Brain damage or brain injury ( BI ) is the destruction or degeneration of brain cells. Brain injury occurs due to various internal and external factors. In general, brain damage refers to significant, non-discriminatory, traumatic damage, whereas neurotoxicity usually refers to naturally selected chemical cell damage.
The general category with the highest number of injuries is traumatic brain injury (TBI) after physical trauma or head injury from an external source, and the term acquired brain injury (ABI) is used in the right circle to distinguish brain injuries that occur after birth from injury, from abnormalities genetic, or from congenital anomalies.
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Signs and symptoms
Symptoms of a brain injury vary based on the severity of the injury or how much the brain is affected. Three categories are used to classify the severity of mild, moderate or severe brain injury.
Mild brain injury
Symptoms of mild brain injury include headaches, confusion, ringing ears, tiredness, changes in sleep patterns, mood or behavior. Other symptoms include problems with memory, concentration, attention or thought. Mental fatigue is a common debilitating experience and may not be linked by the patient to a genuine (small) incident. Narcolepsy and sleep disorders are common misdiagnoses.
Medium/severe brain injury
Cognitive symptoms include confusion, aggression, abnormal behavior, lisp speech, and coma or other disorders of consciousness. Physical symptoms include headaches that are not lost or worsened, vomiting or nausea, convulsions, abnormal eye dilation, inability to wake from sleep, weakness in the extremities and loss of coordination.
Symptoms in children
Symptoms observed in children include changes in eating habits, persistent irritability or sadness, attention changes, disturbed sleep habits, or loss of interest in toys.
Location of brain damage predicting symptoms
Symptoms of a brain injury can also be affected by the location of the injury and as a result a special disorder for the affected part of the brain. The size of the lesion correlates with severity, recovery, and comprehension. Brain injuries often create disorders or defects that can vary greatly in severity.
In cases of severe brain injury, the possibility of areas with large permanent disabilities, including neurocognitive deficits, delusions (often, for specific, monothematic delusions), speech or movement problems, and intellectual disabilities. There may also be a change of personality. The most severe cases lead to coma or even a persistent vegetative state. Even mild incidents can have long-term effects or cause symptoms to appear several years later.
Studies show there is a correlation between brain lesions and language, speech, and specific category disorders. Aphasia Wernicke is associated with anomia, unconsciously composing words (neologism), and problems with understanding. Wernicke's aphasic symptoms are caused by damage to the posterior portion of the superior temporal gyrus.
Broca's area damage usually results in symptoms such as eliminating functional words (agrammatism), changes in sound production, dyslexia, dysgraphia, and problems with understanding and production. Broca's aphasia is an indication of damage to the posterior inferior frontal gyrus of the brain.
A damage after damage to a brain region does not necessarily mean that the damaged area is entirely responsible for the impaired cognitive process. For example, in pure alexia, reading ability is destroyed by lesions that damage both the left visual field and the relationship between the correct visual plane and the language area (Broca's area and Wernicke's area). This does not mean, however, that one suffering of pure alexia is incapable of understanding the conversation - only that there is no connection between the visual cortex and their language area - as indicated by the fact that pure alexics can still write, speak, and even write letters without understanding its meaning.
Lesions to the fusiform gyrus often result in prosopagnosia, the inability to distinguish faces and other complex objects from each other. Lesions in the amygdala will eliminate the enhanced activation seen in the visual areas of occipital and fusiform in response to fear with intact areas. The amygdala lesions change the functional activation pattern to emotional stimuli in areas far from the amygdala.
Other lesions in the visual cortex have different effects depending on the location of the damage. Lesions to V1, for example, can cause blindsight in different areas of the brain depending on the size of the lesion and the location relative to calcarine fissures. Lesions to V4 can cause color blindness, and bilateral lesions on MT/V5 can cause loss of ability to feel movement. Lesions into the parietal lobe can cause agnosia, the inability to recognize complex objects, smells, or forms, or amorphosynthesis, loss of perception on opposite sides of the body.
Body response to brain injury
Unlike some of the more obvious responses to brain damage, the body also has an invisible physical response that is difficult to notice. These will generally be identified by healthcare providers, especially as they are a normal physical response to brain damage. Cytokines are known to be induced in response to brain injury. It has a variety of actions that can cause, worsen, mediate and/or inhibit cell injury and repair. TGF? seems to take mainly neuroprotective measures, while TNF? may contribute to nerve injury and use protective effects. IL-1 mediates ischemic, excitotoxic, and traumatic brain injury, possibly through many actions on glia, neurons, and blood vessels. Cytokines may be useful for finding new therapeutic strategies. By this time, they are already in clinical trials.
Long-term psychological and physiological effects
There are several body responses to brain injury, occurring at different times after initial damage, because neuronal, neural, or brain functioning can be affected by damage. The immediate response can take many forms. Initially, there may be symptoms such as swelling, pain, bruising, or loss of consciousness. Post-traumatic amnesia is also common in brain damage, such as temporary aphasia, or language disorders.
As time passes, and the severity of the injury becomes clear, there are further responses that may become apparent. Due to loss of blood flow or damaged tissue, sustained during injury, amnesia and aphasia may become permanent, and apraxia has been documented in patients. Amnesia is a condition in which a person can not remember something. Aphasia is the loss or disturbance of understanding or the use of words. Apraxia is a motor disorder caused by brain damage, and may be more common in those with left brain damaged, with the loss of critical mechanical knowledge. Headaches, sometimes dizziness, or fatigue, all temporary symptoms of brain trauma, may become permanent, or may not be lost for a long time.
There are also documented cases of long-lasting psychological effects, such as emotional changes that are often caused by damage to different parts of the brain that control human emotions and behavior. Some who experience emotional changes related to brain damage may have emotions that come very quickly and are very intense, but have very little lasting effect. Emotional changes may not be triggered by certain events, and can be a cause of stress for the aggrieved party and their family or friends. Often, counseling is recommended for those who experience this effect after their injury, and may be available as an individual or group session. It may also be covered by insurance, or offered at a discount, or free of charge. Check out the local resource center near you for more information.
It is important to note that long-term psychological and physiological effects will vary by person and injury. For example, perinatal brain damage has been implicated in cases of neurodevelopmental disorders and psychiatric illness. If any symptoms, signs, or behavioral changes are occurring, the health care provider should be consulted. Different types and levels of trauma will have different effects, and if any symptoms, signs, or behavioral changes are occurring, the health care provider should be consulted.
Maps Brain damage
Cause
Brain injury can occur due to a number of conditions including open head injury, closed head injury, retardation injury, exposure to toxic chemicals, lack of oxygen, tumors, infection, stroke. Brain injury occurs due to a wide range of conditions, diseases, and injuries. Possible causes of extensive brain damage include birth hypoxia, prolonged hypoxia (lack of oxygen), poisoning by teratogens (including alcohol), infections, and neurological diseases. Brain tumors can increase intracranial pressure, causing brain damage.
Chemotherapy can cause brain damage to neural stem cells and oligodendrocyte cells that produce mielin. Radiation and chemotherapy can cause brain tissue damage by interrupting or stopping blood flow to the affected area of ​​the brain. This damage may cause long-term effects such as but not limited to; memory loss, confusion, and loss of cognitive function. Brain damage caused by radiation depends on where the brain tumor is located, the amount of radiation used, and the duration of treatment. Radiosurgery can also cause tissue damage that results in about 1 in 20 patients requiring a second operation to remove damaged tissue.
Wernicke-Korsakoff Syndrome can cause brain damage and result from a deficiency of Vitamin B. This syndrome presents with two conditions, Wernicke's encephalopathy and Korsakoff's psychosis. Usually Wernicke's encephalopathy precedes the symptoms of Korsakoff's psychosis. Wernicke encephalopathy causes bleeding in the thalamus or hypothalamus, which controls the nervous and endocrine systems. Because of bleeding, brain damage occurs causing problems with vision, coordination and balance. Korsakoff psychosis usually follows after Wernicke's decline symptoms and results from chronic brain damage. Korsakoff psychosis affects memory. Wernicke-Korsakoff Syndrome is usually caused by chronic alcohol abuse or by conditions that affect the absorption of nutrients, including colon cancer, eating disorders and gastric shortcuts.
Common causes of local or focal brain damage are physical trauma (traumatic brain injury, stroke, aneurysm, surgery, other neurological disorders), and heavy metal poisoning including mercury and its compounds. Disorders of the blood vessels of the brain interfere with blood flow to the brain, resulting in a lesion called infarction. Brain vascular disorders include thrombosis, embolism, angioma, aneurysm, and cerebral arteriosclerosis.
Brain lesions are sometimes deliberately aroused during neurosurgery, such as carefully placed brain lesions used to treat epilepsy and other brain disorders. These lesions are induced by excision or by electric shock (electrolytic lesions) to the exposed brain or usually through the excitotoxins infusion to a particular area.
Diagnosis
Glasgow Coma Scale (GCS) is the most widely used assessment system to assess the severity of brain injury. This method is based on the objective observation of certain traits to determine the severity of brain injury. It is based on three features of eye opening, verbal response, and motor response, measured as described below. Based on the severity of the Glasgow Coma Scale classified as follows, a severely brain injury score of 3-8, a moderate brain injury score of 9-12 and a mild score of 13-15.
There are several imaging techniques that can help in diagnosing and assessing the extent of brain damage, such as computed tomography (CT) scans, magnetic resonance imaging (MRI), diffusion tensor imaging (DTI) and magnetic resonance spectroscopy (MRS), positron emissions. tomography (PET), single photon emission tomography (SPECT). CT scans and MRI are two of the most widely used and most effective techniques. CT scans may show cerebral hemorrhage, skull fracture, fluid formation in the brain that will cause increased cranial pressure. MRI can detect smaller wounds better, detect damage in the brain, diffuse axonal injury, brainstem injury, posterior fossa, and subtemporal and subfrontal areas. However patients with pacemakers, metal implants, or other metals in their bodies can not perform MRI. Usually other imaging techniques are not used in clinical settings due to cost, lack of availability.
Management
Various professions may be involved in medical care and rehabilitation of a person who suffers damage after a brain injury. Neurologists, neurosurgeons, and physiatrists are doctors specializing in treating brain injuries. Neuropsychologists (especially clinical neuropsychologists) are psychologists who specialize in understanding the effects of brain injury and may be involved in assessing severity or creating a rehabilitation strategy. Occupational therapists may be involved in running a rehabilitation program to help restore lost function or help relearn important skills. Registered nurses, such as those working in the hospital's intensive care unit, can maintain health from severe brain injury with continuous drug delivery and neurological monitoring, including the use of Glasgow Coma Scale used by other health professionals to measure as far as orientation.
Physiotherapists also play an important role in rehabilitation after a brain injury. In the case of traumatic brain injury (TBI), physiotherapy treatment during the post-acute phase may include: sensory stimulation, serial casting and splinting, fitness and aerobic exercise, and functional training. Sensory stimulation refers to regaining sensory perception through the use of modalities. There is no evidence to support the efficacy of this intervention. Serial casting and splinting are often used to reduce soft tissue contracting and muscle tone. Evidence-based research reveals that serial casting can be used to increase the range of passive motion (PROM) and reduce flexibility. The study also reported that fitness and aerobic exercise will improve cardiovascular fitness; but the benefits will not be transferred to the functional level. Functional training can also be used to treat patients with TBI. To date, no studies have supported the effectiveness of sit-to-stand training, armory training and weight support systems (BBL). Overall, studies show that patients with TBI who participate in more intensive rehabilitation programs will see greater benefits in functional skills. More research is needed to better understand the effectiveness of the treatments mentioned above.
Other treatments for brain injury include drugs, psychotherapy, neuropsychological rehabilitation, snoezelen, surgery, or physical implants such as deep brain stimulation.
In cases of brain damage from traumatic brain injury, dexamethasone and/or Mannitol may be used.
Prognosis
The prognosis, or the likelihood of advancement of the disorder, depends on the nature, location, and cause of brain damage (see Traumatic Brain Injury, Focal and diffuse Brain Injury, Primary and Secondary Brain Injury).
In general, neuroregeneration can occur in the peripheral nervous system but is much less frequent and more difficult to assist in the central nervous system (brain or spinal cord). However, in neural development in humans, areas of the brain can learn to compensate for other damaged areas, and can increase size and complexity and even alter function, as a person who loses reason can gain increased acuity in another sense - a process called neuroplasticity.
There are many misconceptions that revolve around brain injury and brain damage. One misconception is that if a person suffers brain damage then they can not fully recover. Recovery depends on a variety of factors; such as severity and location. Testing is done to record the severity and location. Not everyone is completely healed of brain damage, but it is possible to have a full recovery. Brain injury is very difficult to predict in results. Many tests and specialists are needed to determine the likelihood of prognosis. People with mild brain damage can have debilitating side effects; not just severe brain damage has a debilitating effect. The side effects of brain injury depend on the location and the body's response to injury. Even a mild concussion can have long-term effects that may not be overcome. Another misconception is that children better recover from brain damage. Children are at greater risk of injury due to lack of maturity. It makes future development difficult to predict. This is because different cortical areas mature at different stages, with some major cell populations and associated cognitive abilities remaining unrefined until early adulthood. In the case of a child with frontal brain injury, for example, the impact of damage may be undetectable until the child fails to develop a normal executive function in late teens and early twenties. This is because different cortical areas mature at different stages, with some major cell populations and associated cognitive abilities remaining unrefined until early adulthood. In the case of a child with frontal brain injury, for example, the impact of damage may be undetectable until the child fails to develop a normal executive function in late teens and early twenties.
History
The foundation for understanding human behavior and brain injury can be attributed to the case of Phineas Gage and the famous case study by Paul Broca. The first case study on a Phineas Gage head injury was one of the most astonishing brain injuries in history. In 1848, Phineas Gage paved the way for a new railway line when he discovered the accidental blast of tamping iron directly through his frontal lobe. Gage was observed intellectually unaffected but exemplified post-injury behavior deficits. These deficits include: being sporadic, disrespectful, profane, and disrespectful to other workers. Gage began having a spasm in February, dying just four months later on May 21, 1860.
Ten years later, Paul Broca examined two patients who showed speech impairment due to frontal lobe injury. Broca's first patient lacked productive speech. He sees this as an opportunity to address language localization. It was not until Leborgne, officially known as "tan", died when Broca confirmed a frontal lobe lesion from an autopsy. The second patient had a similar speech impediment, supporting his findings on language localization. The results of both cases became a vital verification of the relationship between speech and the left hemisphere. Affected areas are known today as Broca and Broca's Aphasia area.
A few years later, a German neurologist, Carl Wernicke, consulted a stroke patient. Patients do not experience speech or hearing impairment, but suffer from some brain deficits. These deficits include: lacking the ability to understand what is being said to him and the words being written. After his death, Wernicke examined an autopsy that found a lesion located in the left temporal region. This area is known as the Wernicke area. Wernicke then hypothesized the relationship between the Wernicke and Broca regions, which proved the fact.
See also
References
External links
- Brain injury in Curlie (based on DMOZ)
Source of the article : Wikipedia
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