For decades, the causes of a serious neurological condition have remained murky. However, University of Iowa researchers have now linked hydrocephalus to a flaw in certain cells crucial to brain development.
Studying mice, they found a cell signaling defect that interrupts the functioning of immature cells necessary for normal brain development. According to ScienceDaily, they were able to treat the defect with a drug, making the hydrocephalus less severe.
Hydrocephalus is marked by excessive accumulation of brain. The "water" on the brain is actually cerebrospinal fluid. Accumulation causes an abnormal widening of the ventricles and abnormal pressure on the brain, says the National Institute of Neurological Disorders and Stroke.
As many as 3 of every 1,000 babies have one of several types of hydrocephalus. Researchers have previously leaned toward inherited genetic abnormalities or development disorders associated with neural tube defects, such as spina bifida, as possible causes.
If the excessive fluid isn't removed from the brain's ventricles, they expand. This can cause serious brain damage or even death. While the disorder is one of the most frequent types of brain abnormalities in newborns, treatment for 50 years has remained brain surgery to remove excess fluid. Complications and repeat surgeries aren't uncommon.
The Iowa researchers identified a new mechanism underpinning the development of neonatal hydrocephalus. They studied a group of immature mouse cells known as neural precursor cells (NPCs). These cells have an important role in the development of most kinds of brain cells.
The team sought to reduce the size of mice ventricles, since such a reduction in humans has produced better patient results. In a subgroup of NPCs important in the development of normal ventricles, they discovered an imbalance in the orderly process of immature cells flourishing, then dying off. This caused a cell signaling flaw and eventual hydrocephalus in their mouse model.
After treating the mice with lithium, the scientists noted a return to the normal cell proliferation and dying process. A reduction in hydrocephalus in the mice followed.
They hope that their identification of cell signaling defects and successful drug therapy will lead to non-invasive treatments for hydrocephalus and other neurological disorders. Their results also suggest that successful treatment will require individualized therapies based on the specific type of hydrocephalus a patient has.
Prior to diagnosis and surgery in his 30s to install a Denver shunt, my husband cannot recall a time when he didn't have symptoms the Mayo Clinic notes as typical of hydrocephalus: a large head, sleepiness, vision problems, short-term memory loss, and poor coordination. Life since surgery has been a struggle of measuring medication levels and worrying about possible shunt malfunction. Some symptoms remain. The development of a non-invasive treatment to correct cellular flaws that cause the signaling malfunction leading to hydrocephalus could someday spare many youngsters a similar ordeal.
Vonda J. Sines has published thousands of print and online health and medical articles. She specializes in diseases and other conditions that affect the quality of life.