Facial muscle rigidity

Introduction Facial muscle rigidity refers to the fact that certain diseases, especially the damage of the facial muscles produced by the damage of the central nervous system, appear to be dull and mask-like, and the facial looking muscles are found to be straight and hard to move.

Cause

Multi-injury damage to the nervous system leads to a pathological change caused by damage to the corresponding nerve or brain region. Skeletal muscle is not easy to relax immediately after contraction or physical stimulation, muscle excitability increases during electrical stimulation and mechanical stimulation, skeletal muscle relaxation after repeated contraction or repeated electrical stimulation, symptoms disappear; strong and straightening in cold environment; electromyography A group of muscle diseases characterized by a continuous high frequency discharge phenomenon.

an examination

Related inspection

EMG

1. Serum CK and LDH and other enzymes are normal or slightly elevated.

2. EMG typical muscle tonic discharge is important for diagnosis. The affected muscles appear to be continuously attenuated by high-frequency strong waves, and the EMG speaker emits a similar sound like a bomber.

3. Muscle biopsy, typical type II muscle fiber hypertrophy, type I muscle fiber atrophy, with a large number of nuclear internal migration, visible muscle mass and ring muscle fibers, as well as muscle fiber necrosis and regeneration.

4. Gene detection The abnormality of the CTG repeat sequence of the 3'-untranslated region of the myotonic kinase gene of chromosome 19q13.3 in patients with chromosome 19q13.3 was more than 40 replicates (normally 5 to 40), which can be confirmed.

5. Brain MRI: MRI studies in the brain of DM1 patients showed a decrease in brain volume, enlarged ventricles, impaired focal white matter, and cortical atrophy. The corpus callosum and pituitary gland were smaller in DM1 patients than in normal subjects, while the parietal cortex volume was not significantly reduced. Fifteen DM1 patients underwent exercise testing, and the right thumb repeatedly touched the remaining four fingers in sequence, while using fMRI to study the patient's brain activity. It was found that the activity of the inferior lobular lobe, basal ganglia, thalamus and ipsilateral anterior region, and supplemental motor area in the bilateral sensorimotor area of DM1 patients was enhanced compared with normal subjects. Analysis of the relationship between disease and age found that DM1 patients with age, their bilateral sensorimotor and contralateral dysfunctional movement activities were greater than the normal control group. The brain of DM1 patients may compensate for the ultrastructural and neurochemical changes that occur during aging of the patient through changes such as recombination and redistribution of the functional zone.

Differential diagnosis

Need to be identified with the following symptoms:

Facial muscle atrophy: facial muscle atrophy refers to dystrophy of striated muscle, muscle volume is reduced compared to normal, muscle fibers become thinner or even disappear. Neuromuscular disease is hypertrophy. In addition to the pathological changes of muscle tissue itself, muscle nutrition is closely related to the nervous system. Spinal cord disease often leads to muscular dystrophy and muscle atrophy.

Facial muscle weakness:

The facial nerve consists of two parts: the motor fiber and the middle nerve that govern the facial expression muscle. The interneuron is composed of sensory and parasympathetic fibers. The damaged part of the face can be in the brainstem, the skull base, the facial nerve canal and its distal end. The nucleus and the pons are adjacent to the facial nucleus. Therefore, brain stem lesions involving the facial nerve are often accompanied by cross-sectional convulsions composed of ocular abduction or lateral paralysis. Facial nerve injury mainly manifests as peripheral facial spasm or hemifacial spasm.

Facial muscle twitching: facial muscle twitching, also known as hemifacial spasm, the common clinical manifestation of the primary facial muscle twitching patients mostly after the onset of middle-aged, more women. When the disease starts, it is mostly intermittent twitching of the orbicularis muscle, which gradually spreads slowly to other facial muscles on one side of the face. The twitching of the horn muscles is most noticeable, and in severe cases, the platysma can be involved in the same side. The degree of convulsions varies, and can be exacerbated by fatigue, mental stress, and autonomous movement, but cannot be imitated or controlled by oneself.

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