Cerebral contusion

Cerebral contusion Cerebral contusion is a traumatic effect immediately and the primary substrate having an organic lesion. It is manifested by loss of consciousness during the variable, being accompanied by neurological signs and vegetative disorders. Cerebral contusion is caused by direct hit or by reaction, as well as concussion, but in this case there is organic brain damage. May occur from an injury so close, and after an open injury.
From anatomical point of view, the substrate is organic contusion, vascular disorders are present and occur early parenchymal lesions that occur secondary vascular disorders. It is found that brain injury bleeding cortical substance, dilacerari tissue and cerebral edema. Following these lesions develop mezodermogliala necrosis. These lesions are usually localized on the face of the frontal lobes and inferior temporal cortex in the region. Deep brain contusion and bleeding occur after cerebral hemispheres moving mechanical forces on the inner surface of the skull. This movement produces hemispheres nerve damage in both substance point of impact, and in the opposite region (contraimpact lesions). Intracerebral hemorrhage with dilacerari of nerve substance occurs when severe trauma. Since the basal surface of the skull is irregular internal, inertial movement of hemispheres in case of sudden deceleration (as in car accidents) produces damage to their lower surface of the sphenoid bone protruding. Front impact hard surfaces results in contusions of the frontal lobes and orbital surface of the anterior and basal portions of the temporal lobes. Lesions appear on the external surface of the hemispheres in case of a side impact.
Classification of cerebral contusion is based on two criteria: - No serious bruises after minor, medium and severe; - Contusion after stretching can be diffuse, circumscribed (the one hemisphere, or focal cerebral lobe) or predominant in some structures (brain stem, diencefal, cerebellum).
Diffuse cerebral contusion occurs as a result of inertial acceleration-deceleration mechanisms, lesions resulting from friction between different brain structures. Circumscribed contusion arises as a result of direct contact or by reaction. Macroscopically, the brain is congested vessels and subpiale leptomeningeene are turgid. It can also be observed blood suffusions purplish color. Section appear on the surface of venous petechial hemorrhages, diffuse or circumscribed, especially in the white matter. If trauma was particularly violent, then these hemorrhages tend to form vesicular and hemorrhagic areas intraparenchimatoase. The microscopic lesions observed in the form of neural cromatoliza, alterations in reticular Golgi apparatus and multinuclear neurons. In severe forms of concussion are of hypoxic neuronal alterations, with vacuoles in the cytoplasm, and in advanced stages of concussion is loss of neuronal populations. Axons of neurons shows the fragmentation of the myelin sheath, myelin in severe cases completely disappeared. Hypertrophy observed at GLIEI microgliei.
Minor cerebral contusion In this case the determinant has a low intensity lesion. Minor cerebral contusion is totally reversible. Clinical manifestations of this form is characterized by the abolition of consciousness for a period of 20 to 30 minutes, but can reach up to 2-3 hours in some cases. There are no neurological signs or symptoms. In a small number of patients may encounter a mismatch diplopia or transient nature miotatice reflexes and signs of meningeal irritation. Autonomic changes are inconstant and transitory, slight changes were found in heart rate, respiration and blood pressure. Defective amnesia that follows this episode cupinde period abolishing consciousness a short time before the traumatic event. Evolution is favorable, the patient recovers completely in about 2-3 weeks. Postcontuzional syndrome is persistence of symptoms as headache, dizziness and fatigue beyond this range for 2-3 weeks. In this case the possible suspected and intracranial hematoma.
Average cerebral contusion In this case suffer brain lesions larger scale and are partially reversible and cleared. Clinical manifestations that accompany brain contusion average are represented by the abolition of consciousness for a period of 2-3 hours to 2-3 days. After the patient recovers from unconsciousness, he may submit a psychomotor agitation, anxiety, retrieval, or dinpotriva hiperemotivitate, can have a state of drowsiness, listlessness, dizziness and confusion. Amnesia is that in minor strokes, including traumatic events before the time period of a loss of consciousness and immediate moments after returning consciousness. Patients can not remember what hit them, I can not tell when the events that precipitated the accident. Neurological signs and symptoms of concussion always meet medium and are represented by changes in miotatice reflexes, bilateral Babinski sign present and signs of meningeal irritation. Changes in autonomic functions are present and consist of changes in heart rate (tachycardia), respiratory rate changes (polipnee), changes in blood pressure. Evolution of concussions is favorable environments, but in some cases patients may die. The patient recovers more difficult after returning consciousness, recovery lasting more than three weeks. Postcontuzional Syndrome meets more frequently.
Severe cerebral contusion This form of concussion involves irreversible brain damage or uncompensated or partially cleared. Clinical manifestations of this form of concussion are the abolition of consciousness that can last from 1-2 weeks until injury time or more. Amnesia is the same as with other forms of concussion. Neurological signs and symptoms are constantly present and consist of muscle tone disorders, disturbances in maintaining posture. Disorders of muscle tone can range from generalized weakness to rigidity by shelling. The rigidity of the upper limbs are shelling triple flexion and extension in the legs. You can meet conjugate deviation of head and eyes, generalized seizures. Changes in autonomic functions are present and consist of tachycardia, polipnee, hyperthermia, hypotensive episodes, vomiting. If achieved, and brainstem, is more severe clinical picture and the more reserved prognosis. Reaching brainstem cause coma, generalized rigidity by cerebration with hypertonic upper limbs in extension and external rotation, and lower limbs in extension and internal rotation. Autonomic disorders are severe and with closure in the brainstem reflexes are abolished.
Diagnostic Laboratory Contusion is distinguished by CT imaging and MRI (magnetic resonance imaging). On CT images damaged areas appear as areas hiperdense and MRI appear as areas hiperintense same areas. These exams objectifies also in most cases, and a degree of subarachnoid hemorrhage. After several hours after the traumatic event, nerve tissue around the lesion is edematiaza and appears at CT as a ring of low density. After a few years after the traumatic event, will highlight the CT scan scar depressions hemosiderin stained cortical surface, which may be a cause of posttraumatic epilepsy.