Etiology: The pathogenesis of lacunar ventricular syndrome is not fully understood. Most believe that it may be due to excessive drainage due to shunt siphoning and increased resistance to cerebrospinal fluid flow in the subarachnoid space of the cerebral cortex. The occurrence of lacunar ventricular syndrome is influenced by several factors. These include hydrocephalus secondary to intracranial infection or cerebral hemorrhage, premature cranial suture closure and narrow craniosynostosis after shunt surgery, and Chiari malformation type II; the younger the patient is at the time of shunt surgery, the more likely it is that a lacunar-like ventricle will occur; the size of the preoperative ventricle and whether or not surgical exploration of the shunt tube is performed to adjust it after shunt surgery; and the type of shunt valve is also a suspected factor. Clinical manifestations: patients’ symptoms are mostly recurrent intermittent headache, nausea and vomiting, impaired consciousness, limb weakness, seizures, and delayed filling of the drainage valve. Some cases have also reported that lacunar ventricular syndrome starts with drowsiness, respiratory distress, and ocular symptoms; once vision is involved, recovery is difficult. The imaging presentation is characterized by a narrowing of the ventricles. Lumbar puncture pressure is significantly elevated during the symptomatic phase. In general, headache worsens on standing and decreases in the recumbent position mostly due to hypocranial pressure from excessive drainage. Patients with chronic or intermittent headache should be differentiated from migraine. Treatment: Surgical treatment is necessary for lacunar ventricular syndrome. The prognosis is good with timely treatment. It has been reported in the literature that progression of lacunar ventricular syndrome can involve vision, and once vision is impaired, it is extremely difficult to recover.