Bell’s palsy is caused by inflammation and swelling of the facial nerve, most likely triggered by a viral infection. The nerve runs through a narrow bony tunnel in the skull, and when it swells, the tight space compresses it, disrupting the signals that control one side of your face. About 23 out of every 100,000 people develop Bell’s palsy each year, giving roughly 1 in 65 people a chance of experiencing it in their lifetime.
The Facial Nerve and Why It’s Vulnerable
The seventh cranial nerve, which controls the muscles of facial expression, travels through a structure called the fallopian canal. This is a narrow bony channel carved through the temporal bone near your ear. The canal has three tight sections: one near the inner ear, one along the middle ear cavity, and one that exits through the base of the skull behind the earlobe.
Because this canal is rigid bone, there’s almost no room for the nerve to expand. When the nerve becomes inflamed for any reason, the swelling has nowhere to go. The result is compression, reduced blood flow, and damage to the nerve’s protective coating. This is the core mechanism behind Bell’s palsy: a swollen nerve trapped in a space that can’t accommodate it.
Herpes Simplex Virus Is the Leading Suspect
The strongest evidence points to herpes simplex virus type 1 (HSV-1), the same virus responsible for cold sores. Most people carry HSV-1 from childhood. The virus stays dormant in nerve cells and can reactivate under stress, illness, or immune suppression. When it reactivates near the facial nerve, the resulting inflammation triggers the chain of compression and damage described above.
In one study, 50% of Bell’s palsy patients were actively shedding HSV-1 in their saliva, compared to just 19% of healthy volunteers. When tested within the first week of symptoms, 40% of Bell’s palsy patients showed signs of active HSV-1 reactivation. This doesn’t mean HSV-1 is the only cause, but it’s by far the most commonly implicated virus.
Bell’s palsy is sometimes confused with Ramsay Hunt syndrome, which is caused by a different virus: varicella-zoster, the one behind chickenpox and shingles. The key difference is that Ramsay Hunt syndrome produces a painful rash in or around the ear, along with more severe facial paralysis and often hearing loss or dizziness. Bell’s palsy has no rash and is typically less severe at onset, though it may be preceded by mild fever, pain behind the ear, or neck stiffness.
The Autoimmune Theory
Some researchers believe Bell’s palsy is not simply a viral infection but an autoimmune reaction triggered by one. In this model, a viral infection or reactivation provokes the immune system into attacking the myelin sheath, the insulating layer around nerve fibers. When the facial nerve loses this protective coating, signals from the brain to the facial muscles are disrupted or blocked entirely.
This mechanism is similar to what happens in Guillain-Barré syndrome, a condition where the immune system attacks peripheral nerves throughout the body. Bell’s palsy may represent a localized version of this process, limited to the facial nerve. The viral trigger essentially confuses the immune system into treating the nerve’s own tissue as a threat.
Common Triggers and Risk Factors
Bell’s palsy often follows a recent cold, flu, or upper respiratory infection. These illnesses can either directly involve HSV-1 reactivation or create the immune conditions that allow it. Anything that suppresses or disrupts immune function raises the risk.
Diabetes is a well-established risk factor. The disease damages small blood vessels throughout the body, including the tiny vessels that supply the facial nerve (called the vasa nervorum). When blood flow to the nerve is already compromised by diabetic vascular changes, it takes less inflammation to cause significant damage. Many Bell’s palsy patients with diabetes show no other signs of nerve problems elsewhere in their body, suggesting the facial nerve’s tight anatomical quarters make it uniquely vulnerable.
Pregnancy
Pregnant women face a higher risk of Bell’s palsy, particularly in the third trimester and the weeks after delivery. Several pregnancy-related changes converge to create this vulnerability. Fluid retention peaks in late pregnancy, and the resulting tissue swelling can compress the facial nerve the same way it causes carpal tunnel syndrome in the wrists. At the same time, elevated cortisol levels suppress the immune system, potentially allowing latent viruses to reactivate. The blood also becomes more prone to clotting in late pregnancy, which can reduce blood flow to the nerve through small vessel clots.
Women with pre-eclampsia face an even higher risk, because the hallmarks of that condition (severe swelling, high blood pressure, and increased clotting) amplify all of these mechanisms.
Genetics Play a Small Role
Bell’s palsy does run in some families, though genetics account for an estimated 4 to 14% of overall risk. A large meta-analysis combining data from Iceland, the UK, Denmark, and Finland (nearly 5,000 cases and over one million controls) identified the first specific genetic variant linked to Bell’s palsy. People carrying this variant had roughly a 23% higher odds of developing the condition. The variant is common, carried by over half the population in the studied groups, so it’s not a strong predictor on its own. But it confirms that some people are genetically more susceptible to the nerve inflammation that drives Bell’s palsy, likely through differences in immune response or nerve structure.
Why No Single Cause Has Been Confirmed
Bell’s palsy is technically a diagnosis of exclusion, meaning doctors diagnose it when no other specific cause of facial paralysis (tumor, stroke, Lyme disease, trauma) can be identified. The “idiopathic” label reflects the reality that multiple pathways can lead to the same outcome: a swollen facial nerve trapped in a bony canal. For some patients, the trigger is clearly viral. For others, it may be vascular compromise from diabetes, immune shifts during pregnancy, or an autoimmune response. In many cases, several of these factors likely overlap, with a viral reactivation igniting inflammation in someone whose anatomy, genetics, or metabolic health already made them vulnerable.