Brain injury is the destruction or degeneration of brain cells, which can impair brain functions. Brain injuries can result from external trauma, such as accidents or falls, or internal factors, such as stroke, infection, or metabolic disorders. In general, brain damage refers to significant, undiscriminating trauma-induced damage.
Traumatic brain injury (TBI) is the most common type of brain injuries, typically caused by external physical trauma or Head injury. Acquired brain injury refers to injuries occurring after birth, in contrast to Genetic disorder or Birth defect brain injuries.
In addition, brain injuries can be classified by timing: primary injuries occur at the moment of trauma, while secondary injuries develop afterward due to physiological responses. They can also be categorized by location: focal injuries affect specific areas, whereas diffuse injuries involve widespread brain regions.
The brain can partially recover function through neuroplasticity, forming new neural connections to compensate for damaged areas. This helps restore some lost abilities, like movement or speech, especially with therapy and practice.
In cases of severe brain injuries, the likelihood of areas with permanent disability is great, including neurocognitive deficits, (often, to be specific, monothematic delusions), speech or movement problems, and intellectual disability. There may also be personality changes. The most severe cases result in coma or even persistent vegetative state. Even a mild incident can have long-term effects or cause symptoms to appear years later.
Studies show there is a correlation between brain lesion and language, speech, and category-specific disorders. Wernicke's aphasia is associated with anomic aphasia, unknowingly making up words (neologisms), and problems with comprehension. The symptoms of Wernicke's aphasia are caused by damage to the posterior section of the superior temporal gyrus.
Damage to the Broca's area typically produces symptoms like omitting functional words (agrammatism), sound production changes, dyslexia, dysgraphia, and problems with comprehension and production. Broca's aphasia is indicative of damage to the posterior inferior frontal gyrus of the brain.
An impairment following damage to a region of the brain does not necessarily imply that the damaged area is wholly responsible for the cognitive process which is impaired. For example, in pure alexia, the ability to read is destroyed by a lesion damaging both the left visual field and the connection between the right visual field and the language areas (Broca's area and Wernicke's area). However, this does not mean one with pure alexia is incapable of comprehending speech—merely that there is no connection between their working visual cortex and language areas—as is demonstrated by the fact that people with pure alexia can still write, speak, and even transcribe letters without understanding their meaning.More Brain Lesions, Kathleen V. Wilkes
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 would eliminate the enhanced activation seen in occipital and fusiform visual areas in response to fear with the area intact. Amygdala lesions change the functional pattern of activation to emotional stimuli in regions that are distant from the amygdala.
Other lesions to the visual cortex have different effects depending on the location of the damage. Lesions to Visual cortex, for example, can cause blindsight in different areas of the brain depending on the size of the lesion and location relative to the calcarine fissure. Lesions to Visual cortex can cause color-blindness, and bilateral lesions to Visual cortex can cause the loss of the ability to perceive motion. Lesions to the parietal lobes may result in agnosia, an inability to recognize complex objects, smells, or shapes, or amorphosynthesis, a loss of perception on the opposite side of the body.Denny-Brown, D., and Betty Q. Banker. "Amorphosynthesis from Left Parietal Lesion". A.M.A. Archives of Neurology and Psychiatry 71, no. 3 (March 1954): 302–13.
Headaches and pain can occur as a result of a brain injury, either directly from the damage or due to neurological conditions stemming from the injury. Due to the changes in the brain as well as the issues associated with the change in physical and mental capacity, depression and low self-esteem are common side effects that can be treated with psychological help. Antidepressants must be used with caution in brain injury people due to the potential for undesired effects because of the already altered brain chemistry.
As time progresses, and the severity of injury becomes clear, there are further responses that may become apparent. Due to loss of blood flow or damaged tissue, sustained during the injury, amnesia and aphasia may become permanent, and apraxia has been documented in patients. Amnesia is a condition in which a person is unable to remember things. Aphasia is the loss or impairment of word comprehension or use. Apraxia is a motor disorder caused by damage to the brain, and may be more common in those who have been left brain damaged, with loss of mechanical knowledge critical. Headaches, occasional dizziness, and fatigue—all temporary symptoms of brain trauma—may become permanent, or may not disappear for a long time.
The long term psychological and physiological effects of brain injury vary depending on the person and the severity of the injury. Brain injury increases the risk of developing depression and aggression. As well as developing , Parkinson's disease, dementia, or hormonal-secreting gland disorders. These patients' monitoring is essential for preventing the development of these symptoms.
Korsakoff psychosis typically follows after the symptoms of Wernicke's decrease. Wernicke-Korsakoff syndrome is typically caused by conditions causing thiamine deficiency, such as chronic heavy alcohol use or by conditions that affect nutritional absorption, including colon cancer, eating disorders and gastric bypass.
There are several imaging techniques that can aid in diagnosing and assessing the extent of brain damage, such as computed tomography (CT) scan, magnetic resonance imaging (MRI), diffusion tensor imaging (DTI) magnetic resonance spectroscopy (MRS), positron emission tomography (PET), and single-photon emission tomography (SPECT). CT scans and MRI are the two techniques widely used and are most effective. CT scans can show brain bleeds, fractures of the skull, fluid build up in the brain that will lead to increased cranial pressure.
MRI is able to better to detect smaller injuries, detect damage within the brain, diffuse axonal injury, injuries to the brainstem, posterior fossa, and subtemporal and subfrontal regions. However, patients with pacemakers, metallic implants, or other metal within their bodies are unable to have an MRI done. Typically the other imaging techniques are not used in a clinical setting because of the cost, lack of availability.
The person may need surgery to remove clotted blood or repair skull fractures, for which cutting a hole in the skull may be necessary. Medicines used for traumatic injuries are , anti-seizure or coma-inducing drugs. Diuretics reduce the fluid in tissues lowering the pressure on the brain.
In the case of brain damage from traumatic brain injury, dexamethasone or mannitol may be used.
Monitoring intracranial pressure is recommended to guide treatment decisions.
Physiotherapists also play a significant role in rehabilitation after a brain injury. In the case of a traumatic brain injury (TBI), physiotherapy treatment during the post-acute phase may include sensory stimulation, serial casting and splinting, fitness and aerobic training, 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 contractures and muscle tone. Evidence based research reveals that serial casting can be used to increase passive range of motion (PROM) and decrease spasticity.
Functional training may also be used to treat patients with TBIs. To date, no studies supports the efficacy of sit to stand training, arm ability training and body weight support systems (BWS). Overall, studies suggest that patients with TBIs who participate in more intense rehabilitation programs will see greater benefits in functional skills. More research is required to better understand the efficacy of the treatments mentioned above.
Other treatments for brain injury can include medication, psychotherapy, neuropsychological rehabilitation, neurotherapy and/or surgery.
In general, neuroregeneration can occur in the peripheral nervous system but is much rarer 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 may increase in size and complexity and even change function, just as someone who loses a sense may gain increased acuity in another sense—a process termed neuroplasticity.
There are many misconceptions that revolve around brain injuries and brain damage. One misconception is that if someone has brain damage then they cannot fully recover. Recovery depends a variety of factors; such as severity and location. Testing is done to note severity and location. Not everyone fully heals from brain damage, but it is possible to have a full recovery. Brain injuries are very hard to predict in outcome. Many tests and specialists are needed to determine the likelihood of the prognosis. People with minor brain damage can have debilitating side effects; not just severe brain damage has debilitating effects.
The side-effects of a brain injury depend on location and the body's response to injury. Even a mild concussion can have long term effects that may not resolve. Another misconception is that children heal better from brain damage. Opposite to some beliefs, children do not always recover better from brain injury; their developing brains are still maturing, making outcomes after mild traumatic brain injury difficult to predict.Lumba-Brown A, Yeates KO, Sarmiento K, et al. Centers for Disease Control and Prevention Guideline on the Diagnosis and Management of Mild Traumatic Brain Injury Among Children. JAMA Pediatr. 2018 Nov 1;172(11):e182853. doi:10.1001/jamapediatrics.2018.2853. Epub 2018 Nov 5. PMID 30193284; PMCID: PMC7006878. In the case of a child with Frontal lobe injury, for example, the impact of the damage may be undetectable until that child fails to develop normal executive functions in his or her late teens and early twenties.
Ten years later, Paul Broca examined two patients exhibiting impaired speech due to frontal lobe injuries. Broca's first patient lacked productive speech. He saw this as an opportunity to address language localization. It was not until Leborgne, informally known as "tan", died when Broca confirmed the frontal lobe lesion from an autopsy. The second patient had similar speech impairments, supporting his findings on language localization. The results of both cases became critical evidence in understanding the left hemisphere's role in speech production. The affected area is known today as Broca's area and the condition as Broca's aphasia.Dronkers, N. F., O. Plaisant, M. T. Iba-Zizen, and E. A. Cabanis. " Paul Broca's Historic Cases: High Resolution MR Imaging of the Brains of Leborgne and Lelong ." Brain: A Journal of Neurology 130.5 (2007): 1432–41. Web. 31 Oct. 2016.
A few years later, a German neuroscientist, Carl Wernicke, consulted on a stroke patient. The patient experienced neither speech nor hearing impairments, but had a few brain deficits. These deficits included lacking the ability to comprehend what was spoken to him and the words written down. After his death, Wernicke examined his autopsy that found a lesion located in the left temporal region. This area became known as Wernicke's area. Wernicke later hypothesized the relationship between Wernicke's area and Broca's area, which was proven fact.
Several studies have examined the history of traumatic brain injury (TBI) among incarcerated populations. A systematic review of 33 papers, covering more than 9,000 prisoners, reported that between 9.7% and 100% of inmates had a past history of TBI, with an average prevalence of 46%. Two meta-analyses included in the review yielded average prevalence rates of 41.2% and 60.3%, considerably higher than those observed in the general population.Durand E, Chevignard M, Ruet A, Dereix A, Jourdan C, Pradat-Diehl P. History of traumatic brain injury in prison populations: A systematic review. Annals of Physical and Rehabilitation Medicine. 2017;60(2):95–101. doi:10.1016/j.rehab.2017.02.003
Most investigations assessed inmates' self-reported history of head injury, though only a few used validated screening tools. The review noted that prisoners with a TBI history were predominantly male, with a mean age of 37 years, and often presented with comorbidities such as mental health disorders and alcohol use disorder. Although the high prevalence of a TBI history in prison populations is well documented, the evidence does not establish a causal link between TBI and criminal behavior, and further research is needed.Durand E, Chevignard M, Ruet A, Dereix A, Jourdan C, Pradat-Diehl P (2017). "History of traumatic brain injury in prison populations: A systematic review". Annals of Physical and Rehabilitation Medicine. 60 (2): 95–101. doi:10.1016/j.rehab.2017.02.003. PMID 28343764.
Signs and symptoms
Severity of injuries
Mild brain injuries
Moderate/severe brain injuries
Symptoms in children
Location of brain damage predicts symptoms
Localizing features
Non-localizing features
Long term psychological
Physiological effects
What can causes Brain injury?
Causes
Chemotherapy
Wernicke–Korsakoff syndrome
Iatrogenic
Diffuse axonal
Diagnosis
Management
Acute
Chronic
Prognosis
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History
See also
Further reading
External links
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