The brain is manifested as transient brain dysfunction, no macroscopic neuropathological changes, and neurological structural disorders can be seen under the microscope. May be related to diffuse brain injury due to inertial forces. The main symptom is a transient disturbance of consciousness immediately at the time of injury, which may be unconscious or completely unconscious, usually for seconds or minutes, usually less than half an hour. Most people who are awake cannot recall the situation at the time of the injury or even the period before the injury, which is called retrograde amnesia. During the period of consciousness disorder, the more severe patients may have ** pallor, sweating, decreased blood pressure, bradycardia, shallow and slow breathing, decreased muscle tone, and various physiological reflexes are dulled or disappeared, but they tend to normal soon with the recovery of consciousness. Symptoms such as headache, dizziness, nausea, and vomiting may occur thereafter, but they may improve on their own in a short period of time. There were no positive signs on neurological examination, no red blood cells on cerebrospinal fluid examination, and no abnormal intracranial findings on CT examination.
The spinal cord is similar to the brain, and the spinal cord is the least severe injury to the spinal cord. Flaccid paralysis occurs immediately after a strong attack on the spinal cord, with loss of sensory, motor, reflex, and sphincter function below the level of injury. Because there are no pathological changes in histomorphology, there is no substantial spinal cord injury, and only temporary functional suppression, which can be fully recovered within minutes or hours. Nerve reflexes above the spinal cord injury segment may also be suppressed. Spinal cord reflexes are always abnormal from foot to head and may be accompanied by abnormal signs such as Babinski's sign and muscle spasms.
In addition, flaccid paralysis below the level of injury can occur immediately after a variety of more severe spinal cord injuries, a pathophysiological phenomenon known as spinal shock in which higher central control is lost. During spinal shock, flaccid paralysis occurs below the level of injury, loss of movement, reflexes, and sphincter function, loss of sensory level, and inability to control bowel and bowel movements. Autonomic reflexes can be affected to varying degrees during spinal shock due to the presence of external dorsal root nodes. After 2 4 weeks, this phenomenon can occur with varying degrees of spastic paralysis below the level of injury, depending on the degree of parenchymal damage to the spinal cord, manifested by increased muscle tone, hyperreflexia, and pathologic pyramidal tract signs. Thoracic spinal cord injuries present as paraplegia, while cervical spinal cord injuries present as quadriplegia. Quadriplegia with upper cervical spine injury is spastic paralysis, and quadriplegia with lower cervical spine injury is flaccid paralysis due to the destruction of spinal cord-neck distension and nerve roots, and the lower limb is still spastic paralysis. Therefore, spinal shock and spinal cord** are two completely different concepts.
Spinal shock was first proposed by Hall 150 years ago to distinguish hemorrhagic shock from hypotension caused by reduced sympathetic tone caused by spinal shock. The latter concept, which refers to the loss of distal spinal nerve reflexes due to spinal cord injury, is actually the same concept. It is currently a clinical phenomenon caused by a temporary loss of reflex activity of the spinal cord below the level of injury caused by anatomical and physiological spinal cord transection injury. Spinal shock can occur immediately after spinal cord injury or may occur several hours later due to a progressive exacerbation mechanism. In general, the more severe the transection injury, the deeper the state of spinal shock. The presence of spinal shock in the same spinal cord injury suggests more rapid progression of the spinal cord injury and a poor prognosis. Nerve reflexes elicited suggest the end of the spinal cord shock phase, but nerve reflexes in the injured segment of the spinal cord may never recover.
Segments adjacent to spinal cord injury are most affected, with loss of nerve reflexes; Segments farther from spinal cord injury are suppressed later. In fact, the farther away from the site of injury, the more some nerve reflexes appear to be preserved. Patients with clinically high spinal cord (cervical) injury may retain sacral reflexes, such as bulbocavernosus reflex and anal reflex, while other nerve reflexes are absent. The lower the segment of spinal cord injury, the less likely it is that distal nerve reflexes will be preserved. Schiff-Sherrington phenomenon: spinal cord injuries as low as lumbar 3 can affect the upper extremities, usually for hours or days. The loss of the nerve reflex arc adjacent to the spinal cord injury segment is based on this phenomenon. In incomplete injury, the retention of anal contraction and partial sensation in the sacrococcygeal region is the basis for distinguishing between complete and incomplete injury, and the bulbocavernosal reflex and anal reflex restriction preserved in high spinal cord injury should not be confused with residual sensation in the sacrococcygeal region.