cerebral palsy
Introduction
Introduction to Cerebral Palsy Cerebral palsy (cerebralpalsy), also known as cerebral palsy, also known as infantile cerebral palsy (infantilecerebralpalsy), is a congenital motor dysfunction and abnormal posture syndrome. Clinically characterized by abnormal posture and muscle tone, muscle weakness, involuntary movement and ataxia, often accompanied by sensation, cognition, communication, behavior and other disorders and secondary skeletal muscle abnormalities, and may have seizures. The cerebral palsy topical symposium (1988) proposed that cerebral palsy is defined as: non-progressive brain damage syndrome in the developmental period from birth to one month after birth, mainly manifested as central dyskinesia and abnormal posture, other The causes of transient dyskinesia, brain-prone diseases, and spinal cord lesions are not within the scope of this disease. basic knowledge The proportion of illness: 0.001% Susceptible people: infants and young children Mode of infection: non-infectious Complications: epilepsy, mental retardation
Cause
Cerebral palsy
Congenital factors (35%):
Including embryonic brain developmental malformations, congenital hydrocephalus, severe early pregnancy infection (especially viral infection), severe nutritional deficiencies, trauma, poisoning (such as pregnancy toxemia) and radiation exposure, genetic factors in the onset The effect is not obvious.
Perinatal injury (20%):
Case analysis shows that premature birth is the definite cause of cerebral palsy. In the United States, about 50,000 premature infants weighing less than 1500 g are born each year. Among 85% of survivors, 5% to 15% suffer from cerebral palsy, 25% to 30%. School-age mental disorder (Volpe, 1989), long delivery time, umbilical cord around the neck, placental abruption, placenta previa, amniotic fluid blockage and meconium inhalation caused by fetal cerebral hypoxia, dystocia or expired infants have too long labor, Broncheter injury and intracranial hemorrhage are common perinatal causes, neonatal hyperbilirubinemia caused by maternal and child blood group incompatibility or other causes, such as serum unconjugated bilirubin >340mol / L may develop into bilirubin encephalopathy And cause cerebral palsy.
Other factors (15%):
Including various infections, trauma, poisoning, intracranial hemorrhage and severe asphyxia, Russman statistics of high risk factors for cerebral palsy include maternal prenatal epilepsy, hyperthyroidism and toxemia, bleeding events within 3 months of the end of pregnancy, delivery period The weakness of the uterus, placental abruption, placenta previa and breech production can also induce the disease.
Pathogenesis
The maintenance of normal muscle tone regulation and posture reflex in human body depends on the dynamic balance between the inhibition of cortical fiber and the facilitation of surrounding Ia afferent fibers. For example, the cortical fiber bundle is damaged, and the inhibition of the lower side is inevitable. The excitatory effect is relatively enhanced, and there may be spastic dyskinesia and posture abnormality. Perceptual ability such as visual acuity, impaired hearing ability may make children with mental retardation, basal ganglia damage may lead to acromegaly, cerebellar damage may occur ataxia Wait.
There are two types of special pathological changes in cerebral palsy:
1 hemorrhagic damage, subependymal hemorrhage or intraventricular hemorrhage, more common in immature children less than 32 weeks of gestation, may be due to relatively large cerebral blood flow, vascular instability, vascular nerve development is imperfect, regulate cerebral blood The ability to flow is poor.
2 ischemic damage, such as white matter softening, cortical atrophy or atrophic lobular sclerosis, etc., more common in infants with hypoxia asphyxia.
In recent years, many countries have adopted the classification of causes, which are mainly divided into the following three types:
1. Premature infants (subependymal) hemorrhage is the hemorrhage near the caudate nucleus of the Monro hole in the cerebral hemisphere. It is located in the subembryonic cell germinal matrix, often involving bilateral and asymmetrical.
The subependymal hemorrhage is supplied by the bean vein artery, the choroidal artery and the Heubner return artery. The venous blood is introduced into the Galen vein through the deep vein. About 25% of the subependymal hemorrhage is divided into small cavity and the rest is broken into the lateral ventricle. Or adjacent to brain tissue, a group of 914 consecutive neonatal necropsy showed that 284 cases of subependymal hemorrhage, accounting for 31% of the total, were low birth weight, the etiology and mechanism of subventricular subcutaneous hemorrhage, It may be related to the significant increase of venous pressure in the stromal layer and the lack of adequate support tissue. The increase of blood pressure or venous pressure may be related to lung lesions in premature infants.
2, ventricle white matter softening, is a white matter banded necrosis occurring in the watershed branch of the cortical branch and deep perforating artery, located in the lateral and posterior lateral part of the lateral ventricle, may involve occipital radiation and radiation crown sensory motor fiber, Sweden survey Reports show that 55% of spastic bilateral twins are due to subependymal hemorrhage, white matter softening or both, children often have bilateral bilateral paralysis and mental retardation, dyskinesia is often more important than cognitive and speech Dysfunction, seen in 1/3 of cases of subependymal hemorrhage, can also occur in premature or full-term infants with hypotension and dyspnea, Chaplin et al observed 20 patients with hydrocephalus after hemorrhage, 40% of dyskinesia, More than 60% of the children had an IQ of less than 85. Victor et al. observed 12 cases of light cases. The average weight of the child after birth was 1.8kg, and the average gestational age was 32.3 weeks. Only 1 case had residual bilateral sputum and 9 cases of IQ. Under the low and normal or normal IQ range, the average survival age is 8.5 years.
3, hypoxic-ischemic encephalopathy (hypoxic-ischemic encephalopathy) is a clinical syndrome of various causes of hypoxia, ischemia, brain damage, although many newborns have different degrees in the perinatal period Asphyxiation, but only a small number of brain damage, many children with cerebral palsy can safely pass through the perinatal period, indicating that some prenatal and postpartum pathogenic factors also play an important role, animal experiments confirmed that the baby just after birth CNS Tolerant to hypoxia, the ability to ischemia is the strongest in life, only when the arterial oxygen partial pressure drops to 10% to 15% of the normal value, brain damage occurs, and other organ dysfunction will also aggravate the degree of brain damage. For example, myocardial injury and arrhythmia cause hypotension, a reasonable explanation is that hypoxic-ischemic encephalopathy usually occurs in the uterus, and clinical symptoms appear after the baby is born.
Prenatal risk factors for hypoxic-ischemic encephalopathy may include pregnancy toxemia, prenatal uterine bleeding or dysplasia such as micro-babies, the main cause of which is abnormal labor and prenatal pathogenic factors such as uterine hypoxia, ischemia Etc., as well as abnormal mental development of the mother, birth weight less than 2000g, fatal malformation and breech production, about 1/3 of the breech-produced infants have no brain abnormalities, Nelson and Ellenberg observed 189 children with cerebral palsy, 21% have some degree of asphyxia, and other factors related to pathogenesis include mothers with epilepsy, siblings with motor dysfunction, two or more siblings prematurely, mothers with hyperthyroidism, preeclampsia or eclampsia, etc. The pathogenic factors of children with bilateral cerebral bilateral hernias vary. Nearly half of the cases are caused by pregnancy toxemia, malnutrition and low body weight, placental infarction and intrauterine asphyxia. Serious neonatal asphyxia is full term. Or premature infants have an important cause of spastic-myodystonic-ataxic syndrome, often accompanied by epileptic seizures and abnormal mental status.
Children with cerebral palsy without common causes such as hypoxia-ischemia, matrix hemorrhage and white matter softening should consider other reasons. Symmetrical brain penetrating malformation brain defects are often located in one frontal lobe, which can lead to congenital hemiplegia, such as lesions located in double Side may have hemiparesis and severe mental development disorder; hydrocephalus without brain deformity, most of the hemispheres are replaced by a membrane, leaving only the lower temporal lobe, occipital lobe, thalamus and basal ganglia, the skull can be intact or enlarged The child can survive for weeks, months or years to preserve the basic functions of the brain stem.
Prevention
Cerebral palsy prevention
Pay attention to maternal and perinatal health care and neonatal feeding care, prevent premature babies, low birth weight, hypoxia and postpartum jaundice, and the prognosis usually depends on the type of cerebral palsy and the severity of cerebral palsy. More than 90% of children with cerebral palsy Survival to adulthood, only the most severely affected children, that is, those without any ability to live, have a shorter life span.
Complication
Cerebral palsy complications Complications, epilepsy, mental retardation
The clinical signs and symptoms are complex and diverse, and their performances are different. For details, please refer to the various types of clinical manifestations, which are not described here.
Some children may have hyperbilirubinemia, low birth weight, enamel green pigmentation, myocardial damage and arrhythmia. Often accompanied by mental retardation and seizures. There are obstacles to sight and hearing.
Neonatal neonatal cortical dysplasia due to different factors, resulting in "cortical blindness." After early childhood, the most common intraocular strabismus and refractive errors, such as myopia, amblyopia, strabismus and so on. A few have nystagmus, and even blind. There are also cases where it is difficult to distinguish the rhythm of the sound.
Seizure
Epilepsy is a very dangerous form of cerebral palsy, which may be life threatening. Clinically, at least 10% to 40% of children have seizures at different ages. It is more common in patients with spastic quadriplegia, hemiplegia, single limb paralysis and mental retardation. Children with dysregulation are rare.
Feelings and perceptions will be abnormal
The children lacked the correct visual space and stereoscopic feeling, and their cognitive function defects were more prominent. The children's recognition of complex graphics is poor, and the relationship between the shape of the object and the background of the space is not clear, and the recognition of the color is also poor.
Mental retardation
About 2/3 of the children are intelligently backward, about 1/4 are severely intelligent and backward, and the squat type quadriplegic and tonic cerebral palsy are often worse, and the children with hand and foot pulsation are seriously inferior.
Symptom
Cerebral palsy symptoms Common symptoms Irritability, fatigue, fatigue, long-term illness, loss of response, slow weight, weight gain, convulsions
The clinical classification of cerebral palsy is complicated. In the past, Minear clinical symptom classification was used. The characteristics are clear definition and easy to apply. It can be divided into:
1 spastic type: the most common, accounting for 50% to 70% of children with cerebral palsy, including diplegic lower limbs, quadriplegic, hemiplegic, bilateral Double hemiplegic.
2 dyskinetic: including hyperkinetic or athetoid, myodystic.
3 ataxia type (ataxic).
4 mixed (mixed), according to Nelson (1978) statistics, sputum double lower extremity sputum accounted for 32%, hemiplegia accounted for 29%, quadriplegia accounted for 24%, exercise difficulty and ataxia type only accounted for 14%.
The clinical manifestations of cerebral palsy vary, and the severity of the disease varies. Severe symptoms appear in the days after birth. The symptoms are difficulty in sucking and muscles. Most cases are found only after months of family members trying to lift up. The main clinical types are The specific performance is as follows.
Cerebral spasm
Cerebral spastic diplegia can affect the extremities, the lower extremities are heavier, can exist independently, or with subependymal hemorrhage or lateral ventricle white matter softening, the incidence is closely related to the degree of preterm birth, since the use of newborns After the monitoring, the incidence rate decreased significantly, the genetic factors can not be ignored, the disease was first proposed by Ingram (1964), and Litter (1862) first proposed the concept of hypoxia-ischemic birth injury, it is also known as Litter disease.
(1) Initially, the muscle tension is reduced, the tendon reflex is weakened, and the weakness and convulsions appear after several months. The lower limbs are more obvious than the upper limbs. The weakness is first involving the adductor muscles, the tendon reflexes are active, and the children's legs are stiff and clumsy. When the child is lifted under the armpit, there is no leg movement, and the leg is still stretched or flexed. Most of the children have an extensor response, and the child has a late toddler, showing characteristic posture and gait. When the small step is slightly bent, the legs are more rigid, the muscles of the femoral adduct are strong, the calves are crossed, the step is curved (cross gait), the flexion of the foot is adducted, the heel can not touch the ground, and the legs can be adolescent or adult. Become thin and short, no obvious muscle atrophy, passive movement of the limbs can feel extensor and flexor rigidity, upper limbs are slightly affected or not tired, such as clums and rigidity of the fingers, some patients appear weakness and paralysis, can reach beyond when reaching for items The target, the face can be seen with a smile, the pronunciation is clear or vague, one third of the children have seizures, some can have hand and foot hyperactivity, face, tongue and hand involuntary movement, ataxia and muscle tension reduction.
(2) Scoliosis is very common, can compress the spinal cord, nerve roots or affect breathing, patients learn to urinate spontaneously very late, but the sphincter function is usually not tired, the subtype of sputum bilateral sputum may be associated with mild head and intelligence low.
2. Infant hemiparesis, paraplegia and quadriplegia
(1) congenital infantile hemiplegia: usually after birth, parents observe different physical activities on both sides of the child. If you only use one hand to pick things or grab things, it often does not attract attention until 4-6. Only when the month is aware of the seriousness of the problem, the lower extremity is usually found when the baby learns to stand or walk. The child can sit and walk on his own, but several months later than the normal baby; the examination shows that the child's tendon reflex is obviously hyperactive, usually Babinski sign ( ), the upper limbs are flexed, adducted and pronated, the foot is clubfoot, some children may have sensory disturbances and visual impairment, and those with mental disorders are more cerebral bilateral and bilateral Hemiplegia is rare, there may be slow language, attention should be paid to mental retardation and bilateral motor abnormalities, 35% to 50% of children may have convulsions, some children last for life, may be systemic seizures, common hemiplegic side focal Sexual seizures, Todd paralysis after seizures, Gastaut et al. have described hemiplegia-hemiplegic syndrome. After months or years, the patient has atrophy and progressive paralysis due to delayed development of the limbs and muscles of the hemiplegia.
(2) Acquired infantile hemiplegia: Hemiplegia that occurs in normal infants within 3 to 18 months, usually with or without aphasia, often with epileptic seizures, may be unconscious after seizures To the occurrence of hemiplegia, the language recovery is relatively complete, the ability to receive education can be reduced to varying degrees, the degree of recovery of motor function is not the same, when the functional impairment is heavier, there may be hand and foot movement, tremor and ataxia, etc. .
(3) infantile paraplegia (infantile paraplegia): manifested as lower extremity muscle weakness and sensory disturbances, sphincter dysfunction and sensory loss below the trunk level often suggest spinal cord lesions.
(4) infantile quadriplegia (infantile quadriplegia): The difference between the two sides of the spasm is that the latter often have medullary muscle involvement, and mental retardation is more serious.
3. Congenital extrapyramidal syndrome
Congenital extrapyramidal syndrome can be gradually evolved from cerebral palsy bilateral sputum. According to pathological basis and course of disease, it can be divided into prenatal-producing extrapyramidal syndrome and acquired or postpartum cone. In vitro syndrome, the former usually has obvious symptoms and signs in the first year after birth; the latter symptoms appear later, including familial acromegaly, dystonia musculorum deformans and hereditary cerebellum Arrhythmia, etc., common diseases due to severe hypoxia during birth, polycythemia with bilirubin encephalopathy, etc. The most common lesion in the brain is the putamen, the white marble-like appearance of the junction of the thalamus and cerebral cortex, the disappearance of nerve cells. Glial cell hyperplasia and medullary fiber condensation.
(1) double athetosis (also known as dyskinesia cerebral palsy), is the most common congenital extrapyramidal lesion, due to hyperbilirubinemia, Rh factor incompatibility, lack Blood hypoxic encephalopathy, etc., congenital non-hemolytic jaundice or glucose-6-phosphate dehydrogenase deficiency can be caused.
Patients often have a random combination of dance and hand and foot movements, or other involuntary movements such as dystonia, ataxia tremor, myoclonus and hemiplegia, for months or years after birth. All patients with bilateral acromegaly have primary autonomous dyskinesia and no pyramidal tract sign. The severity of the disease is very different between infants and children with dyskinesia. The abnormal movement of the mild person can be mistaken for anxiety. The autonomous movement of severely ill patients can cause intense involuntary movements. Individual patients continue to progress during puberty or early adulthood. They should be differentiated from hereditary metabolic or degenerative diseases, extrapyramidal diseases, etc., and patients with early manifestations of low muscle tone, Then there is motor developmental delay, usually up to 3 to 5 years old when walking upright or not standing upright, tendon reflexes are mostly flex, no sensory disturbances, may have mental defects or completely normal, a few can accept higher level education Some patients misunderstood mental retardation due to motor and language disorders. The diagnosis of CT/MRI is of little significance. Some have mild brain atrophy and basal ganglia become small, some serious. Ataxia seen in patients with lacunar lesions, unless seizures, EEG is usually not helpful in the diagnosis.
With growth and development, the patient's posture and athletic ability will improve. Those who are light can engage in certain occupations. Those who are severe can rarely exercise independently. They often cannot live independently. Some have reported that they have tried physical therapy and sensory integrative therapy. Such rehabilitation measures, progressive progression of procedural exercise can promote neuromuscular development, but with little effect.
(2) bilirubin encephalopathy (nuclear jaundice, kernicterus): is a serious neonatal disease characterized by congenital and/or neonatal physical factors caused by jaundice and a large number of nucleated red blood cells in the blood, is an extrapyramidal disease The rare cause, serum bilirubin content >25mg / dl usually produces central nervous system toxic effects, causing neurological symptoms, low birth weight or transparent membrane disease in infants in the case of acidosis and hypoxia, even serum Very low levels of bilirubin can also cause bilirubin encephalopathy.
1 mild nuclear jaundice: may be due to various blood types incompatible and physiological reasons, often in the 24 ~ 36h after birth, jaundice and liver, splenomegaly, after the fourth day, jaundice gradually subsided, no obvious neurological symptoms.
2 severe jaundice: jaundice occurs rapidly at birth or several hours after birth, often with liver, splenomegaly and heart expansion, with edema and anemia, skin and mucous membrane bleeding, etc.; 3 to 5 days baby becomes Burnout, sucking weakness and difficulty breathing, may have vomiting, lethargy, muscle rigidity, angular arch reversal, eyeball upturn, seizures and breath holding bruises, as well as dance or hand and foot movements, fingering movements, muscle tension Obstruction and other extrapyramidal symptoms, some cases may have spastic paralysis, if not treated in time, most cases can die within a few days to 2 weeks, even if the child survives often left mental retardation, deafness and muscle tension, etc. Can not sit, stand and walk, after the teeth, the enamel can have green pigmentation, neonatal extrapyramidal symptoms with bilateral deafness and upper vision paralysis, should consider the possibility of bilirubin encephalopathy.
3 Premature infants with jaundice caused by physiological jaundice: Symptoms often appear 2 days after birth, peak at 8 to 10 days, can also be delayed until several weeks after birth, showing glucuronyltransferase deficiency and hyperbilirubin Blood.
4 laboratory examination showed that there were a lot of nucleated red blood cells in the blood, moderate white blood cells, decreased platelets and hemoglobin; increased serum total bilirubin, indirect reaction of bilirubin qualitative test, strong urinary urinary biliary, positive mother and newborn blood type The examination is helpful for diagnosis, Rh or other rare blood type incompatibility direct anti-human globulin test (), ABO blood group compatibility bilirubin qualitative direct test (-), indirect test ().
4. Congenital ataxia
Congenital ataxias can be the only symptom of neonatal hypoxic ischemic encephalopathy. The cause is unknown. It may be related to genetic factors, intrauterine mercury poisoning, and radiation exposure of the mother 3 months before pregnancy. Cerebellar sclerosing lesions, congenital atrophy and hypoplasia, the brain can be damaged.
The child initially showed reduced muscle tone and decreased activity. When the child grew up, when the body and the limbs were to coordinate movement, such as sitting, standing and walking, there was obvious cerebellar dysfunction, which was characterized by sitting instability and reaching for the object. Uncoordinated movements, gait awkward and often fall, walking when the torso is unstable with a slightly rhythmic movement of the head ( gait), muscle strength, sputum reflex, sacral reflex or extensibility, no muscle atrophy In some cases, ataxia with tendon, no muscle tone reduction, called spastic-ataxic diplegia, may improve with the growth and development of patients, older children can see cerebellum gait, limbs Ataxia, nystagmus and incoherent pronunciation need to be differentiated from myoclonus, chorea, hand and foot, dystonia and tremor. CT and MRI can be seen in cerebellar atrophy.
5. flaccid paralysis
Flaccid paralysis includes the following types:
(1) Cerebral form of flaccid paralyses: first described by Foerster, called cerebral atonic diplegia, posture reflex, sputum reflex retention, and motor development Hysteresis should be differentiated from paralysis caused by the spinal cord and peripheral nerves, congenital muscular dystrophy.
(2) syndrome of infantile spinal muscular atrophy: is a typical lower motor neuron disorder, also known as Werding-Hoffmann disease, the mother can feel contraction reduction during pregnancy, most children after birth It manifests as obvious motor deficit or joint flexion deformity at birth. Other types of familial progressive muscular atrophy can occur in early or late childhood, puberty and early adulthood. It manifests as muscle weakness, muscle atrophy and tendon reflex disappear, but no sensory disturbance. A small number of suspected infants or childhood muscular atrophy, follow-up observation found that not love activities, caused by physical weakness, need to be identified with polymyositis or acute idiopathic polyneuritis.
(3) brachial plexus palsy (brachial plexus palsy): is a common complication of twins, because the hips first pull the shoulder or shoulder when the first exposed, the head is in the pulled state and tilt position, sometimes damage can be Sustained for life, small limb development after birth, skeletal dysplasia, upper brachial plexus (neck 5 ~ 6) and lower brachial plexus (7 ~ 8 cervical nerve, first thoracic nerve) nerve root can be involved, there are reports The upper brachial plexus is 20 times more likely to be damaged than the lower brachial plexus, and sometimes the entire brachial plexus is involved.
(4) facial paralysis: is a common neonatal peripheral neuropathy, involving the unilateral side, the forceps of the facial nerve is caused by the far-end fiber of the stem of the stalk, which is characterized by side closure and suction weakness. It needs to be differentiated from congenital bilateral paralysis (Möbius syndrome), which is often accompanied by external rectus paralysis. Most cases recover after a few weeks, and a few lifetime unhealed and left facial asymmetry.
Examine
Examination of cerebral palsy
1, neonatal routine hematuria examination, biochemical electrolyte examination.
2, mother and newborn blood type test, bilirubin qualitative test, serum total bilirubin quantification.
3, maternal prenatal amniotic fluid gene, chromosome, immunological examination.
4, cranial CT is mainly used to identify the presence or absence of organic lesions and lesions, common abnormalities include extensive brain atrophy, brain softening and white matter dysplasia, etc., for some cases can be used to suggest the cause, such as congenital brain development Malformations, intrauterine infections, etc.
5, EEG because children with cerebral palsy have more epilepsy, it should be routinely performed EEG to rule out the complication, common abnormalities include slowing of background activity, limited slow wave foci or epileptic seizure discharge.
6, IQ measurement: evaluation of intelligence and social adaptation, to determine whether the child has combined mental retardation.
7. Evoked potentials: Children with suspected vision and abnormal hearing function can do visual and auditory evoked potentials to detect abnormalities early and intervene in time.
Diagnosis
Diagnosis of cerebral palsy
diagnosis
At present, the lack of specific diagnostic indicators for cerebral palsy, mainly based on clinical symptoms and signs, the three diagnostic criteria developed in China (1988) Pediatric Cerebral Palsy Conference are:
1 Central paralysis occurs in infancy.
2 with mental retardation, convulsions, abnormal behavior, sensory disturbances and other abnormalities.
3 Except for the progressive disease caused by central sputum and normal children with transient movement development.
If you have any of the following conditions, you should be highly alert to the possibility of cerebral palsy:
1 premature infants, low birth weight infants at birth, severe hypoxia at birth and neonatal period, convulsions, intracranial hemorrhage and bilirubin encephalopathy.
2 mental retardation, emotional instability and easy to panic, etc., sports retardation.
3 There are limb and trunk muscle tension and typical performance of sputum;
4 extrapyramidal symptoms with bilateral deafness and upper paralysis.
Differential diagnosis
1. Acute disseminated myelitis
Most of the disease occurs in young and middle-aged adults. Most of the patients have symptoms or vaccination history in the first few days or 1 to 2 weeks. Cold, overwork, trauma, etc. are often the cause of the disease. The onset is urgent, and the first symptoms are mostly double. The lower extremity is numb, weak, the corresponding part of the lesion is painful, and the lesion segment has a sense of bandage, which often reaches a peak within 2 to 3 days. Clinically, the limbs are below the lesion level, and the sensory loss and sphincter disorders are the main features. The acute phase can be expressed as Spinal cord shock, there are many autonomic neurological disorders below the plane of damage. The disease can enter the recovery period after 3 to 4 weeks. Most of them recover after 3 to 6 months after the onset. A few cases have different degrees of sequelae, but many are not accompanied. There are convulsions, involuntary movements, mental disorders and seizures.
2, optic neuromyelitis
The onset age of the disease is between 20 and 40 years old. The incidence of under 10 years old is rare. It is a subtype of multiple sclerosis. It is acute or subacute. The first symptom is mostly back pain or shoulder pain, followed by partial or Complete spinal cord transverse damage, and can show visual acuity such as decreased vision before or after symptoms of transverse spinal cord injury, but the condition is often relieved and recurred, and other multifocal signs such as nystagmus may also appear one after another. , double vision, ataxia and so on.
3, myasthenia gravis
The disease is more than 20 to 60 years old, the child is less common, the onset is concealed, the first symptoms are mostly the weakness of the extraocular muscles, including the ptosis, limited eye movement and double vision, other skeletal muscles can also Involved, such as masticatory muscles, throat muscles, facial muscles, sternocleidomastoid muscles, trapezius muscles and limb muscles, etc., can affect daily activities, severe cases are forced to stay in bed, the above symptoms usually increase after activities, can be different after rest The degree of relief, with the characteristics of stagnation and heaviness, some cases with thymic hypertrophy or thymoma, and some other autoimmune diseases such as hyperthyroidism.
4, periodic paralysis
The disease is characterized by recurrent skeletal muscle flaccid paralysis, more than adolescent onset, and the onset is gradually reduced after middle age. The incidence of infants and young children is extremely rare, which can be induced by factors such as overwork, food, cold, anxiety, etc. More than the rest after a meal or after strenuous exercise, the onset of the disease, mostly from the lower limbs, the extension and the upper limbs, bilateral symmetry, the proximal end is heavier, the attack generally lasts 6 to 24 hours, the elderly can reach more than 1 week Irregular recurrent episodes, most of which have changes in blood potassium (increased or decreased), some cases of heart rhythm disorder, increased blood pressure, intermittent muscle strength, according to the onset process, clinical signs, laboratory tests and family History is not difficult to identify with this disease.
5, progressive muscular dystrophy
A disease is a group of genetic diseases that originate in the muscles. Most of them have a family history. The clinical features are characterized by slow progressive progressive symmetry muscle weakness and muscle atrophy. Individual types may have myocardial involvement, and different types often show different onset. Age, clinical features and diseased muscle distribution, but generally more common in children and adolescents, visible "winged scapula", "free shoulder", "calf muscle pseudohypertrophy", "Gowers" sign and other characteristic performance, with Progressive symptoms, age of onset, clinical features and family history can be identified with the disease.
6, acute epidural abscess
The disease is due to purulent lesions in other parts of the body, such as bloated skin, tonsil purulent lesions, etc., or due to infections in adjacent tissues, such as acne, sputum or perirenal abscess, pathogens reach the dura through blood or tissue spread. Abscess is formed in the outer adipose tissue, and many of the sudden onset occurs several days or weeks after the primary infection. Sometimes the primary lesion is often neglected. The first symptom is severe pain in the back or both lower extremities. Fever, general weakness, severe tenderness and snoring of the spine in the corresponding part of the lesion. If not treated in time, the lower extremity paralysis can occur quickly. Laboratory examination shows a slight increase in cerebrospinal fluid leukocytes and a significant increase in protein content, vertebral obstruction, peripheral blood. Increased white blood cells, CT and MRI also help to identify.
7, Greene-Barre syndrome
Most of the symptoms of upper respiratory tract or digestive tract infection 1 to 4 weeks before onset, a small number of patients have a history of immunization, mostly with symmetry weakness of the limbs as the first symptom, can develop from the distal end to the proximal end or vice versa, or at the same time Affected, and can affect the trunk, severe cases can involve respiratory muscles and respiratory paralysis, sputum is flaccid, severe cases of muscle atrophy at the distal end of the limb, may be accompanied by paresthesia of the distal part of the limb and glove-like, sock-like feeling Decreased, the lesions are more extensive, cranial nerve damage is more common in adults with bilateral sputum, more common in children with medullary paralysis, but also eye movement, sublingual and trigeminal nerve paralysis, can have more sweat, skin flushing Symptoms of autonomic nerve damage such as swelling of the hands and feet and nutritional disorders, the symptoms progress rapidly, about half of the cases reach a peak within a week, the longest can reach 8 weeks, usually resume after 1 to 4 weeks of symptom stabilization, cerebrospinal fluid examination shows protein A cell separation phenomenon, the prognosis is generally better.
8, small chorea
In addition to a few cases of acute onset of mental irritation, most of the onset is slow, most of the age of onset is between 5 and 15 years old. Both mental stimulation and pregnancy can be induced. Clinically, irregular, non-repetitive, and uncertain. The sudden incessant dance-like involuntary movement is characterized by the appearance of the face, upper limbs, and trunk, but the movement of the lower limbs is less, the involuntary movements of the face and the trunk are both bilateral, and the involuntary movements are in the emotional stress. Intensified, disappeared during sleep, casual movement showed ataxia, often accompanied by emotional instability, distracted attention, cries and laughter and other mental symptoms, severe cases may have illusion, even paralysis and mania, the disease and cerebral palsy dance There are many similarities in the clinical manifestations of the Xudong disease type, but the disease often shows various rheumatic fever manifestations before, during or after the disease, which can be identified.
9. Subacute combined degeneration of the spinal cord
It is a degenerative disease of the nervous system caused by vitamin Blz deficiency, which is more sub-acute or chronic in the course of middle-aged disease. It is clinically characterized by deep sensory loss, sensory ataxia and spastic paralysis, often accompanied by Sexual sensory disturbance, most patients have burnout, fatigue, glossitis, diarrhea and other manifestations before the onset of neurological symptoms. The earliest neurological symptoms are abnormalities in the extremities of the extremities, such as tingling, numbness and burning sensation, etc., mostly persistent. And symmetry, often from the toe gradually involving the upper limbs, may have the distal limbs of the glove-like, socks-like feelings decline, with the progress of the disease gradually appear lower limb weakness, stiffness, walking instability, such as stepping on cotton, such as pyramidal bundles If the damage is severe, the muscle tension of the lower limbs is increased. If the posterior or (and) peripheral nerve degeneration is severe, the muscle tension is reduced, the tendon reflex is weakened, the pyramidal tract sign and pathological reflex are positive, and the bladder sphincter is often accompanied. There are irritating, drowsiness, suspicious, emotional instability and other mental symptoms, or mental decline or even dementia, serum vitamin B12 decreased, Schilling test found dimension Defective pixel B12 absorption.
10, multiple neuropathy
The clinical manifestations of the disease are characterized by limb symmetry of peripheral sensory disturbance, lower motor neuron sputum and autonomic dysfunction. Due to different etiology, onset may have acute, subacute, chronic, recurrent, and various functions. The degree of damage is also different. The end of the limb is glove-like, the sore-like shape is deep and shallow, and the symmetry of the lower motor neuron is present at the distal end of the limb. The distal end is heavier than the proximal end, and may be accompanied by muscle atrophy and reduced tendon reflex. The patient also has various manifestations of autonomic nerve involvement such as cold at the distal end of the limb, dry skin, desquamation, sweating, etc. The patient has obvious diabetes, poisoning, taking furan drugs and isoniazid, uremia, pregnancy, surgery. After, chronic gastrointestinal diseases, malignant tumors, connective tissue diseases and vaccination history, according to their medical history and typical clinical manifestations, it is not difficult to identify this disease.
