What Is Facial Nerve Palsy?
Facial nerve palsy refers to weakness or complete loss of motor function in the muscles on one side of the face as a result of injury to the seventh cranial nerve.
The most common form is Bell’s palsy, also known as idiopathic facial paralysis. It develops suddenly and is thought to result from inflammation and swelling of the nerve, often following a viral infection. Other causes include herpes zoster infection, known as Ramsay Hunt syndrome, trauma, surgical complications, tumors and bacterial infections.
The clinical presentation is characteristic and may include drooping of the corner of the mouth, an inability to close the eye, loss of forehead wrinkles and an asymmetrical smile.
More severe cases may also involve hearing disturbances, altered taste and changes in tear production. Prompt treatment is essential, as delays may increase the risk of permanent neurological impairment or abnormal reinnervation.
Characteristics and Prognosis of Facial Nerve Palsy
The facial nerve passes through the narrow bony facial canal and exits the skull through the stylomastoid foramen. This anatomical arrangement means that even mild inflammation-related swelling can exert significant pressure on the nerve, reducing its blood supply and oxygenation.
The resulting ischaemia within the confined canal may further aggravate the nerve injury, even after the initial cause, such as a viral infection, has been brought under control.
The prognosis of facial nerve palsy depends largely on the extent of axonal injury. Mild injury, known as neurapraxia, generally resolves completely, whereas more severe injury, such as axonotmesis or neurotmesis, may leave permanent neurological deficits.
The primary objective of treatment is therefore to minimize the duration of ischaemia and create the most favorable possible conditions for neurological recovery.
Clinical Studies
Clinical studies and case series have evaluated the use of hyperbaric oxygen therapy in patients with facial nerve palsy, particularly in cases that do not respond adequately to conventional treatment with corticosteroids and antiviral medication.
The findings indicate faster recovery of motor function, a lower risk of permanent neurological deficit and a reduced likelihood of abnormal reinnervation in patients who received hyperbaric oxygen therapy as an adjunct to standard treatment.
The mechanism of action is clear. Increased oxygenation reduces swelling of the nerve within the facial canal, restores its blood supply, stimulates neurotrophic factors and accelerates axonal regeneration—processes that conventional pharmacological treatment cannot directly influence.
The Role of Hyperbaric Oxygen Therapy
In facial nerve palsy, hyperbaric oxygen therapy may be incorporated as an adjunctive treatment, particularly in patients with severe paralysis, classified as House–Brackmann grade V or VI, those with Ramsay Hunt syndrome, which carries a less favourable prognosis, and patients whose treatment was delayed.
Early intervention is crucial. The sooner treatment begins after the onset of paralysis, the greater the likelihood of preserving nerve tissue that remains in a state of ischaemic dysfunction rather than irreversible injury.
Each session helps reduce swelling within the facial canal and restore oxygen delivery to the nerve, creating conditions that support axonal recovery.
A typical treatment course consists of 15 to 20 sessions and is planned in collaboration with the neurologist or otorhinolaryngologist.