Upper motor neuron paralysis
Upper motor neuron paralysis, also known as central paralysis, is caused by the damage of cortical motor projection area and upper motor neuron pathway (cortical spinal cord bone marrow tract and cortical brain stem tract). Because the muscle tension of paralyzed muscles increases, it is also called spastic paralysis or hard paralysis. Because the fibers and cells of the fiber bundle are arranged quite closely, the paralysis of upper motor neurons is mostly extensive, affecting the whole limb or one side of the body.
Etiology, pathology and pathogenesis
Any damage to cortical motor projection area and upper motor neuron pathway may lead to upper motor neuron paralysis. The common causes are craniocerebral trauma, tumor, inflammation, cerebrovascular disease, degeneration and poisoning, as well as some diseases in internal medicine, such as diabetes, hematoporphyrin disease, erythrocytic anemia and vitamin B 12 deficiency.
clinical picture
Different types of paralysis, such as paralysis, hemiplegia, paraplegia, quadriplegia, etc. Clinically, it can occur due to different lesion sites. Although the manifestations of paralysis are different, they all have the same characteristics, that is, increased muscle tension, hyperactivity of tendon reflexes, disappearance of shallow reflexes, so-called joint (joint) movements and pathological reflexes, no atrophy of paralyzed muscles, and no denaturalization reaction in electrical tests.
Diagnosis and differential diagnosis
Transient ischemic attack
Transient ischemic attack. TIA refers to the temporary and limited loss of brain function caused by transient cerebral ischemia. Paralysis of upper motor neurons is characterized by sudden disappearance of symptoms, which usually lasts for several minutes to tens of minutes, and can be relieved within 24 hours without any sequelae.
(2) Cerebral hemorrhage
Cerebrovascular hemorrhage refers to hemorrhage caused by rupture of blood vessels in brain parenchyma. Typical upper motor neuron paralysis occurs. Patients have a history of hypertension and atherosclerosis, mostly middle-aged and elderly people over 55 years old, and most of them are in a state of dynamic and exertion. Headache, dizziness and unconsciousness often occur a few hours to a few days before onset. Acute onset, rapid progress, often appear disturbance of consciousness, hemiplegia, early vomiting and other focal symptoms of the nervous system. Cerebrospinal fluid pressure increased, 80% of cerebrospinal fluid was mixed with blood, and 50% of patients showed bloody appearance. CT examination showed high density shadow of intracranial hematoma.
(3) Cerebral thrombosis
Cerebral vascular thrombosis is the most common acute cerebrovascular disease. Symptoms and signs of upper motor neuron paralysis often appear in a quiet state, and 25% patients have a history of transient ischemic attack. The onset is slow, mostly progressive or staged, and it is more common in atherosclerosis, arteritis and hematological diseases. Generally, consciousness is clear or slightly disordered within 12 days after onset. Cerebrospinal fluid examination is normal, and brain CT or MRI examination can obviously increase the location and scope of infarction. Cerebral angiography can show the stenosis or occlusion of diseased arteries.
cerebral embolism
Cerebral embolism refers to emboli from all parts of the body, which enter the skull through carotid artery and vertebral artery, blocking the cerebral vessels and causing brain dysfunction. It is characterized by primary diseases of embolus origin, such as rheumatic valvular disease, subacute bacterial endocarditis, acute myocardial infarction and atrial fibrillation. The onset is sudden, mostly without premonitory symptoms, and the symptoms peak after a few seconds or minutes. How strong your consciousness is, or have a temporary disturbance of consciousness. The symptoms of the lesion are obvious, and most of them are symptoms of internal carotid artery involvement. There was no obvious change in cerebrospinal fluid, CT showed low density area consistent with arterial distribution, and cerebral angiography showed vascular occlusion.
(5) Brain tumor
Intracranial tumors can cause localized epilepsy and contralateral limb paralysis to varying degrees. Tumors in frontal lobe, parietal lobe and temporal lobe can sometimes cause upper motor neuron paralysis, and brain stem tumors often cause cross paralysis. Most of them have slow onset, headache, vomiting, nipple edema? Three characteristics? And symptoms of local neurological dysfunction at the tumor site. The content of protein in cerebrospinal fluid increased, and the number of cells was normal. However, lumbar puncture is prohibited for patients with increased intracranial pressure to avoid cerebral hernia. CT and MRI can confirm the diagnosis.
(vi) Acute myelitis
Acute mgelitis is more common in young adults, with sudden onset, symptoms and signs of systemic infection and spinal cord transection injury, and increased protein and cells in cerebrospinal fluid. First of all, limb paralysis is characterized by relaxation paralysis, decreased muscle tension, weakened or disappeared tendon reflex, and no pathological reflex (spinal shock phenomenon). After a few weeks, the phenomenon of spinal cord shock gradually decreased, muscle tension and tendon reflex recovered, and pathological reflex appeared. Urinary retention becomes urinary incontinence and reflex urination occurs.
(7) Spinal arachnoiditis
The onset of spinal arachnoiditis can be acute or chronic, which can be secondary to infection, trauma, intrathecal injection of drugs, spinal cord or spinal cord lesions. Symptoms such as fever or cold may appear first, and then symptoms such as nerve root pain and spinal cord compression may appear, manifested as paraplegia or quadriplegia, as well as sensory disturbance and sphincter dysfunction. This disease often has the characteristics of multiple lesions; Long course of disease; The condition is good and bad, and sometimes it will be relieved or relapsed. Protein content in cerebrospinal fluid is increased, and white blood cells are increased or normal. Iodine angiography of spinal cord can show partial or complete obstruction.
(8) Tumors in spinal cord and spinal canal
The early symptoms of extramedullary tumors are nerve root pain, which can be aggravated by cough, defecation and exertion. With the progress of the disease, symptoms such as spinal cord compression, numbness and abnormal sensation appear at the distal end of the lower limb, which gradually develops to the lesion plane, and paraplegia or quadriplegia occurs at the same time. Pain symptoms of intramedullary tumors are rare, which often lead to segmental dissociative sensory disturbance and early urinary incontinence. The content of protein in cerebrospinal fluid is increased, and it can be separated into protein cells. There is obstruction in the spinal canal. X-ray film of spinal cord, lipiodol myelography and CT examination are helpful for diagnosis.
(9) Amyotrophic lateral sclerosis
The prominent pathological phenomena of this disease are degeneration of corticobulbar tract and corticospinal tract, loss of anterior horn cells of spinal cord and damage of motor nucleus of brain stem. Clinically, it often begins with local atrophy and weakness of one small muscle, gradually spreads to the opposite side, and then spreads upward to the forearm, upper arm and shoulder strap muscles. The muscle strength of both upper limbs decreases, and obvious muscle bundle tremor often appears in the affected muscles. With the development of muscle atrophy in upper limbs, muscle weakness, increased muscle tension, hyperreflexia and pyramidal tract sign gradually appear in lower limbs. The symptoms of progressive bulbar palsy often appear in the later stage.
(10) syringomyelia
Syringomyelia (syngomyelia) When the cavity involves the pyramidal tract, limb weakness, increased muscle tone, hyperreflexia of tendon and upper motor neuron paralysis with positive pathological reflex appear below the involved spinal cord segment. Most of its paralysis is bilateral asymmetry. There is also a kind of separation sensory disorder between semi-mandarin jacket and mandarin jacket, that is, the pain and temperature sensation disappear, and the touch and deep sensation are relatively normal. Spinal cord lipiodol angiography showed that the spinal cord was swollen at the lesion site, and CT or MRI examination clearly showed that the lesion spinal cord was swollen and there were strip cavities in the spinal cord.
(1 1) Sporadic encephalitis
Sporadic encephalitis is a common infectious disease of central nervous system in neurology. When the vertebral tract is damaged, hemiplegia or positive pyramidal tract sign of both limbs appears. However, there was a history of infection before the disease, and there were symptoms and signs of diffuse brain parenchymal damage. Most patients are accompanied by mental disorders of different degrees. Cerebrospinal fluid is normal or mild inflammation, EEG is diffuse abnormal, skull CT shows scattered or a large number of low-density shadows in brain parenchyma, and skull MRI shows large edema areas and softening foci.
Paralysis of lower motor neuron
Lower motor neuron paralysis, also known as peripheral paralysis. It is the result of the damage of the motor fibers of the anterior horn cells of the spinal cord (or motor nucleus cells of the brain), the anterior root of the spinal cord, the peripheral nerves of the spine and the peripheral nerves of the brain.
Etiology of lower motor neuron paralysis
The common causes of lower motor neuron paralysis are: peripheral nerve injury, such as laceration, contusion, compression, brachial plexus injury, electric injury, radiation injury, burn and so on; Toxic damage, including drugs, organic substances, inorganic substances, bacterial toxins, etc. ; Peripheral neuritis, including infectious, post-infection and allergic diseases, connective tissue diseases and nodular peripheral neuropathy; Peripheral neuropathy in metabolic diseases; Peripheral neuropathy in malignant diseases; Peripheral nerve tumors, primary peripheral neuropathy related to heredity, etc.
Clinical manifestations of lower motor neuron paralysis
The clinical features of lower motor neuron paralysis are decreased muscle tone (so it is also called flaccid paralysis), weakened or disappeared tendon reflex, muscle atrophy and degeneration reaction in electrical test. The characteristics of lesions in different parts are as follows:
1. Lesions of spinal cord anterior horn cells: Lesions confined to anterior horn cells cause flaccid paralysis without sensory disturbance, and the distribution of paralysis is segmental, such as deltoid paralysis and atrophy caused by cervical spinal cord anterior horn injury.
2. Anterior root lesion: The distribution of paralysis is also segmental, and root pain and segmental sensory disturbance occur due to frequent invasion of posterior root at the same time.
3. Neuropathy: Injury usually leads to paralysis and sensory disturbance of most peripheral nerves of limbs.
4. Peripheral neuropathy: The distribution of paralysis and sensory disturbance is consistent with the innervation of each peripheral nerve.
Differential diagnosis of lower motor neuron paralysis
(1) Acute polio usually begins with symptoms such as fever, sore throat, anorexia, nausea, vomiting, constipation and diarrhea. Generally, limb paralysis occurs on the 3rd to 5th day after the onset of fever. Paralysis is more common in one lower limb, both lower limbs or limbs involved, which is characterized by asymmetric flaccid paralysis, relaxation of muscle tension and weakening or disappearance of tendon reflex. Feelings exist. The number of cells in cerebrospinal fluid increased, and the content of protein increased slightly.
(2) Acute infectious polyneuritis is also called acute polyradiculitis or Guillain-Barre syndrome. History of nonspecific infection within 0 ~ 3 weeks before onset of 65438+. Acute onset, muscle weakness of lower limbs, rapid upward development, quadriplegia 1 ~ 2 days. Paralysis and relaxation, tendon reflex weakened or disappeared. The muscles are tender. Distal muscle atrophy, no obvious sensory disturbance. It is often accompanied by cranial nerve damage, especially unilateral or bilateral facial nerve damage. In severe cases, symptoms of bulbar palsy such as hoarseness and dysphagia may occur, and respiratory muscle paralysis may occur. Is cerebrospinal fluid protein with increased protein and normal or near normal cell count? Cell separation phenomenon.
(3) Brachial plexus injury is an acute onset, and upper limb pain is the characteristic of the disease. First at the root of the neck, above the clavicle, and then quickly spread to the shoulders, back, arms and hands. The pain started intermittently and then became persistent. Most of them disappeared within 1 ~ 2 weeks. The muscle strength of the affected upper limb is weakened, tendon reflex is reduced or disappeared, the superficial feeling of hands and fingers is reduced, and muscle atrophy is not obvious. There is tenderness in the nerve trunk during physical examination, which is characterized by paralysis of the upper arm and normal muscle function of hands and fingers; The main manifestations of lower brachial plexus injury are paralysis of distal upper limbs and muscular atrophy of small hands. Eagle claw hand? Ulnar sensory and autonomic nerve dysfunction in forearm and hand. EMG lost nerve potential, decreased motor unit, increased polyphase potential and prolonged duration.
(4) Polyneuritis mainly manifested as sensory disturbance of symmetrical distal limbs, paralysis of lower motor neurons and autonomic nerve disturbance. Its paralysis is characterized by symmetrical motor neuron paralysis at the distal end of the limb, which can range from paraplegia to total paralysis according to the severity of nerve involvement. Muscle tension decreases, tendon reflex weakens or disappears, and ankle reflex weakens earlier than knee reflex. Muscle atrophy may occur, showing that the distal end is heavier than the proximal end. The tibialis anterior muscle, fibula muscle, interosseous muscle, lumbricoid muscle, thenar muscle and thenar muscle of lower limbs are obviously atrophied, their hands and feet can droop, and they can walk with a cross-threshold gait.
(5) Radial nerve paralysis The main manifestations of radial nerve paralysis are that the wrist, fingers and thumb cannot be straightened, that is, the wrist droops, and the sensation on the back of the thumb and the first and second metacarpal bones weakens or disappears. According to different injured parts, it has different effects. Axillary injury, except wrist droop, elbow joint can not be straightened because of triceps brachii paralysis, forearm can not bend elbow because of brachioradialis paralysis. For example, in humeral injury, triceps brachii functions well. When the injury is at the lower end of humerus or arm 1/3, the functions of brachioradialis muscle, supinator muscle and extensor muscle are preserved, and when the injury is below arm 1/3, only the finger extension function is lost, and there is no wrist droop. If the injury is in the wrist joint, symptoms of dyskinesia may appear.
(6) Ulnar nerve paralysis When ulnar nerve paralysis occurs, the fingers are radial, the ulnar abduction is weakened, the movement of the little finger is impaired, and the thenar muscle and interosseous muscle atrophy. The ulnar side of the palm and the back of the hand, and the ulnar half of the whole little finger and ring finger are sensory disorders.
(7) caypal tunnel syndrome can be caused by fracture, trauma or thickening of transverse carpal ligament that compresses median nerve. The main manifestations are that the flexion function of fingers is weakened, the thumb and forefinger can't bend, the thumb can't move against the palm, and the thenar muscle is obviously atrophied. Finger 1 ~ 3, little finger and half finger, palmar and radial sensory disturbance. Symptoms of autonomic nervous dysfunction such as dry skin, cold skin and fragile nails appear.
(8) Paralysis of peroneal muscle and tibialis anterior muscle group occurred after peroneal nerve paralysis. It is characterized by drooping feet, inability to bend back when practicing feet and soles, and difficulty in walking heels. When walking, lift your feet. When the feet land, the toes droop and the whole sole touches the ground, which is similar to the gait of a chicken. This is the so-called cross-threshold gait. Sensory disturbance of anterolateral calf and dorsum of foot.
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4. What is motor neuron disease?
5. What is lower motor neuron injury?
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7. What are the sequelae of cerebral hemorrhage?