Our facial nerve can be easily compared to a thick telephone cable that connects the telephone station (nerve nucleus in the brain) with the neighborhood of the town (our face). Large bundles of wires split to reach separate apartment blocks (parts of the face). Then they go to various floors of the apartment blocks (facial muscles). Finally the individual wires supply phone signals to each separate apartment (muscle fibers, lacrimal gland and taste sensors).
Although our facial nerve is less than 1 millimeter thick, it contains 10,000 nerve cells (neurons).
There are 3 sorts of neurons in the facial nerve.
Sensory neurons are responsible for the taste receptors in a part of our tongue. That is why when Bell’s palsy happens, some patients have a weird taste sensation or a loss of taste on one side of the tongue (anterior two thirds).
Parasympathetic fibres are responsible for the function of the tear gland. During the acute phase of Bell’s palsy our affected eye becomes dry because the tear production signals cannot reach the lacrimal gland.
Motor neurons are very important. They connect our brain to the facial muscles, so we can blink, reflect our emotions and produce articulated speech. Motor neurons are combined in bundles that supply mimetic signals to various parts of the face. Those bundles are divided into smaller ones to manage individual facial muscles, and then further divided into very small bunches that regulate the function of parts of muscles. Individual neurons (nerve fibres) supply mimetic signals to single muscle strands, just like phone calls that arrive to your home or to a mobile phone. There are about 7000 motor neurons in the facial nerve.
Motor neuron consists of 3 important parts: cell body (soma), dendrites (numerous branch-like connections to exchange signals between individual neurons) and the axon – a long “wire” that connects the cell body with the corresponding muscle fibre. Axons are the highways between the brain and the facial muscles. They conduct finely coordinated actuating (efferent) signals from the facial nerve nucleus to various groups of muscle fibres to produce our facial expressions.
The axon ends at the so called neuromuscular junction. It is the very narrow gap between the nerve and muscle tissue, where the electric signal passes on from the nerve fibre to the muscle fibre and excites it. Excitation results in contraction.
Just like any electric wire, each individual nerve fibre (axon) is electrically insulated with the sheath made of special protein called myelin. It is also mechanically protected by a tube-like endoneurium. When Bell’s palsy happens, myelin gets damaged firstly from a mechanical compression by the swollen tissue, electrical insulation is lost, and mimetic signals cannot reach the facial muscles. This is called a conduction block.
Conduction block can also be a result of the effect of toxins. For example, botulinum toxin permanently blocks neuromuscular junctions. This damage is irreversible, and to recover its function, the affected axon needs to grow (generate) side-terminals to regain the connection with the corresponding muscle fibres. This explains why the effect of Botox injections is only temporary. Depending on the regenerative capacity of the body, within 2 to 5 months facial nerve branches re-connect to ”their” facial muscles and restore their functions.
Here it is worth mentioning that during the whole period after Botox injection, mimetic signals from the brain are produced normally, and even sometimes more actively (we will discuss this topic later). They go all the way along the axons to the muscles, but cannot pass the blocked neuromuscular junctions.
Speaking about the recovery after Bell’s palsy, we must thoroughly understand the construction of the facial nerve and the mechanism of conduction block. Only then we can analyze and choose proper rehabilitation methods that are able to provide the desired results.
– Alex Pashov
Crystal Touch Bell’s palsy clinic