What is the pathogenesis of cranial nerve hyperexcitability disorders

  Facial myoclonus and trigeminal neuralgia are the most common of the cranial nerve hyperexcitability disorders. Facial myoclonus is characterized by paroxysmal involuntary twitching of one side of the facial muscles, while trigeminal neuralgia is characterized by paroxysmal episodes of severe pain on one side of the face, both of which are not fatal but seriously affect patients’ quality of life. Traditional treatment is unable to cure this stubborn disease, and can only treat the symptoms but not the root of the problem.  Why is traditional treatment unsatisfactory for patients? The reason why traditional treatment is unsatisfactory is that the root cause of the disease has not been found.  Traditional treatment 1: drugs Some patients will have some relief at the beginning of the disease, but the required dose will increase, and later the patient will have to terminate the medication because they cannot tolerate the side effects. In addition, these drugs are anti-epileptic drugs, which have a great impact on the central nervous system, liver and kidney function and hematopoietic system, and can cause allergies, resulting in a generalized rash, etc.  Traditional treatment II: Destructive surgery For facial muscle spasm, local injection of botulinum toxin is commonly used to cause perceived mild facial paralysis, but the efficacy is maintained for a short period of time, and repeated multiple injections will eventually cause irreversible facial paralysis. For trigeminal neuralgia, radiofrequency destruction and balloon compression are commonly used to destroy the trigeminal nerve, but this will cause numbness of half of the face, including the tongue, and the symptoms will recur soon after nerve repair.  Etiological analysis We know that the sensation and movement of the face are innervated by the trigeminal nerve and facial nerve respectively. The role of the trigeminal nerve is mainly to perceive the pain and touch of the skin of the face, the oral mucosa and the tongue and cornea. For example, when the face is bitten by mosquitoes or traumatized, the trigeminal nerve will send pain signals to the brain, telling us that we are in danger, and we will make avoidance actions to avoid further damage or prompt us to go to the doctor. In fact, the function of people to perceive pain is very beneficial. And by blocking the function of the trigeminal nerve, people may bite their tongue while eating, or dust may get into their eyes without knowing it, or facial burns without knowing it. Instead, the role of the facial nerve is to innervate the orbicularis oris muscle and the orbicularis oculi muscle, which are instructed by the brain to control the rich expressive activity of the face.  So how does the nerve work? Let’s say: when someone rings the doorbell, the wire connected to the button will send an electrical signal to the house bell and make a sound to tell the owner that a guest is coming, and we will go to open the door. If the owner does not want to be disturbed, the button can be removed or the wire cut. This is how the clinical “disruption” works, but the nerve fibers have a repair function and will heal after a period of time, so they will soon relapse! Medication is akin to reducing the volume of the doorbell.  A large number of experimental studies have found the following characteristics: 1. race: more common in the East; 2. age: most people develop the disease after middle age; 3. gender: slightly higher in women than in men; 4. anatomy: almost all patients have cerebrovascular compression of the trigeminal nerve/facial nerve root; 5. precipitating factors: emotional stress such as excitement and anxiety are prone to seizures.  It was concluded from a large number of animals that the essence of this type of disease is due to pathological changes in the nerve itself, not a problem with its receptors (skin of the face) – it is the wire that short-circuits, not the button. If the wire is shorted, the doorbell will ring without pressing the button! So the essence of trigeminal neuralgia or facial spasm is that the nerves entering and leaving the brainstem are “short-circuited” by the compression of the surrounding cerebral vessels.  The reason for these five characteristics is as follows: the trigeminal nerve or facial nerve is fixed in the face (like a dark wire buried in the wall), while in the skull it is relatively free and the outer membrane of the nerve is thin and less resistant to abrasion (like an electric wire that is easily broken because it does not have a protective coat). Due to the anatomical characteristics of the skull base of Oriental people, especially Oriental women, the trigeminal or facial nerve is very close to the surrounding cerebral vessels in the skull. With age, the brain tissue gradually shrinks while the cerebral vessels sclerosis, making them closer to each other or even in contact with each other, and with the pulsation of the vessels, they rub against each other, causing the contact surface to break and exposing the nerve fibers. In addition, the outer membrane of the cerebrovascular wall is rich in sympathetic nerve network, which is used to control the change in the diameter of cerebrovascular vessels and regulate cerebral blood flow. However, when the membrane is broken, the sympathetic nerves of the vessel wall are exposed and come into direct contact with the trigeminal nerve or facial nerve fibers where the outer membrane of the nerve is broken, resulting in a “short circuit” of the nerve. The sympathetic nerve endings release a large amount of norepinephrine when the patient is agitated, causing abnormal impulses in the trigeminal nerve and producing pain in the face (which is actually a hallucination). As to how sympathetic nerves act on trigeminal neuralgia, this involves very complex molecular biology and electrophysiological responses.  Based on the initial clarification of the etiology of trigeminal neuralgia, neurosurgery currently treats patients mainly by minimally invasive surgery. By making a small incision in the hairline behind the patient’s ear and drilling a hole in the occipital bone, the responsible blood vessel compressing the trigeminal or facial nerve root is moved away under a microscope, and the patient’s symptoms disappear immediately after surgery. This surgical method is also the most reasonable and effective treatment method available.