Epstein-Barr Virus-associated Encephalitis and Lumbosacral Radiculitis, Evolved to Normal Pressure Hydrocephalus in an Immunocompetent Adult: A Case Report

Most people know the Epstein-Barr virus as the common germ that causes mononucleosis, often called "the kissing disease." It is so widespread that nearly everyone carries it in their bodies after childhood, usually hiding quietly inside certain immune cells without causing any trouble. For the vast majority of people, this virus remains a dormant passenger. However, in rare instances, it can wake up and invade the central nervous system, the body's command center made up of the brain and spinal cord. When this happens, the virus can trigger inflammation that damages brain tissue or the nerves that control movement and sensation. While doctors generally expect such infections to be a single, short-lived event that clears up once the immune system fights it off, the long-term behavior of the virus in the brain remains a mystery. Understanding whether the virus can linger and cause problems months or years later is crucial, because it changes how doctors monitor patients and decide on treatments.

This story begins with a seventy-one-year-old man who was admitted to a hospital in Shanghai with a sudden inability to speak clearly and a low-grade fever. He was alert but struggled to find words and understand what he heard, symptoms pointing to a problem in the left front part of his brain. Medical scans revealed swelling and inflammation in that specific area, and a detailed analysis of the fluid surrounding his brain and spinal cord confirmed the presence of the Epstein-Barr virus. The medical team treated him with a standard combination of antiviral medication to attack the virus, along with immune therapies to calm the body's overactive response. Within a short time, his fever went away, and his ability to speak returned to normal. It seemed the battle was won.

But the story did not end there. A few days after finishing his initial treatment, the man developed a new and alarming set of symptoms. He lost control of his bladder and, shortly after, his legs became weak and paralyzed. Tests on his spinal fluid showed a strange pattern: the protein levels were very high, but the number of immune cells was low, a sign that the nerve roots in his lower back were being attacked. Further testing confirmed that the insulation around his nerves had been damaged, a condition known as demyelination. Because his body was not producing the usual antibodies that cause such damage, doctors suspected the Epstein-Barr virus was still driving the inflammation. He received a second round of immune therapy, which helped his legs regain strength, but the underlying issue was not fully resolved.

As the months passed, the man's condition took another unexpected turn. Even though he had no fever and no new signs of brain infection, tests continued to find the virus's genetic material in his spinal fluid. The virus had not been cleared; it was still replicating inside his central nervous system, keeping the area in a state of low-level inflammation. This persistent activity eventually led to a third complication. The man began to stumble, his walk became shuffling and unsteady, and he developed memory problems. Scans of his brain showed that the fluid-filled spaces inside the skull had enlarged, a condition called normal pressure hydrocephalus. This happens when the brain cannot properly absorb or circulate its protective fluid, often due to scarring or blockage from past inflammation. To fix this, surgeons placed a small tube to drain the excess fluid from his spine into his abdomen. While this surgery improved his ability to walk, he was left with lasting weakness in his limbs and some cognitive difficulties.

This case challenges the traditional view that viral brain infections are simple, one-time events. The researchers found that in this patient, the virus did not just cause a single episode of sickness and then disappear. Instead, it caused a sequence of different problems: first an inflammation of the brain, then an attack on the nerve roots in the lower back, and finally a blockage of fluid flow that led to hydrocephalus. The key discovery was that the virus remained active in the spinal fluid for months, long after the initial symptoms had faded. This suggests that for some patients, the virus can hide and continue to cause damage even after the acute phase of the illness seems to be over. The authors suggest that when a patient shows signs of persistent virus in the spinal fluid, doctors might need to consider longer-term treatments that combine antiviral drugs with therapies to calm the immune system, rather than stopping treatment as soon as the patient feels better.

The case also highlights a serious, delayed risk that doctors should watch for. Because the chronic inflammation from the virus can eventually disrupt how the brain handles fluid, patients who survive a severe viral brain infection should be monitored for signs of hydrocephalus, even if they seem to have recovered. While the man in this report did not make a full recovery, his journey provides a clear warning that the aftermath of a viral infection can be complex and long-lasting. It suggests that the virus can leave a trail of damage that unfolds in stages, requiring careful observation and perhaps different treatment strategies than what is currently standard for most viral infections.