Peripheral nerves [PNS]

peripheral nerve disease

Overview

Cause and pathogenesis

clinical manifestations

Auxiliary inspection

Diagnosis and identification

treat

Overview

Cause and pathogenesis

pathology

clinical manifestations

Auxiliary inspection

Diagnosis and differential diagnosis

treat

prognosis

Overview

Cause and pathogenesis

pathology

clinical manifestations

Auxiliary inspection

Diagnosis and differential diagnosis

treat

prognosis

concept

Cause and pathogenesis

clinical manifestations

Auxiliary inspection

Diagnosis and Differential Diagnosis

treat

prognosis

Chapter 17 Peripheral Nerve Diseases Overview Peripheral nerve refers to the cranial and spinal nerves, autonomic nerves and their ganglia except the optic nerve. week Peripheral neuropathy is a general term for diseases that damage the structure or function of the peripheral nervous system caused by various causes. Peripheral nerves are functionally divided into sensory afferents and motor efferents. The former consists of dorsal roots of spinal nerves, dorsal root ganglia, and distal sensory It is composed of nerve afferent fibers and brain sensory nerves. The latter is composed of the anterior roots and distal motor fibers of the spinal nerves arising from the anterior and lateral horns of the spinal cord and the It is composed of cranial nerves emanating from the motor nuclei of the brainstem and terminating in muscle fibers. Autonomic nerves are composed of sympathetic and parasympathetic nerves, and the peripheral part includes Visceral motor (efferent) and visceral sensory (afferent) nerves regulate the activity and secretion of viscera, blood vessels, smooth muscles and glands. Peripheral nerve fibers can be divided into two types: myelinated and unmyelinated. The myelin sheath surrounding the axon of myelinated nerve fibers is composed of Schwann cells (Schwann cell), the unmyelinated part between the two myelin sheaths is a segmental structure formed by the myelination of each cell called the node of Ranvier. (Ran vier node). The myelin sheath acts as an insulator and allows nerve impulses to jump rapidly between the nodes of Ranvier. There are several unmyelinated fibers The axon is wrapped in a Schwann cell and is not surrounded by myelin. The nerve impulse is conducted along the surface of the nerve fiber at a slower speed. cranial nerves and The motor and deep sensory fibers of the spinal nerves are mostly myelinated nerve fibers, while the pain and temperature sensation and autonomic nerves are mostly unmyelinated nerve fibers. peripheral nerves It is protected by the perineurium and epineurium, and the membranotrophic arteries send out abundant communicating branches. The perineurium and capillary endothelium are tightly connected to ensure blood circulation. Macromolecules in the tube are not easy to leak out of the capillaries, forming a blood-nerve barrier. However, there is no such barrier at nerve roots and ganglia, which is caused by some immune or Reasons why toxic diseases easily invade this area The causes of peripheral nerve diseases are complex and may be related to nutritional metabolism, drugs and poisoning, vasculitis, tumors, heredity, trauma or mechanical compression, etc. Because related. They selectively damage different parts of peripheral nerves, leading to corresponding clinical manifestations. Due to the cause of the disease, scope of involvement and The course of the disease is different, the classification standards for peripheral nerve diseases have not yet been unified, and it is difficult for a single classification method to cover all diseases. First, it can be divided into genetic Sexual and acquired, the latter is divided into nutritional deficiency and metabolic, toxic, infectious, immune-related, ischemic, paraneoplastic, Mechanical trauma, etc.: According to the pathological changes of the damage, it can be divided into primary neuropathy (the lesion originates in axons and nerve fibers) and Interstitial neuropathy (lesions are located in the perineurium and epineurium surrounding nerve fibers); according to the clinical course, it can be divided into acute and subacute Sexual, chronic, recurrent and progressive neuropathy, etc.; according to the involved nerve distribution pattern, it is divided into mononeuropathy, multiple mononeuropathy, polyneuropathy, etc. Sexual neuropathy, etc.: According to symptoms, it is divided into sensory, motor, mixed, autonomic neuropathy, etc.: According to the anatomical location of the lesion, it is divided into neurological types. Radiculopathies, plexopathies, and truncal diseases. Peripheral nerve diseases have many unique symptoms and signs. Sensory disorders mainly include sensory loss, paresthesias, pain, and sensory disturbances. Ataxia; movement disorder including symptoms of motor nerve stimulation (abnormal excitement) and paralysis. Symptoms of irritation mainly include muscle fascicles shaking the face, muscles Fiber inflammation, painful pain, etc., while muscle weakness or loss of muscle atrophy are symptoms of motor nerve paralysis. In addition, patients with peripheral nerve disease Patients are often accompanied by weakened or disappeared tendon reflexes. Damage to autonomic nerves often manifests as anhidrosis, piloerection disorder, and orthostatic hypotension. In severe cases, No tears, no boundaries, impotence and bladder and rectal dysfunction. Medical history description, clinical physical examination and necessary auxiliary examinations are the main basis for the diagnosis of peripheral nerve diseases. nerve conduction measurement (Nerve conduction studies, NC S) and electromyogram (EM G) examinations are very valuable in the diagnosis of peripheral neuropathy. Peripheral nerve tissue biopsy is generally used for patients with difficulty in qualitative clinical and other laboratory examinations. It can determine the location of peripheral nerve damage and clarify the disease. nature. The treatment of peripheral neuropathy is first to treat the cause; secondly to provide symptomatic support, such as giving analgesics and B vitamins etc. Rehabilitation, acupuncture, physiotherapy, and massage are important measures during the recovery period and help prevent muscle shrinkage and joint deformation. 387

388 Chapter 17 Peripheral Nerve Diseases Section 1 Cranial Nerve Diseases There are 12 pairs of cranial nerves in total. The optic nerve and OH nerve are part of the brain. The remaining 10 pairs of cranial nerve nuclei are all in the brainstem, with peripheral branches. It originates from the brainstem and controls the organs of the head and face. Cranial nerve diseases may involve one or more nerves. 1. Trigeminal neuralgia Trigeminal neuralgia (trigeminal neuralgia) is the abbreviation of primary trigeminal neuralgia, which manifests as transient pain in the distribution area of ​​the trigeminal nerve. Recurrent severe pain. 【Cause】 The cause of primary trigeminal neuralgia is not yet fully understood. The peripheral theory believes that the lesion is located between the semilunar ganglion and the pons and is caused by Caused by compression caused by various reasons; the central theory believes that trigeminal neuralgia is a sensory epileptic seizure, and the abnormal discharge site may In the spinal trigeminal tract nucleus or brainstem. 【Pathogenesis】 The pathogenesis is still under discussion. Many scholars believe that various reasons cause local demyelination of the trigeminal nerve to produce ectopic impulses. Movement, pseudo-synapses of adjacent axonal fibers form or produce short circuits, slight pain stimulation is transmitted to the brain through short circuits, and central outgoing impulses also pass through short circuits. Passing on from the road, this superposition causes an attack of trigeminal neuralgia 【pathology】 Trigeminal nerve sensory rhizotomy biopsy showed disappearance of ganglion cells, infiltration of inflammatory cells, irregular thickening of the nerve sheath, and myelin sheath tiles. Solution, axonal segmental degeneration, exposure, distortion, deformation, etc. Under the electron microscope, a large number of mitochondria can still be seen in the axon near the node of Ranvier, which can Can be related to mechanical compression of nervous tissue [Clinical manifestations] It is more common in adults and the elderly, with 70% to 80% of patients over 40 years old, and more women than men. Trigeminal neuralgia is often localized to the trigeminal nerve The distribution area of ​​meridian is 2 or 3 branches, most common in the maxillary branch and inferior collar branch. During the attack, the symptoms are obvious severe electric shock-like sensations on the upper and lower collars of the cheeks and tongue, Pain like acupuncture, cutting or tearing, lasts for a few seconds or 1 to 2 minutes, stops suddenly, and the intermission period is completely normal. The patient's mouth corners, nose, The cheeks or tongue are sensitive areas that can be triggered by light touch and are called trigger points or trigger points. In severe cases, facial muscle reflex taps may occur due to pain. The corner of the mouth is pulled toward the affected side, causing painful twitching (tic do ul our eux). The course of the disease is cyclical, with attacks lasting days, weeks, or months, and remission periods Like ordinary people. As the course of the disease progresses, the number of attacks gradually increases, the attack time is prolonged, the intermission period is shortened, and even the attacks become persistent and rarely occur spontaneously. Get better. Nervous system physical examination generally shows no positive signs. The main symptoms of patients are that they dare not wash their face, brush their teeth, eat, and maintain facial and oral hygiene due to fear of pain. Poor, complexion, depressed mood. 【Auxiliary inspection】 1. Neuroelectrophysiological examination By electrically stimulating the branches of the trigeminal nerve and observing the surface electrical activity of the oculoid muscles and masticatory muscles, the three The function of the branchial nerve's transmission from human to brain to the central path of the trigeminal nerve is mainly used to rule out secondary trigeminal neuralgia. V1 reflex for electrical stimulation III Blink reflex occurs in the ophthalmic branch of the trigeminal nerve. V 2 reflex and V 3 reflex respectively stimulate the maxillary branch and mandibular branch of the trigeminal nerve to produce masseter muscle inhibitory reflex. 2. Imaging examination, MRI examination of the head and face can rule out secondary trigeminal neuralgia caused by organic lesions, such as facial base tumors, multiple Sclerosis, cerebral vascular malformation, etc. 【diagnosis】 Typical primary trigeminal neuralgia is not difficult to diagnose based on the location and nature of the pain, trigger points on the face, and lack of positive signs in the nervous system. Confirmed. 【Differential Diagnosis】 This disease needs to be differentiated from the following diseases: 1. The pain of secondary trigeminal neuralgia is persistent, accompanied by facial hypoesthesia on the affected side, slow corneal reflex, etc., and is often combined with other brain disorders. Symptoms of damage. Commonly seen in multiple sclerosis, bulbar syrinx, primary or metastatic tumors, etc.

389 Chapter 17 Peripheral Nerve Diseases 2. Toothache: Toothache is often a persistent dull pain, limited to the gums, and can be aggravated by eating cold or hot food. X-ray examination can reveal Teeth, tumors, etc. are helpful for identification. 3. Glossopharyngeal neuralgia is less common and is more common in young women. Confined to the tonsils, tongue base, pharynx and deep part of the ear canal, that is, the distribution of the glossopharyngeal nerve Paroxysmal pain in the area, similar in nature to trigeminal neuralgia. Swallowing, talking, yawning, and coughing can often trigger it. In the throat, base of tongue, tonsillar fossa, etc. Spraying trigger points with 4% cocaine or 1% tetracaine can stop attacks. 【treat】 Drug therapy is the first choice, and other therapies are used when they are ineffective or ineffective. 1.Drug treatment (1) Carbamazepine: The first choice treatment drug, with an effective rate of 70% to 80%. First dose 0.1 g, 2 times/ daily, increase by 0.1 g daily until pain is controlled, and the maximum dose does not exceed 1.0 g/d. After maintaining treatment at an effective dose for 2 to 3 weeks, gradually Reduce to the minimum effective dose and continue taking it for several months. Adverse reactions include dizziness, drowsiness, dry mouth, nausea, indigestion, etc. Most of them disappear after stopping the drug. lose. The drug must be discontinued immediately if rash, ataxia, aplastic anemia, insomnia, impaired liver function, angina pectoris, or psychiatric symptoms occur. pregnant woman Avoid use. (2) Phenytoin sodium (phenytoin sodium): initial dose 0.1 g, taken orally, 3 times/day. If it is ineffective, the dose can be increased. The maximum dose No more than 0.4 g/d. If poisoning symptoms such as dizziness, unsteady gait, and nystagmus occur, the dose should be reduced until the poisoning reaction disappears. If there is still The effect is to use this as the maintenance amount. Gradually reduce dosage after pain subsides 3) Gabapentin: 0.3 g orally once on the first day. After that, the dosage can be gradually increased according to the clinical efficacy and enzyme status. Generally, the most The maximum dose is 1.8 g/d. Common side effects include drowsiness, dizziness, and unsteady gait. With continued use of the drug, the symptoms may be reduced or disappeared. pregnant Women should not use it. (4) Pregabalin: The starting dose can be 75 mg twice a day, or 50 mg three times a day. Available in 1 Within weeks, increase to 150 mg twice daily based on efficacy and tolerability. Pain improved in 74% of patients. The most common adverse reactions are Dizziness, drowsiness, and ataxia are dose-dependent. If you need to stop using it, it is recommended to gradually reduce it for at least 1 week. 2. For those whose closed treatment is ineffective or has obvious side effects, who refuse surgical treatment or are not suitable for surgical treatment, absolute ethanol can be tried. sensory loss 3. Percutaneous semilunar ganglion radiofrequency electrocoagulation therapy. Under X-ray monitoring or CT guidance, a radiofrequency needle is inserted percutaneously into the trigeminal ganglion. select Selectively destroys the unmyelinated A8 and C fibers (conducting pain and temperature sensation) in the postganglionic semilunar ganglion, while retaining the myelinated Aα and β thick fibers (conducting touch sensation). sleep), the efficacy reaches more than 90%. It is suitable for the elderly, frail, systemic diseases and those who cannot tolerate surgery. About 20% of patients who use this therapy develop Complications such as facial paresthesia, keratitis, masticatory muscle weakness, diplopia, and herpes zoster are present. The recurrence rate in long-term follow-up is 21% to 28%, and severe Valid for repeated applications. 4. Surgical treatment: Partial sensory rhizotomy of the trigeminal nerve or gamma knife treatment can be used, which has a definite analgesic effect. There are also surrounding branches cut Surgery and trigeminal tractotomy are currently rarely used. In recent years, microvascular decompression of the trigeminal nerve has been recommended to relieve pain without causing labor. It is the safest and most effective surgical method that is widely used to treat sensory and motor disorders. However, hearing loss, air embolism, pulley, atrophy, and Complications such as temporary facial nerve paralysis 【Prognosis】 The prognosis of this disease is good. When drug control is poor, closure, percutaneous semilunar ganglion radiofrequency electrocoagulation, and trigeminal nerve microvascular debulking can be considered. With surgical treatment such as compression, the symptoms of most patients can be effectively controlled 2. Idiopathic facial nerve palsy Idiopathic facial palsy (idiopathic facial palsy) is also called facial neuritis (facial neuritis) or Bell's palsy (Bell's palsy) Palsy) is peripheral facial paralysis caused by non-specific inflammation of the facial nerve in the stylomastoid foramen. 【Cause】 The cause of facial neuritis is unknown, but it is currently believed to be related to neurotropic virus infection. Often develops after catching a cold or upper respiratory tract infection

390 Chapter 17 Peripheral Nerve Diseases 【Pathogenesis】 Since the bony facial nerve canal can only accommodate the passage of the facial nerve, ischemia and edema of the facial nerve will inevitably lead to nerve compression. viral sensation Infection can lead to autoimmune reactions of local nerves and nutritional vascular disease, nerve ischemia, edema, and facial paralysis. 【pathology】 The early pathological changes of facial neuritis are mainly nerve edema and demyelination. In severe cases, axonal degeneration may occur, especially the stylomastoid foramen and facial nerve canal. The inner part is particularly noticeable. [Clinical manifestations] It can occur at any age, but is more common in 20 to 40 years old, more often in men than women. Usually acute onset, facial nerve paralysis lasts for several hours to several The main symptoms include paralysis of facial expression muscles on the affected side, disappearance of forehead lines, inability to frown and eyebrows, and inability or incomplete closure of eye fissures. Some patients have persistent pain behind the ear and mastoid tenderness on the affected side 1 to 2 days before the onset of symptoms. During physical examination, it can be seen that the eyeball of the affected side moves toward The outer and upper parts are rotated to expose the white sclera, which is called Bell sign; the nasolabial fold becomes shallower, the corners of the mouth droop, and the corners of the mouth are tilted to the healthy side when teeth are exposed; from Oral orochondrial muscle paralysis, air leakage when blowing or whistling; buccal muscle paralysis and phlegm, food tends to remain in the gums of the affected side; facial paralysis is more common on one side, and if it is bilateral, examination is required Consider whether it is other diseases such as Guillain-Barre syndrome (GBS). In addition, facial neuritis can also be caused by facial nerve Some other clinical manifestations may occur depending on the damaged part. For example, neuropathy above the chorda tympani may cause loss of taste in the front 2/3 of the tongue on the same side; orange bone Damage to areas above the muscles and nerves will result in loss of taste in the front 2/3 of the tongue and hyperacusis: when the geniculate ganglion is involved, in addition to peripheral facial paralysis, In addition to loss of taste in the front 2/3 of the tongue and hyperacusis, patients may also have mastoid pain, hypoesthesia in the ear gallery and external auditory canal, and scars in the external auditory canal and tympanic membrane. rash, called Hunt syndrome 【Auxiliary inspection】 1. Electromyography and facial nerve conduction measurement can help determine temporary conduction disorder or permanent denervation of the facial nerve. like If the M-wave amplitude of myoelectric action potential evoked on the affected side of a patient with complete facial paralysis in the early stage (within 7 days after the onset of illness) is 30% or more of that on the normal side, then Complete recovery is possible within 2 months; if denervation potential occurs within 10 days of illness, recovery will be slow. 2. Imaging examination is not used as a routine examination for this disease, but when clinical organic lesions in the face are suspected, head MRI or CT should be performed examine. 【diagnosis】 Based on the acute onset and clinical manifestations of this disease, which are mainly peripheral facial paralysis and no other positive signs of the nervous system, organic diseases within the face are excluded. change, the diagnosis can be confirmed. 【Differential Diagnosis】 Pay attention to the identification of the following diseases: 1. Guillain-Barré syndrome, mostly bilateral peripheral facial paralysis, accompanied by symmetric limb flaccid paralysis and sensory impairment, cerebrospinal fluid examination shows Characterized protein-cell separations. 2. Otogenic facial nerve paralysis Otitis media, labyrinthitis, and mastoiditis are often complicated by otogenic facial nerve paralysis, and can also be seen in adenitis, swelling tumors and purulent mandibular lymphadenitis, etc., often with a clear history of the original disease and special symptoms. 3. Peripheral facial paralysis caused by posterior fossa tumors or meningitis has a slow onset and is often accompanied by other symptoms of cranial nerve damage and various characteristics of the primary disease. Special performance. 4. NeuroLyme disease is unilateral or bilateral facial nerve paralysis, often accompanied by fever and migrating erythema of the skin, and can often involve other cranial nerves. 【treat】 The treatment principle is to improve local blood circulation, reduce facial nerve edema, relieve nerve compression, and promote nerve function recovery. 1.Drug treatment (1) Corticosteroids: Use corticosteroids as early as possible in the acute phase. Prednisone 30 to 60 mg/d is often used, daily Take it once and for 5 days, then gradually stop using it within 7 days. 2) B vitamins: Vitamin B, 100 mg, Vitamin B 2500 ug, intramuscular injection, once a day, to promote nerve marrow recovery (3) Acyclovir (a cy clo vi r): Patients in the acute phase can use a combination of glucocorticoids and antiviral drugs according to their condition, such as Hunt syndrome Patients with combined syndrome can take acyclovir 0.2~0.4 g orally, 3~5 times a day, for 7~10 days

391 peripheral nerve disease Chapter 17 2. Physiotherapy_ In the acute stage, ultrashort wave diathermy, infrared irradiation or local hot compress can be performed near the breast extraction port, which will help improve the condition. Improve local blood circulation and reduce nerve edema. 3. Eye protection. Because patients cannot close their eyes for a long time, the cornea will be exposed and dry, which may easily lead to infection. They can wear eye masks for protection, or use levofluoride Floxacin eye drops, etc. prevent infection and protect the cornea 4. Rehabilitation treatment: Iodide ion permeation therapy, acupuncture or electro-acupuncture treatment can be used during the recovery period. 【Prognosis】 Patients with incomplete facial paralysis may recover or recover within 1 to 2 months, while patients with complete facial paralysis generally need 2 to 8 months or even 1 year. It takes time to recover and often leaves sequelae. Recovery of taste within 1 week indicates a good prognosis. Young patients have a good prognosis, while older patients have mastoid pain or Patients with diabetes, hypertension, arteriosclerosis, myocardial infarction, etc. have a poor prognosis 3. Facial muscle pain Facial spasm, also known as facial spasm, refers to intermittent involuntary or painless twitching of facial muscles on one side. Ankylosis. 【Cause】 The cause of this disease is unknown, but it is often caused by abnormal arteries or veins, rare basilar artery aneurysms, acoustic neuromas, brainstem infarction, or multiple sclerosis. In recent years, it has been reported at home and abroad that most facial muscle diseases have faulty blood vessels that compress the facial nerve root, and can be cured after microsurgical decompression, suggesting that It has a similar basis to trigeminal neuralgia, and a small number of patients may also suffer from the sequelae of Bell's palsy. 【Pathogenesis】 The pathogenesis of facial muscle disease is speculated to be caused by ectopic excitation of the facial nerve or pseudosynaptic transmission. 【pathology】 Secondary demyelination changes caused by compression of facial nerve fibers can be seen [Clinical manifestations] It usually starts after middle age, and is more common in women. In the early stage of the disease, it is mostly caused by intermittent sampling of the eyeball muscles, and then gradually spreads to other parts of the face on one side of the face. Among other facial muscles, the muscles at the corners of the mouth are the most obvious, and in severe cases, the platysma on the same side can be involved. The symptoms of nervousness, fatigue, and voluntary movements are aggravated, and people It stops after sleeping, and it is rare for patients to have sampling on both sides of the facial muscles. A few patients may suffer from mild paralysis of the facial muscles in the late course of the disease. 【Auxiliary inspection 1. Electromyography examination Electromyography examination shows characteristic high-frequency radiation associated with unilateral extension reaction and panocular reflex and other associated movements. Electricity helps to distinguish facial muscle disease from other involuntary movements 2. Imaging examination Magnetic resonance tomo graphic angiography (MRT A) display surface The nerve is obviously compressed. 【diagnosis】 This disease is based on the medical history and paroxysmal twitching of facial muscles, no other positive signs of the nervous system, and electromyography showing muscle fiber tremors and muscle fascicle tremors. Wave, diagnosis is not difficult. [differential diagnosis Need to be differentiated from the following diseases 1. Functional facial dysplasia is common in middle-aged and older female patients. It is often bilateral and is limited to the pain of the eye and facial muscles, without affecting the lower facial muscles. twitch. 2. Habitual tics It is common in children and young adults. It has obvious muscle contraction and is mostly related to mental factors. 3.Meige syndrome Wang, also known as facial dystonia Li-oromandibular dystonia syndrome, is more common in older women, mainly bilateral facial dystonia. Li, with dystonia of the oral and tongue, facial, mandibular, laryngeal and cervical muscles 【treat】 1. Botulinum toxin A (B TX-A) local injection At present, the preferred method for treating facial muscle disease is safe, effective, simple and easy to implement. During the epidemic Inject B TX-A 2.5~5 U into the obvious part of the body. Each injection is about 50 U. It takes effect in 3 to 5 days. If there is residual infection one week after the injection, additional injections can be made.

392 Chapter 17 Peripheral Nerve Diseases injection, the curative effect can last for 3 to 6 months. Those who relapse can be injected with the original dose or doubled dose, but the total dose of each injection should not be higher than 200 U. bad Reactions include short-term drooping of the eyes and face, blurred vision, and coagulation, which can disappear in a few days. This drug can be used to treat a variety of focal dystonias. One of the major advances in the treatment of neurological diseases in recent years. 2. For drug treatment, a variety of sedatives and anti-epileptic drugs can be used, which can alleviate symptoms in some patients. Carbamazepine 0.6～1.0 g/d 2/3 patients are effective, and clonazepam (clo naze pam), gabapentin, etc. can also be tried. 3. For patients with poor efficacy of B TX-A injection in surgical treatment, such as facial muscle pain caused by vascular compression, microvascular decompression of the facial nerve can be used. surgery, peripheral neurotomy may also be effective. 【Prognosis】 The prognosis of this disease is good, and local injection of BTX-A has good therapeutic effects on most patients. 4. Multiple cranial nerve damage Multiple cranial nerve damage refers to unilateral or bilateral cranial neuropathy caused by various causes. Often caused by tumors, such as nasopharyngeal carcinoma and meningioma etc.: vascular diseases, such as aneurysms, vasculitis, etc.; infections, such as localized meningitis, spread of sinusitis, arachnoiditis, etc.; and trauma, such as facial base. Caused by fractures, hematoma, bleeding, etc. The main clinical manifestations are a variety of cranial nerve damage syndromes. The key lies in treating the cause. Now clinical practice A summary of common multiple cranial nerve damage syndromes is shown in Table 17-1 Table 17-1 Common multiple cranial nerve damage syndrome syndrome Lesion clinical manifestations Involving cranial nerves Common causes cavernous sinus cavernous sinus syndrome Ⅲ, IV, V, Vth Damage to III, IV, and VI causes damage to the affected side Cavernous sinus thrombophlebitis: neck (Foix I syndrome) 1 branch, the lesion is posterior internal arterial cavernous sinus failure; cavernous sinus Droopy face, dilated pupils, eyeballs The person may have V's Internal aneurysm; within or adjacent to the cavernous sinus Dyskinesia, diplopia; V impairment Causes regional sensory impairment, angle 2 or 3 branches involved nearby tumor The membrane reflex disappears and the conjunctiva is filled with blood edema supraframe cleft syndrome Near the crack on the frame m, IV, V, Vth I, IV and VI are damaged and all eye muscles appear Tumors such as nasopharyngeal carcinoma and pituitary gland tumor 1 stick (Roc hon-Du vigne aud etc; vascular lesions such as arteries Paralysis, abduction paralysis appears early; tumors, vasculitis; infections such as localized Sensory disturbances in the trigeminal region; syndrome) Corneal reflex is dull or disappears; may Dural meningitis, supraperiosteum Ipsilateral Horner syndrome occurs inflammation, etc.; bones near the lesser wing of the sphenoid bone Fracture, bleeding, hematoma, etc. Ⅱ, Ⅲ, I, VI, Eyeballs appear when III, IV, VI are damaged sleep peak syndrome Wangjian area Swelling at the tip of sleep and nearby areas V branch 1 Tumor, vascular disease, trauma, infection Limited movement, double vision, upper and lower face (Roll et syndrome) Vertex; trigeminal nerve innervated area Hyperesthesia, hypoesthesia; optic nerve Damage resulting in decreased vision, visual acuity Meridian shrinkage, peripheral vision loss petrous tip Abducens nerve paralysis on the affected side causes esotropia petrous apex syndrome V VI Inflammation of the petrous part of the metatarsal bone is characterized by acute and moderate Vision and diplopia: affected side tricuspid Otitis is most common: tumors such as epidermis (Grade ni go syndrome) Pain and fear in the area controlled by the ophthalmic branch Tumors, meningiomas, etc.: trauma, bone Decreased light and corneal sensation Folding and bleeding ipsilateral progressive neurological deafness cerebellopontine syndrome Acoustic schwannoma is the most common tumor pontocerebellar peduncles V, VI, V, sometimes With impaired vestibular function; face common, followed by meningiomas, (Cushing I syndrome) With VI, IX, X Hypoesthesia, pain, corneal reaction Dermoid cysts, etc.; arachnoiditis, vascular malformation Reduction or disappearance of ejaculation; ipsilateral eye Esotropia, mild peripheral facial paralysis: ipsilateral cerebellar ataxia May have frequent high voltage performance; rear group cranial nerve palsy symptoms

Section 2, Spinal Nerve Diseases 1. Mononeuropathy and neuralgia Mononeuropathy (mon on europa thy) refers to damage to a single nerve resulting in loss of motor and sensory functions consistent with the innervation range of that nerve. Symptoms and signs. Neuralgia is pain in the distribution of damaged nerves. Causes include trauma, ischemia, tumor infiltration, physical injury,

394 Chapter 17 Peripheral Nerve Diseases Systemic metabolic diseases (such as diabetes) or poisoning (ethanol, lead), etc. The clinical manifestations depend on the affected nerves. The common features are sensory, motor and autonomic nervous system dysfunction in the affected nerve distribution area, accompanied by reflex symptoms. The radiation weakens or disappears. Electromyography and nerve conduction measurements aid in diagnosis. Neurogenic damage changes appear in EMG 2 to 3 weeks after nerve injury. Changes, such as a large number of fiber potentials and positive sharp waves, a significant reduction in motor units when muscles contract vigorously, etc. At the same time, nerve conduction velocity may appear Slowing down to varying degrees, action potential amplitude reducing or disappearing to varying degrees. Monitoring nerve conduction velocity is useful for localization and determining the extent of nerve damage. degree and estimate prognosis are of great significance (1) Burn nerve paralysis The radial nerve originates from the posterior bundle of the brachial plexus and is composed of nerve root fibers from Cs to T. Its motor branches innervate the triceps and supination muscles. extensor carpi ulnaris, extensor digitorum communis, index finger and little finger proper extensor muscles, abductor pollicis longus and pollicis longus, The main function of the extensor brevis is to extend the elbow, wrist and fingers; the sensory branches are distributed on the upper arm, the back of the forearm and the back of the hand, and the proximal back of the fingers. 【Cause】 The circumferential nerve is the most vulnerable branch of the brachial plexus and has many causes. Pressure on the armpit or upper limb, infection, shoulder joint discoloration, peptide bone Fractures, penetrating injuries to the upper limbs, lead and ethanol poisoning, excessive abduction of the upper arm for a long time during surgery, or the umbilical cord wrapping around the upper arm in newborns can cause nerve burns. damaged. [Clinical manifestations] Radial paralysis mainly manifests as wrist ptosis, which is caused by extensor muscle paralysis and the inability to extend the wrist and fingers. Cannot supinate. Clinical manifestations vary depending on the site of injury. 1. High-level injury (axillary) damages the area above the triceps branch of the axillary nerve, resulting in complete nerve paralysis. The extensor muscles of the upper limbs are completely paralyzed. The elbow, wrist, and metacarpophalangeal joints cannot be straightened. The forearm cannot be supinated in the extended position, and the hand is usually in a pronated position. 2. 1/3 of the bone is damaged, and the area below the triceps branch is damaged. The triceps function is normal, and the rest is extensor paralysis. 3. The function of the triceps, circumflex, supinator and wrist extensor muscles will be preserved if the lower end of the bone or the upper 1/3 of the forearm is injured. 4. If less than 1/3 of the forearm is injured, only the finger extension function is lost without wrist droop. Due to the overlap of adjacent nerves, the sensory impairment of Xiaoxiao nerve palsy is limited to the thumb on the back of the hand and the "tiger's mouth area" on the dorsal side of the space between the first and second metacarpal bones. Skin (Figure 17-1). -Xiao Nervous ulnar nerve -ulnar nerve median nerve median nerve B Figure 17-1 Distribution of sensory impairments caused by damage to the Xiaoxiao nerve, median nerve and ulnar nerve A. Sensory disturbances (back of hand) when the dawn, median and ulnar nerves are damaged B. Burn, median and ulnar nerve damage Sensory disturbance during injury (palm surface) 【diagnosis】 The clinical diagnosis was based on the inability to straighten the elbow, wrist, and fingers, the inability to straighten and abduct the thumb, and a decrease in sensation around the back of the hand and the proximal dorsum of the thumb and index finger. Not difficult

395 Chapter 17 Peripheral Nerve Diseases 【treat】 In addition to the treatment of the cause, nutritional neurotherapy can also be supplemented. The circumferential nerve has good regeneration ability, and the functional recovery after treatment is better than that of other upper limbs. Nervousness is better (2) Median nerve palsy The median nerve originates from the medial and lateral bundles of the arm. It is composed of C, ~T and nerve root fibers. It innervates the pronator teres muscle. Almost all the flexors and thenar muscles of the forearm, including the flexor carpi lateralis, flexors of each finger, opponens pollicis, flexor pollicis brevis, etc. Main function is to control the forearm Pronate, flex the wrist, and flex the fingers. The sensory branches of the median nerve are distributed in the palm half, the palm surface of the three and a half fingers of the dawn half, and the middle and distal fingers. back skin 【Cause】 Dislocations secondary to shoulder and elbow joints are mostly caused by traction injuries. For example, peptide bone fractures and lunate dislocations are often accompanied by median nerve contusion or extrusion. Crushing. Because the median nerve is most superficial at the wrist during its entire course, it is easily injured by amputation or cutting with sharp instruments, and is often accompanied by flexor tendons. damaged. [Clinical manifestations] Movement disorders mainly manifest as impairment of grip strength and forearm pronation. Damage to the upper arm resulting in complete median nerve palsy, manifesting as forearm Inability to pronate, unable to abduct and flex the wrist, unable to flex the thumb, index, and middle fingers, unable to make a fist, unable to palm, abduct, and flex the thumb; especially muscle atrophy The thenar muscle is prominent, and the palm is flat: the thumb is adducted, showing a "guessing hand" deformity. When the middle 1/3 or lower 1/3 of the forearm is injured, the movement disorder is limited to Thumb abduction, flexion and palm opposition, etc. Sensory impairment manifests as burning around the side half of the palm, the palm surface of the thumb, middle finger and index finger, burning of the side half palm surface of the ring finger, the distal segments of the index finger, middle finger and ring finger. Sensation decreases or disappears on the dorsal side of the burned side, often accompanied by caustic neuralgia (Figure 17-1) Median nerve injury is common in carpal tunnel syndrome (CT S). The carpal tunnel is composed of 8 carpal bones and the upper wrist The transverse ligament forms a bony fiber tunnel, through which the median nerve and nine muscle legs pass. Various internal diseases cause water in carpal tunnel contents Swelling, venous stasis, repeated force or trauma on the wrist, etc. cause the median nerve to be compressed in the carpal tunnel, resulting in abnormal sensation and numbness in the three fingers on the side. Wood, pain, and atrophy of the thenar muscles are called carpal tunnel syndrome 【diagnosis】 This disease can be diagnosed based on motor and sensory impairment in the area innervated by the median nerve, and neuroelectrophysiological testing indicating damage to the median nerve. 【treat】 The treatment of carpal tunnel syndrome includes wrist joint immobilization, local physical therapy, taking indomethacin, ibuprofen and other non-steroidal anti-inflammatory drugs, and can also be used on the wrist. Inject 0.5 ml of prednisolone plus 0.5 ml of 2% procaine into the tube, once a week, and 4 to 6 times constitute a course of treatment. If it fails more than 2 times, Electromyography shows that the thenar muscle is denervated and the transverse carpal ligament can be incised to release the nerve. (3) Ulnar nerve numbness and thinness The ulnar nerve originates from the medial bundle of the arm and is composed of C and T nerve root fibers. It innervates the flexor carpi ulnaris and flexor digitorum profundus muscles on the ulnar side. Half, hypothenar muscle, interosseous muscle, spiral muscle, adductor pollicis muscle, palmar flexor muscle of little finger, etc. The main function is to flex the wrist to tilt the hand to the ulnar side, with the little finger outside Extension, palm alignment and flexion, etc. The sensory branch is mainly distributed on the ulnar side of the hand below the wrist and the ulnar half of the little finger and ring finger. 【Cause】 Ulnar nerve injury is common in trauma, compression, inflammation, fracture, leprosy, etc. It is also seen in improper hanging posture, abnormal intraosseous development and Elbow deformity. The ulnar nerve runs superficially behind the ureteral bone and at the olecranon of the ulna. It is a common site for injuries such as impaction. [Clinical manifestations] Dyskinesia typically manifests as atrophy and weakness of small muscles in the hands, and a decrease or inability to move fine fingers. Flexor carpi ulnaris paralysis, side Antibacterial wrist flexor muscles cause the hand to turn sideways; paralysis of the adductor pollicis muscle and antibacterial abductor pollicis muscles cause the thumb to maintain an abducted position; hypoflexion and excessive contraction of the extensor muscles cause the palm to The finger joints are hyperextended, and the distal phalanx is flexed into a "claw-shaped hand", accompanied by atrophy of the hypothenar and interosseous muscles. The middle 1/3 and lower 1/3 of the ulnar nerve in the forearm are injured Sometimes only the small muscles of the hands are paralyzed. Sensory impairment mainly manifests as hypoaesthesia on the ulnar side of the dorsum of the hand, the hypothenar muscle, the little finger and the ulnar half of the ring finger or Disappear (Figure 17-1).

396 Chapter 17 peripheral nerve disease 【diagnosis】 The diagnosis can be made based on the history of wrist and elbow trauma, typical motor and sensory impairment in the innervated area of ​​the ulnar nerve, and electromyography. 【treat】 Mainly targeting the cause of the disease, neurotrophic drugs and steroid drugs can also be used, supplemented by physical therapy and functional exercise. (4) Common row nerve palsy The common per one al nerve originates from L 4 to S, the nerve root, and is the main branch of the sciatic nerve. It is responsible for dorsiflexion, abduction, and flexion of the foot. Adduction and extension of toes, etc. The common drainage nerve branches from the sciatic nerve at the lower 1/3 of the thigh, and branches around the outside of the small head of the rib bone to branch into the lateral drainage cutaneous nerve. It controls the sensation on the lateral surface of the calf. The medial branch divides into the superficial nerve and the deep nerve. The former sends out muscle branches to innervate the long muscle and short muscle of the calf. The skin The branches are distributed on the lateral side of the calf, the dorsum of the foot and the skin of the dorsum of the 2nd to 5th toes. The latter innervates the coelophysis premuscle, extensor longus, extensor brevis and extensor digitorum brevis, and branches out. Cutaneous branch to the skin of the opposite edge of the 12th toe 【Cause】 The common pelvic nerve is most vulnerable to damage when it goes around the neck of the pelvic bone. Trauma and compression are common, such as surgery, compression during sleep, fracture of the pelvic bone head, and long-term trauma. Habit of sitting cross-legged and waiting, diabetes, lead poisoning and bursitis can also cause paralysis of the common excretory nerve [Clinical manifestations] Common drainage nerve palsy manifests as inability to dorsiflex the feet and toes, foot drop, walking with a straddle gait, and sensation on the anterolateral side of the calf and dorsum of the foot. obstacle. 【Diagnosis and Treatment】 Diagnosis is based on medical history, detailed neurological examination, and neuroelectrophysiological data. Pay attention to the differentiation from sciatic neuropathy. remove In addition to treating the cause, neurotrophic agents and local physical therapy can be added. (5) Cavalal nerve palsy The tibia l nerve originates from the L-S nerve roots. After branching off from the sciatic nerve at the upper corner of the thoracic fossa, it goes straight down the back of the calf. Equipped with the intestinal tract muscle, soleus muscle, coelophysis muscle, flexor digitorum longus and all brevis muscles of the foot. The main functions are knee flexion, plantar flexion, inversion and toe spacing. Wait. [Clinical manifestations] The embryonic nerve is damaged, the feet and toes cannot flex, the knee flexion and foot adduction are limited, and the Achilles tendon reflex is weakened or disappeared. Foot eversion and abduction, interosseous muscles Paralysis causes a claw-like posture of the toes, with the heels touching the ground when walking. Sensory disturbances in the back of the calf, soles, and lateral edges of the feet, and occasionally pain and burning in the toes and soles of the feet. Abnormal sensations such as burning sensation. 【Diagnosis and Treatment】 Diagnosis is mainly based on medical history, clinical manifestations and neuroelectrophysiological examination. In addition to treating the cause of the disease, corticosteroids and neurological medications can be used in the acute phase. Nutritional medicines, B vitamins, nerve growth factors, etc. can also be used, acupuncture, physical therapy and drug iontophoresis can also be used. Limb deformity is obvious and preserved Surgical correction is possible if conservative treatment is ineffective (6) Occipital neuralgia Occipital neuralgia is a general term for pain in the distribution areas of the greater occipital nerve, lesser occipital nerve, and greater auricular nerve. Three pairs of nerves come from C and C Distributed in the occiput. 【Cause】 Common causes of occipital neuralgia include cervical spondylosis, cervical tuberculosis, trauma, spinal cord tumors, osteoarthritis, cervical and occipital myositis, meningitis and metastasis Tumors, etc., mostly secondary nerve damage, may also be caused by respiratory infection or tonsillitis or the cause is unknown. [Clinical manifestations] The clinical manifestations are mostly one-sided persistent dull pain originating from the occipital region and extending toward the top of the head (greater occipital nerve), mastoid (lesser occipital nerve) or external ear. (Greater auricular nerve) radiation, which can be exacerbated in paroxysms, aggravated by head and neck movements and coughing, and is often accompanied by cervical muscle inflammation. Check that there is often tenderness under the external occipital protuberance. Hypoesthesia or hypersensitivity often occurs in the occipital nerve distribution area 【treat】 The first is to treat the cause. Symptomatic treatments such as analgesics, sedatives, and neurotrophic drugs, local sealing, and physical therapy can also be used. If the effect is not good, surgery can be used.

397 Chapter 17 Peripheral Nerve Diseases treat. (7) Brachial plexus pain The brachial plexus is composed of C, ~T, and the anterior branches of the spinal nerves. It mainly controls movement and sensation of the upper limbs. When damaged, it often causes pain in the innervated area, so it is called for “brachial neuralgia” 【Cause】 Brachial plexus pain is usually divided into two categories: idiopathic and secondary, with the latter being more common. The cause of idiopathic brachial plexus pain is unknown, but it may be An allergic disease related to viral infection, vaccination, separation, surgery, etc. Secondary brachial plexus neuralgia is usually caused by the brachial plexus It is caused by the compression of tissue lesions and is divided into radicular brachial plexus neuralgia and dry brachial plexus neuralgia. The common causes of the former include cervical spondylosis, cervical tuberculosis, and bone disease. fracture, dislocation, cervical spinal cord tumors, etc. The latter is often caused by thoracic outlet syndrome, trauma, clavicle fracture, superior sulcus tumor, metastatic cancer, etc. [Clinical manifestations] Idiopathic brachial neuralgia is more common in adults, with an acute or subacute onset. Fever, fatigue, and muscle aches may occur before the disease or in the early stages of the disease. and other systemic symptoms, followed by shoulder and upper limb pain, upper limb muscle weakness, tendon reflex changes, and sensory impairment within a few days. secondary arm syndrome Menstrual pain manifests as varying degrees of pins and needles, burning or soreness in the shoulders and upper limbs, starting in the shoulders and neck, spreading to the upper limbs on the same side, and may be persistent or intermittent. Symptoms aggravate, obvious at night or when upper limbs move, arm movement and sensory impairment from the distribution area, localized muscle atrophy, tendon reflexes weaken or disappear, neck Spondylosis is the most common cause of secondary brachial plexus pain. Elderly people may have autonomic nervous system dysfunction during the course of the disease. brachial plexus stretch test and straight arm raising test are mostly positive. [Diagnosis and differential diagnosis] Clinical diagnosis can be made mainly based on clinical manifestations, electromyography, nerve conduction measurement and other neurophysiological examinations, but attention should be paid to the shoulder joint Differentiation of arthritis and periarthritis of shoulder. The pain in the latter is generally limited to the shoulder or upper arm, the pain does not dissipate, and the pain does not worsen with neck movement. check The movement of the shoulder joint is limited, there is tenderness in the joint muscles, and there are no signs of nerve damage. Cervical spine and shoulder joint X-rays and CT can be used for differential diagnosis. 【treat】 Treatment of the cause is the first choice, followed by non-steroidal anti-inflammatory drugs such as ibuprofen, acetaminophen, etc. To reduce nerve edema and relieve pain The pain points can be partially closed with 2% procaine and prednisolone. Depending on the situation, local physical therapy, acupuncture, cervical traction and other comprehensive treatments can be tried. treat. (8) Intercostal neuralgia Intercostal neuralgia (intercostal neuralgia) refers to the pain syndrome in the area innervated by the interaided nerve 【Cause】 Primary is rare, mostly secondary intercostal neuralgia, often caused by herpes zoster, pleurisy, pneumonia, thoracic spine or rib trauma, tumors, etc. cause. 【Clinical manifestations The pain is distributed along one or several intercostal spaces, showing persistent stinging and burning pain, which is aggravated by breathing, coughing, and wheezing. Physical examination can reveal corresponding help Hyperesthesia in intercutaneous areas and tenderness at rib edges. In herpetic intercostal neuralgia, scars can be seen in the corresponding intercostal space, and the pain appears before the scars. The pain may persist for some time after the rash disappears. 【treat】 The treatment of intercostal neuralgia mainly includes etiological treatment such as tumor removal, anti-infection, anti-virus, etc. Symptomatic treatment can include analgesics, sedatives, B Vitamins, partial sealing, physical therapy, etc. (9) Lateral femoral cutaneous neuritis Lateral femoral cutaneous neuropathy (lateral femoral cuta neo us n europa thy) is also called mer al gia pares the ti- ca), is the most common clinical cutaneous neuritis and is caused by damage to the lateral femoral cutaneous nerve. The lateral femoral cutaneous nerve is a purely sensory nerve that originates from the lumbar The plexus, composed of the anterior branch of the LL nerve root, passes below the inguinal ligament and is distributed in the skin of the anterolateral thigh 【Cause】 Damage to the lateral femoral cutaneous nerve is mainly seen in local compression, retroperitoneal tumors, abdominal tumors, pregnancy uterine compression, etc. Other causes include Obesity, trauma, alcohol and drug poisoning, etc. Diabetic mononeuropathy tends to involve this nerve.

398 Chapter 17 peripheral nerve disease [Clinical manifestations] Common in men, mostly affected on one side, manifested by abnormal sensation in the lower 2/3 areas of the anterolateral thigh, such as numbness, pain, ant walking sensation, etc., standing for a long time Or symptoms may worsen after walking for a long time. Physical examination shows hypersensitivity, decrease or disappearance of the outer thigh, without muscle atrophy or weakness, showing a chronic course. It can occur repeatedly and the prognosis is good. 【treat】 The first choice is to treat the cause, such as treating diabetes, arteriosclerosis, poisoning, etc. Obese people should lose weight, and alcoholics should quit drinking. People with severe pain can take it orally Analgesics, sedatives or carbamazepine, large doses of B vitamins or 2% procaine local sealing may be effective. Severe pain, conservative treatment If treatment fails, fascia lata or inguinal ligament incision can be considered to relieve nerve compression. (10) Sciatica Sciatica refers to a pain syndrome along the path of the sciatic nerve and its branches. The sciatic nerve arises from the plexus It consists of L to S nerve roots, which are the longest and thickest nerves in the body. They exit the pelvis through the inferior foramen of the piriformis muscle and are distributed throughout the lower limbs. 【Cause】 Primary sciatica is clinically rare, also known as sciatic neuritis, and its cause is unknown. May be related to colds, colds, teeth, sinuses, tonsils Infection invades the epineurium of peripheral nerves and causes interstitial neuritis, often accompanied by myositis or fibrositis. Secondary sciatica is common clinically and is caused by the compression or stimulation of the sciatic nerve pathway by surrounding tissues or lesions. A small number of cases are secondary to sciatica. Systemic diseases such as diabetes, gout, connective tissue diseases, etc. can be divided into radicular and dry sciatica according to the damaged part. root sciatica Menstrual pain is more common than dry sciatica and is often caused by intraspinal diseases (inflammation of the spinal cord and cauda equina, tumors of the lumbar spinal cord and spinal canal, trauma, and vascular malformation). etc.) and spinal diseases (lumbar disc herniation, lumbar spondylitis, spinal stenosis, lumbar osteoarthrosis, spinal tuberculosis, tumors, etc.). That Lumbar disc herniation is the most common cause. Dry sciatica is often caused by hypoarthritis, myeloid arthritis, lumbar skin swelling, pelvic Caused by tumors, uterine adnexitis, pregnancy uterine compression, improper injection site of gluteal muscle [Clinical manifestations] It is more common in young adults and is mostly unilateral. The pain mainly radiates along the path of the sciatic nerve from the waist and buttocks to the posterior thigh, posterolateral side of the calf, and lateral side of the foot. shoot. The pain is often persistent and dull, exacerbating in paroxysms. It can also be electric shock, cutting or burning pain, and pain when walking and pulling the sciatic nerve. obvious. Radical pain worsens when coughing, sneezing, or exerting force. In order to reduce the pain or pain caused by activities, the patient slightly flexes the affected limb and Lie on the unaffected side, bend the knee joint on the affected side first when standing up on your back, apply force on the buttocks on the unaffected side first when sitting down, and flex the spine toward the affected side when standing upright, etc. Physical examination It can be found that the straight leg raising test (La segue sign) is positive. The patient lies on his back with the lower limbs straightened. The examiner raises the affected limb. If the patient is within 70°, It is considered positive when the patient feels pain, which is caused by the reflex reaction of the parathoracic muscles; sensory impairment may occur on the outer side of the calf and the dorsum of the foot on the affected side; the stepping reflex is weakened or Disappearance: There are tender points on L, L, paraspinous process, low parailiac, and intestinal muscle. X-ray films of the lower back, medullary bones, and medullary joints are useful for detecting fractures, dislocations, and Innate spinal deformities are helpful. CT, MRI, and myelography are helpful in the diagnosis of spinal and spinal canal diseases. B-ultrasound can detect pelvic related diseases. Electromyography and nerve conduction measurement are meaningful for determining the location, extent and prognosis of sciatic nerve damage. [Diagnosis and differential diagnosis] According to the medical history, clinical symptoms, and physical signs such as pain distribution range, triggers for exacerbation and alleviation, tender points, La segue sign, weakened stepping reflex, and Imaging examination can diagnose this disease. Pay attention to the identification of the following diseases: 1. Acute lumbar muscle sprain, with a history of trauma, obvious local pain in the waist, no radiating pain, and tenderness points on both sides of the waist. There is also pain in the lower back, buttocks and lower limbs, but the pain and tenderness are not localized. 2. Lumbar muscle strain, hip fibrositis, body arthritis Diffusion, no sensory impairment, muscle weakness, etc., stepping reflex is generally normal. Possible identification by X-ray, CT, MRI examination 【treat】 1. Cause treatment Different treatment plans are adopted for different causes. For example, patients with lumbar disc herniation sleep on a hard bed in the acute stage and rest for 1 to 2 weeks. Many symptoms are stable. 2. Drug treatment - If the pain is obvious, analgesics such as indomethacin, ibuprofen, and carbamazepine can be used. For muscle pain, you can use Dixiban 5~ 10 mg orally, 3 times/day. Neurotrophic agents, such as vitamin B, can also be added, 100 mg each time, once a day, intramuscular injection Paravertebral closure can also be performed with 1%~2% procaine or 1 ml each of prednisolone. 3. Occluded therapy , Ultrashort wave and infrared irradiation can be used in the acute stage. After the pain is relieved, induction electricity, iodine ion penetration and hyperthermia can be used. 4.Physiotherapy

399 peripheral nerve disease Chapter 17 etc. Acupuncture, massage, etc. can also be used 5. Surgical treatment may be considered in cases of poor efficacy of surgical treatment or chronic recurrence. (11) Femoral neuralgia The femoral nerve is composed of the anterior branch of the Lz-a nerve root and is the longest branch in the lumbar plexus. Femoral neuralgia neuralgia) is also called Wasserman's n sign. 【Cause】 Common causes include pelvic and femoral fractures, gunshot wounds, stab wounds and poisoning, diabetes, infectious diseases, pelvic tumors, thick swelling, and varicose veins and femoral artery aneurysm, etc. [Clinical manifestations] The main manifestation of femoral nerve injury is weakness of the lower limbs. Try to avoid the special gait of bending the knees. When walking, take small steps. Extend the good foot first, then the disease. I can't move forward with my feet dragging my feet, and I can't run or jump. Skin branch injuries cause severe neuralgia and hyperalgesia in the distribution area, and there is reduced pain sensation in the front and inner thighs and inner calves. Retreat or disappear; knee reflex weakens or disappears; may be accompanied by nutritional changes such as edema and cyanosis. 【treat】 1. Treatment of the cause: Femoral nerve dissection requires nerve suturing, scar compression requires neurolysis, and pelvic tumors or femoral aneurysms require surgery. surgical resection. 2.Drug treatment Corticosteroids can eliminate local nerve edema and adhesions and facilitate recovery from trauma. Use Somitron tablets, aspirin Lin and ibuprofen have obvious analgesic effects. Neurotrophic drugs include vitamin B, vitamin B, vitamin B, vitamin B, and nerve growth factor, etc. 3. Femoral nerve sealing If the pain is severe and unbearable, 2% procaine plus lysine, vitamin B or absolute ethanol can be used. The nerves are sealed and the analgesic effect is good. Acupuncture, physical therapy, and acupoint sealing can help relieve adhesions and promote nerve regeneration. 2. Polyneuropathy Polyneuropathy (poly n europa thy) is a multiple nerve damage that mainly affects the distal parts of the limbs. The clinical manifestation is that the limbs are opposite to each other Asymmetric motor sensory impairment and autonomic nervous system dysfunction. 【Cause】 There are many causes, including drugs, chemicals, heavy metals, alcoholism, metabolic disorders, paraneoplastic syndromes, etc. 1. Poisoning by isoniazid, dermatoid drugs, phenytoin, organophosphorus pesticides, heavy metals, etc. 2. Nutritional disorders B vitamin deficiency, chronic alcoholism, chronic gastrointestinal disease or after surgery, etc. 3． Metabolic disorders Lyme disease, diabetes, uremia, amyloidosis, gout, myxedema, acromegaly, cachexia, etc. 4. Infectious or inflammatory Acute or chronic inflammatory demyelinating polyneuropathy, serum or following vaccination. 5. Autoimmune diseases Connective tissue diseases such as lupus erythematosus, sarcoidosis, polyarteritis nodosa, and rheumatoid arthritis 6. Other cancer-related distal axonopathy, cancerous sensory neuronopathy, subacute sensory neuronopathy, POEMS syndrome and other tumor-related disease. 【Pathogenesis】 Depending on the cause, the pathogenesis is different and non-specific. 【pathology】 Pathological changes mainly include peripheral nerve axonal degeneration, segmental demyelination, and neuronal degeneration. 【Clinical manifestations In polyneuropathy, there is usually symmetrical sensory, motor, and autonomic dysfunction in the distal limbs. Affected distal limb In the early stage, irritating symptoms such as paresthesia, such as pins and needles, ant walking, burning, tenderness and hyperesthesia, may occur. As the disease progresses, limb distance gradually occurs End-symmetrical depth sensation is reduced or absent, with a glove-sock-like distribution. Lower motor neuron paralysis of the limbs, distal symmetrical muscle weakness Strength, may be accompanied by muscle atrophy, muscle fascicle changes, etc. Muscle atrophy is evident in the interosseous muscles, screw-shaped muscles, and thenar muscles in the upper limbs, and in the lower limbs, the anterior chamber muscles and pelvic muscles Significantly, the wrists and feet may be drooped, and in the late stage, the muscles may shrink significantly and deformities may occur. Tendon reflexes in the limbs weaken or disappear, usually in the early stages of the disease Performance.

400 Chapter 17 Peripheral Nerve Diseases Autonomic nervous system dysfunction manifests as thin, dry, pale, cold, sweet skin on the extremities, excessive sweating or no sweating, and thick fingernails. Rough, crispy, piloerection disorder, hypertension and orthostatic hypotension, etc. The above symptoms usually appear at the same time, are symmetrically distributed in the limbs, and extend from the distal end to the proximal end. Laboratory cerebrospinal fluid examinations vary in different diseases, and some diseases may have elevated cerebrospinal fluid protein levels. Electromyography as neurogenic Due to sexual damage, nerve conduction velocity may be reduced to varying degrees. Nerve biopsy may reveal segmental demyelination or axonal degeneration of peripheral nerves 【Auxiliary inspection】 Neurogenic changes can be seen on electromyography, including slowed conduction velocity or reduced amplitude. Nerve tissue biopsy can be performed if necessary. Because there are many causes, auxiliary examinations should be carried out based on medical history and clinical manifestations. If tumor-related diseases are considered, serum tumor markers can be improved. biomarkers, paraneoplastic syndrome antibodies, and imaging examinations of the head, chest and abdomen, etc. When considering autoimmune diseases, rheumatic immunity, lupus, ANA antibody spectrum testing, etc. Considering the lack of B vitamins, serum vitamin level determination should be improved, etc. 【diagnosis】 The diagnosis is mainly based on symmetrical sensory impairment with a glove-sock-like distribution in the distal limbs, obvious flaccid paralysis at the distal end, and autonomic nervous system Functional impairment, electromyography and nerve conduction measurement can help in diagnosis, and nerve tissue biopsy can be performed if necessary. Nerve conduction measurement may help with dryness Diagnosis of subclinical cases at early stage. 【Differential Diagnosis】 Mainly differentiated from the following diseases 1. Acute myelitis, paraplegia or quadriplegia, urinary and defecation disorders, conductive tract sensory impairment and pyramidal tract signs, spinal cord visible on MRI lesions. 2. Acute poliomyelitis It is more common in children. The paralysis has asymmetric segmental characteristics, flaccid paralysis, and no sensory impairment. 3. Periodic paralysis, recurrent attacks of limb weakness and flaccid paralysis. During the attack, blood potassium is significantly reduced, but returns to normal after potassium supplementation. 【treat】 1. When treating diabetic polyneuropathy, patients should pay attention to controlling blood sugar and delaying the progression of the disease; those caused by drugs should stop taking the drug immediately. Drugs; heavy metal and chemical poisoning should be removed from the poisoning environment immediately, timely application of antidote and rehydration, diuresis, and laxatives to eliminate the poison as soon as possible; Uremic polyneuropathy can be treated with hemodialysis or kidney transplantation; patients with nutritional deficiency and metabolic disorder polyneuropathy should be actively treated Primary disease; those with ethanol poisoning need to stop drinking. 2. General treatment can include supplementing B vitamins and other neurotrophic drugs such as coenzyme A, ATP, etc. For those with severe pain, various painkillers can be used Painkillers, carbamazepine or phenytoin can be used in severe cases. Patients in the acute stage should rest in bed, strengthen nutrition, and strengthen care for severe patients. Patients with the disease should turn over frequently, and splints or braces should be used to maintain functional positions of paralyzed limbs to prevent joint shrinkage and deformity. Acupuncture and physiotherapy can be used during the recovery period and rehabilitation training. 【Prognosis】 The prognosis varies according to the cause and duration of the disease, such as early poisoning, B vitamin deficiency, peripheral nerve damage caused by infection, etc. Nervous function can be partially or fully restored after the cause is removed. Malignant tumor-related diseases or long-term autoimmune, genetic, and metabolic diseases Irreversible neurological deficits may occur 3. Guillain-Barré syndrome Guillain-Barre syndrome (GBS) is an autoimmune-mediated peripheral neuropathy that mainly damages Most spinal nerve roots and peripheral nerves, and cranial nerves are also often involved. The clinical characteristics are acute onset, with symptoms reaching their peak in about 2 weeks. Presently, multiple nerve roots and peripheral nerves are damaged, often with cerebrospinal fluid protein-cell separation. Most of them have a single-phase self-limiting course. Intravenous injection Immunoglobulin (intravenous immunoglobulin, I VIG) and plasma exchange (plasma exchange, PE) treatments are effective. The disease includes Acute inflammatory demyelinating polyradiculoneuropathy (A IDP), acute inflammatory demyelinating polyradiculoneuropathy (A IDP) Acute motor a xona ln europa thy, A MAN, acute motor-sensory axonal neuropathy (acute motor- sensory axon al n europa thy (AM SAN), Miller-Fisher syndrome (MFS), acute pan-autonomic Menopausal disease (acute pan autonomic n europa thy, A PN) and acute sensory neuropathy (acute sensory n europa thy, AS N) and other subtypes.

401 Chapter 17 peripheral nerve disease 【Cause】 The exact cause of GB S is unknown. Clinical and epidemiological data show that the onset of some patients may be related to Campylobacter jejuni (campylobacter). jeju ni,C) related to infection. The CJ infection rate in GB S patients with diarrhea as the prodromal symptom is as high as 85%, which often causes acute motor axonal neuropathy. Menstrual illness. CJ is a gram-negative microaerophilic Campylobacter with multiple serotypes. Patients often develop symptoms after diarrhea has stopped. In addition, GB S may also be related to Cytomegalovirus, Epstein-Barr virus, varicella-zoster virus, Mycoplasma pneumoniae, hepatitis B virus, and HIV infection. Most reports refer to Bleeding leukemia, lymphoma, use of immunosuppressants after organ transplantation, or patients with autoimmune diseases such as systemic lupus erythematosus, Hashimoto's thyroiditis, etc. The disease is often complicated by GB S 【Pathogenesis Molecular mimicry is currently considered to be one of the most important mechanisms that may lead to the pathogenesis of GBS. This theory holds that Some components of the pathogen have the same structure as some components of the peripheral nerves. The body's immune system recognizes errors, and autoimmune cells and autoimmune cells The body's antibodies attack normal peripheral nerve components, causing peripheral nerve demyelination. Different types of GB S can identify different parts of Nervous tissue units, clinical manifestations are also different. 【pathology】 The main pathological changes are lymphocyte and giant cell infiltration around small blood vessels in peripheral nervous tissue, demyelination of nerve fibers, and severe cases. Axonal degeneration may ensue. 【Classification and diagnosis】 1.A IDP is the most common type of GB S, also called classic GB S. The main lesions are multiple nerve roots and peripheral nerve segments. Demyelination. (1) Clinical manifestations 1) It can occur at any age and in any season. 2) Frequently have respiratory or gastrointestinal infection symptoms or vaccination history 1 to 3 weeks before illness 3) Acute onset, the condition usually reaches its peak in about 2 weeks. 4) The first symptom is mostly symmetrical flaccid muscle weakness of the limbs, which gradually develops from the distal end to the proximal end or worsens from the proximal end to the distal end, often from both sides. The lower limbs begin to gradually involve trunk muscles and cranial nerves. It may reach its peak within a few days to 2 weeks. In severe cases, the synergistic muscles and diaphragm muscles may be involved, causing respiration. paralysis. Tendon reflexes in the limbs are often weakened, and 10% of patients show normal or active tendon reflexes. 5) During the onset of the disease, patients often experience abnormal limb sensations such as burning, numbness, tingling, and discomfort, which may occur before or at the same time as motor symptoms. now. Sensory loss is relatively mild, with a glove-sock pattern. A few patients may have muscle tenderness, especially tenderness in the bowel muscles, which is more common. Occasionally, Nerve root irritation symptoms such as Kern ig sign and La segue sign occur 6) Bilateral facial nerve paralysis is the most common form of cranial nerve involvement, followed by glossopharyngeal, vagus nerve, oculomotor, abductor, hypoglossal, and trigeminal nerve palsy. Rarely, some patients seek treatment with cranial nerve damage as the first symptom. 7) Some patients have autonomic nervous system dysfunction, manifested by skin flushing, increased sweating, tachycardia, arrhythmia, and orthostatic hypoemia. Pressure, swelling of hands and feet, nutritional disorders, urinary and defecation disorders, etc. 8) The disease course is mostly monophasic, and there may be short-term fluctuations during the course of the disease. (2) Auxiliary inspection 1) Cerebrospinal fluid examination: ① Cerebrospinal fluid protein-cell separation is one of the characteristics of GBS. Most patients have normal protein content within a few days of onset. Usually, protein increases to varying degrees within 2 to 4 weeks, but rarely exceeds 1.0 g/L; sugar and chloride are normal; white blood cell count is generally <10×10/L; ② Some patients have oligocl on al bands (OB) in their cerebrospinal fluid, but they are not characteristic changes; ③ Some patients have cerebrospinal fluid resistant to Ganglioglyceride antibodies were positive. 2) Serological examination: Some patients are positive for anti-ganglioglyceride antibodies in blood, and the positive rate is higher than that in cerebrospinal fluid. 3) Campylobacter jejuni can be isolated and cultured from the stool of some patients, but it is not currently routinely tested in China. 4) Neuroelectrophysiology: Motor nerve conduction measurement shows prolonged distal latency and slowed conduction velocity, and F wave shows slowed conduction velocity. Or the occurrence rate decreases, suggesting the presence of demyelinating lesions in peripheral nerves, and the presence of conduction block or abnormal waveform dispersion in non-entrapment parts is detrimental to diagnosis. Demyelinating lesions are more valuable.

402 Chapter 17 Peripheral Nerve Diseases 5) Intestinal nerve biopsy: It can be used as an auxiliary diagnostic method for GBS, but it is not a necessary examination. Biopsy shows demyelination of myelinated fibers Infiltration of phagocytes may occur in some parts, and inflammatory cells may infiltrate around small blood vessels. (3) Diagnostic criteria 1) There is often a history of prodromal infection, with an acute onset and progressive aggravation, usually reaching a peak in about 2 weeks. 2) Symmetrical weakness of muscles innervated by limbs and cranial nerves. Severe cases may have respiratory muscle weakness and weakened or disappeared tendon reflexes in the limbs. 3) May be accompanied by mild sensory abnormalities and autonomic nervous system dysfunction. 4) Protein-cell separation occurs in cerebrospinal fluid 5) Electrophysiological examination shows prolonged distal motor nerve conduction latency, slowed conduction velocity, abnormal F waves, conduction block, and abnormal waves. Discrete shapes, etc. 6) The course of the disease is self-limiting (4) Differential diagnosis: If the following symptoms occur, the diagnosis of GBS is generally not supported: ① Significant and persistent asymmetrical limb insemination ② Bladder or rectal dysfunction as the first symptom or persistent bladder and rectal dysfunction: ③ The number of cerebrospinal fluid mononuclear cells exceeds 50×10°/L: ④ There are lobulated nuclear leukocytes in the cerebrospinal fluid; there is a clear sensory plane. Diseases that need to be identified include: myelitis, periodic paralysis, polymyositis, poliomyelitis, myasthenia gravis, acute rhabdomyolysis Diphtheria neuropathy, Lyme disease, Lyme disease, peripheral neuropathy, schizophrenia, and toxic peripheral neuropathy. 1) Poliomyelitis: Fever usually occurs at the onset, and limb paralysis is often limited to one lower limb without sensory impairment. 2) Acute transverse myelitis: There is a history of fever 1 to 2 weeks before the onset, the onset is sudden, paraplegia occurs in 1 to 2 days, and movement below the plane is impaired. The disorder is accompanied by tract sensory impairment, early urinary and defecation disorders, and the cranial nerves are not affected. 3) Hypokalemic periodic paralysis: rapid onset of flaccid paralysis of the limbs, no sensory impairment, respiratory muscles and cranial nerves generally not affected, cerebrospinal Fluid examination is normal, serum potassium is reduced, and there may be a history of recurring attacks. Potassium supplementation is effective 4) Myasthenia gravis (MG): The affected skeletal muscles suffer from morbid fatigue, fluctuating symptoms, lightness in the morning and weight in the evening, neostigmine test Testing can assist in identification. 2.A MAN" is mainly characterized by extensive motor cranial nerve fibers and spinal nerve anterior roots and motor fiber axonal lesions. (1) Clinical manifestations: ① It can occur at any age, and is more common in children. The prevalence is similar in men and women. Domestic patients are more likely to develop the disease in summer and autumn; ② Prodromal symptoms: diarrhea and upper respiratory tract infection are common, with Campylobacter jejuni infection being the most common; ③ Acute onset, reaching symptoms in an average of 6 to 12 days Peak, a few patients can reach the peak within 24 to 48 hours; ④ Symmetrical limb weakness, some patients have impaired cranial nerve motor function In severe cases, respiratory muscle weakness may occur. The weakening or disappearance of tendon reflexes is consistent with the degree of muscle weakness. No obvious sensory abnormalities, none or only Have mild autonomic nervous system dysfunction (2) Auxiliary examination: ① cerebrospinal fluid examination: same as A IDP; ② serum immunological examination: anti-ganglionic antibodies can be detected in the serum of some patients Antibodies to GM 1 and GD 1 a in lipids, and some patients had positive serum Campylobacter jejuni antibodies; ③Electrophysiological examination: Motor nerves are mainly affected, and motor nerves are mainly affected. Significant damage to motor nerve axons (3) Diagnostic criteria: Refer to the A IDP diagnostic criteria. The prominent feature is that neuroelectrophysiological examination shows almost pure motor nerve involvement, and is characterized by Significant damage to motor nerve axons. 3. AM SAN. Mainly axonal degeneration of extensive nerve roots and motor and sensory fibers of peripheral nerves (1) Clinical manifestations: ① Acute onset, reaching the peak in 6 to 12 days on average, and a few patients reach the peak within 24 to 48 hours: ② Symmetrical limb weakness, often involving cranial nerve motor function, severe cases may have respiratory muscle weakness and respiratory failure. The patient also feels Disorders, and even partial sensory ataxia. Autonomic dysfunction often occurs (2) Auxiliary examination: ① cerebrospinal fluid examination: same as A IDP; ② serum immunological examination: anti-ganglionic antibodies can be detected in the serum of some patients Glyceride antibodies: ③Electrophysiological examination: Except for the decrease in the amplitude of the sensory nerve action potential or the inability to elicit the waveform in the sensory nerve conduction measurement, Others are the same as A MAN: ④ Intestinal nerve biopsy: axonal degeneration and nerve fiber loss can be seen, but it is not a necessary condition for diagnosis. (3) Diagnostic criteria: refer to the A IDP diagnostic criteria, the prominent feature is that neuroelectrophysiological examination shows damage to sensory and motor nerve axons obvious. Different from classic GB S, the main clinical features are ophthalmoplegia, ataxia and loss of tendon reflexes. 4.MFS

403 Chapter 17 Peripheral Nerve Diseases (1) Clinical manifestations: ① It can occur at any age and season: 2 Prodromal symptoms: There may be diarrhea and respiratory tract infection, usually jejunal flexure Bacterial infection is common; ③ acute onset, the condition reaches its peak within days to weeks; ④ usually starts with diplopia, but also myalgia, numbness of limbs, glue Onset of dizziness and ataxia. Symmetrical or asymmetrical external ophthalmoplegia occurs one after another. Some patients have ptosis of the eyes and face, and a few patients have mydriasis. Large, but the pupil's light reflex is normal. There may be trunk or limb ataxia, tendon reflexes weakened or disappeared, muscle strength is normal or slightly reduced, and some Divided into swallowing and facial muscle weakness, numbness and hypoesthesia of the distal limbs and face, and bladder dysfunction (2) Auxiliary examination: ① Cerebrospinal fluid examination: same as A IDP: ② Serum immunological examination: jejunal curvature can be detected in the serum of some patients bacterial antibodies. Most patients have positive serum GQ 1 b antibodies: ③ Neuroelectrophysiological examination: Action potential amplitude can be seen in sensory nerve conduction measurement Decrease and conduction velocity slow down: patients with cranial nerve involvement may experience a decrease in facial nerve C MAP amplitude: the blink reflex can show prolonged R 1 and R 2 latencies. Or the waveform disappears. Motor nerve conduction and electromyography are generally unremarkable. Electrophysiological testing is not required to diagnose MFS. (3) Diagnostic criteria: ① Acute onset, the condition reaches its peak within days or weeks: 2 Clinically, extraocular muscle paralysis and ataxia The three main symptoms are the disappearance of tendon and tendon reflexes, normal or mild loss of limb muscle strength: 3. Protein-cell separation in cerebrospinal fluid: 4. The course of the disease is spontaneous. Limitations. (4) Differential diagnosis: Diseases that need to be differentiated include Bickerstaff brainstem encephalitis and acute external ophthalmoplegia related to GQ 1 b antibody Brainstem infarction, cerebral hemorrhage, neuromyelitis optica, multiple sclerosis, myasthenia gravis, etc. 【treat】 1.General treatment (1) Anti-infection: Patients with gastrointestinal CJ ​​infection can be treated with macrolide antibiotics (2) Respiratory tract management: Severe patients can have respiratory muscles involved and cause respiratory failure. They should be placed in the intensive care unit, their breathing conditions should be closely observed, and respiratory tract treatment should be performed regularly. Blood gas analysis. When the vital capacity drops to 25% to 30% of normal, and the blood oxygen saturation and blood oxygen partial pressure decrease significantly, tracheal intubation should be performed as soon as possible. Tube or tracheotomy, mechanically assisted ventilation. Strengthen airway care, turn over regularly, pat the back, and promptly aspirate respiratory secretions to maintain respiratory tract health. Unobstructed and prevent infection. (3) Nutritional support: People with paralysis of the medullary muscles have difficulty swallowing and coughing when drinking water. Nasal feeding nutrition is required to ensure adequate daily intake. Calories, vitamins, prevent electrolyte imbalance. For patients with gastrointestinal bleeding or gastrointestinal paralysis, intravenous nutritional support will be provided (4) Symptomatic treatment and prevention of complications: If urine is dissolved and retained, the lower abdomen can be massaged with pressure. When ineffective, catheterization can be performed. For constipation, laxatives and moisturizers can be given. Enteral agents. Antibiotics prevent and control pneumonia, urinary tract infections, etc. 2. Immunotherapy (1) Plasma exchange (PE): It can quickly reduce antibodies and other inflammatory factors in plasma. It is recommended that those with conditions apply it as soon as possible. every time The replacement volume is 30 to 50 ml/kg, and it is carried out 3 to 5 times within 1 to 2 weeks according to the severity of the disease. Contraindications include serious infection, cardiac arrhythmia, cardiac dysfunction Insufficiency and coagulation dysfunction, etc. PE is most effective when used within 7 days after the onset of GBS, but PE treatment is still effective within 30 days after the onset of GBS. efficient. (2) Intravenous immunoglobulin (IVIG): can compete with a large number of antibodies to prevent the binding of antigens to antigen receptors on the surface of lymphocytes achieve therapeutic effect. Adult dose: 0.4 g/(kg·d). Use for 5 days. Contraindicated in patients with immunoglobulin allergy or congenital IgA deficiency Fever and flushing are common adverse reactions, which can be alleviated by slowing down the infusion rate. Occasionally, aseptic meningitis, renal failure, and cerebral infarction have been reported, which may be related to blood associated with increased liquid viscosity. PE and I VIG are the first-line treatments for A IDP, but combined treatment does not increase the efficacy. Using PE after I VIG will It will cause the infused gamma globulin to be cleared, so it is recommended to use it alone. I VIG is best used within two weeks of onset of illness. (3) Glucocorticoids: Currently, domestic and foreign guidelines do not recommend glucocorticoids for the treatment of GBS. But for unconditional row I VIG and PE treatment or severe patients in the early stage of the disease can try methylprednisolone 500 mg/d, intravenous drip, continuous use for 5 days and then gradually reduce the dose, or dexamethasone 10 mg/d, intravenous infusion, 7 to 10 days as a course of treatment. 3. Neurotrophic application of B vitamins, including vitamin B, vitamin B2, and vitamin B2. wait 4. After rehabilitation treatment, after the condition is stabilized, early formal neurological rehabilitation exercises should be carried out, including passive or active exercise, physical therapy, and acupuncture. Moxibustion and massage, etc., to prevent disuse of muscle atrophy and joint traction. 【Prognosis】 The disease is self-limiting and has a good prognosis. Paralysis usually begins to recover after 3 weeks, and most patients return to normal within 2 months to 1 year, about

404 Chapter 17 Peripheral Nerve Diseases 10% of patients have serious sequelae. The mortality rate of GB S is about 5%, mainly due to respiratory failure, infection, hypotension, severe arrhythmia, etc. complication. Being over 60 years old, rapidly progressing disease, requiring assisted breathing, and reduced motor nerve amplitude are risk factors for poor prognosis. 4. Chronic inflammatory demyelinating polyradiculoneuropathy Chronic inflammatory demyelinating polyradiculoneuropathy (chronic inflammatory demyelinating polyradiculoneuropathy) CID P is a group of immune-mediated inflammatory demyelinating diseases with a chronic progressive or relapsing course. The incidence of CID P is lower than that of A IDP. The classification includes classic type and variant type. The latter type is rare, such as pure motor type, pure sensory type, and distal acquisition. distal acquired demyelinating symmetric neuropathy (DADS), multifocal acquired demyelinating neuropathy Myelinating sensorimotor neuropathy (multi focal acquired de myelin a ting sensory and motor n europa thy, MAD SAM, or Lewis-Sumner syndrome), etc. 【Cause】 The cause is unknown. B-tubulin antibodies and myelin-binding glycoprotein antibodies can be found in patients with CID P, but they have not been found to be related to A IDP. Evidence of immune responses against infectious agents such as Campylobacter jejuni and cytomegalovirus that are closely related to the disease. 【Pathogenesis Similar to A IDP, it is an immune-mediated peripheral neuropathy. It is currently believed that the possible pathogenesis is activation of CD 4*T cells by foreign antigens. Cell proliferation activation mediates cellular immunity and autoimmune antibodies mediate humoral immunity, leading to immune damage to Schwann cells or myelin sheaths, thus Causes peripheral nerve demyelination and axonal damage. Contact protein 1 (contact in-1.CNT N 1) and neurofascin 155 (neuro f as c in 155, NF 155) is an important component protein of the node of Ranvier. In recent years, it has been found that the autoantibodies CNT N 1 IgG 4 and NF 155 IgG 4 interact with CID P associated with the onset of certain subtypes. Some patients may be positive for ganglioglyceride antibodies in their serum and cerebrospinal fluid. 【pathology】 The inflammatory reaction is not as obvious as that of A IDP, and the pathology shows characteristics such as multifocal demyelination of myelinated fibers, endoneurial edema, and inflammatory cell infiltration. Demyelination and remyelination coexist, and Schwann cell regeneration can show "onion-like" changes, and axonal damage is also common. [Clinical manifestations] It can occur in all age groups, with similar incidence rates in men and women. Precursor infection is rare before the disease, the onset is hidden and gradually progresses, reaching a maximum of 2 months or more. At the peak, about 16% of patients had a subacute onset. The main clinical manifestations are symmetrical distal or proximal weakness of the limbs, mostly from distal to proximal develop. There is generally no dysphagia, and dyspnea is even rarer. Some patients may be accompanied by autonomic nervous system dysfunction, manifesting as orthostatic hypoemia. pressure, sphincter dysfunction and arrhythmia, etc. Physical examination showed decreased muscle strength and low muscle tone in the limbs, with or without muscle atrophy, and decreased tendon reflexes in the limbs. Weakness or disappearance, peripheral sensory loss or disappearance in the limbs, tenderness in the bowel muscles, and positive Kern ig sign. 【Auxiliary inspection】 1. In cerebrospinal fluid examination, 80% to 90% of patients have cerebrospinal fluid protein-cell separation, and the protein content fluctuates between 0.75 and 2 g/L. There is a positive correlation between the severity of the disease and the protein content of cerebrospinal fluid. A small number of CID P patients have normal protein content, and some patients have positive oligoclonal bands. 2. Electrophysiological examination and electrophysiological manifestations include slowing down of peripheral nerve conduction velocity, conduction block and abnormal waveform dispersion. Early line EM G The examination showed slowed nerve conduction velocity and prolonged F wave latency, suggesting demyelinating disease. 3. Biopsy of the intestinal nerve shows "onion-like" changes formed by repeated segmental demyelination and regeneration, which is highly suggestive of CID P 【diagnosis】 The diagnosis of CID P is still a diagnosis of exclusion. This disease can be considered if the following conditions are met: ① The symptoms progress for more than 8 weeks, and the symptoms progress chronically. ② The clinical manifestations are varying degrees of limb weakness, most of which are symmetrical, and a few are asymmetrical, both proximal and distal. Involved, tendon reflexes in the limbs are weakened or disappeared, accompanied by deep and superficial sensory abnormalities: ③ cerebrospinal fluid protein-cell separation: ④ Electrophysiological examination indicates peripheral Slowed nerve conduction velocity, conduction block, or abnormal waveform dispersion; 5 peripheral neuropathy caused by other causes is excluded; glucocorticoid treatment Treatment is effective 【Differential Diagnosis】 Pay attention to the identification of the following diseases 1. Multifocal motor neuropathy (MM N) mainly affects motor nerve terminals

405 Chapter 17 peripheral nerve disease Progressive peripheral neuropathy, clinically manifested as chronic asymmetric distal limb weakness, mainly in the upper limbs, with normal sensation 2. Progressive spinal muscular atrophy (P SMA) is also a slowly progressive disease. However, the distribution of movement disorders is asymmetric, with muscle fascicles trembling, but no sensory impairment. Nerve electrophysiology showed normal NCS, and EMG showed extensive nerve sources. sexual harm. 3． Hereditary motor and sensory neuropathy (HMS N) manifests as many Idiopathic sensorimotor peripheral neuropathy generally has a genetic family history and is often associated with hand and foot deformities. Diagnosis requires genetic testing, if necessary Perform a nerve biopsy. 4. About 1/4 of other CID P patients may be accompanied by connective tissue disease or other diseases, such as systemic lupus erythematosus, vasculitis, and Sjogren's disease syndrome, paraproteinemia, lymphoma, etc. For patients with CID P manifestations, M protein measurement should be routinely performed. Should we be frightened by blood at the same time? Differentiating between disease, chronic metabolic neuropathy and diabetic peripheral neuropathy 【treat】 1. Glucocorticoids are the preferred treatment for CID P. Methylprednisolone 500-1000 mg/d, intravenous infusion, gradually increase after 3-5 days Reduce the dosage or directly switch to oral prednisone 1 mg/(kg·d), take it once in the morning, maintain it for 1 to 2 months and then gradually reduce the dosage; or dexamethasone 10~ 20 mg/d, intravenous infusion, for 7 consecutive days, then changed to prednisone 1 mg/(kg·d), taken as a quick meal in the morning, maintained for 1 to 2 months and then gradually reduced; Prednisone 1 mg/(kg·d) can also be taken orally directly. Take it once in the morning, maintain it for 1 to 2 months and then gradually reduce the dose. Oral prednisone for the above treatments The dose should be reduced to a low dose (5 to 10 mg) and maintained for more than half a year before stopping the drug due to enzyme conditions. 2. Plasma exchange (PE) and intravenous immunoglobulin (I VIG) PE are administered 3 to 5 times per course, with an interval of 2 to 3 days, each time The exchange volume is 30 ml/kg, and one course of treatment is carried out every month. About half of the patients are effectively treated with high-dose I VIG, generally 0.4 g of I VIG is used (kg·d), 3 to 5 consecutive days constitute a course of treatment. Repeat once a month for 3 consecutive months. The number of applications can be extended if conditions or illness require it. moon. It should be noted that PE treatment cannot be performed within 3 weeks after application of IVIG. 3. For those who have unsatisfactory results from the above treatments, or who develop hormone dependence or hormone intolerance, immunosuppressants such as cyclophosphamide and sulfate can be tried. Azole bleach, cyclosporine A, methotrexate, etc. The most commonly used clinical method is thiazoline, and the usage method is 1 to 3 mg/(kg, d), divided into 2 to 3 times. Oral administration. 4. Neuronutrition B vitamins can be used for treatment, including vitamin B, vitamin B, vitamin B, vitamin B, etc. 5. Symptomatic treatment For those with neuralgia, carbamazepine, amitriptyline, tramadol, gabapentin, pregabalin, etc. can be used 6. Rehabilitation treatment After the condition is stable, formal neurological rehabilitation exercises should be carried out early to prevent disuse of muscle atrophy and joint shrinkage. 【Prognosis】 About 10% of CID P patients died 2 to 19 years after onset due to various complications, and only 4% fully recovered, with relatively low neurological symptoms. Mild, about 60% of the cases are able to live and work normally, 8% are unable to work and live normally, and 8% are bedridden or need to rely on a wheelchair. Accounted for 18%. (Xiao Bo) Thinking questions 1. What is the definition of peripheral nerves? 2. What are the clinical manifestations of trigeminal neuralgia and how to choose drug treatment? 3. What are the common causes of polyneuropathy? 4. Diagnostic criteria and treatment principles of Guillain-Barré syndrome. 5. How is chronic inflammatory demyelinating polyradiculoneuropathy diagnosed and what diseases need to be differentiated from it? 6. Briefly describe the treatment principles of chronic inflammatory demyelinating polyradiculoneuropathy. references [1] Neuromuscular Disease Group, Neurology Branch, Chinese Medical Association, Electromyography and Clinical Neuroelectrophysiology Group, Neurology Branch, Chinese Medical Association, China Neuroimmunology Group of the Neurology Branch of the Chinese Medical Association. Guidelines for Diagnosis and Treatment of Guillain-Barré Syndrome in China. Chinese Journal of Neurology, 2010, 43: 583-586