apraxia
Introduction
Introduction Neurological insufficiency is one of the clinical symptoms of spinal neuropathy in a single neuropathy. Neurological insufficiency is a temporary block of nerve trauma, which can be divided into two types: one is transient ischemia and no anatomical change, causing mild transient conduction block; the other is staged demyelination, axonal normal, Symptoms can be restored within 2-3 weeks. Single neuropathy is a single neuropathy that produces clinical symptoms consistent with this neural distribution. Neuralgia is pain in the area of damaged nerves and is divided into two categories: idiopathic and symptomatic. Idiopathic neuralgia is a paroxysmal pain in the area of damaged nerves. Normally, nerve conduction function is normal and there is no pathological change. Symptomatic neuralgia is an early symptom of various etiological neuropathies. There is no obvious sensation and lack of motor function. A lesion adjacent to the tissue on the spinal or neural pathway.
Cause
Cause
Mainly due to local causes such as trauma, ischemia, tumor invasion and physical damage, it can also be caused by systemic metabolic (such as diabetes) or toxic (such as lead poisoning) diseases.
Pathophysiology
Nerve trauma leads to temporary block, axonal injury, and nerve injury; oppressive neuropathy is peripheral nerve injury caused by compression of tumor, epiphysis, synovial membrane and fibrous band. Slight compression causes demyelination, and severe cases lead to axonal degeneration.
Examine
an examination
Related inspection
Electromyography F-wave
According to clinical manifestations and pathological findings can be divided into:
(1) Neurological disability: It is a temporary block of nerve trauma, which can be divided into two types: one is transient ischemia and no anatomical change, causing mild transient conduction block; the other is staged demyelination, The axon is normal and the symptoms can be recovered within 2-3 weeks;
(2) Axonal injury: Axonal degeneration causes Huale degeneration at the distal end, the basal layer of the Schwann cell surrounding the axon, the connective tissue of the endometrium is normal, and the axonal regenerative recovery function;
(3) nerve injury: the axon and surrounding connective tissue scaffolds are disconnected, only a small number of axons can regenerate to reach the original target organ, and most of the axonal buds become neuromas due to vagus, so the recovery surface is not complete. Compressive neuropathy is a peripheral nerve injury caused by compression of tumors, epiphyses, synovial membranes, and fibrous bands. Slight compression causes demyelination, and severe cases lead to axonal degeneration. Nerve through a narrow anatomical passage and undergoing repeated constrictive compression can lead to demyelination, known as invasive neuropathy.
Diagnosis
Differential diagnosis
Differential diagnosis of neurological disorders:
(1) Peripneral paciacial paraysis has a history of cold and infection. All facial muscles are paralyzed on the same side of the lesion, and the mouth is drooping and the sail is positive. The eyebrows are restricted, the frontal lines become shallow or disappear, the eyelids cannot be fully closed, and the scleral band is exposed at the lower edge of the cornea, and the eyeball moves up from the healthy side. The contralateral platysma contraction, the paralysis side does not contract. Due to the styloid and genioglossus, the tongue is biased to the healthy side. Occasionally, hypersensitivity, paralysis of the occipital rim of the eyelid, reflex of the orbicularis oculi muscle, blinking of the eye, reflection of the eye, and low reflex of the palmar palpebral. 2/3 wow sensation in front of the lateral tongue, tears sometimes overflow, the sucking of the facial nerve is limited when the baby is paralyzed, and the salivation of the paralyzed side is reduced.
(B) bulbar paralysis (bulbar paralysis) more bilateral medullary nerve motor function loss and autonomic dysfunction, increased salivary secretion, due to poor swallowing and lip paralysis. Peripheral paralysis of the soft palate, pharyngeal muscles, laryngeal muscles, and lingual muscles. Early speech disorder, tongue muscle fibrillation, accompanied by atrophy of the tongue muscle, the tongue gradually becomes smaller, the tongue tendon is severe, and the facial and orbicularis muscles are involved. Due to the spasm of the muscle, the pronunciation is ambiguous due to the tongue muscle. The contraction of the lips is thin, the lips are weak, the lips are wrinkled, and the whistle cannot. The paralysis of the soft palate and the pharyngeal muscles, and the occurrence of throat sounds and vocal disorders. Then there is a nasal sound. Due to the loss of motor function of the vagus nerve, the pronunciation is difficult, the difficulty of swallowing occurs when the condition is aggravated, the drinking water convulsions, the pharyngeal reflex disappears and the chewing is weak. Invading the facial nucleus, there are bilateral facial expressions around the muscles, and the face is dull and expressionless, and the palmar reflex is reduced. Respiratory rhythm disorders occur as the condition worsens. There are even phenomena such as Chao's breathing and apnea. Late circulatory failure and death.
(C) polyneuritis (polyneuritis) affected limbs have pain or sensorimotor dysfunction, the lesion area has tenderness or tenderness, sputum reflexes disappear, deep and shallow sensation diminished or disappeared. Symmetrical lower motor neuron spasm, decreased muscle tone, decreased tendon reflexes earlier than knee reflexes, and muscle atrophy distal to be more proximal. Lower extremity muscle atrophy with the tibialis anterior and tibialis anterior muscles, the upper limbs with interosseous muscles, sacral muscles, and large and small fishes are obvious, and the hands and feet can sag. The skin of the distal part of the limb is symmetrical, smooth, thin or dry, without sweat or sweating, and affects the afferent or efferent nerves, and the palmar reflex is reduced.
(D) cerebral infarction (cerebral infarction) This disease is more common in patients over 50 to 60 years old, patients with hypertension, arteriosclerosis or diabetes. More men than women, mostly in a quiet state or at rest. In the frontal and internal sac lesions, mental symptoms and hemiplegia, partial sensory disturbance and hemianopia, dominant hemispheric lesions accompanied by aphasia, non-dominant side involvement of contralateral sensory dysfunction and somatosensory disturbance. The frontal lobe lesions are sometimes positive for the contralateral palmar palsy.
(5) Cerebral arteriosclerosis (cere bral arteriosclerosis) Age more than 45 years old, early can be similar to neurasthenia, headache, head sinking, dizziness, tinnitus, numbness, tremors, insomnia, forgetting, slow thinking, attention Inconsistent, poor computational power, poor work efficiency, memory loss, brain-like mental symptoms and dementia as the disease progresses, with personality changes, apathy, carelessness, childishness, no hygiene, more words, repeated language,? or speech is reduced. The superficial temporal artery is fusiform, with asymmetry of tendon reflex, positive palmar and sucking reflex.
(6) Multiple enephalomalacia is more than 50 years old, accompanied by a history of hypertension. There are multiple irregular small cysts in the brain, and the diameter is 0.5-1.5mm. Poor memory, low intelligence, low computing power, laughter for no reason, loss of orientation, uncertainty, and even dementia. There were cerebellar ataxia and mild paralysis on one side of the upper and lower limbs, hyperreflexia, Babinski sign positive and ipsilateral palmar reflex. There may be cerebellar ataxia, but not caused by cerebellar damage, but by cortical bridge brain lesions, only mild hemiplegia, and no sensory disturbances and aphasia. There may be dysarthria, central facial paralysis and tongue sputum, difficulty swallowing, poor hand grip, and positive finger test.
