Disease name:
Introduction:
Multiple sclerosis (MS) is an autoimmune disease characterized by demyelinating white matter of the central nervous system (CNS) and genetically susceptible individuals and environmental factors. MS is the most common and most common disease in the central nervous system demyelinating disease. It is more common in young and middle-aged patients. The clinical features are widespread spread of lesions. The brain, spinal cord and optic nerve damage are often relieved during the course of the disease.
Cause:
(1) Causes of the disease
In the initial description of MS, the cause was classified as inhibition of sweat glands. There were multiple speculations about the cause of MS at the time. Many of the early theories are ridiculous now. Although the exact cause of MS is not yet certain, a large number of epidemiological data that are clearly identified are consistent with the hypothesis of the following etiology.
1. Genetic factors MS is known to have a family predisposition. About 15% of MS patients have at least one relative who is sick and has the highest recurrence rate (5%) in the patient's siblings. About 20% of the probands have at least one affected relative, of which the patient has the highest risk.
2. Epidemiological data on infection and immune factors reveals the relationship between MS and some environmental factors, indicating that certain environmental factors encountered during childhood may induce morbidity or become the cause of morbidity after several years of incubation. In recent years, it has been increasingly recognized that this environmental factor is an infection, presumably a viral infection. A large number of indirect facts support this view. MS patients have been shown to produce humoral and cell-mediated immune changes to viral infections. However, despite a great deal of effort, no virus has been isolated from MS patient tissues (including various human T-lymphocyte retroviruses), and there is no satisfactory experimental model for virus-infected MS animals. However, the fact that retroviruses cause typical tropical paralysis and successful use of transgenic mice that express T-cell receptors that bind to basic myelin proteins to make experimental models of demyelinating diseases The study of the etiology of viral infection as a MS continues to deepen.
If the viral infection is indeed the primary cause of MS, then some secondary factors must play a role in the later life to activate the nervous system lesions or cause deterioration. The most popular view is that this secondary mechanism is an autoimmune response characterized by attacking certain components of the myelin, severely destroying all nerve fibers including axons. There are several theories that support this view. For example, it has been found that MS lesions are roughly similar to those of disseminated encephalomyelitis, while the latter is almost certainly a delayed allergic autoimmune disease (see below); it has been found in serum and cerebrospinal fluid of MS patients. Specific antibodies such as basic myelin protein (MBP). These antibodies act on MB and other intact myelin phospholipid proteins with the involvement of T cells; these antibody activities increase with disease activity. In addition, MBP interacts with mumps virus antibodies. Viral infection in susceptible populations is the initial process of MS, and this theory is more convincing than the theory that chronic viruses persist.
How body fluids and cytokines cause MS plaques remains unclear. Evidence for humoral immunity is evidenced by the presence of oligoclonal immunoglobulins in CSF in most patients, the latter being the product of B-lymphocytes in the cerebrospinal fluid.
(two) pathogenesis
1. The molecular mimicry theory of viral infection and autoimmune reaction suggests that the virus infected by the patient may have a common antigen with the CNS myelin protein or oligodendrocytes, ie, the viral amino acid sequence and the neuromyelin component of MBP. The amino acid sequences of a certain polypeptide are identical or very similar. It is speculated that activation of T cells in vivo and production of antiviral antibodies after viral infection can cross-react with the myelin polypeptide fragments, leading to demyelinating lesions.
Johnson suggested that the autoimmune response of the nervous system caused by viral infection is related to the abnormal expression of autoantigen in CNS cells. He found that several different viruses (measles, rubella, varicella) can cause T cells to respond to autoimmune responses to basic myelin proteins. This means that T cells recognize identifiable structures on the virus and myelin. Once in childhood, this autoimmune response is triggered by a virus that can later be reactivated by any common virus, which is more pronounced in the higher north-south latitudes. This molecular similarity (the virus has the same antigen as the CNS myelin or oligodendrocytes) is the pathogenesis of several diseases, such as rheumatic fever and the Guillain-Barré syndrome, which is highly valued in theory.
Supporting MS as a classic experiment of autoimmune diseases, immunizing Lewis rats with myelin antigen, such as myelin basic protein (MBP), can cause experimental autoimmune encephalomyelitis in experimental animal models of MS (experimental autoimmune) Encephalomyelitis, EAE). Moreover, transduction of a sensitized cell line that recognizes an MBP polypeptide fragment in an EAE rat to a normal rat can also cause EAE, demonstrating that MS is a T cell mediated autoimmune disease.
Tissue damage and neurological symptoms of MS are thought to be caused by an immune response directed against the myelin antigen. Viral infection or other stimulating factors can cause T cells and antibodies to enter the CNS by destroying the blood-brain barrier, leading to increased expression of cell adhesion molecules, matrix metalloproteinases, and pro-inflammatory cytokines, which together act to attract other immune cells and break down cells. The outer matrix facilitates the migration of immune cells and activates autoimmune responses against autoantigens such as MBP, myelin-binding glycoprotein (MAG), oligodendrocyte glycoprotein (MOG) and lipid-containing protein (PLP), αB- Crystalline protein (αB-crystallin), phosphodiesterase and S-100. The binding of these target antigens to antigen-presenting cells triggers autoimmune responses that may be involved in cytokines, macrophages, and complement, particularly helper T cell type 1 (Th1) cytokines such as IL-2 and IFN-γ. Related to the onset of MS. Because the immune attack can exfoliate the myelin, the nerve conduction velocity is slowed down and the neurological symptoms are caused.
2. Genetic factors MS genetic susceptibility may be determined by the interaction of most weakly acting genes to determine the risk of MS. Information on genetics comes mainly from studies of twins. One of the most detailed studies reported that there were 12 (34%) pairs of 35 pairs of twins confirmed by MS, and only 2 pairs (4%) of 49 pairs of twins. There are two pairs of clinically normal single-oval twins, and MRI shows lesions. In a family with more than one member of the disease, no genetic pattern was found. In most cases, the high incidence of a disease in a family is considered hereditary, but sometimes it may only reflect that several members of the same family are exposed to a common environmental factor under the same conditions.
Some tissue-associated antigens (HLA) have been found to be more common in MS patients, suggesting a genetic role for the pathogenic role of MS. Closer is the DR site on chromosome 6. HLA antigens are abundantly present in MS (HLA-DR2) and rare HLA-DR3, HLA-B7 and HLA-A3 are considered to be markers of MS susceptibility genes. If one body carries one of these antigens, the susceptibility to MS increases by a factor of three to five. These antigens have been shown to be involved in the pathogenesis of MS, but their exact role is poorly understood.
3. Pathological changes The appearance of the brain is generally normal, but the surface of the spinal cord may be uneven. The brain and spinal cord sections showed a large number of white matter lesions scattered and slightly depressed, and starred pink due to loss of myelin. The lesions range in size from 1 mm to several centimeters; these lesions are located in the white matter of the brain and spinal cord and do not exceed the entry zone of the spinal nerves and cranial nerve roots. Because of its obvious outline, French pathologists call it a hardened plaque.
The distribution of lesions has a certain regularity, and the lesions are mostly located around the ventricles, especially in the subventricular zone around the ventricles (mainly near the ventricle and the lateral ventricle). Other vulnerable structures are the optic nerve and optic chiasm (but rarely affecting the optic tract), and the soft veins of the spinal cord are adjacent to the white matter. The lesions are randomly distributed in the brainstem, spinal cord, and cerebellar arm without being biased toward a certain fiber. In the cerebral cortex, central nucleus and spinal cord structure, the lesion destroys the myelin sheath but the nerve cells remain relatively intact.
The manifestation of the histology of the lesion depends on the time of the lesion. Relatively new lesions are composed of a number of focal demyelinating regions located around the vein. Some or all of the myelin sheath in the lesion area is destroyed or lost, while the axons are relatively retained. There are varying degrees of oligodendrocyte degeneration, glial cell responses (stellate cells) and perivascular, paramembrane mononuclear cells and lymphocytes. In the later stage, a large number of small colloidal phagocytic cells (macrophages) infiltrated, and the volume of astrocytes in and around the lesion increased and the number increased. On the other hand, the old lesions are composed of densely thickened glial plaques, and lymphoid and macrophages are occasionally visible around the blood vessels; the axons are still relatively intact. The retention of axons prevents Wallerian degeneration. Undiminished axons produce partial remyelination, a histological cause of "shadow repair" of imaging demyelinating spots. Shape, size, and histology were seen throughout the clinical course to alter both old and new lesions.
symptom:
The majority of lesions scattered in the central nervous system and the remission of recurrence in the course of the disease, the spatial multiple of symptoms and signs and the multiple duration of the disease constitute the main clinical features of MS.
MS can be acute, subacute or chronic onset. MS patients in China have more acute or subacute onset, and MS has complicated clinical manifestations.
1. First symptoms include one or more limbs with local numbness, tingling or single limb instability, single eye sudden vision loss or blurred vision (opic neuritis), diplopia, balance disorder, bladder dysfunction (urgency or Some patients have acute or progressive progression of spastic paraplegia and loss of sensation. These symptoms usually last for a short period of time and disappear after a few days or weeks, but some residual signs can still be found after careful examination.
2. After the first onset, there may be several months or years of remission, and new symptoms or recurrence of the original symptoms may occur. Infection can cause recurrence, and women are more likely to relapse about 3 months after delivery. The increase in body temperature can temporarily worsen the stable condition. The number of relapses can be as many as 10 times or more. After multiple recurrences and incomplete remission, the patient's weakness, stiffness, sensory disturbance, limb instability, visual impairment and urinary incontinence can be heavier and heavier.
3. Clinical common symptoms and signs MS patients with more signs than symptoms are important clinical features, the patient complained of one side of lower limb weakness, gait instability and numbness, but may find bilateral pyramidal tract signs or Babinski sign. The coexistence of nystagmus and internuclear ophthalmoplegia is indicated as a brainstem lesion and is a two-symptom of MS.
(1) Limbs are more common, and common asymmetry is mild and paraplegic, showing weakness or heavy feeling of lower limbs.
(2) About half of the cases can be seen with visual impairment, starting from one side and invading the other side at intervals, or two eyes are involved in a short time. The onset is more urgent, often with multiple remissions - recurrence, which can begin to recover after a few weeks.
(3) The nystagmus is mostly horizontal or horizontal plus rotation, and diplopia accounts for about 1/3. Invasion of the medial longitudinal bundle causes internuclear ophthalmoplegia, invasion of the anterior reticular formation (PPRF) leads to a semi-syndromic; other cranial nerve involvement is rare, such as central or peripheral facial paralysis, deafness, tinnitus, dizziness, biting Weak muscles, dysarthria, and difficulty swallowing.
(4) More than half of patients have sensory disturbances, including deep sensory disturbances and Romberg signs.
(5) Ataxia is seen in about half of the cases, but Charcot's three main signs (eye, intentional tremor, and sinusoidal language) are only found in some patients with advanced MS.
(6) Neurophysiological examination confirmed that MS can be combined with peripheral nerve damage (such as polyneuropathy, multiple mononeuropathy), may be due to peripheral nerve P1 protein and the central nervous system MBP as the same component, both demyelination To.
(7) There may be pathological emotions such as euphoria and excitement. Most cases show depression and irritability, as well as mental disorders such as apathy, lethargy, strong crying, slow response, repeated language, suspicion and persecution.
Optic atrophy, nystagmus, and dysarthria are often found in advanced case examinations, and pyramidal tract signs, sensations, or cerebellar signs may occur in some or all of the limbs. It has been confirmed that certain symptoms are extremely rare in MS, such as aphasia, hemianopia, extrapyramidal dyskinesia, severe muscle atrophy, and fasciculation, which are often used as exclusion criteria for MS.
4. In addition to the above mentioned neurological deficit symptoms, the paroxysmal symptoms of MS can not be ignored. For example, the Lhermitte sign is an abnormal acupuncture-like pain when the neck is excessively flexed, and is released from the neck along the spine to the thigh or foot, which is a sign of cervical spinal cord involvement. Posterior optic neuritis and transverse myelitis are usually seen as manifestations of MS onset, as well as common painful seizures, anterior flash, tonic seizures, paroxysmal itching, extensive facial muscle twitching, dysarthria, and total Loss of relief and so on. However, these rarely appear as first-episode symptoms, and tend to re-emerge frequently in a fixed pattern for days, weeks, or longer, and can be completely relieved. Some cases of MS with rare or unconventional onset often make diagnosis difficult, such as typical trigeminal neuralgia in young patients, especially bilateral should be highly suspected of MS.
5. Two special syndromes of optic neuromyelitis and transverse myelitis are the most typical pathogenesis of MS and a specific basis for establishing MS diagnosis. Of course, the above syndrome can itself be an independent disease, and the diagnosis of MS can only be hypothesized for a period of time.
(1) Optic neuritis: About 25% of MS patients (with a larger proportion of children) or optic neuritis are the first symptoms. It is characterized by acute development, with partial or total blindness in a single eye for hours or days. Some patients have periorbital pain 1 to 2 days before vision loss, and the pain can be aggravated by eye movement or touching the eyeball. A small number of patients with visual loss develop progressively within a few months, similar to the performance of oppressive lesions or optic nerve intrinsic tumors. Dark spots and blind spots (eccentricity) in the macula are often found. Other fields of vision defects are also common, and may even be hemianopia and blindness of the same quadrant. In some cases, bilateral optic nerve involvement is occurring at the same time or within a few days or weeks. One in eight patients will re-send. About half of the patients have optic disc swelling and edema (opic discitis). The presence or absence of optic discitis depends on the distance of the demyelinating lesion from the optic disc. Optic discitis and optic disc edema due to increased intracranial pressure, the former often manifests as severe and sudden loss of vision. The optic nerve is actually part of the brain's conduction beam. Optic nerve involvement is consistent with the principle that MS only infringes on CNS.
About one-third of patients with optic neuritis recover completely, and most of the rest can be significantly improved even with severe vision loss and pale optic disc. Color vision disorders often persist. Vision improvement is generally 2 weeks after onset, or shortly after corticosteroid therapy. Once the neurological function begins to improve, it will continue to improve within a few months.
1/2 or more patients with simple optic neuritis eventually develop other symptoms and signs of MS. If the first optic neuritis occurs in childhood, the risk of developing MS is lowest (indicating that some types of disease occur in childhood). In a prospective survey, Rizzo and Lessel found that 74% of women and 34% of men developed MS after 15 years of vision loss. The longer the observation time, the more detailed the inspection, the higher the proportion of the final development into MS. Most of the other symptoms appear within 5 years of the first episode. In fact, many patients with clinical optic neuritis, MRI found MS lesions in the white matter of the brain, indicating that asymptomatic disseminated lesions already exist.
Whether or not simple optic neuritis is not accompanied by other demyelinating evidence is a localized MS or another disease process is still controversial. The pathological basis of common optic neuritis is demyelinating changes. Vasculitis injury or compression of the optic nerve by tumors, cysticercosis rarely causes central or eccentric blind spots.
(2) Acute transverse myelitis: a common acute inflammatory demyelinating disease involving spinal cord involvement, whether it is a single acute course or a chronic (multiple) course type, which is considered a manifestation of MS in most cases. form. In this sense, spinal cord lesions and optic neuritis are equivalent. The use of transverse to describe myelitis is inaccurate, meaning that the structure of the cross-section of the spinal cord is involved, generally with a short range of influence on the vertical axis. But in most cases, the symptoms of the spinal cord are asymmetrical and incomplete.
The clinical features of the disease are rapid paralysis of the lower extremities, sensory plane of the trunk, sphincter dysfunction, and pyramidal tract signs. CSF is moderately elevated in lymphocytes and elevated in protein, but cerebrospinal fluid can be normal in the early stages of the disease. One-third of patients have a history of infectious diseases within a few weeks before onset, which is mostly a single-phase demyelinating disease caused by infection. Less than half of the patients had other neurological asymptomatic lesions at the same time as the spinal cord, or found to have diffuse clinical symptoms within 5 years. Therefore, acute transverse myelitis is less associated with optic neuritis than MS. Another view is that most transverse myelitis develops into MS, and this relationship can only be discovered by long-term follow-up.
In the same site of recurrent myelitis, patients with demyelinating lesions in other sites were not noticed by careful MRI. In some cases, oligoclonal bands appeared even in the cerebrospinal fluid. This situation is not uncommon in clinical practice. Most people agree that this is a localized, recurrent spinal cord MS. It is worth mentioning that simple recurrent myelitis is occasionally accompanied by lupus erythematosus with connective tissue disease, antiphospholipid antibody syndrome or other autoantibodies. Similarly, optic neuritis also has multiple recurrences that are confined to the optic nerve.
Once the diagnosis of MS is established, several clinical syndromes can be found to occur regularly. About 1/2 of the patients are mixed or systemic, with clinical manifestations of symptoms and signs of optic nerve, brainstem, cerebellum, and spinal cord injury; another 30% to 40% of patients show varying degrees of spastic ataxia and extremity extremities Deep sensory impairment, basically in line with spinal cord MS. Asymmetric spastic paraparesis is the most common form of progressive MS. The cerebellum or pons of the medulla cerebellum and the total blind type each accounted for 5%. Therefore, mixed and spinal type accounts for about 80% of clinical cases.
MS patients often show mental disorders, and some cases show euphoria. More cases are characterized by depression, irritability, and temper. Other mental disorders such as retention of memory loss, generalized dementia, or mental disorder can occur regularly in the later stages of the disease. The cognitive impairment of MS is more consistent with the "subcortical dementia" described above. Frontal lobe syndrome with severe loss of will is a common feature of advanced MS. 2% to 3% of MS patients have a one-time or repeated epileptic seizure at a certain stage of their disease, which is caused by a condition in the cerebral cortex or adjacent to the cortex.
6. Other variant MS
(1) Acute multiple sclerosis: a rare malignant type of MS, manifested by the combined involvement of the brain, brainstem, and spinal cord within a few weeks, resulting in a patient with stupor, coma, or denervation, with obvious cranial and corticospinal bundles. Abnormalities, progressive development of symptoms can die within weeks or months. The autopsy found typical acute MS spots visible to the naked eye. The only difference from the general type of MS is that the majority of the sclerosing plaques are identical, and many of the venous demyelination areas around the veins are well integrated. Usually CSF cells are active (increased number of cells).
(2) Multiple sclerosis complicated with peripheral neuropathy: MS patients can be accompanied by multiple peripheral neuropathy or a variety of single neuropathy. This relationship brings some speculation and contradictions. The sporadic association of this combination suggests that MS and peripheral neuropathy may occur coincidentally, but it is difficult to explain why the latter is a very characteristic peripheral neuropathy. Both autonomic and peripheral nerves can undergo autoimmune demyelination, which occurs in the latter leading to chronic, inflammatory multiple peripheral neuropathy. Of course, root and peripheral neurological movements and/or sensory symptoms can also be caused by fibers that are involved in the spinal nerve root entry zone or in the ventral white matter of the spinal cord. In the late stage of MS, there is the possibility of suffering from vitamin-deficient peripheral neuropathy.
diagnosis:
1. The lesion has two or more objective signs of lesions such as optic nerve, spinal cord and brain stem in the white matter of the central nervous system.
2. The course of the disease is relieved and relapsed. The second episode is at least one month apart, each lasting more than 24 hours, or the stage of progression is more than half a year.
3. The onset age is between 10 and 50 years old.
4. Exclusion of other causes such as brain tumor, cerebrovascular disease, cervical spondylosis, etc.
If all four criteria are available, they can be diagnosed as “clinical diagnosis”; if one or two are missing, the diagnosis “clinical may be multiple sclerosis”; if only one predileous site occurs for the first time, it can only be used as “ Clinically suspicious." Increased IgG index in other cerebrospinal fluids, the appearance of IgG monoclonal bands, serum antiphospholipid antibody positive, liver disease necrosis factor activity, and myelin basic protein increase can be used as a reference.
Identification
MS is often identified with the following diseases:
1. Disseminated encephalomyelitis is an acute disease with extensive scattered lesions, which is self-limiting and mostly a single disease course. In addition, the disease often has fever, stupor and coma, and these features are rare in MS.
2. Systemic lupus erythematosus and other rare autoimmune diseases (mixed connective tissue disease, Sjogren's syndrome, hard skin sign, primary biliary cirrhosis) There may be multiple lesions in the CNS white matter. The CNS damage of these diseases is parallel to the activity of a potential immune disease or the level of autoantibodies such as against their own DNA or phospholipids. There are many other systemic lesions that have been or have been combined, but there are also examples of demyelination or cerebral hemisphere lesions that precede other systemic organs. 5% to 10% of MS patients carry anti-nuclear or anti-double-stranded DNA antibodies without lupus or other systemic damage.
In addition, it has been pointed out that the prevalence of various autoimmune diseases in relatives of MS patients is higher than expected. This suggests an unproven link between MS and autoimmune disease. The lesions of lupus erythematosus on MRI are very similar to sclerosing plaques. The optic nerve and myelin sheath can be involved, and can even be repeated continuously, much like MS, but the pathology is small area vasculitis or embolization caused by small area of infarct necrosis. Instead of demyelinating inflammatory, individual inflammatory demyelinating lesions can be seen without vascular changes. It is currently considered that the above-mentioned similar MS condition is regarded as a specific manifestation of lupus erythematosus or related diseases.
3.Behcet disease Recurrent iridocyclitis, meningitis, mucosa and genital ulcers; joint, kidney, lung symptoms and multiple brain lesions are identified.
4. Spinal cord compression simple spinal cord MS is often accompanied by varying degrees of posterior cord involvement. The diagnosis of simple spinal cord MS with progressive spastic paraplegia is particularly difficult. As mentioned above, spinal cord MS is particularly prone to affect older women, and this situation should be carefully excluded from spinal cord compression due to tumor or cervical joint disease. Root pain during a certain period of time is often a manifestation of spinal cord compression, which is rare in MS. Neck pain, limited mobility, and severe muscle atrophy caused by nerve root involvement can be seen in spondyloarthropathy and MS rarely has the above symptoms. As a general rule, abdominal reflexes disappear in the early stage of demyelinating myelopathy, impotence and bladder dysfunction occur in men, and in the cases of cervical joint hyperplasia, the above symptoms appear in the late stage, or do not appear at all. The CSF protein content can be significantly increased in the spinal cord compression sign. However, there are no abnormalities of other MS-specific proteins. The most valuable method of identification is MRI and CT spinal cord imaging. Any neurological signs are limited to progressive spastic paraplegia of the spinal cord, and spinal cord imaging should be performed.
5. Skull base depression and flat skull base This patient has a short neck, and radiological examination can confirm the diagnosis. Neurological syndromes caused by malformation of the skull base and skull holes, cerebellopontine angles, slopes, and other posterior fossa tumors can also be misdiagnosed as MS. In the above situation, an isolated and special lesion can cause neurological symptoms and signs of the brain stem, cerebellum, posterior group and upper cervical spinal cord, and is easily considered as a disseminated lesion. If all of the patient's symptoms and signs can be explained by a lesion in a certain area of the nerve axis, MS should not be diagnosed, which is a clinical rule.
6. Hereditary ataxia Occasionally MS can be confused with hereditary ataxia. The latter often has a family history and its associated genetic traits, with occult onset, chronic persistent progression, and a symmetrical and specific clinical approach. Abdominal wall reflexes and sphincter function, arched foot, posterior scoliosis, and heart disease are some of the common features that support hereditary diseases.
7. Posterior optic neuritis Posterior optic neuritis is the simultaneous onset of both eyes, manifested as a sharp decline in vision, accompanied by eye pain, no symptoms and signs of central nervous system damage, as well as visual papilledema, generally no recurrence after healing . MS often invades the optic nerve during the course of the disease, leading to visual impairment. Early is easy to be confused with simple posterior optic neuritis. Most scholars believe that 25% to 35% of optic neuritis can develop into MS. However, optic neuritis often damages the monocular, often accompanied by central dark spots plus peripheral visual field defects, and there is no remission in the course of the disease. MS often suffers from both eyes, with few central dark spots, with obvious relief and recurrence.
As mentioned earlier, the widespread use of evoked potentials, oligoclonal bands in CSF, and MRI expands the diagnostic criteria for MS. These tests often reveal the presence of multiple sclerotic plaques that are undetectable by clinical examination. Diagnosing MS requires the requirement of "multiple time and space" evidence, and has gone through the test of time and is still valid today. But the difference is that the evidence is no longer just pure clinical findings, but also includes some laboratory findings. It should be noted that no laboratory test can be considered as a credible indicator of MS alone.
complication:
1. Urinary dysfunction in different stages of multiple sclerosis, if the bilateral pyramidal tract is damaged, it is easy to bring urinary dysfunction. In the early stage, the nerve function was suddenly damaged, and the urine could not be discharged smoothly, resulting in retention of urine. In the later stage, a neurogenic bladder is formed, and urgency, frequent urination, overflow of urine, and residual urine in the bladder increase. In both cases, it is easy to cause urinary tract infection.
2. Spastic spasm is a prominent feature of central nervous system damage in patients with multiple sclerosis. Due to the loss of control of upper motor neurons, lower neurons are hyperfunctioning, muscle tension is increased, often accompanied by muscle weakness, and patient activity is limited. . Muscle spasm in the throat forms pseudo-ball paralysis, difficulty in swallowing, drinking water, and speaking is not fluent. The presence of double upper limb paralysis makes the hand activity inflexible. Both lower extremity paralysis, patients have more balance disorders, gait instability, easy to fall to injury.
3. Paroxysmal symptoms, painful tonic spasm, skin burning and pain. It is thought to be caused by a short circuit between the nerves leading to the loss of myelin. The lesion occurs in the upper cervical spinal cord, and the sympathetic nerve center is stimulated to cause sweating of the hands and feet. When the nerves are damaged, the hands and feet are dry and sweat-free.
4. Depression Because the pathological process of multiple sclerosis can cause psychological problems, the disability of the disease makes the patient's movement disorder, limits their activities, is isolated from the society, and gradually develops neuropsychological defects and depression. Recommendation: Correct treatment of illness, early recurrence, neurological function is not affected, patients should get out of bed as soon as possible, and actively participate in social activities and family labor. Patients with limited mobility, if they have residual limb function, should also actively perform functional exercise to enhance self-confidence. Patients with more obvious effects can use antidepressants under the guidance of a doctor.
5. If hemorrhoids damage occurs in the hemorrhoids, the patient has paraplegia below the level of the lesion, prolonged bed rest, poor dysfunction of the blood circulation, lack of nutrition, and the skin is easily crushed to form hemorrhoids, which is difficult to heal.
treatment:
Western medicine treatment
Most of the treatment experiments in recent years have been based on anti-inflammatory and immunosuppressive drugs. Clinically controlled studies have shown that only corticotropin (Adrenocorticotropic hormone),Methylprednisolone(methylprednisolone),Prednisone(prednisone),CyclophosphamideAnd interferon (--interferonIt works well for improving clinical and MRI lesions. With the intervention of anti-inflammatory factors, patients recover faster from each episode. However, in acute malignant MS, anti-inflammatory treatment is ineffective in most patients; the efficacy of a small number of patients can only be maintained for more than one month. It has not been proven that steroid hormones can shorten the entire course of the disease, or can prevent recurrence, so its long-term efficacy is difficult to determine.
1. Corticosteroids For the application of corticosteroids, the first large dose is crucial. Intravenous administration of large doses of methylprednisolone (methylprednisolone) (500 mg / d, 3 to 5 days), after oral administration of a larger dose of prednisone (prednisone) can effectively alleviate acute or subacute MS and optic nerve Inflammation can shorten the course of the disease. If you can not use intravenous methylprednisolone (methylprednisolone), you can use oral prednisone (prednisone) instead, starting from 60 ~ 80mg / d, this can avoid hospitalization. For severe attacks, especially myelitis responds more quickly to large doses of intravenous medication.
Beck et al. cautioned in the clinical treatment report of optic neuritis: avoid oral administration in the treatment of acute optic neuritis. A randomized, controlled study of 457 patients with optic neuritis found intravenous injection of methylprednisolone (methylprednisolone) followed by oral prednisone (prednisone), although at 6 months compared with placebo Big, but it does accelerate the recovery of vision. However, treatment with oral (prednisone) alone increases the risk of recurrent optic neuritis. The efficacy of intrathecal injection of prednisolone (prednisolone) is highly controversial and is generally not recommended.
It is recommended to limit the treatment of corticosteroids to 3 weeks, and if the symptoms are repeated, the process of reducing the weight will be extended. This short-term corticosteroid treatment has fewer side effects, but some patients may have insomnia, and some may have symptoms of depression or mania. Patients who have been treated for more than a few weeks are prone to hypertension, hyperglycemia and loss of diabetes, osteoporosis, aseptic necrosis of the hip, cataracts and rare gastrointestinal bleeding, active tuberculosis. Proper potassium supplementation is necessary. The authors believe that steroid hormone therapy is not a great benefit, and short-term daily high-dose shock therapy can prevent some patients from recurrence, so hormone tolerance is better than long-term oral medication.
2. Immunomodulatory drugs have tried a variety of immunomodulatory drugs, only a few drugs such as azathioprine and cyclophosphamide are effective, and the administration of systemic lymphatic radiation therapy to a small number of patients seems to improve some conditions. These treatments can improve clinical symptoms and support the mechanism of CNS damage in MS is the doctrine of autoimmune processes. However, the dangers of long-term immunosuppressive drug applications, such as cancer, have greatly limited the widespread use of such drugs. In the UK and the NetherlandsAzathioprinetreatmentMultiple sclerosisA detailed experimental study showed that the drug had no significant effect on MS. According to a MS research team, after two years of chronic and advanced disease, prednisone (prednisone) and cyclophosphamide treatment can delay the deterioration of the disease, they also pointed out that this treatment should bring patients The burden and potential toxic effects. At least one double-blind, placebo-controlled study showed no effect of cyclophosphamide.
There are two new treatments that promise to change the natural course of MS. Initial clinical trials have shown that subcutaneous injection of interferon (beta-interferon) can reduce the frequency and severity of MS recurrence and reduce the number of MS lesions. There is evidence that interferon (beta-interferon) reduces demyelination in the cerebral hemisphere. Whether the drug can suppress the progression of neurological dysfunction needs further verification. However, the clinical efficacy is not exciting. Bornstein et al also reported that MBP multimers and complex multimer I (Cop I) are effective for relapsing-remitting MS. This drug is still subject to FAD approval. Experiments on desensitization of myelin by oral bovine myelin have not been concluded.
3. Others There is no reliable controlled study of whether a low-fat, gluten-free diet or supplemental flaxseed has a therapeutic value for MS. The significance of synthetic peptides and hyperbaric oxygen therapy is not clear. Plasmapheresis may have an effect on fulminant acute patients, but there are still rigorous trials that are not effective in chronic cases.
4. General treatment general measures include ensuring proper bed rest time, avoiding excessive fatigue and reducing infection, and seeking maximum recovery from the first time or worsening of the condition. Use possible rehabilitation measures (such as pull belts, wheelchairs, slides, elevators, etc.) to minimize the bedtime of the disease. Careful care, use of changing pressure mattresses, silicone pads and other special equipment to prevent bed sore acne. Fatigue is a common complaint in MS patients, especially during acute attacks.Amantadine(100mg morning and evening) or pemoline (20-75mg once a day) can alleviate fatigue symptoms.
Bladder dysfunction is a more difficult problem to treat. The main symptom is urinary retention, which may be helpful in clofibrate. In the case of urinary retention, the residual urine volume should be monitored to avoid infection, and the residual urine volume should not exceed 100 ml. Another common problem is urgency, frequent urination (bladder spasm). Bromopropylamine (bromoquinone bromide, profenozin) orOxibutin(Urine, chlorinated, Ditropan) can relax the detrusor to alleviate this symptom, these drugs are best used intermittently. Intermittent catheterization is essential for patients with severe bladder dysfunction, especially urinary retention. Patients can learn to catheterize themselves, reducing the risk of infection by retaining the catheter. For severe constipation, it is best to enema. Regular rectal training helps to keep the stool smooth.
For patients with severe spastic paraplegia and painful flexion of the lower extremities, as well as other paralysis, intrathecal injection through a retention tube or burial pumpBaclofen(Bachlorophenol) has a certain effect. Mild warts can be taken orally with baclofen. When the above methods are ineffective, surgical methods such as dorsal spinal nerve rootectomy, spinal cordectomy, and obturator nerve compression can alleviate symptoms for a long time.
A very severe, disabling tremor induced by mild movement of the lower extremities is feasible for ventrolateral resection of the thalamus. Carbamazepine,Clonazepam(clodroxetine) also has a certain effect on this symptom.
The understanding and compassion of the doctor is crucial to the treatment of MS patients. Patients should be advised on issues of concern in daily life, marriage, pregnancy, drug use, vaccination, etc. Do not tell the patient a possible diagnosis of “multiple sclerosis” until a positive diagnosis. Once the diagnosis is established, the patient should be given a balanced explanation that emphasizes the optimistic aspects of the disease.
prevention:
In daily life, patients with multiple sclerosis are treated according to their daily work and learning needs, and they are arranged in order to prevent and regulate them:
1. First of all, pay attention to saving physical fitness. Patients should have a schedule every day, and arrange their daily life or work, including the order, in order to save physical fitness. Some jobs must be done on the same day, and those that can be slowed down can be postponed until tomorrow or the day after tomorrow. Some things don't have to be done every day. They can't be extended for a long time. When and how to do it should never cause fatigue and energy conservation. What a person can't do or can barely accomplish, it is best to have someone else help to complete, to avoid excessive consumption of physical fitness. For example, when preparing three meals, you can collect all the ingredients you need in advance, put them in a position that you can reach them, and then sit in the position, and strive to complete the flow from the raw materials to the finished product line. When washing and drying clothes, don't have to do too much at one time. When ironing, you can sit in the seat.
2. Multiple sclerosis diet: For patients with multiple sclerosis, a balanced diet is important to maintain a good physical condition. In the past, some foreign scholars believed that inappropriate diet may be one of the causes of multiple sclerosis, such as intake of animal fat, meat products and milk. Therefore, a variety of dietary recipes have been recommended to patients to help them treat multiple sclerosis, which has proven to be ineffective. Patients should ensure a balanced diet, no picking, and multiple classes. There is evidence that cod liver oil and plant unsaturated fatty acids may have the effect of preventing recurrence of multiple sclerosis, so as with cardiovascular disease, patients are advised to take a low-fat, high-fiber diet.
3. In addition, patients with recurrent episodes often use a large number of hormone shock treatments, or with small doses of hormones, while hormones can stimulate gastric acid secretion and increase the appetite of patients, then patients should pay attention to control food intake to avoid induced obesity, leading to high Blood lipids, high blood pressure, diabetes, etc. Because gastric acid secretion increases, it has an adverse effect on the mucosa of the digestive tract, so patients should avoid eating too spicy food. Some patients need to use acid-suppressing drugs and gastric mucosal protective agents while using hormones.
简体中文