Duck gait

Introduction Severe pseudo-fat large malnutrition is a clinical manifestation of muscular dysfunction. It is characterized by two feet open and a slow swing, showing a special "duck step" gait. Muscular dystrophy is a group of primary skeletal muscle necrotic diseases characterized by progressive skeletal muscle weakness caused by genetic factors. It is clinically characterized by progressive and aggravated skeletal muscle atrophy and weakness in varying degrees and distribution. . Can also affect the heart muscle. Muscular dystrophy includes congenital muscular dystrophy and other types of BECKER-type MD.

Cause

The cause of the "duck step" gait

The cause of this disease is genetic abnormality, which can be carried out in different ways in different types, but the mechanism by which genetic factors ultimately cause muscle degeneration is still unclear. The pelvic girdle and the thigh muscles are weak, the progress is slow, the course of disease is long, and it is not possible to walk 25 or 25 years after the symptoms appear. Most of them do not occur when they are 30-40 years old, and the prognosis is good.

an examination

Related inspection

Duck step detection of serum aldolase serum aldolase (ALD)

Serum enzyme assay

(1) Serum creatine phosphokinase (CPK): Increased CPK is an important and sensitive indicator for the diagnosis of this disease. It can be increased after birth or clinical symptoms, and the activity of the disease is gradually decreased. Can also be used to check gene carriers, the positive rate is 60 ~ 80%.

(2) Serum myoglobin (MB): Significantly increased in the early stage of the disease and in the carriers of the gene.

(3) Serum pyruvate enzyme (PK) is sensitive. The serum PK value of normal male and female under 20 years old is 119.00, 84.30 for males over 20 years old, and 77.50 for females. The positive rate of CRK and PK in the above three serum enzymes is higher than Mb. The three comprehensive detection rates are around 70%.

(4) Other enzymes: such as aldolase (ADL), lactate dehydrogenase (LDH), aspartate aminotransferase (GOT), alanine aminotransferase (GPT), etc., can also be increased, but they are not specific changes in myopathy, Not sensitive.

2. Urine examination: increased creatinine excretion and decreased creatinine.

3. Electromyography: EMG findings of myogenic damage were observed in all types of muscular dystrophy. Including the average time limit of the exercise unit is shortened, the average amplitude of the exercise unit potential is decreased, the multi-phase potential is increased, the interference phase occurs during re-contraction, the range of the motion unit is reduced, the maximum amplitude of the unit potential of the motion is decreased, and the fibrillation potential and the positive phase potential are also seen. and many more.

4. Muscle biopsy: visible pathological changes as described above, X-CT or MRI can be used when conditions are available, the extent and extent of muscle degeneration can be found, and the preferred site for muscle biopsy is provided clinically.

Differential diagnosis

"Duck step" gait confusing symptoms

1. Juvenile proximal spinal muscular atrophy: This disease is also known as (Kugelberg-welder, progressive muscular atrophy), an autosomal dominant genetic disease. The onset of adolescents is mainly characterized by proximal muscle atrophy of the extremities, symmetric distribution, similar to myopathy, but fasciculation, electromyography is neurogenic damage, and muscle pathology is group atrophy, consistent with denervation.

2. Chronic polymyositis: no history of genetic disease, the disease progresses slowly, the symptoms often have ups and downs, and the degree of muscle weakness is more obvious than muscle atrophy. There is often pain and tenderness, and the blood sedimentation increases. Serum muscle enzymes are normal or slightly elevated, muscle pathology is consistent with changes in myositis, and corticosteroids are better.

3. Myasthenia gravis: Myasthenia gravis is aggravated after exercise, relieved after rest, no muscle atrophy and pseudo-muscle hypertrophy. Anticholinergic esterase agents are effective. Electromyography and muscle biopsy help to identify.

4. Myotonic dystrophy: The disease is rare and is autosomal dominant. Any age can be ill, first involving the small muscles of the distal hand and foot, no pseudo-hypertrophy, early manifestations of weakness in the distal part of the limb, occasionally facial muscle, eye muscle or throat muscle weakness. Progression is slow, and muscle rigidity and muscle atrophy gradually appear. Muscle atrophy is mainly at the distal end of the extremities, and can be developed to the facial muscles, masseter muscles, diaphragm muscles, and sternocleidomastoid muscles. Therefore, the patient's face is elongated and has an axe face and a gooseneck. Some patients may also have unclear speech and difficulty swallowing. Most patients have cataracts, alopecia, sexual dysfunction, infertility, and mental retardation. In the advanced stage, sputum and myocardial damage may occur, and serum enzymes may be normal or slightly elevated. Electromyography and muscle pathology help to identify.

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.