What can be the manifestation of excessive shunt after hydrocephalus surgery? What is the best treatment? Excessive shunting after hydrocephalus can cause subdural hemorrhage, low intracranial pressure syndrome or ventricular fissure syndrome. Subdural hematoma is caused by the collapse of the ventricles, which causes the cerebral cortex to be pulled down from the dura and the pontine vein to tear and bleed. Although subdural hematomas can resolve on their own without treatment, surgery is still required for symptomatic or progressively increasing subdural hematomas to facilitate ventricular re-expansion. The surgical approach is either external drainage by drilling a hole or internal drainage by burying a low-pressure shunt in the subdural space. What are the symptoms associated with excessive shunts in patients with hydrocephalus? Excessive shunts can cause hypocranial pressure syndrome, resulting in headache, nausea, vomiting, tachycardia, and lethargy, which are particularly likely to occur with changes in position. In patients with hypocranial pressure syndrome, when the patient presents in an upright position, it can cause excessive shunting, resulting in negative intracranial pressure and severe postural headaches that must be relieved by lying down. If symptoms persist or are frequent and interfere with normal life and school, a shunt repair is required to reinsert a higher pressure shunt, or an anti-siphon tube or a higher pressure anti-siphon shunt. Excessive shunts can also cause lacunar ventricles, where the ventricles become very small and lacunar-like after a shunt has been placed. Most patients with lissencephaly can be completely asymptomatic, and only a few patients with recurrent symptoms require surgical intervention. Symptoms of lacunar brain syndrome occur occasionally and present as intermittent vomiting, headache, and lethargy. Imaging shows very small ventricles with reduced extraventricular cerebrospinal fluid gaps, thickened skull, and no space for intracranial cerebrospinal fluid to accumulate. At this point, the ventricular wall collapses, encasing and obstructing the intracerebroventricular shunt, making it impossible to drain. Subsequently, intracerebroventricular pressure rises, the ventricles expand slightly, and the shunts resume work. The intermittent obstruction and working of the shunts cause fluctuations in elevated intracranial pressure, resulting in acute impairment of neurological function. Moreover, due to intracranial space limitations, there is no additional space left to allow for increased intracranial volume, including increased cerebral blood volume. As a result, any factor that can cause cerebral vasodilation (e.g., migraine) or increased cerebral blood flow (e.g., exercise, swimming outdoors in the hot summer sun) can cause increased intracranial pressure and produce symptoms. How are patients with hydrocephalus treated for excessive postoperative shunts? Treatment includes medication such as tachyphylaxis, a dehydrating agent, and acetazolamide, a drug that reduces cerebrospinal fluid secretion to lower intracranial pressure. If medication is not effective, surgical intervention is required. Surgical approaches include repair of the shunt at the ventricular end, upward pressure adjustment of the shunt valve to increase resistance, placement of an anti-siphon or flow control valve, decompression of the subtemporal flap ipsilateral to the shunt, and a combination of these approaches. The application of an intracranial pressure monitor is recommended to discriminate between cranial hypertension headaches caused by high cranial pressure fluctuations and hypocranial headaches caused by negative intracranial pressure due to true overshunting. Intracranial pressure monitors are also useful in identifying other causes of headaches with normal intracranial pressure unrelated to shunt surgery.