Blepharospasm is what we call “eyelid hopping”. Idiopathic blepharospasm is a spontaneous spasmodic contraction of the orbital and periorbital orbicularis muscles of unknown origin, which can be of long or short duration, and is characterized by the constant repetition of strong non-volitional eye closure. The disease occurs in middle-aged and older women, often with bilateral lesions that progress progressively, 2/3 are women, and most stabilize within 3-5 years, manifesting as frequent and involuntary transients, bilateral tight frowning, and spastic or tonic lid closure in both eyes, while secondary lesions such as brow ptosis, ptosis, and eyelid skin laxity can be caused by prolonged and intense spasm of the orbicularis oculi. These patients often have good vision, but are unable to use it well because their eyes close involuntarily, resulting in what is known medically as “functional blindness”: that is, “blindness” that is not due to organic eye disease, and which Patients often cannot open their eyes the more they try to use them, but they can open them well when they are relaxed and do not use them. In some patients, the eyelid spasm gradually extends to the corners of the mouth and the entire half of the face, and the spasm can be triggered or aggravated by facial movements such as talking and eating. The incidence of blepharospasm is still very high, and it has been reported that there are at least 50,000 cases of blepharospasm in the United States, with more than 2,000 new cases born each year, representing an incidence of about 5 per 1,000 of the total population. The etiology of this disease is unclear, and in the past many physicians believed that blepharospasm could be psychogenic, as they found that chronic mental stress could trigger or exacerbate blepharospasm with psychiatric disorders, while at the same time, it increased the patient’s mental anxiety and stress as a chronic progressive disease. Modern medicine, on the other hand, considers blepharospasm to be a functional disorder of the nervous system that may be caused by multiple factors, but its exact mechanism is still unknown. The latest popular hypothesis is that the spasm is caused by increased neuroexcitability due to vascular compression at the beginning of the facial nerve (at the exit of the brainstem), which is manifested by thickening of the arteries there, which travel abnormally and form vascular climbs that ride across and compress the root of the facial nerve. Although these arterial variants are congenital, the hardened vessels can gradually aggravate the compression of the facial nerve as we age and the degree of arteriosclerosis increases, thus The age of onset of this disease is mostly in the elderly. In response to this hypothesis, hemifacial spasm has been treated with microvascular decompression, in which the responsible vessel is found by craniotomy and a spacer is placed between the vessel and the facial nerve, with satisfactory early postoperative results and generally no severe facial paralysis. However, a significant proportion of patients are found to have no vascular compression at the time of craniotomy, and because many patients have a fear of craniotomy, fewer patients are able to undergo surgery, and more patients seek conservative treatment to relieve symptoms and resume normal life and work before new radical treatments become available. The most effective conservative treatment with few side effects is topical botulinum toxin A (Botox) injections. Botulinum toxin is designed to reduce the excitatory transmission of local nerves. It acts on the cholinergic motor nerve endings, antagonizing the effect of calcium ions in some way, interfering with the release of acetylcholine from the motor nerve endings, making the muscle fibers unable to contract, thus relieving the symptoms of spasm. However, since the toxin is gradually metabolized in the body, 4-5 months after injection, the motor end plate regenerates, nerve excitability is restored, and the spasm recurs, so Botox treatment is not a once-and-for-all solution, and repeated injections are needed. The treatment of blepharospasm and facial spasm by local injection of botulinum toxin was first reported by Frueh et al. in 1984. In the 1990s, China developed its own botulinum toxin product and applied it clinically, and it has become one of the preferred, fastest and most effective treatments due to its high efficacy and few side effects. Occasional complications are ptosis, diplopia, dry eye, mild facial paralysis on the injection side, etc. These symptoms often subside gradually in 1-6 weeks. These symptoms often subside within 1-6 weeks. Individual patients may develop resistance to the drug after prolonged use. Some scholars have followed 178 patients treated with botulinum toxin A for more than 20 years, and the results showed that 93% of the patients obtained symptomatic improvement, of which 76% obtained significant and stable improvement after receiving more than 14 treatments, and 1.7% of the patients were completely cured. We have not experienced any unacceptable side effects in the past 3 years of clinical application, and most patients have experienced a significant reduction in the degree of flare-ups after botulinum toxin injections compared to the pre-injection period, even if they relapse. Although this injection treatment can be repeated many times over, it should be spaced out for a certain period of time so as not to cause toxicity. Here you may be a little worried about the so-called “talk of toxicity” and whether this treatment will cause poisoning. We can answer this question with certainty: Botox injections are very safe because its semi-lethal dose for a human is 40 units per kilogram of body weight, i.e., 2000 units for a 50 kg person. For patients with blepharospasm who do not do well with botulinum toxin injections, we can surgically remove most of the orbicularis oculi muscle, but although this procedure provides short-term relief, it has a high recurrence rate. The results can be very good.