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TCEs occur when an external force injures the brain. Trauma can be classified according to severity, mechanism (closed or penetrating brain injury) or other characteristics. A head injury can involve damage to various structures, such as the scalp and the skull. The ECT can lead to physical, cognitive, social, emotional and behavioral symptoms, and the results may vary from complete recovery to permanent disability or death.
Current medical techniques allow many injured patients to be saved, but this has significantly increased the number of people with disabilities.
- 1 Causes of TBI
- 2 Closed injuries
- 3 penetrating injuries
- 4 Consequences of TCE
Causes of TBI
The causes of a TCE are very varied, from falls, to car accidents or violence, among others. Brain trauma occurs as a result of a sudden acceleration or deceleration within the skull or a complex combination of sudden movement and impact. In addition to the damage caused at the time of the injury, a variety of events in the minutes or days after the injury can cause secondary injuries. These processes include alterations in cerebral blood flow and pressure inside the skull.
In general, the TCE are divided into open, when there is skull fracture, and closed, when it is not fractured.
The brain damage seen after a closed injury can be divided into primary damage and secondary damage.
We can observe three types of primary lesions:
- Diffuse Axonal Injury
When the brain is hit a bruise occurs. Contusions are focal lesions caused by a blow or kickback.
Image obtained by CT, where one is seen as cerebral contusion produced by kickback in the right hemisphere. The exact place of the blow can be determined by the inflammation of the tissues in the right part of the image (arrow).
That is, we will observe bruises both in the area of the brain that receives an impact (blow), and in the opposite areas where the brain is struck against the inner walls of the skull (kickback).
For a bruise to occur, however, it is not necessary for the head to physically strike an object.
Sudden decelerations can cause bruises due to the impact of the brain against the inner walls of the skull. These bruises are preferably located in the frontal and temporal lobes.
Representation of the size and location of the contusions in a series of forty patients. The most common location in the frontal lobes, especially the orbital and temporal part, can be clearly observed.
This is the case, for example, of the majority of TCE caused by traffic accidents. Even if the person is not hit with any object, they may suffer a severe TBI due to sudden deceleration. The arrangement of the cranial bones makes the frontal and temporal lobes the ones that most frequently receive these bruises.
The main non-focal primary damage is diffuse axonal injury.
The intense and abrupt movement of the brain inside the skull stretches, can even break, axons and small blood vessels. This causes diffuse axonal injury (LAD) and minor bleeding.
Although it is not a focal lesion, the LAD shows a preference for the frontal and temporal lobes, for the white substance located around the ventricles and basal ganglia, for the corpus callosum and for the fiber tracts of the brain stem. These diffuse lesions disconnect the cortex from subcortical structures.
The involvement of the white matter by the movement of the brain causes a concussion syndrome, or concussion.
If the concussion is mild it will not be accompanied by loss of consciousness, although the person may be disoriented ("see the stars" phenomenon). The most severe concussions are accompanied by loss of consciousness, which can be resolved in minutes, hours or days. Even the slightest concussions they can leave permanent cognitive sequelae.
Apart from the small hemorrhages that accompany the LAD, large hemorrhages can occur due to the rupture of large blood vessels. These hemorrhages can be located intracerebrally or meningeal spaces. In any case, its presence complicates the patient's prognosis.
These are injuries not directly caused by TBI, but sometimes they can be more serious than primary injuries.
In closed ECT, hemorrhages, whether they are intracerebral or meningeal, displace and compress nerve tissue. This, in a closed space like the skull, causes a increased intracranial pressure (ICP).
As a result of primary damage or compression of the brain, a physiological reaction of fluid accumulation in the tissue, which is known as edema. Edema, especially if it is diffuse, increases the ICP.
If the ICP increases greatly, there is a risk of compression of vital structures of the brain stem, which will cause the death of the patient.
In these conditions the arteries can also be affected and normal blood circulation through the brain is prevented. This will cause episodes of ischemia and hypoxia.
Episodes of ischemia or hypoxia can cause multiple cerebral infarctions, which worsens the patient's prognosis.
Penetrating injuries are those caused by an object, for example, a bullet, which penetrates strongly into the skull.
By definition, penetrating injuries are open lesions. In addition to the skull fracture, laceration of brain tissue is observed, that is, rupture of the meninges and brain tissue that is traversed by the object. Brain tissue is usually found, in addition, inclusions of bone fragments.
The relative specificity of penetrating lesions has sadly allowed neuropsychology to have developed greatly in times of war. In the wars of the first half of the twentieth century, projectiles were not fast enough to cause widespread damage throughout the brain. From this important sample of patients who knew how to take advantage of important neuropsychologists, such as the Russian AR Luria, who studied the location of the lesions and their neuropsychological consequences.
When the injury does not directly affect any vital structure, patient evolution will depend on the structures affected by the impact. Objects that penetrate the skull at low speed tend to leave less sequels than those that penetrate at high speed.
Consequences of TCE
Coma, confusional syndrome and posttraumatic amnesia
Loss of consciousness after a TBI is not directly related to its severity. Thus, trauma with loss of consciousness can leave sequels less important than trauma without loss of consciousness.
The prolonged coma they are produced by lesions that affect the brain stem or by diffuse bilateral lesion of the subcortical white matter.
Cases of lesions that exclusively affect the motor pathways of the brain stem have been described. These patients are fully aware, but cannot issue any type of motor response. This is known by the state name locked-in or locked in oneself, since patients cannot speak or move any part of their body.
The severity of coma is measured with the Glasgow scale. This scale assesses different degrees of ocular opening (spontaneously, in response to pain ...), motor response and verbal response. The score ranges from 3 (deep coma) to 15 (normal). With a score of 8 or less, the TBI is considered to be severe, 9 to 12, moderate, and 13 to 15, mild. Serious scores have a mortality of 40%.
Injuries to the brain stem, and sometimes to the thalamus, occur as a result of the involvement of the reticular formation, so that the cortex loses the activating signals from the brain stem. In some cases, patients may be in a coma for months or years. This is known as vegetative state. After a year in a coma, some patients may open their eyes and recover some functions, such as chewing, drinking or emitting some noise, but they do not regain consciousness.
The confusional syndrome observed in patients recovering from coma or in minor trauma. The patient is disoriented (generally it is not known to orient in time and / or space, and in some cases in person), and it is difficult to pay attention to environmental stimuli.
The phase of post-traumatic amnesia is not considered overcome until the patient can continuously remember the events that happen around him. If you only remember isolated facts, it is considered that you are still in posttraumatic amnesia. Post Traumatic Amnesia It can be accompanied by agitation, aggressive behavior and / or paranoid ideation.
Posttraumatic amnesia refers to the period of time that passes between the accident and the recovery of memory in a continuous way. After a concussion with loss of consciousness, the patient usually presents a picture of anterograde and retrograde amnesia, which includes the hours before the accident. It can be resolved in hours, days or months.
The duration of the post-traumatic amnesia phase is an important prognostic factor for patient recovery.
Neuropsychological consequences of moderate and severe TBI
After a moderate or severe TBI, they are usually observed memory problems, anomie and cognitive slowdown.
Memory problems can be both at the level of consolidation of the information, due to injuries in the medial temporal structures, and at the level of evocation of the information, due to the involvement of the white subcortical substance.
Some patients have speech disorders, such as joint problems (dysarthria), or swallowing problems (dysphagia). This is usually due to brain stem injuries.
Except in the case of focal lesions in language areas, linguistic alteration is usually limited to naming problems. Language alteration, unlike memory impairment, usually improves over time.
Cognitive slowdown can be observed by the increase in reaction time. It is usually accompanied by concentration problems, and is a consequence of the involvement of the white subcortical substance.
After a severe or moderate TBI, patients also usually present behavioral disturbance, in the form of irritability, anxiety and lack of initiative.
It is believed that this is due to the injury of frontal and temporal structures.
In cases where the patient presents a chronic alteration of multiple cognitive and behavioral functions, we talk about posttraumatic dementia.
Neuropsychological consequences of mild TBI
After minor trauma, some patients have memory complaints, attention problems, irritability, lack of initiative, fatigue, hypersensitivity to noise and light or a high frequency of headache episodes. This is known by the name of post-concussion syndrome, and usually remit in six months.
The accumulation of trauma, mild and moderate, is usually common in some sports. This is the case, for example, of American football or boxing. The pugilistic dementia It is a form of posttraumatic dementia that affects some boxers and that, in addition to cognitive deficit, is characterized by tremors and other symptoms of motor involvement.
The accumulation of minor trauma, however, can cause chronic cognitive and behavioral involvement..
Diamond, M.C .; Scheibel, A.B. and Elson, L.M. (nineteen ninety six). The human brain Work book. Barcelona: Ariel.
Guyton, A.C. (1994) Anatomy and physiology of the nervous system. Basic Neuroscience Madrid: Pan American Medical Editorial.
Martin, J.H. (1998) Neuroanatomy. Madrid: Prentice Hall.
Nolte, J. (1994) The human brain: introduction to functional anatomy. Madrid: Mosby-Doyma.Related tests
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