Eat

Introduction Eating and eating is also called difficulty in pronunciation. It is caused by muscle atrophy, paralysis, motor coordination disorder or convulsions of the vocal organs, causing inaccurate speech, uneven rhyme, slow speech flow and disordered rhythm. Clinically, according to anatomical and physiological changes, there are two types of paralytic eating and mediating. Mainly due to cerebral blood diseases, intracranial tumors, inflammation, toxic diseases, multiple sclerosis, myasthenia gravis, medullary cavity, amyotrophic lateral sclerosis. The primary disease should be actively treated, and certain functions should be restored through certain rehabilitation training.

Cause

The pathological basis of paralytic eating is in the muscles, cranial nerves, cranial nerves or pyramidal bundles. The main diseases are cerebral blood diseases, intracranial tumors, inflammation, toxic diseases, multiple sclerosis, myasthenia gravis, medullary cavity, amyotrophic lateral sclerosis.

Regulatory eating is the vocal organ in addition to the nerve impulses issued by the cortical-nucleus-peripheral nerve pathway, the regulation of extrapyramidal and cerebellum is also important. When the extrapyramidal and cerebellum develop lesions, they are eaten due to the regulation of dysfunction. Cerebellar nevus is common in multiple sclerosis, hereditary ataxia, cerebellar trauma, and tumors. It is more common in the extrapyramidal lesions to be seen in the Wilson's disease, hand and foot hyperkinesia, torsion sputum, Parkinson's syndrome, and chorea.

an examination

Related inspection

Otolaryngology CT examination of serum lipase serum lipase (LPS)

Paralytic eating can have different clinical manifestations due to different damaged parts. For example, when VII brain damage occurs, it causes lip weakness or paralysis. When the buccal buccal and whistling, the labial muscles are found, affecting the lip tooth sound b , p, m such as bag (bo), toss (páo), cat (máo) and lip sound f such as flying (fi); in IX, X brain innervation of the pharyngeal muscle - soft sputum weakness or paralysis, when speaking The nasal sound is very heavy, and the pronunciation of the breath is short due to the leaking of the nose, and the pronunciation is ambiguous. The pronunciation of the initials g, k, h is particularly difficult. At the same time, accompanied by difficulty swallowing, eating cough, soft palate rise, incomplete pharyngeal reflex or disappear. When the XII cranial nerve dominates the lingual tendon, the tongue is skewed and has atrophy of the tongue muscle and muscle fiber tremor; when the bilateral lesions are not able to stretch the tongue, the tongue sounds S and Z sounds are ambiguous.

Regulatory neat can vary depending on the location of the lesion. Cerebellar palpebral lesions can make the articulated muscles coordinate disorders, dysarthria, ambiguous speech, intermittent stagnation or bursting, beat-like and sinister words, accompanied by unstable standing, gait, easy Dumping, posture tremors, limb ataxia, and nystagmus. Extrapyramidal lesions can cause changes in vocal muscle tone or involuntary movement. When the muscle tension is enhanced, such as Parkinson's syndrome, the speech is slow, the pitch is low, the sentence is monotonous, and the vibrato and the first word are often repeated, saying that the exercise is too vocal. The pronunciation muscles are involuntarily exercised, such as chorea, and the speech is high and low. The time is fast, the time is slow, the length is different, the tone is inlaid, the language is repeated, and the speech can be suddenly interrupted or started.

Differential diagnosis

First, paralyzed

(a) cerebrovascular disease (cerebrovascular disease): vertebral-basal artery occlusion can cause paralytic eating, but also dizziness, tinnitus, difficulty swallowing, ataxia, cross sputum and other performance. More common in cerebral thrombosis and cerebral embolism, according to medical history, clinical manifestations, laboratory tests can make a preliminary diagnosis, CT and MRI have a diagnostic value.

(B) inflammation (inflammation): inflammatory damage to medullary poliomyelitis, brain stem inflammation, acute infection, polyneuritis and so on. Medullary poliomyelitis is more common in children aged 1 to 5 years who do not prevent oral vaccines. More frequent in summer and autumn, there are fever and respiratory tract, digestive tract, prodromal symptoms, 3 to 8 days after onset, one or both sides of the asymmetrical asymmetry of the temperate medullary type of children with common XII, X, XII on the cranial nerve damage. There are eating and corresponding symptoms. The cerebrospinal fluid cell count can be increased to 50-500/mm3, with more lymphocytes and a slight increase in protein. A virus can be isolated from the nasopharynx and feces within one week of onset. Serological tests such as neutralization test, complement fixation test, and hemagglutination inhibition test are helpful for diagnosis. Acute infectious polyneuritis mostly occurs in acute subacute onset. 80% of patients have symptoms of upper snoring and intestinal infection before the disease, and the limbs rapidly appear symmetry, flaccid paralysis, and proximal end. More than half of the cranial nerve palsy occurs. There are symptoms of deafness and other cranial nerve damage, cerebrospinal fluid shows cell protein separation, and electromyography shows neuronal damage. There is a tendency to relapse. In addition to intracranial inflammation, brain stem inflammation has cranial nerve symptoms and even respiratory and circulatory disorders.

(3) Poisoning: Organophosphorus poisoning, organic mercury poisoning, botulism, etc. can cause paralysis. Botulism poisoning generally has suspicious foods such as canned food and a history of collective disease, clinical symptoms such as ophthalmoplegia, speech, swallowing, difficulty in breathing, etc., and detection of exotoxin and animal inoculation test from the gastrointestinal contents of patients. Positive can confirm the diagnosis. Diagnostic evidence for exposure history or history of exposure to organic phosphorus, organic mercury poisoning, clinical manifestations, decreased bile lipase activity, and elevated blood mercury.

(4) bulbar tumour: medullary tumor is common in children, may have symptoms of increased intracranial pressure, there is a posterior group of cranial nerve damage and contralateral limb cross sputum, the symptoms are progressively aggravated.

(5) Muscular disease: Myasthenia gravis starts from 20 to 30 years old, and there are more women. The affected muscles are weak and the morning light is heavy and heavy. After fatigue, it is aggravated and recovered after rest. Patients with medullary type have low nasal sounds, difficulty in swallowing, difficulty in articulation, weakness in masticatory muscles and facial expression, and drinking water flowing out of the nostrils. Fatigue tests and anti-cholinesterase drug tests can help diagnose. In addition to necrosis, there are eyelid dysfunction, difficulty in swallowing, slow progressive atrophy of the pharyngeal muscles, mild involvement of the muscles of the face and limbs, and chronic progressive progression of the disease. Polymyositis, dermatomyositis can invade the throat muscles, and even become the sole complaint, with systemic muscle atrophy, weakness and myalgia, and can be positive for rheumatoid factor, urinary creatine is easy to increase (24 hours discharge is higher than 200 mg has diagnostic value), EMG and muscle biopsy can help diagnose.

(6) syringitis (syringitis): mostly for the continuation of cervical medullary cavity to the brainstem, often damage one side of the cranial nerve or conduction beam, common symptoms are nystagmus, one side vocal cords and soft palsy, tongue muscle atrophy and fiber Trembling. The medullary CT scan shows a high-density cavity scene, and MRI can clearly show the location and size of the cavity in the longitudinal and transverse sections.

(7) Multiple sclerosis (MS): characterized by demyelinating diseases of the central nervous system, characterized by multiple lesions and alternating remission in the course of disease. Mainly manifested as nystagmus, vision loss, lower limb paralysis, deep sensory disturbance, disappearance of parietal wall reflex, positive Pap smear. Brain stem damage can be eaten, tinnitus, deafness and so on. In the cerebrospinal fluid examination, the number of cells, protein increased slightly, and r globulin increased. The oligoclonal test was positive and the somatosensory evoked potential was abnormal. A CT scan of the head showed plaque around the ventricles. Demyelinating antibodies can be found in tissue cultured acute patient sera.

(8) Motor neuron disease: The dysphonic difficulty of amyotrophic lateral sclerosis is a chronic progressive disease course. Due to lesions, the anterior horn cells and pyramidal tracts of the spinal cord are damaged. . 1 to 2 years after the disease, there is a manifestation of medullary damage. In addition to eating neat, there may be difficulty in swallowing, drinking water and cyanosis. In the examination, the soft palate and the muscle strength of the throat were poor, and the pharyngeal reflex disappeared. Tongue muscle atrophy is early and obvious, there is fasciculation, and the cortical medulla oblongata appears strong crying and strong laughter. The mandibular reflex is hyperthyroidism, and the pouting reflex is obvious, which constitutes a pseudo-balloon paralysis syndrome. Progressive medullary (ball) paralysis is rare. The lesions are mainly cerebral pons, medullary cranial nerves, and involve the cortical brain stem and other sports fibers, which are characterized by difficulty in pronunciation and other symptoms. Progressed rapidly and died of lung infection within 13 years.

Congenital medullary sacral deformity, skull base concealment, inflammation near the occipital foramen, fractures, etc. can also appear paralyzed and other craniocerebral dysfunction.

Second, regulatory stammering (regulatory stammering)

(a) cerebellar lesions

1. Hereditary ataxia (heredoataxia): juvenile myeloid hereditary ataxia is the most common type of disease, usually starting at about 10 years old, the main symptoms are ataxia of lower limbs, loss of tendon reflex Deep sensory disturbance and damage to the pyramidal tract. It has the characteristics of sensory ataxia in the early stage. The characteristics of cerebellar ataxia with the increase of degeneration of the cerebellar tract of the spinal cord from 15 to 20 years old may have mild involuntary movements due to uncoordinated movements. Cerebellar dysarthria is a prominent clinical sign of the disease. Some patients have optic atrophy and retinitis pigmentosa. Intelligent barriers, cardiac hypertrophy, murmurs, bundled conduction stagnation and T wave inversion. Late systemic weakness and muscle atrophy, fasciculation can be seen. All cases had progressive bone deformities. Biochemical examination showed that the pyruvate dehydrogenase activity decreased (generally 50% of normal), and the nerve conduction velocity test showed that the conduction velocity slowed down. Hereditary spastic ataxia, often with blasting speech, increased muscle tone, hyperreflexia, disappearance of abdominal wall reflex, positive pathological reflex, optic atrophy, dying. No skeletal deformities. Late onset cerebellar cortical atrophy is rare, more sensitive to onset after 30 years of age, clinical features of walking and standing instability, upper limb symptoms are relatively light, head and trunk static tremor and difficulty in articulation. In the later stage, there may be nystagmus, no extrapyramidal symptoms, and other such as olive bridge cerebellar atrophy may also cause regulatory necrosis.

2. Multiple sclerosis: 10% to 15% of patients have a regulation of nephropathy and ataxia. The clinical features have a tendency to aggravate and relapse in the course of the disease. Cerebrospinal fluid gamma globulin and IgG increase and protein electrophoresis with less clonotype are important laboratory tests, EEG and CT scan can help diagnosis. Cerebellar trauma, cerebellar tumor, cerebellar abscess, etc. are rare to eat.

(two) extrapyramidal lesions

1. Hepatolenticular degeneration: between 10 and 20 years of age, there may be a family history. The initial symptoms are gross tremors on one or both sides of the limbs, and the head may be extended to the head and torso. Mental abnormalities can be the first symptom, and some patients have muscle rigidity, reduced movement, dysarthria, "mask face", and do not self-defective crying and other symptoms. Late limb flexion contracture, difficulty swallowing, sputum outflow and mental decline. At the junction of the posterior border of the cornea and the sclera, a green-brown pigment ring can be seen, which increases the increase of urinary copper, decreases the total amount of serum copper and serum ceruloplasmin, increases the amount of serum direct anti-Qing and increases the serum copper oxidase activity. At the beginning of the patient, only the speech was uneven, and the evaluation of the progress of the disease gradually became vague. Some rhymes cannot be correctly expressed, and late speech is extremely difficult, and even public can express individual words.

2. Atherosclerosis (athletosis): a clinical syndrome caused by striatum degeneration. Common causes are basal ganglia marble-like degeneration, encephalitis, and nuclear jaundice. A few months after birth, there is a pulsating action, starting from the finger, which can affect the facial muscles, lower limb muscles, throat muscles, and tongue muscles. Intensified when the spirit is tense, disappears after falling asleep. Feeling normal, intelligence can be reduced. The course of disease can range from several years to several decades. Electroencephalography CT and MRI can assist in diagnosis.

3. Chorea: Choral disease is often manifested by the rheumatic fever nervous system, with slow onset, involuntary movements, low muscle tone, mood changes, and rheumatic activity symptoms. Laboratory examination showed increased erythrocyte sedimentation rate, increased anti-"O", and increased serum mucin. Difficulty swallowing due to involuntary movement invading the tongue and pharyngeal muscles. Chronic progressive chorea usually eats in adulthood, with a distinct family history, mainly characterized by dance-like movements and mental retardation, and the condition is chronic progressive deterioration. The language is very early, and the voice is monotonous. Pregnancy chorea is more common in women with first-episode pregnancy with a history of rheumatism. Symptoms can disappear after termination of pregnancy.

4. Paralysis: After more than 50 years of age, the main clinical manifestations are reduced joint movement of the limbs, muscle rigidity and tremor. The language is reduced, low, and monotonous. The dopamine metabolites in the patient's cerebrospinal fluid have a high content of vanillic acid and 5-hydroxyindole acetic acid. Pediatric dopamine and high vanillic acid are also reduced.

5. Torsion spasm: rare in clinical practice. Mainly manifested as the body and involuntary distorted movements of the trunk and limbs, accompanied by increased muscle tone, increased urinary dopamine discharge, and slow progression. Hemifacial spasm, difficulty swallowing, and dysarthria occur when the facial muscles, pharynx, and laryngeal muscles are involved. Paralytic eating can have different clinical manifestations due to different damaged parts. For example, when VII brain damage occurs, it causes lip weakness or paralysis. When the buccal buccal and whistling, the labial muscles are found, affecting the lip tooth sound b , p, m such as bag (bo), toss (páo), cat (máo) and lip sound f such as flying (fi); in IX, X brain innervation of the pharyngeal muscle - soft sputum weakness or paralysis, when speaking The nasal sound is very heavy, and the pronunciation of the breath is short due to the leaking of the nose, and the pronunciation is ambiguous. The pronunciation of the initials g, k, h is particularly difficult. At the same time, accompanied by difficulty swallowing, eating cough, soft palate rise, incomplete pharyngeal reflex or disappear. When the XII cranial nerve dominates the lingual tendon, the tongue is skewed and has atrophy of the tongue muscle and muscle fiber tremor; when the bilateral lesions are not able to stretch the tongue, the tongue sounds S and Z sounds are ambiguous.

Regulatory neat can vary depending on the location of the lesion. Cerebellar palpebral lesions can make the articulated muscles coordinate disorders, dysarthria, ambiguous speech, intermittent stagnation or bursting, beat-like and sinister words, accompanied by unstable standing, gait, easy Dumping, posture tremors, limb ataxia, and nystagmus. Extrapyramidal lesions can cause changes in vocal muscle tone or involuntary movement. When the muscle tension is enhanced, such as Parkinson's syndrome, the speech is slow, the pitch is low, the sentence is monotonous, and the vibrato and the first word are often repeated, saying that the exercise is too vocal. The pronunciation muscles are involuntarily exercised, such as chorea, and the speech is high and low. The time is fast, the time is slow, the length is different, the tone is inlaid, the language is repeated, and the speech can be suddenly interrupted or started.

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