Scissors gait

Introduction The lower limbs are scissor gait is the clinical manifestation of bilateral cerebral palsy. The gait of the scissors is due to the increase of muscle tension in the lower limbs, especially in the muscles of the extension muscles. When the steps are taken, the lower limbs are over-exposed and the legs are scissor-like. Suffering from cerebral palsy or paraplegia. Due to brain damage or congenital dysplasia, infection, etc. caused by asphyxia during childbirth, it is a manifestation of spastic paralysis, that is, increased muscle tone, hyperreflexia, manifested as hip flexion, adduction, internal rotation, and foot drop And inversion, the knees rub each other while walking, and even the legs completely cross, showing a typical "scissors" gait.

Cause

Suffering from cerebral palsy or paraplegia.

Common causes of cerebral palsy are as follows:

First, prenatal factors

1. Abnormal brain development during embryonic period such as small head deformity, congenital hydrocephalus, giant brain disease or no brain malformation.

2, maternal pregnancy, trauma, pregnancy toxemia, diabetes and radiation exposure can affect fetal brain development and cause permanent brain damage.

3, early pregnancy, rubella, toxoplasmosis affect the development of the fetal central nervous system and cause disease.

4, premature infants, small samples, the smaller the gestational age, the incidence of more. It is associated with hypoplasia of the nervous system in premature infants, easy bleeding and hypoxia.

5, expired birth placenta degeneration and necrosis, causing hypoxemia, resulting in fetal hypoxia.

Second, the cause of birth

1, cerebral hypoxia labor time is too long, prenatal use of anesthetics, sedatives can inhibit fetal hypoxia caused by fetal respiration, in addition to the umbilical cord around the neck, placenta early stripping, pre-position can cause fetal brain hypoxia.

2, cerebral hemorrhage birth, emergency, dystocia and bleeding disorders can cause intracranial hemorrhage.

3, postpartum causes neonatal hyperbilirubin-induced nuclear jaundice, meningitis, encephalitis or severe infection caused by toxic encephalopathy, head trauma, carbon monoxide poisoning, etc., can also be diagnosed as a sequela of a disease.

Pathogenesis of cerebral palsy

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 spastic dyskinesia and posture abnormalities may occur. Impaired ability of perception, such as visual and auditory ability, can make children with mental retardation, basal ganglia damage can lead to acromegaly, cerebellar damage can occur ataxia.

There are two types of special pathological changes of cerebral palsy: 1 hemorrhagic damage, subependymal hemorrhage or intraventricular hemorrhage, more common in immature children less than 32 weeks gestation, may be due to relatively large cerebral blood flow, blood vessels Vulnerable, vascular nerve development is not perfect, the ability to regulate cerebral blood 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

It is the hemorrhage near the caudate nucleus of the Monro hole in the cerebral hemisphere, which is located in the subependymal cell germplasm matrix, often involving bilateral and asymmetrical.

The subependymal hemorrhage is supplied by the bean vein artery, the choroidal artery and the Heubner return artery, and the venous blood is introduced into the Galen vein through the deep vein. About 25% of the subependymal hemorrhage is divided into small cavities, and the rest break into the lateral ventricle or adjacent to the brain tissue. A group of 914 consecutive neonatal necropractors showed 284 cases of subependymal hemorrhage, accounting for 31% of the total, were low birth weight children. The etiology and mechanism of subependymal hemorrhage are unclear, which may be related to the significant increase of stromal layer venous pressure and 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

It is a white matter banded necrosis that occurs in the watershed branch of the cortical branch and the deep perforating artery. It is located in the lateral and posterior lateral parts of the lateral ventricle and may involve occipital radiant and radiographic sensory motor fibers. According to a Swedish survey, 55% of spastic bilateral hernias are due to subependymal hemorrhage, white matter softening, or both. Children often have bilateral cerebral palsy and mental retardation. Movement disorders are often more important than cognitive and speech dysfunction. 1/3 of cases of subependymal hemorrhage can also occur in premature infants with hypotension and dyspnea. Full-term baby. Chaplin et al observed 20 patients with hydrocephalus after hemorrhage, 40% had significant dyskinesia, and more than 60% had IQ below 85. Victor et al observed 12 cases of light cases, the average weight of the child after birth was 1.8kg, the average gestational age was 32.3 weeks, only 1 case left bilateral spastic paralysis, 9 cases of IQ were between low and normal or normal IQ. The average survival age is 8.5 years.

3. Hypoxia-ischemic encephalopathy

(hypoxic-ischemic encephalopathy) is a clinical syndrome that causes hypoxia and ischemia in newborns and causes brain damage. Although many newborns have varying degrees of asphyxia during the perinatal period, only a few have brain damage. Many children with cerebral palsy can also survive the perinatal period safely, indicating that some prenatal and postnatal pathogenic factors also play an important role. Animal experiments have confirmed that the ability of CNS to tolerate hypoxia and ischemia is the strongest in life. Brain damage occurs only when the arterial oxygen partial pressure drops to 10% to 15% of the normal value. Other organ dysfunction can also aggravate the degree of brain damage, such as myocardial injury and arrhythmia caused by hypotension. A reasonable explanation is that hypoxic-ischemic encephalopathy usually occurs in the uterus and shows clinical symptoms after the baby is born.

Prenatal risk factors for hypoxic-ischemic encephalopathy may include pregnancy toxemia, prenatal uterine bleeding or dysplasia such as miniature infants. The main causes are abnormal labor and prenatal pathogenic factors such as uterine hypoxia, ischemia, etc., as well as maternal mental dysplasia, birth weight less than 2000g, fatal malformation and breech production, about 1/3 of breech production. The baby has no brain abnormalities. Nelson and Ellenberg observed 189 children with cerebral palsy, 21% had some degree of asphyxia, and other factors associated with pathogenesis included mothers with epilepsy, siblings with motor dysfunction, two or more siblings, and mothers. Suffering from hyperthyroidism, pre-eclampsia or eclampsia. The pathogenic factors of children with bilateral cerebral palsy were different. Nearly half of the cases were caused by pregnancy toxemia, malnutrition and low body weight, placental infarction and intrauterine asphyxia. Severe neonatal asphyxia is an important cause of spastic-myodystonic-ataxic syndrome in term or preterm infants, often accompanied by epileptic seizures and abnormal mental status.

Other causes should be considered when there are no common causes of hypoxia-ischemia, matrix hemorrhage, and white matter softening in children with cerebral palsy. Symmetrical brain penetrating malformation of the brain defect is often located in one side of the frontal lobe, which can lead to congenital hemiplegia. For example, the lesion may be located on both sides with hemiparesis and severe mental development disorder; hydrocephalus without brain malformation. Substrate membrane replacement, only the lower part of the temporal lobe, occipital lobe, thalamus and basal nucleus, the skull can be intact or enlarged, the child can survive for weeks, months or years, can preserve the basic functions of the brain stem.

an examination

Related inspection

Bone and joint MRI

The performance of cerebral palsy varies depending on the cause and type, but it is more common in the early stage: (early symptoms of the first half of the cerebral palsy (within 6 months).)

1, the body is soft and spontaneous exercise is reduced, this is a symptom of low muscle tone, can be seen in a month. If it lasts for more than 4 months, it can be diagnosed as severe brain injury, mental retardation or muscle system disease.

2, the body is hard, this is the symptoms of hypertonic muscle, can be seen in a month. If it lasts for more than 4 months, it can be diagnosed as cerebral palsy.

3, slow response and no name, this is an early manifestation of mental retardation, generally considered to be slow at 4 months, no response at 6 months, can be diagnosed as mental retardation.

4, head circumference abnormalities: head circumference is an objective indicator of the development of the brain's morphology, brain damage children often have head circumference abnormalities.

5, poor weight gain, breastfeeding weakness.

6, fixed posture, often due to brain damage caused by abnormal muscle tension, such as angular arch reversal, frog position, inverted U-shaped posture. It can be seen in one month after birth.

7, do not laugh: If you can't smile for 2 months, you can't laugh out loud for 4 months, you can diagnose it as mental retardation.

8, hand fist: If 4 months still can not open, or thumb adduction, especially the presence of one side of the upper limbs, has important diagnostic significance.

9, body twist: 3-4 months of babies if the body is reversed, often suggesting extrapyramidal injury.

10, head instability: such as 4 months prone can not raise the head or sit when the head can not be vertical, often an important sign of brain damage.

11, strabismus: 3-4 months of babies with strabismus and poor eye movements, can indicate the presence of brain damage.

12, can not reach out to grab things: such as 4-5 months can not reach out to grab things, can be diagnosed as mental retardation or cerebral palsy.

13, gaze hands: 6 months later still exist, can be considered for mental retardation. Some brain damage is mild, and there are often no obvious symptoms in the early stages of the baby, but in the second half of the baby (6-12 months).

Cerebral palsy

1. Ask whether there is a history of dysplasia or impaired motor neuron, such as premature birth, dystocia, high fever, cerebral ischemia, cerebral hypoxia, craniocerebral injury, brain infection, etc.

2, check for sputum sputum, muscle movement disorders, muscle tension, hyperreflexia, muscle atrophy, joint deformity, ataxia and mental retardation.

Auxiliary inspection

Children diagnosed with cerebral palsy according to clinical manifestations must also undergo the following supplementary examinations:

1. Intelligence test.

2. EEG examination.

3. Determination of brainstem auditory evoked potentials.

4, imaging and other examinations confirmed.

Differential diagnosis

Differential diagnosis of lower limbs with scissors gait:

1. Hemiplegia gait: When walking, the upper limbs flexed, the swing disappeared, the thighs and calves were straight, and the feet were drawn outwards, so it was also called the gait of the circle, which was seen after the stroke.

2, panic gait: the body leans forward, the start is slow, and then gradually faster, the faster and faster it is difficult to "quick brake", its flustered Zhang, seen in Parkinson's disease.

3, drunken gait: the foot is slow, landing like a lame, the upper limbs shaking before and after, the gait is not stable can not go straight like drunk, seen in cerebellar tumors, inflammation and lost disease.

4, duck gait: walking waist and bulging, hips swinging like ducks, is a manifestation of progressive muscular dystrophy, can also be seen in rickets, congenital dislocation of the hip.

5, across the gait: walking hip joints, knee joints raised too high to avoid the toe touch the ground, seen in the common peroneal nerve paralysis, sciatic nerve palsy, polyneuritis patients.

6. Rooster gait: When standing, the two thighs are close, the calves are slightly separated, and the feet stand like toes. When walking, they are like a ballet-like walk, which is more common in spinal cord lesions, such as inflammation and paraplegia.

Diagnosis: Main symptoms: can not stand and walk alone, muscle tension in both lower limbs, parent support standing, double lower limbs in scissors gait, double hip, knee flexion, ankle joint flexion, bipedal varus deformity, toe walking .

The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments.