A new study led by a neurosurgeon at Stony Brook Medicine appears in the Journal of Neurosurgery: Pediatrics and challenges the older view that hydrocephalus is mainly due to CSF malabsorption. The authors argue that the key problem is a failure of the brain to absorb pulsatile energy from the heartbeat, and that this explanation fits a wide range of experimental and clinical evidence.
The team used an electrical circuit model of pulsatile CSF dynamics to simulate hydrocephalus caused by subarachnoid obstruction. Their results support the idea that an impaired cerebral windkessel system cannot remove heartbeat pulsations, which then alters capillary blood flow and CSF dynamics.
Hydrocephalus affects people of any age and can follow birth defects, prematurity bleeding, head trauma, aneurysms, strokes, or tumors. Symptoms range from high pressure to walking problems, bladder control issues, and memory loss. Current treatment is surgical, usually a shunt from the brain to the abdomen, but shunts have high malfunction rates and often require repeat surgery. The authors call for more imaging studies and new shunt designs.
Difficult words
- neurosurgeon — a doctor who operates on the brain
- hydrocephalus — a condition with excess fluid in the brain
- malabsorption — failure to absorb substances into the body
- pulsatile — having regular pulses or rhythmic beating
- windkessel — a system that reduces heartbeat pressure changes
- capillary — the smallest blood vessel in the body
- shunt — a tube that moves fluid to another body partshunts
Tip: hover, focus or tap highlighted words in the article to see quick definitions while you read or listen.
Discussion questions
- Do you think new shunt designs could reduce repeat surgeries? Why or why not?
- How might better imaging studies change the treatment of hydrocephalus in patients?
- What concerns would you have if a family member needed brain surgery for hydrocephalus?
Related articles
New device measures blood viscosity in real time
Researchers at the University of Missouri created a non-invasive device that monitors blood viscosity and density in real time using ultrasound and software. It can read blood without drawing samples and may help in diseases like sickle cell.
Antibody and EGFR–STAT1 pathway point to new fibrosis treatments
Researchers at Yale found a human antibody that blocks epiregulin and lowers fibrosis markers. They also show EGFR activates STAT1 in fibroblasts, suggesting two treatment paths: block epiregulin or target the EGFR–STAT1 pathway.