The so-called oculomotor palsy is peripheral oculomotor palsy: impaired muscle movement, autonomic and reflex movements of a single muscle or of the same innervation, rarely accompanied by other neurological symptoms. Clinical features: the onset of the disease is usually preceded by infection/cerebrovascular disease, diabetes, tumors, peripheral neuropathy and other triggers, and can be acute, subacute, chronic or recurrent in onset. Clinical manifestations include diplopia, dilated or narrow pupils, and impaired eyelid or eye movement. How should intraocular muscle palsy be diagnosed? Intraocular muscle palsy is characterized by ptosis, downward strabismus, dilated pupils, and loss of light and adjustment reflexes. 1. Suprachoroidal muscle palsy: The symptoms produced are ptosis and downward strabismus of the affected eye, the vision of the affected eye is obscured by the drooping upper lid, and diplopia is usually not felt. 2. Ciliary muscle palsy: Symptoms include impaired lens accommodation, blurred near vision, dilated pupils, and loss of light and accommodation reflexes. 3, extraocular muscle paralysis: the chance of six extraocular muscles paralysis at the same time is very small, most of them are one or two extraocular muscles paralysis; the performance of paralysis is various. There are various manifestations of paralysis, such as inward, outward, downward, and upward movement of the eye, resulting in strabismus, diplopia, and confusion. Diplopia, strabismus, and visual confusion cause vertigo. When the eye moves, the strabismus angle changes constantly and the object seen cannot be stabilized, causing vertigo, and in severe cases, nausea and vomiting. The palsy of the muscles in the eye is characterized by dilated pupils, loss of light reflexes and modulation reflexes, and diplopia. 4. Palsy of the talocrural nerve, mostly combined with palsy of the oculogyric nerve, and rare with palsy of the talocrural nerve alone, manifests as restricted outward and downward movement of the eye, diplopia, and strabismus when gazing downward and outward. 5. Abducens nerve palsy, which produces strabismus and diplopia when gazing inward and outward. What symptoms are easily confused with ocular muscle palsy? 1. Peripheral ophthalmic muscle palsy: motor nerve palsy, manifesting as paralysis of all the innervated ophthalmic muscles, limited inward, downward and upward eye movements, ptosis and exotropia; intraocular muscle palsy, manifesting as pupil dilatation, loss of light and adjustment reflexes, and diplopia; talocrural nerve palsy, mostly combined with motor nerve palsy, and rarely talocrural nerve damage alone, manifesting as limited outward and downward eye movements, and diplopia; adductor nerve palsy, manifesting as limited outward and downward eye movements, and diplopia. Abducens nerve palsy, showing internal strabismus, the eye cannot turn outward, with diplopia, mostly seen in inflammation, skull base tumor, aneurysm compression of the oculomotor nerve, peripheral neuropathy, multiple sclerosis (MS), paraneoplastic syndrome, etc. 2, nuclear ocular muscle palsy: nuclear damage is manifested as paralysis of the innervated part of the eye muscles, mostly bilateral, and can have the manifestation of adjacent structural damage, with crossed paralysis, mostly seen in cerebrovascular disease, inflammation, tumors. The former is damage to the medial longitudinal bundle, which shows that the ipsilateral eye can be abducted and the contralateral side cannot be inwardly retracted, and there can be nystagmus on the abducted side, and the collecting reflex is normal; the latter is damage to the fibers between the pontocerebellar lateral visual center and the ipsilateral abducens nucleus, which shows that the ipsilateral eye cannot be abducted and the contralateral side can be inwardly retracted. It is mostly seen in cerebrovascular disease, multiple sclerosis (MS), and brainstem tumors. Supranuclear oculomotor palsy: manifests as conjugate motor deficits in both eyes. 1. Oculomotor palsy: The three pairs of cranial nerves, motoneurotic (III), gliding (IV) and abduction (VI), are all motor nerves that innervate the eye muscles. Cranial injury can affect the extraocular muscles and the III, IV and VI pairs of cranial nerves and cause various forms of oculomotor palsy. Oculomotor disorders (oculomotor paralysis) and abnormal pupil dilation occur when the nerves are damaged. Damage to the oculomotor nerve can be divided into peripheral, nuclear and supranuclear types. Ophthalmologic examination and cranial CT should be performed to exclude intracranial organic lesions. 2. Supranuclear vertical ophthalmoplegia: It is seen in juvenile type (C chronic neurological type) Niemann-Pick disease, mostly in children, and a few young children or adolescents with the onset of cherry erythema or supranuclear vertical ophthalmoplegia. Juvenile (type C chronic neurological type) Niemann-Pick disease is usually seen in children, with a few cases in young children or adolescents. Postnatal development is mostly normal, with a few having early jaundice. Hepatosplenomegaly is often the first sign, and neurological symptoms appear in most children between the ages of 5 and 7 years (or earlier or as late as young adulthood). Mental retardation, language disorders, learning difficulties, emotional changes, unsteady gait, ataxia, tremor, hypertonia and tendon reflexes, convulsions, dementia, and cherry erythema or supranuclear vertical oculomotor paresis are seen in the fundus. SM accumulation is 8 times higher than normal and enzyme activity is up to 50% of normal or close to normal or normal. 3. Ptosis: A partial or total failure to lift the upper lid due to incomplete or lost function of the levator muscle, or other causes, obscuring part or all of the pupil is called ptosis. In normal individuals, the upper lid margin covers 2 mm of the superior cornea and the average width of the lid fissure is approximately 7.5 mm. To estimate the function of the levator muscle, the position of the upper lid margin can be measured when the eye is gazing extremely upward and downward, respectively, with the frontalis muscle contraction force offset. In normal individuals, the difference should be more than 8 mm. If the difference is less than 4 mm between the front and back, this indicates severe insufficiency of the levator muscle. Simultaneous horizontal leftward, rightward, or vertical movements; without diplopia, both eyes are involved at the same time, but reflex movements are still present, mostly in cerebrovascular disease, tumors, and inflammatory conditions. Diabetes mellitus combined with ocular muscle palsy mostly presents with extraocular muscle palsy, i.e., 80% intraocular muscle palsy and 20% intraocular muscle palsy; aneurysm compression mostly presents with intraocular muscle palsy, and with progression of the disease, extraocular muscle palsy may appear; brainstem tumor may present with nuclear, inter-nuclear and supranuclear ocular muscle palsy; paraneoplastic syndrome may present with various forms of ocular muscle palsy; multiple sclerosis (MS) inter-nuclear and peripheral ocular muscle palsy, which may be accompanied by visual Inflammatory diseases can present with nuclear and peripheral ocular muscle palsy; cerebrovascular diseases can present with nuclear, inter-nuclear, and supranuclear ocular muscle palsy; and ocular muscle palsy of peripheral nerve damage are all peripheral ocular muscle palsy. The so-called oculomotor palsy is peripheral oculomotor palsy, in which a single muscle or the same nerve innervated muscle movement disorder, voluntary movement and reflex movement are impaired, rarely accompanied by other neurological symptoms. Clinical features: the onset of the disease is usually preceded by infection/cerebrovascular disease, diabetes, tumor, peripheral neuropathy, and other triggers, and can be acute, subacute, chronic, or recurrent in onset. Although the causes of ocular muscle paralysis in the elderly are complex, in terms of pathology and physiological changes, diabetes, hypertension, and brainstem infarction all share the same pathophysiological changes, namely, small vessel occlusion and microthrombosis on the basis of microvascular sclerosis and vascular damage, causing pathophysiological changes of ischemic vascular disease. It is also not difficult to find that various etiologies can act alone in a particular patient, while most of them are multiple etiologies co-existing. Systemic diseases: such as diabetes mellitus, ocular muscle palsy due to myasthenia gravis, ocular muscle palsy due to ocular trauma, infectious diseases: rabies, neuroinflammatory diseases cause, and then treated for the cause. Therefore, for elderly people with ocular muscle palsy, both diagnosis and treatment should be more comprehensive and detailed. The treatment of ophthalmoplegia 1, the current application of compound camptothecin injection for the treatment of ophthalmoplegia clinical efficacy. The method is to use 2 ml of compound camptothecin injection for subcutaneous injection of the lesion side or bilateral superficial temporal artery, once a day, 10 times as a course of treatment, 2 consecutive courses of injection. 2.For inflammatory extraocular muscle paralysis, dexamethasone injection can be added for paralytic muscle injection. 3, oral nerve nutrition and blood circulation drugs. 4.Acupuncture treatment. 5.Chinese herbal medicine treatment.