Multiple sclerosis

Introduction

Introduction to multiple sclerosis Multiple sclerosis (MS) is an autoimmune disease characterized by central nervous system (CNS) white matter demyelinating lesions, genetically susceptible individuals and environmental factors. MS is the most common and most common disease in the central nervous system demyelinating diseases. 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. basic knowledge The proportion of illness: the incidence rate is about 0.0001%-0.0002% Susceptible people: no specific population Mode of infection: non-infectious Complications: hemorrhoids urinary tract infections

Cause

Cause of multiple sclerosis

Genetic factors (35%)

MS is known to be family-oriented, with approximately 15% of MS patients having at least one relative who is ill, with the highest recurrence rate in the patient's siblings (5%), and about 20% of the probands have at least one affected relative. Among them, the patient's siblings are the most dangerous.

Infection and immune factors (30%)

Viral infection is indeed the initial cause of MS, so some secondary factors must play a role in the later life to activate the nervous system lesions or cause deterioration. The most popular opinion is that this secondary mechanism is to attack the myelin sheath. Certain components, in severe cases, destroy autoimmune responses characterized by all nerve fibers including axons, and several theories support this view.

Genetic factors (20%)

MS genetic susceptibility may be determined by the interaction of most weakly acting genes to determine the risk of MS. The genetic information is mainly from the study of twins. One of the most detailed studies reports the diagnosis of MS in 35 pairs of monozygotic twins. There are 12 (34%) pairs, only 2 pairs (4%) of the 49 pairs of double-oval twins, there are two pairs of clinically normal single-oval twins, MRI shows lesions, in families with more than one member of the disease A certain genetic pattern has not been found. In most cases, the high incidence of a disease in a family is considered to be hereditary, but sometimes it may only reflect several members of the same family and be exposed to some common under the same conditions. Environmental factors.

Pathogenesis

Some tissue-associated antigens (HLA) were found to be more common in MS patients, suggesting that the genetic factors are involved in the pathogenesis of MS, and the more closely related is the DR site on chromosome 6, and HLA antigens are abundant in MS (HLA- DR2) and rare HLA-DR3, HLA-B7 and HLA-A3 are considered to be markers of MS susceptibility genes. If one organism carries one of these antigens, the susceptibility to MS increases by 3 to 5 times. These antigens have been Proof is related to the onset of MS, but its exact role is still poorly understood.

The appearance of the brain is generally normal, but the surface of the spinal cord may be uneven, the brain and spinal cord sections appear scattered, slightly depressed, and the white pink lesions of the star pink due to the loss of myelin sheath, the lesion size ranges 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 their distinct contours, French pathologists call them sclerosing plaques.

The distribution of lesions has a certain regularity. The lesions are mostly located around the ventricles, especially in the subventricular zone around the ventricles (mainly near the ventricle and lateral ventricle). Other vulnerable structures are optic nerves and Optic chiasm (but rarely affects the optic tract), the soft vein of the spinal cord is adjacent to the white matter, and the lesion is randomly distributed in the brainstem, the spinal cord and the cerebellar arm without focusing on a certain fiber, in the cerebral cortex, the central nucleus In the group and spinal cord structure, the lesion destroys the myelin sheath but the nerve cells remain relatively intact.

The histological manifestations of the lesion depend on the time of the lesion. The relatively new lesion is composed of many focal demyelination areas around the vein. Some or all of the myelin sheath in the lesion area is destroyed or lost, while the axon is relatively retained. There are varying degrees of oligodendrocyte degeneration, glial cell reactions (stellate cells) and perivascular, paracranial mononuclear cells and lymphocytes exuding, late, a large number of small glial phagocytic cells (macrophages) Infiltration, the size of the astrocytes in and around the lesion increases, and the number increases. 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; Axons are still relatively intact, axon retention prevents Wallerian degeneration, and undamaged axons can produce partial remyelination, which is the histological cause of "shadow repair" of imaging demyelinating spots. The shape, size, and histology of the new and old lesions at various levels can be seen throughout the clinical course.

Prevention

Multiple sclerosis prevention

This disease usually occurs in people aged 25-40. It slowly evolves and may disappear for a period of time, with intermittent recurrence, and the symptoms of recurrence tend to be more severe. Stress, stress and malnutrition are likely to cause this disease. Therefore, it is especially important to prevent the recurrence of multiple sclerosis and avoid various causes.

Daily protective health measures

1 Prevention of colds and colds is a major cause of repeated illness in MS patients. Therefore, when weather changes, timely addition and subtraction of clothing to avoid exposure to influenza is particularly important. In addition, appropriate diet can be selected to prevent colds.

2 Avoid fatigue, excessive fatigue, and overload exercise is not advisable for patients with MS.

3 Avoid high temperature, avoid extremely hot water bath, or excessive warm environment, so as not to cause this disease.

Complication

Multiple sclerosis complications Complications acne urinary tract infection

1. Urinary dysfunction In the 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 is suddenly damaged, the urine can not be discharged smoothly, resulting in urinary retention, late , the formation of a neurogenic bladder, urgency, frequent urination, urine overflow, increased residual urine in the bladder, in both cases, are likely to cause urinary tract infection.

2. is a prominent feature of central nervous system damage in patients with multiple sclerosis, due to loss of control of upper motor neurons, lower neuronal function, increased muscle tone, often accompanied by muscle weakness, making patients restricted Muscle spasm in the throat area forms pseudobulbar paralysis, difficulty in swallowing, drinking water, fluent speech, and the presence of double upper limb paralysis, making hand movements inflexible, lower limb paralysis, patients with balance disorders, gait instability, It is easy to fall to the point of injury.

3. Hereditary symptoms, painful tonic spasm, skin burning pain, is considered to be caused by myelin degeneration caused by nerve conduction short circuit, the lesion occurs in the upper cervical spinal cord, the sympathetic nerve is stimulated, there may be sweating of hands and feet, subject to When the damage is broken, 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. Suggestions: Correct treatment of illness, early recurrence The neurological function is not affected. Patients should get out of bed as soon as possible, actively participate in social activities and family labor. Patients with limited activities, if they have residual limb function, should also actively perform functional exercise to enhance self-confidence and influence more obvious patients. You can use antidepressants under the guidance of a doctor.

5. Hemorrhoids If spinal cord transection injury occurs, the patient has paraplegia below the level of the lesion, prolonged bed rest, poor neurological dysfunction, poor nutrition, and lack of nutrients. After the skin is compressed, it is easy to ulcerate and form hemorrhoids, which is difficult to heal.

Symptom

Symptoms of multiple sclerosis Common symptoms Cerebral white matter degeneration Pathological laughter and crying reaction Slow twitching gait instability Distressed lips often weak but can not be demented dementia tinnitus tinnitus

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 time, 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 symptoms may occur. The infection may cause recurrence. Women may relapse more easily after 3 months of delivery, and elevated body temperature can stabilize the condition. Temporary deterioration, the number of recurrences can be as many as 10 times or more, the patient's weakness, stiffness, sensory disturbance, limb instability, visual impairment and urinary incontinence can be heavier after multiple recurrences and incomplete remission.

3. Clinical common symptoms and signs MS patients with more signs than symptoms is an important clinical feature, the patient complained of one side of the lower extremity weakness, gait instability and numbness, but may find bilateral pyramidal tract signs or Babinski signs, eyeballs The coexistence of tremor and internuclear ophthalmoplegia is indicative of a brainstem lesion and is a two-dimensional indication 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 visually impaired, starting from one side, and then invading the other side at a time, or two eyes are involved in a short period of time, the incidence is more urgent, often multiple remissions - recurrence, after several weeks Start to recover.

(3) The nystagmus is mostly horizontal or horizontal plus rotation, and the diplopia accounts for about 1/3. The lesion invades the medial longitudinal bundle and causes internuclear ophthalmoplegia. Invading the anterior reticular formation (PPRF) leads to a half syndrome. Other brain nerve involvement is rare, such as central or peripheral facial paralysis, deafness, tinnitus, dizziness, weak muscle mass, 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, 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, irritability, and also can be seen in apathy, lethargy, strong crying, slow response, repeated language, suspicion and persecution and delusion.

Opal atrophy, nystagmus and dysarthria are often found in advanced case examinations. Some or all limbs may have pyramidal tract signs, sensation or cerebellar signs. It has been confirmed that certain symptoms are extremely rare in MS, such as aphasia, hemianopia, extrapyramidal It is a dyskinesia, severe muscle atrophy and fasciculation, which can often be used as an exclusion criterion 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 abnormal acupuncture-like pain when the neck is excessively flexed, and is released from the neck along the spine to the thigh or foot. Posterior myelopathy, retrobulbar optic neuritis and transverse myelitis can usually be regarded as the performance of MS onset, but also common painful seizures of the limbs, flashes of the eyes, tonic seizures, paroxysmal itching, extensive facial muscle twitching, construction Sound disorders and ataxia, etc., but these rarely appear as first-episode symptoms, tend to re-emerge in a fixed pattern for several days, weeks or longer, and can be completely relieved, some in rare or unconventional ways Sick MS cases often make diagnosis difficult, such as typical trigeminal neuralgia in young patients, especially bilateral should be highly suspected 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. The diagnosis of MS within the time can only be assumed.

(1) Optic neuritis: About 25% of MS patients (in the case of a larger proportion of children) or optic neuritis are the first symptoms, characterized by acute development, partial or total blindness in a few hours or days, some patients in One to two days before vision loss, there is periorbital pain. Pain can be aggravated by eye movement or touching the eyeball. A small number of patients have progressive vision development within a few months. Similar to oppressive lesions or optic nerve intrinsic tumors, macular spots are often found. Area dark spots and blind spots (eccentricity), other common field defects are also common, even hemianopia, blindness of the same quadrant, some cases of bilateral optic nerve involvement at the same time or days or weeks, 1 / 8 of the patients will Recurrence, about half of patients have optic disc swelling, edema (opic discitis), optic discitis depends on the distance of demyelinating lesions from the optic disc, optic discitis and optic disc edema due to increased intracranial pressure, the former Often manifested 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 invades the CNS.

About one-third of patients with optic neuritis recover completely, and most of the remaining patients can have significant improvement even if they have severe vision loss and pale optic disc. Color vision disorder often persists. Visual acuity improvement usually occurs 2 weeks after onset, or in the classic Shortly after treatment with corticosteroids, once 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 the lowest (indicating that some types of diseases occur in childhood), Rizzo In a prospective survey with Lessel, 74% of female patients and 34% of male patients developed MS after 15 years of visual loss. The longer the observation period, the more detailed the examination revealed the higher the proportion of MS eventually developed into MS. Most of the other symptoms occurred 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 evidence of demyelination is a localized type of MS or another disease process is still controversial. The pathological basis of common optic neuritis is demyelinating changes, vasculitis damage or due to Tumors, cysticercosis oppression of the optic nerve rarely cause 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 affected, generally on the vertical axis has a shorter range of influence However, 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 dysfunction. CSF has moderate lymphocyte elevation and protein elevation, but cerebrospinal fluid can be normal in the early stage of the disease, 1/3 The patient has a history of infectious diseases within a few weeks before the onset of the disease, which is mostly caused by single-phase demyelinating lesions after infection. Less than half of the patients have other neurological asymptomatic lesions at the same time as the spinal cord. Or the clinical symptoms of diffuseness are found within 5 years. Therefore, acute transverse myelitis is less correlated with optic neuritis than MS. Another view is that most transverse myelitis develops into MS, which can only be found after long-term follow-up. a relationship.

In the same site of recurrent myelitis, patients with demyelinating lesions in other sites have not been noticed by careful MRI. Some cases even have oligoclonal bands in the cerebrospinal fluid. This 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 associated with lupus erythematosus, with connective tissue disease, antiphospholipid antibody syndrome or other autoantibodies. Existence, too, 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, and the clinical manifestations are symptoms and signs of optic nerve, brain stem, cerebellum and spinal cord injury; another 30% ~40% of patients showed different degrees of spastic ataxia and deep sensory disturbance at the extremities, which basically accorded with spinal cord MS. Asymmetric spastic parastomal paralysis is the most common manifestation of progressive MS, cerebellum or pons medullary cerebellum The total and blind type each accounted for 5%, so mixed and spinal type accounted for about 80% of clinical cases.

MS patients often show mental disorders, some cases are euphoric, more cases are characterized by depression, irritability and temper, other mental disorders such as retention of memory loss, general dementia or mental disorder can be regular In the later stage of the disease, the cognitive impairment of MS is more consistent with the "subcortical dementia" described above. The frontal lobe syndrome with severe will is a common feature of advanced MS, and 2% to 3% of MS patients have their disease course. There is a one-time or repeated epileptic seizure at a certain time, 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, which manifests itself in the brain, brainstem, and spinal cord in a few weeks, causing the patient to be stupor, coma or denervated, 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 MS is that the majority of the sclerosing plaques are the same, many of the perivascular demyelination areas The fusion is obvious, and 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 mononeuropathy. This relationship leads to some speculation and contradiction. The occasional suggestion of this combination is MS and its surroundings. The occurrence of neuropathy may be coincidental, but it is difficult to explain why the latter is a very characteristic peripheral neuropathy. Both central and peripheral nerves can undergo autoimmune demyelinating changes, which occur 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 the involvement of fibers in the spinal cord nerve root entry zone or the ventral white matter of the spinal cord, which may be associated with vitamin-deficient peripheral neuropathy in the late stage of MS.

Examine

Multiple sclerosis examination

1. Cerebrospinal fluid routinely about 1/3 of MS patients, especially acute onset, worsening cases, cerebrospinal fluid often have mild to moderate mononucleosis (usually less than 50 × 106 / L), in the progressive optic nerve In patients with myelitis and certain brainstem demyelinating diseases, the total number of cells can reach 100×106/L. In the acute peak condition, the proportion of cells can be multi-nuclear white blood cells, and the increase or decrease of cell number reflects the activity of the disease.

In about 40% of patients, the total protein content in CSF is increased, the protein increase is mild, and the protein concentration exceeding 100 mg/dl is rare in MS, and more importantly, in 2/3 patients -globulin. The proportion of (mainly IgG) increased (more than 12% of total protein).

2. Another diagnosis is to measure the ratio of albumin and -globulin in serum and cerebrospinal fluid. The IgG index IgG index is obtained by the following formula: CSFIg ÷ serum Ig / CSF albumin ÷ serum albumin, the ratio is greater than 1.7 is possible MS, it has been proved that -globulin in CSF of MS patients is synthesized in CNS. Abnormal bands are separated in agar electrophoresis, called oligoclonal bands (IgG). This oligoclonal band can also be found in syphilis and sub- CSF in patients with acute cirrhosis of encephalitis.

The oligoclonal bands present in CSF do not appear in the blood, which is of special significance for the early diagnosis of atypical MS. The first episode of MS with oligoclonal bands can be predicted as chronic recurrent MS, and many patients in acute phase CSF High concentration of myelin basic protein (MBP); MBP content is low or normal in chronic advanced phase; normal MBP content during remission of disease, other lesions that destroy myelin (such as infarction) can also increase MBP levels, Therefore, this measurement is not specific to the diagnosis. Considering the number of cells, total protein, -globulin and oligoclonal bands, most patients will find abnormalities in cerebrospinal fluid. Currently, -globulin and oligoclonal bands, which are a component of total protein in CSF, are MS. The most reliable chemical detection method.

3. Electrophysiological examination When clinical data suggest that there is only one lesion in the CNS, several physiological and radiological examinations may indicate the presence of asymptomatic lesions, which are common in the early stages of the disease or in the spinal cord type MS. Auditory and somatosensory evoked responses; electro-eye diagram; blink reflex changes; visual fusion of flash fusion, it is reported that 50% to 90% of patients with MS have one or more abnormalities, and the rate of visually induced abnormalities is diagnosed 80% of MS patients, 60% of possible or suspected MS; somatic-induced abnormal rate was 69% and 51% in both groups; brainstem auditory induced abnormal rate (general inter-wave latency extension or wave) 5 peak reductions were 47% and 20%, respectively.

4. Imaging examination MRI is more sensitive than CT to show asymptomatic multiple sclerosis in the brain, brain stem, optic nerve and spinal cord. 80% of MS cases have multiple lesions. It should be noted that signal enhancement around the ventricles can be seen in various pathologies. The process, even seen in normal people, especially the elderly, in the latter, the changes around the ventricles are milder than MS, the borders are smoother, and there are no specific MRI findings in the scattered multiple sclerosis lesions, visible in T2-weighted images. Several asymmetry, clear boundaries, close to the lesions on the surface of the ventricle, usually suggest Ms, corresponding to the fiber travel, the demyelinative changes of the radial distribution particularly support the diagnosis, some lesions can be double or triple normal in the acute phase The amount of gadolinium showed intensification, and continuous MRI examination showed the development of the disease.

Diagnosis

Multiple sclerosis diagnosis

diagnosis

1. The lesion has two or more objective signs of lesions in the white matter of the central nervous system, such as the optic nerve, spinal cord, and brain stem.

2. The course of the disease is remission and recurrence. The second episode is at least one month apart, each time 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 1,2 is missing, the diagnosis clinical may be multiple sclerosis; if only one predileous site occurs for the first time, it can only be used as Clinical suspicious", increased IgG index in other cerebrospinal fluid and the appearance of IgG monoclonal band, serum antiphospholipid antibody positive, liver disease necrosis factor activity increased, myelin basic protein increased, etc. can be used as a reference.

Differential diagnosis

1. Disseminated encephalomyelitis is an acute disease with extensive scattered lesions. It is self-limiting and mostly a single course. In addition, the disease often has fever, stupor and coma, and these characteristics 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 are multiple lesions in the CNS white matter, these diseases The CNS injury is parallel to the activity of a potentially immunological disease or the level of autoantibodies, such as against its own DNA or phospholipids, with or without other systemic damage, but also with demyelination or cerebral hemispheres. In the case of other systemic organs, 5% to 10% of MS patients carry anti-nuclear or anti-double-stranded DNA antibodies without the performance of 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, indicating that there is an unproven link between MS and autoimmune diseases. The lesions of lupus erythematosus on MRI are much like sclerosis. The plaque, optic nerve and myelin 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, rather than demyelinating inflammation, individual can also be seen Inflammatory demyelinating lesions without vascular changes, it is currently considered that the above-mentioned MS-like condition is considered to be a specific manifestation of lupus erythematosus or related diseases.

3. Behcet's disease with recurrent iridocyclitis, meningitis, mucosa and genital ulcers; joint, kidney, lung symptoms and multiple brain lesions are the distinguishing features.

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. In this case, the spinal cord compression syndrome caused by tumor or cervical joint disease should be carefully excluded. Root pain is often manifested in spinal cord compression at certain time of the disease. It is rare in MS, neck pain, limited activity and cause. Severe muscle atrophy caused by nerve root involvement can be seen in spinal joint lesions and MS rarely has the above symptoms. As a general rule, abdominal reflexes disappear in the early stage of demyelinating myelopathy, and impotence and bladder dysfunction occur in men. In the case of 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, but there is no abnormality of other MS-specific proteins. The most valuable identification method is MRI and CT spinal cord imaging. Surgery, any signs of the nervous system are limited to the progressive spastic paraplegia of the spinal cord, and spinal cord development should be performed.

5. Skull base depression and flat skull base This patient has a short neck, radiological examination can confirm the diagnosis, due to skull base development malformation and skull hole, pons cerebral angle, slope and other posterior fossa tumors and other neurological syndrome Can be misdiagnosed as MS, in the above situation, an isolated and special lesions can cause brain symptoms, signs in the brain stem, cerebellum, posterior group and upper cervical spinal cord, and easy to be considered as a disseminated lesion, such as 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. It is a clinical rule.

6. Hereditary ataxia Occasionally MS can be confused with hereditary ataxia, which often has a family history and its associated genetic characteristics, with occult onset, chronic persistent progression, symmetry and specific clinical approach, abdominal wall Reflex and sphincter function is intact, 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. It is easy to be confused with simple posterior optic neuritis. Most scholars believe that 25% to 35% of optic neuritis can develop into MS, but optic neuritis often damages monocular, often accompanied by center. Dark spots plus peripheral visual field defects, and no remission in the course of the disease, MS often suffered from both eyes, few central dark spots, significant relief and recurrence.

As mentioned earlier, evoked potentials, the widespread use of oligoclonal bands and MRI in CSF expand the diagnostic criteria for MS, which often reveal the presence of multiple sclerosis plaques that are undetectable by clinical examination. The requirement of multiple "evidence" has gone through the test of time and is still valid today, but the difference is that the evidence is no longer only pure clinical findings, but also includes some laboratory findings. It should be noted that there is no laboratory. The check can be considered as a credible indicator of the MS alone.

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