dementia, and Adam reported 3 cases a year later, after which the number of reported cases in the literature increased. Pathophysiology: In cases of NPH with a clear etiology, the mechanism causing hydrocephalus is easy to understand, such as tumors can block the cerebrospinal fluid circulation pathway causing obstructive hydrocephalus. Subarachnoid hemorrhage causes obstruction of cerebrospinal fluid reabsorption causing traffic hydrocephalus. However, the pathogenesis of idiopathic NPH is still unclear. Symon and Dorsch observed that many patients with idiopathic NPH have intermittent increased intracranial pressure, which is often not detected during first and second lumbar punctures, and Hakin and Adam observed that patients with increased intracranial pressure and ventricular enlargement at the beginning of the disease return to normal pressure (Laplace’s law). Although the cranial pressure was normal, the ventricular enlargement indicated that the pressure on the ventricular wall was still increased. Recent studies have found abnormalities in the brain parenchyma of NPH, and Sklar et al. found altered brain elasticity in these patients, which may be related to ventricular enlargement. It was also found that patients with idiopathic NPH have diffuse reduction in cerebral blood flow, which can be improved after shunt. III. Clinical manifestations: The course of the disease is long, and many years can be experienced from the onset to the enlargement of the ventricles. Symptoms can often worsen progressively and can have different rates of progression. Gait instability is the first symptom to appear, but it may also appear simultaneously with cognitive dysfunction, urinary incontinence, etc. Occasionally, it may appear after mental decline and urinary incontinence, and gait instability can be manifested as a slight walking imbalance, small steps with wide base and Parkinson’s disease gait is not changed walking rhythm. There is no panic gait, which is present in all cases. There is often a history of falls, and in severe cases, an inability to walk or stand. Mental symptoms are mainly cognitive dysfunction and vary in severity from mild memory loss (especially near memory) to slowed thinking, and in severe cases patients become unconscious (abulic), inattentive or mildly demented. About 2/3 of patients develop varying degrees of psychiatric symptoms. About half of the patients present with urinary incontinence mainly because they do not know to urinate and therefore wet the bed or pants. IV. Diagnosis: The diagnosis of NPH mainly relies on clinical manifestations, based on medical history and neurological examination, and the application of head CT or MR to confirm the diagnosis of clinical impression. (a), 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 ventricular enlargement can be judged. Sometimes the cause of hydrocephalus can be found, and the degree of ventricular shrinkage after cerebrospinal fluid shunt can also be observed with or without complications. CT and MRI show significant ventricular enlargement but less significant cerebral cortex atrophy, and MRI can be helpful in understanding the cause by observing 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 scan often sees a smaller cerebrospinal fluid gap (obstruction) in the convex surface of the brain, according to which it can be differentiated from cerebral atrophy. (b) Lumbar puncture: pressure does not exceed 180 mmH2O (24 Kpa), and glycoprotein quantification is often at normal levels. The cell count is normal. In some cases there is significant improvement in symptoms after lumbar puncture releasing 20-30 ml of cerebrospinal fluid, and the effect can last 12-36 hours. This test is called Tap-test. A positive Tap-test is an indication that cerebrospinal fluid shunts are effective, but a negative Tap-test is not an indication that cerebrospinal fluid shunts are necessarily ineffective, and such patients can slowly improve several months after shunt surgery. (iii) Intracranial pressure monitoring: Routine intracranial pressure measurements are often in the normal range, but 24-hour continuous intracranial pressure monitoring may show scattered high pressure waves. (iv) Other examinations: cerebral blood flow, radioisotope multi, brain pool imaging, and electroencephalography can be used as parameters to determine changes after cerebrospinal fluid shunt. Figure 108-1-1 shows the guidelines for the treatment of idiopathic normal cranial pressure hydrocephalus. V. Treatment: Once the diagnosis of NPH is established, ventriculoperitoneal shunt surgery should be performed as early as possible. The literature reports that according to the characteristics of normal cranial pressure hydrocephalus with intracranial pressure at normal level, it is therefore appropriate to choose a low pressure shunt tube of 60~90 mmH2O. The improvement rate after cerebrospinal fluid shunt is 93%. The literature reports that the operative mortality rate is 0-9% and the complications are 5-25%. The common complications are subdural hematoma (3-23%), epilepsy (0-10%) and shunt device infection (2-5%).