This is the sixth meeting within the neurological diseases course presented by Dr. Fawzi Abu Khalil and interviewed by Prof. Dr. Eyad Qunaibi. You can find the lecture slides here: https://jpuedu-my.sharepoint.com/:b:/g/personal/eyad_aqunaibi_jpu_edu_jo/EQ-FbSYa1gBJgVtRzf0cGQUBCmg4K3kL7fFOerEQHoNzsw?e=puV2YS
Peace be upon you and God’s mercy and blessings. Today we will discuss Bell’s Palsy. We will begin by reviewing the anatomy of the seventh cranial nerve, then move on to the definition of the condition, its causes, symptoms, diagnosis, and treatment options.
The seventh cranial nerve originates from the upper motor neuron in the primary motor cortex of the brain and extends to the pons region of the brainstem, where the facial nerve nucleus is located. From this nucleus, nerve fibers extend toward the face.
An important anatomical fact: the upper part of the face (forehead and eyes) receives nerve supply from both sides of the brain (right and left). Therefore, in the event of a stroke on one side, the muscles of the forehead are not affected because the other side of the brain compensates for the deficit. However, the lower part of the face receives nerve supply from only one side of the brain, which is why weakness or paralysis becomes clearly apparent in this area during a stroke.
The seventh cranial nerve has an intracranial and an extracranial pathway. It runs very close to the eighth cranial nerve, which is responsible for hearing. The nerve exits the skull through the stylomastoid foramen. Upon reaching the face, it divides into five main branches:
The seventh cranial nerve is a mixed nerve, responsible for:
Bell’s Palsy is an acute and sudden weakness in the facial muscles, not gradual in onset. The paralysis must be peripheral, affecting the entire half of the face (upper and lower), with the absence of "red flags" that may indicate other diagnoses.
Most cases improve spontaneously within the first few weeks. The incidence is estimated at 40 cases per 100,000 people annually, with an average age of onset around 40 years. Diabetes, hypertension, and sometimes pregnancy are considered risk factors.
This is a critical diagnostic point:
There is no single, definitive cause known with 100% certainty, but studies suggest a role for the herpes simplex virus and its reactivation in the nerve ganglion.
Symptoms include:
The presence of any of the following signs warrants further investigation (such as MRI) as they rule out a simple diagnosis of Bell’s Palsy:
Once a patient is clinically diagnosed with Bell’s Palsy (after ruling out red flags), treatment should begin immediately, preferably within the first 72 hours of symptom onset:
Let us discuss a tragic case involving a 34-year-old female patient with uncontrolled diabetes (HbA1c = 18). She began experiencing facial pain and difficulty moving her eye.
The patient was actually suffering from mucormycosis (a fungal infection of the nasal and sinus cavities) that had spread to the cavernous sinus in the brain. The cavernous sinus contains cranial nerves III, IV, and VI (responsible for eye movement) and the fifth cranial nerve (responsible for facial sensation and pain).
Administering steroids in the presence of a fungal infection was like "pouring oil on fire," leading to the spread of the fungus and the patient’s death, may God have mercy on her.
A physician must always correlate the medical history with the clinical examination. Bell's palsy is a diagnosis of exclusion; that is, after ensuring the absence of a stroke, tumor, or serious infection.
We ask God for safety for all, and we hope this lecture has clarified the key differences in managing cases of facial nerve palsy (Bell's palsy).
Note: Due to the approaching last ten nights of Ramadan and the blessed Eid al-Fitr, lectures will be temporarily suspended and will resume after Eid, God willing.
A blessed Eid to all, and may you have a prosperous year ahead.