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Brain damage

Neurotrauma, brain damage or brain injury (BI) is the destruction or degeneration of brain cells. Brain injuries occur due to a wide range of internal and external factors. In general, brain damage refers to significant, undiscriminating trauma-induced damage.

Brain damage
A CT of the head years after a traumatic brain injury showing an empty space where the damage occurred, marked by the arrow

A common category with the greatest number of injuries is traumatic brain injury (TBI) following physical trauma or head injury from an outside source, and the term acquired brain injury (ABI) is used in appropriate circles to differentiate brain injuries occurring after birth from injury, from a genetic disorder (GBI), or from a congenital disorder (CBI).[1] Primary and secondary brain injuries identify the processes involved, while focal and diffuse brain injury describe the severity and localization.[citation needed]

Recent research has demonstrated that neuroplasticity, which allows the brain to reorganize itself by forming new neural connections throughout life, provides for rearrangement of its workings. This allows the brain to compensate for injury and disease.

Signs and symptoms edit

Symptoms of brain injuries vary based on the severity of the injury or how much of the brain is affected. The three categories used for classifying the severity of brain injuries are mild, moderate or severe.[2]

Severity of injuries edit

Mild brain injuries edit

Symptoms of a mild brain injury include headaches, confusions, tinnitus, fatigue, changes in sleep patterns, mood or behavior. Other symptoms include trouble with memory, concentration, attention or thinking.[3] Mental fatigue is a common debilitating experience and may not be linked by the patient to the original (minor) incident.

Moderate/severe brain injuries edit

Cognitive symptoms include confusion, aggressiveness, abnormal behavior, slurred speech, and coma or other disorders of consciousness. Physical symptoms include headaches that worsen or do not go away, vomiting or nausea, convulsions, brain pulsation, abnormal dilation of the eyes, inability to awaken from sleep, weakness in extremities and loss of coordination.[3]

Symptoms in children edit

Symptoms observed in children include changes in eating habits, persistent irritability or sadness, changes in attention, or disrupted sleeping habits.[3]

Location of brain damage predicts symptoms edit

Symptoms of brain injuries can also be influenced by the location of the injury and as a result impairments are specific to the part of the brain affected. Lesion size is correlated with severity, recovery, and comprehension.[4] Brain injuries often create impairment or disability that can vary greatly in severity.

In cases of severe brain injuries, the likelihood of areas with permanent disability is great, including neurocognitive deficits, delusions (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.[5]

Studies show there is a correlation between brain lesion and language, speech, and category-specific disorders. Wernicke's aphasia is associated with anomia, 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.[6][7]

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.[8]

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, however. 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.[9]

Lesions to the fusiform gyrus often result in prosopagnosia, the inability to distinguish faces and other complex objects from each other.[10] 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.[11]

Other lesions to 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 location relative to the calcarine fissure.[12] Lesions to V4 can cause color-blindness,[13] and bilateral lesions to MT/V5 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.[14]

Non-localizing features edit

Brain injuries have far-reaching and varied consequences due to the nature of the brain as the main source of bodily control. Brain-injured people commonly experience issues with memory.[15] This can be issues with either long or short-term memories depending on the location and severity of the injury. Sometimes memory can be improved through rehabilitation, although it can be permanent. Behavioral and personality changes are also commonly observed due to changes of the brain structure in areas controlling hormones or major emotions.

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.

Long term psychological and physiological effects edit

There are multiple responses of the body to brain injury, occurring at different times after the initial occurrence of damage, as the functions of the neurons, nerve tracts, or sections of the brain 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.[16] Post-traumatic amnesia is also common with brain damage, as is temporary aphasia, or impairment of language.[17]

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.[18] 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.[19] Headaches, occasional dizziness, and fatigue—all temporary symptoms of brain trauma—may become permanent, or may not disappear for a long time.

There are documented cases of lasting psychological effects as well, such as emotional changes often caused by damage to the various parts of the brain that control human emotions and behavior.[20] Individuals who have experienced emotional changes related to brain damage may have emotions that come very quickly and are very intense, but have very little lasting effect.[20] Emotional changes may not be triggered by a specific event, and can be a cause of stress to the injured party and their family and friends.[21] Often, counseling is suggested for those who experience this effect after their injury, and may be available as an individual or group session.

The long term psychological and physiological effects will vary by person and injury. For example, perinatal brain damage has been implicated in cases of neurodevelopmental impairments and psychiatric illnesses. If any concerning symptoms, signs, or changes to behaviors are occurring, a healthcare provider should be consulted.

Causes edit

 
A coup injury occurs under the site of impact with an object, and a contrecoup injury occurs on the side opposite the area that was hit.

Brain injuries can result from a number of conditions, including:[22]

Chemotherapy edit

Chemotherapy can cause brain damage to the neural stem cells and oligodendrocyte cells that produce myelin. Radiation and chemotherapy can lead to brain tissue damage by disrupting or stopping blood flow to the affected areas of the brain. This damage can cause long term effects such as but not limited to; memory loss, confusion, and loss of cognitive function. The brain damage caused by radiation depends on where the brain tumor is located, the amount of radiation used, and the duration of the treatment. Radiosurgery can also lead to tissue damage that results in about 1 in 20 patients requiring a second operation to remove the damaged tissue.[27][28]

Wernicke–Korsakoff syndrome edit

Wernicke–Korsakoff syndrome can cause brain damage and results from a Vitamin B deficiency (specifically vitamin B1, thiamine).[29][30] This syndrome presents with two conditions, Wernicke's encephalopathy and Korsakoff psychosis. Typically Wernicke's encephalopathy precedes symptoms of Korsakoff psychosis. Wernicke's encephalopathy results from focal accumulation of lactic acid, causing problems with vision, coordination, and balance.[29]

Korsakoff psychosis typically follows after the symptoms of Wernicke's decrease.[29][30] 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.[29]

Iatrogenic edit

Brain lesions are sometimes intentionally inflicted during neurosurgery, such as the carefully placed brain lesion used to treat epilepsy and other brain disorders. These lesions are induced by excision or by electric shocks (electrolytic lesions) to the exposed brain or commonly by infusion of excitotoxins to specific areas.[medical citation needed]

Diffuse axonal edit

Diffuse axonal injury is caused by shearing forces on the brain leading to lesions in the white matter tracts of the brain.[31] These shearing forces are seen in cases where the brain had a sharp rotational acceleration, and is caused by the difference in density between white matter and grey matter.[32]

Body's response to brain injury edit

Unlike some of the more obvious responses to brain damage, the body also has invisible physical responses which can be difficult to notice. These will generally be identified by a healthcare provider, especially as they are normal physical responses to brain damage. Cytokines are known to be induced in response to brain injury.[33] These have diverse actions that can cause, exacerbate, mediate and/or inhibit cellular injury and repair. TGFβ seems to exert primarily neuroprotective actions, whereas TNFα might contribute to neuronal injury and exert protective effects. IL-1 mediates ischaemic, excitotoxic, and traumatic brain injury, probably through multiple actions on glia, neurons, and the vasculature. Cytokines may be useful in order to discover novel therapeutic strategies. At the current time, they are already in clinical trials.[34]

Diagnosis edit

Glasgow Coma Scale (GCS) is the most widely used scoring system used to assess the level of severity of a brain injury. This method is based on the objective observations of specific traits to determine the severity of a brain injury. It is based on three traits: eye opening, verbal response, and motor response, gauged as described below.[35] Based on the Glasgow Coma Scale severity is classified as follows, severe brain injuries score 3–8, moderate brain injuries score 9–12 and mild score 13–15.[35]

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.[36]

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.[37]

Management edit

Acute edit

The treatment for emergency traumatic brain injuries focuses on assuring the person has enough oxygen from the brain's blood supply, and on maintaining normal blood pressure to avoid further injuries of the head or neck. 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 diuretics, anti-seizure or coma-inducing drugs. Diuretics reduce the fluid in tissues lowering the pressure on the brain. In the first week after a traumatic brain injury, a person may have a risk of seizures, which anti-seizure drugs help prevent. Coma-inducing drugs may be used during surgery to reduce impairments and restore blood flow.

In the case of brain damage from traumatic brain injury, dexamethasone and/or Mannitol may be used. [38]

Chronic edit

Various professions may be involved in the medical care and rehabilitation of someone with an impairment after a brain injury. Neurologists, neurosurgeons, and physiatrists are physicians specialising in treating brain injury. Neuropsychologists (especially clinical neuropsychologists) are psychologists specialising in understanding the effects of brain injury and may be involved in assessing the severity or creating rehabilitation strategies. Occupational therapists may be involved in running rehabilitation programs to help restore lost function or help re-learn essential skills. Registered nurses, such as those working in hospital intensive care units, are able to maintain the health of the severely brain-injured with constant administration of medication and neurological monitoring, including the use of the Glasgow Coma Scale used by other health professionals to quantify extent of orientation.[39]

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.[40] Sensory stimulation refers to regaining sensory perception through the use of modalities. There is no evidence to support the efficacy of this intervention.[41] 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.[41]

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).[42][43] Overall, studies suggest that patients with TBIs who participate in more intense rehabilitation programs will see greater benefits in functional skills.[44] More research is required to better understand the efficacy of the treatments mentioned above.[45]

Other treatments for brain injury can include medication, psychotherapy, neuropsychological rehabilitation, and/or surgery.[46]

Prognosis edit

Prognosis, or the likely progress of a disorder, depends on the nature, location, and cause of the 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 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.[47]

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.[48]

The side-effects of a brain injury depend on location and the body's response to injury.[48] Even a mild concussion can have long term effects that may not resolve.[49] Another misconception is that children heal better from brain damage. Children are at greater risk for injury due to lack of maturity. It makes future development hard to predict.[49] [dead link] This is because different cortical areas mature at different stages, with some major cell populations and their corresponding cognitive faculties remaining unrefined until early adulthood. In the case of a child with frontal brain 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.[50]

History edit

The foundation for understanding human behavior and brain injury can be attributed to the case of Phineas Gage and the famous case studies by Paul Broca. The first case study on Phineas Gage's head injury is one of the most astonishing brain injuries in history. In 1848, Phineas Gage was paving way for a new railroad line when he encountered an accidental explosion of a tamping iron straight through his frontal lobe. Gage observed to be intellectually unaffected but was claimed by some to have exemplified post-injury behavioral deficits.[51][failed verification]

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 a vital verification of the relationship between speech and the left cerebral hemisphere. The affected areas are known today as Broca's area and Broca's Aphasia.[52]

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.[53]

See also edit

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Further reading edit

  • Sam Kean (2015). The Tale of the Dueling Neurosurgeons: The History of the Human Brain as Revealed by True Stories of Trauma, Madness, and Recovery. Back Bay Books. ISBN 978-0316182355.

External links edit

  • Brain damage at Curlie
  • Brain injury at Curlie
  • International Brain Injury Association

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For other uses see Brain damage disambiguation For the scientific journal on brain injuries see Brain Injury journal See also Acquired brain injury and Traumatic brain injury This article needs more reliable medical references for verification or relies too heavily on primary sources Please review the contents of the article and add the appropriate references if you can Unsourced or poorly sourced material may be challenged and removed Find sources Brain damage news newspapers books scholar JSTOR January 2019 Neurotrauma brain damage or brain injury BI is the destruction or degeneration of brain cells Brain injuries occur due to a wide range of internal and external factors In general brain damage refers to significant undiscriminating trauma induced damage Brain damageA CT of the head years after a traumatic brain injury showing an empty space where the damage occurred marked by the arrowA common category with the greatest number of injuries is traumatic brain injury TBI following physical trauma or head injury from an outside source and the term acquired brain injury ABI is used in appropriate circles to differentiate brain injuries occurring after birth from injury from a genetic disorder GBI or from a congenital disorder CBI 1 Primary and secondary brain injuries identify the processes involved while focal and diffuse brain injury describe the severity and localization citation needed Recent research has demonstrated that neuroplasticity which allows the brain to reorganize itself by forming new neural connections throughout life provides for rearrangement of its workings This allows the brain to compensate for injury and disease Contents 1 Signs and symptoms 1 1 Severity of injuries 1 1 1 Mild brain injuries 1 1 2 Moderate severe brain injuries 1 2 Symptoms in children 1 3 Location of brain damage predicts symptoms 1 4 Non localizing features 1 5 Long term psychological and physiological effects 2 Causes 2 1 Chemotherapy 2 2 Wernicke Korsakoff syndrome 2 3 Iatrogenic 2 4 Diffuse axonal 3 Body s response to brain injury 4 Diagnosis 5 Management 5 1 Acute 5 2 Chronic 6 Prognosis 7 History 8 See also 9 References 10 Further reading 11 External linksSigns and symptoms editSymptoms of brain injuries vary based on the severity of the injury or how much of the brain is affected The three categories used for classifying the severity of brain injuries are mild moderate or severe 2 Severity of injuries edit Mild brain injuries edit Symptoms of a mild brain injury include headaches confusions tinnitus fatigue changes in sleep patterns mood or behavior Other symptoms include trouble with memory concentration attention or thinking 3 Mental fatigue is a common debilitating experience and may not be linked by the patient to the original minor incident Moderate severe brain injuries edit Cognitive symptoms include confusion aggressiveness abnormal behavior slurred speech and coma or other disorders of consciousness Physical symptoms include headaches that worsen or do not go away vomiting or nausea convulsions brain pulsation abnormal dilation of the eyes inability to awaken from sleep weakness in extremities and loss of coordination 3 Symptoms in children edit Symptoms observed in children include changes in eating habits persistent irritability or sadness changes in attention or disrupted sleeping habits 3 Location of brain damage predicts symptoms edit Symptoms of brain injuries can also be influenced by the location of the injury and as a result impairments are specific to the part of the brain affected Lesion size is correlated with severity recovery and comprehension 4 Brain injuries often create impairment or disability that can vary greatly in severity In cases of severe brain injuries the likelihood of areas with permanent disability is great including neurocognitive deficits delusions 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 5 Studies show there is a correlation between brain lesion and language speech and category specific disorders Wernicke s aphasia is associated with anomia 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 6 7 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 8 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 however 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 9 Lesions to the fusiform gyrus often result in prosopagnosia the inability to distinguish faces and other complex objects from each other 10 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 11 Other lesions to 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 location relative to the calcarine fissure 12 Lesions to V4 can cause color blindness 13 and bilateral lesions to MT V5 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 14 Non localizing features edit Brain injuries have far reaching and varied consequences due to the nature of the brain as the main source of bodily control Brain injured people commonly experience issues with memory 15 This can be issues with either long or short term memories depending on the location and severity of the injury Sometimes memory can be improved through rehabilitation although it can be permanent Behavioral and personality changes are also commonly observed due to changes of the brain structure in areas controlling hormones or major emotions 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 Long term psychological and physiological effects edit There are multiple responses of the body to brain injury occurring at different times after the initial occurrence of damage as the functions of the neurons nerve tracts or sections of the brain 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 16 Post traumatic amnesia is also common with brain damage as is temporary aphasia or impairment of language 17 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 18 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 19 Headaches occasional dizziness and fatigue all temporary symptoms of brain trauma may become permanent or may not disappear for a long time There are documented cases of lasting psychological effects as well such as emotional changes often caused by damage to the various parts of the brain that control human emotions and behavior 20 Individuals who have experienced emotional changes related to brain damage may have emotions that come very quickly and are very intense but have very little lasting effect 20 Emotional changes may not be triggered by a specific event and can be a cause of stress to the injured party and their family and friends 21 Often counseling is suggested for those who experience this effect after their injury and may be available as an individual or group session The long term psychological and physiological effects will vary by person and injury For example perinatal brain damage has been implicated in cases of neurodevelopmental impairments and psychiatric illnesses If any concerning symptoms signs or changes to behaviors are occurring a healthcare provider should be consulted Causes edit nbsp A coup injury occurs under the site of impact with an object and a contrecoup injury occurs on the side opposite the area that was hit Brain injuries can result from a number of conditions including 22 trauma multiple traumatic injuries can lead to chronic traumatic encephalopathy A coup contrecoup injury occurs when the force impacting the head is not only strong enough to cause a contusion at the site of impact but also able to move the brain and cause it to displace rapidly into the opposite side of the skull causing an additional contusion open head injury closed head injury penetrating when a sharp object enters the brain causing a large damage area Penetrating injuries caused by bullets have a 91 percent mortality rate deceleration injuries poisoning for example from heavy metals including mercury and compounds of lead Genetic disorder hypoxia including birth hypoxia 23 tumors infections stroke leading to infarct which may follow thrombosis embolisms angiomas aneurysms and cerebral arteriosclerosis 24 neurological illness or disorders such as cerebral palsy Parkinson s disease etc surgery Substance use disorder neurotoxins pollution exposure or biological exposure Annonaceae rotenone 25 Aspergillus spores West Nile fever Viral meningitis suicide attempt such as hanging falling off from height and even on rare occasion getting shot by a firearm etc acute total or REM sleep deprivation lasting longer than a day 26 Chemotherapy edit Chemotherapy can cause brain damage to the neural stem cells and oligodendrocyte cells that produce myelin Radiation and chemotherapy can lead to brain tissue damage by disrupting or stopping blood flow to the affected areas of the brain This damage can cause long term effects such as but not limited to memory loss confusion and loss of cognitive function The brain damage caused by radiation depends on where the brain tumor is located the amount of radiation used and the duration of the treatment Radiosurgery can also lead to tissue damage that results in about 1 in 20 patients requiring a second operation to remove the damaged tissue 27 28 Wernicke Korsakoff syndrome edit Wernicke Korsakoff syndrome can cause brain damage and results from a Vitamin B deficiency specifically vitamin B1 thiamine 29 30 This syndrome presents with two conditions Wernicke s encephalopathy and Korsakoff psychosis Typically Wernicke s encephalopathy precedes symptoms of Korsakoff psychosis Wernicke s encephalopathy results from focal accumulation of lactic acid causing problems with vision coordination and balance 29 Korsakoff psychosis typically follows after the symptoms of Wernicke s decrease 29 30 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 29 Iatrogenic edit Brain lesions are sometimes intentionally inflicted during neurosurgery such as the carefully placed brain lesion used to treat epilepsy and other brain disorders These lesions are induced by excision or by electric shocks electrolytic lesions to the exposed brain or commonly by infusion of excitotoxins to specific areas medical citation needed Diffuse axonal edit Diffuse axonal injury is caused by shearing forces on the brain leading to lesions in the white matter tracts of the brain 31 These shearing forces are seen in cases where the brain had a sharp rotational acceleration and is caused by the difference in density between white matter and grey matter 32 Body s response to brain injury editUnlike some of the more obvious responses to brain damage the body also has invisible physical responses which can be difficult to notice These will generally be identified by a healthcare provider especially as they are normal physical responses to brain damage Cytokines are known to be induced in response to brain injury 33 These have diverse actions that can cause exacerbate mediate and or inhibit cellular injury and repair TGFb seems to exert primarily neuroprotective actions whereas TNFa might contribute to neuronal injury and exert protective effects IL 1 mediates ischaemic excitotoxic and traumatic brain injury probably through multiple actions on glia neurons and the vasculature Cytokines may be useful in order to discover novel therapeutic strategies At the current time they are already in clinical trials 34 Diagnosis editGlasgow Coma Scale GCS is the most widely used scoring system used to assess the level of severity of a brain injury This method is based on the objective observations of specific traits to determine the severity of a brain injury It is based on three traits eye opening verbal response and motor response gauged as described below 35 Based on the Glasgow Coma Scale severity is classified as follows severe brain injuries score 3 8 moderate brain injuries score 9 12 and mild score 13 15 35 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 36 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 37 Management editAcute edit The treatment for emergency traumatic brain injuries focuses on assuring the person has enough oxygen from the brain s blood supply and on maintaining normal blood pressure to avoid further injuries of the head or neck 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 diuretics anti seizure or coma inducing drugs Diuretics reduce the fluid in tissues lowering the pressure on the brain In the first week after a traumatic brain injury a person may have a risk of seizures which anti seizure drugs help prevent Coma inducing drugs may be used during surgery to reduce impairments and restore blood flow In the case of brain damage from traumatic brain injury dexamethasone and or Mannitol may be used 38 Chronic edit Various professions may be involved in the medical care and rehabilitation of someone with an impairment after a brain injury Neurologists neurosurgeons and physiatrists are physicians specialising in treating brain injury Neuropsychologists especially clinical neuropsychologists are psychologists specialising in understanding the effects of brain injury and may be involved in assessing the severity or creating rehabilitation strategies Occupational therapists may be involved in running rehabilitation programs to help restore lost function or help re learn essential skills Registered nurses such as those working in hospital intensive care units are able to maintain the health of the severely brain injured with constant administration of medication and neurological monitoring including the use of the Glasgow Coma Scale used by other health professionals to quantify extent of orientation 39 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 40 Sensory stimulation refers to regaining sensory perception through the use of modalities There is no evidence to support the efficacy of this intervention 41 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 41 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 42 43 Overall studies suggest that patients with TBIs who participate in more intense rehabilitation programs will see greater benefits in functional skills 44 More research is required to better understand the efficacy of the treatments mentioned above 45 Other treatments for brain injury can include medication psychotherapy neuropsychological rehabilitation and or surgery 46 Prognosis editThis section needs more reliable medical references for verification or relies too heavily on primary sources Please review the contents of the section and add the appropriate references if you can Unsourced or poorly sourced material may be challenged and removed Find sources Brain damage news newspapers books scholar JSTOR September 2016 nbsp Prognosis or the likely progress of a disorder depends on the nature location and cause of the 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 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 47 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 48 The side effects of a brain injury depend on location and the body s response to injury 48 Even a mild concussion can have long term effects that may not resolve 49 Another misconception is that children heal better from brain damage Children are at greater risk for injury due to lack of maturity It makes future development hard to predict 49 dead link This is because different cortical areas mature at different stages with some major cell populations and their corresponding cognitive faculties remaining unrefined until early adulthood In the case of a child with frontal brain 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 50 History editThe foundation for understanding human behavior and brain injury can be attributed to the case of Phineas Gage and the famous case studies by Paul Broca The first case study on Phineas Gage s head injury is one of the most astonishing brain injuries in history In 1848 Phineas Gage was paving way for a new railroad line when he encountered an accidental explosion of a tamping iron straight through his frontal lobe Gage observed to be intellectually unaffected but was claimed by some to have exemplified post injury behavioral deficits 51 failed verification 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 a vital verification of the relationship between speech and the left cerebral hemisphere The affected areas are known today as Broca s area and Broca s Aphasia 52 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 53 See also edit nbsp Medicine portal nbsp Philosophy portal nbsp Psychology portalCerebral palsy Group of movement disorders that appear in early childhood Encephalopathy Disorder or disease of the brain Epilepsy Group of neurological disorders causing seizures Fetal alcohol spectrum disorder Group of conditions resulting from maternal alcohol consumption during pregnancy Frontal lobe injury Type of brain injury Head injury Serious trauma to the cranium Infinity Walk Therapeutic method for progressively developing coordination Lobotomy Neurosurgical operation Myogenesis Formation of muscular tissue particularly during embryonic development Nerve injury Damage to nervous tissue Neurocognition Cognitive functions related to a brain region Neurology Medical specialty dealing with disorders of the nervous system Primary and secondary brain injury Medical condition Rehabilitation neuropsychology Therapy to regain or improve neurocognitive function that has been lost or diminished Synaptogenesis Formation of neuronal junctions in the nervous system Traumatic brain injury Injury of the brain from an external sourceReferences edit What is an Acquired Brain Injury PDF Headway Archived from the original PDF on 2016 07 05 Retrieved 19 September 2016 Traumatic Brain Injury Information Page National Institute of Neurological Disorders and Stroke NINDS www ninds nih gov Retrieved 2018 11 09 a b c Traumatic brain injury Symptoms Mayo Clinic www mayoclinic org Retrieved 2016 11 15 Stefaniak James D Halai Ajay D Lambon Ralph Matthew A 2019 The neural and neurocomputational bases of recovery from post stroke aphasia Nature Reviews Neurology 16 1 43 55 doi 10 1038 s41582 019 0282 1 ISSN 1759 4766 PMID 31772339 S2CID 208302688 Traumatic Brain Injury Signs and Symptoms BrainLine 2017 12 01 Retrieved 2020 01 23 Superior Temporal Gyrus DNA Learning Center www dnalc org Retrieved 2016 12 09 Wernicke s Aphasia National Aphasia Association Retrieved 2016 12 09 Kean Mary Louise Broca s and Wernicke s Aphasia www rohan sdsu edu Archived from the original on 2017 01 04 Retrieved 2016 12 09 More Brain Lesions Kathleen V Wilkes Purves Dale Augustine George J Fitzpatrick David Katz Lawrence C LaMantia Anthony Samuel McNamara James O Williams S Mark 2001 Lesions of the Temporal Association Cortex Deficits of Recognition Neuroscience 2nd Edition Diano Matteo Celeghin Alessia Bagnis Arianna Tamietto Marco 2017 Amygdala Response to Emotional Stimuli without Awareness Facts and Interpretations Frontiers in Psychology 7 2029 doi 10 3389 fpsyg 2016 02029 ISSN 1664 1078 PMC 5222876 PMID 28119645 Celesia Gastone G 2010 01 01 Visual Perception and Awareness Journal of Psychophysiology 24 2 62 67 doi 10 1027 0269 8803 a000014 ISSN 0269 8803 Jaeger W Krastel H Braun St 1988 12 01 Cerebrale Achromatopsie Symptomatik Verlauf Differentialdiagnose und Strategie der Untersuchung Klinische Monatsblatter fur Augenheilkunde in German 193 12 627 34 doi 10 1055 s 2008 1050309 ISSN 0023 2165 PMID 3265459 S2CID 260195187 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 Vakil Eli 2005 11 01 The Effect of Moderate to Severe Traumatic Brain Injury TBI on Different Aspects of Memory A Selective Review Journal of Clinical and Experimental Neuropsychology 27 8 977 1021 doi 10 1080 13803390490919245 ISSN 1380 3395 PMID 16207622 S2CID 17967490 What Happens Immediately After the Injury 2008 07 25 Retrieved 2016 11 12 Aphasia Definitions National Aphasia Association Retrieved 2016 11 12 Definition of Amnesia www merriam webster com Retrieved 2016 11 12 Baumard Josselin Osiurak Francois Lesourd Mathieu Le Gall Didier 2014 01 01 Tool use disorders after left brain damage Frontiers in Psychology 5 473 doi 10 3389 fpsyg 2014 00473 PMC 4033127 PMID 24904487 a b Emotional Problems After Traumatic Brain Injury www msktc org Retrieved 2016 11 12 Wahrborg Peter 1991 Assessment amp Management of Emotional Reactions to Brain Damage amp Aphasia Far Communications Ltd TBI Causes of Traumatic Brain Injury www traumaticbraininjury com Retrieved 2016 11 15 Birth Hypoxia and Brain Damage to Newborns Michael E Duffy Archived from the original on 2013 08 05 Retrieved 2013 07 27 Overview of Brain Dysfunction Brain Spinal Cord and Nerve Disorders Merck Manuals Consumer Version Retrieved 2016 12 09 Pamies David Block Katharina Lau Pierre Gribaldo Laura Pardo Carlos A Barreras Paula Smirnova Lena Wiersma Daphne Zhao Liang Harris Georgina Hartung Thomas 2018 09 01 Rotenone exerts developmental neurotoxicity in a human brain spheroid model Toxicology and Applied Pharmacology 354 101 14 doi 10 1016 j taap 2018 02 003 ISSN 0041 008X PMC 6082736 PMID 29428530 Owen Jessica E Veasey Sigrid June 2020 Impact of Sleep Disturbances on Neurodegeneration Insight from Studies in Animal Models Neurobiology of Disease 139 104820 doi 10 1016 j nbd 2020 104820 ISSN 0969 9961 PMC 7593848 PMID 32087293 Prevention Cancer Resources from OncoLink Treatment Research Coping Clinical Trials Possible Side Effects of Radiation Treatment for Brain Tumors OncoLink www oncolink org Retrieved 2016 09 22 a href Template Cite web html title Template Cite web cite web a CS1 maint multiple names authors list link Long Term Side Effects of Brain Tumour Radiotherapy Cancer Research UK October 22 2015 Archived from the original on September 23 2016 Retrieved September 22 2016 a b c d Butterworth Roger F 1981 07 01 Effects of Thiamine Deficiency on Brain Metabolism Implications for the Pathogenesis of the Wernicke Korsakoff Syndrome Alcohol and Alcoholism 24 4 271 279 doi 10 1093 oxfordjournals alcalc a044913 PMID 2675860 Retrieved 2022 11 26 a b Wernicke Korsakoff syndrome MedlinePlus Medical Encyclopedia medlineplus gov Retrieved 2016 11 15 Vieira RC Paiva WS de Oliveira DV Teixeira MJ de Andrade AF de Sousa RM 2016 10 20 Diffuse Axonal Injury Epidemiology Outcome and Associated Risk Factors Frontiers in Neurology 7 178 doi 10 3389 fneur 2016 00178 PMC 5071911 PMID 27812349 Gaillard F Diffuse axonal injury radiopaedia org Radiopaedia Retrieved 2018 01 07 Dammann Olaf O Shea Michael 2016 11 12 Cytokines and Perinatal Brain Damage Clinics in Perinatology 35 4 643 v doi 10 1016 j clp 2008 07 011 ISSN 0095 5108 PMC 3657129 PMID 19026332 Zhang Jun Ming An Jianxiong 2007 01 01 Cytokines Inflammation and Pain International Anesthesiology Clinics 45 2 27 37 doi 10 1097 AIA 0b013e318034194e ISSN 0020 5907 PMC 2785020 PMID 17426506 a b What Is the Glasgow Coma Scale Retrieved 2016 11 15 Watanabe Thomas Marino Michael 2014 Current Diagnosis amp Treatment Physical Medicine amp Rehabilitation McGraw Hill Education ISBN 978 0 07 179329 2 via Access Medicine page needed Watanabe Thomas Marino Michael 2014 Current Diagnosis amp Treatment Physical Medicine amp Rehabilitation McGraw Hill Education ISBN 978 0 07 179329 2 via Access Medicine page needed Alderson P Roberts I 1997 Corticosteroids in acute traumatic brain injury systematic review of randomised controlled trials BMJ 314 7098 1855 59 doi 10 1136 bmj 314 7098 1855 PMC 2126994 PMID 9224126 Bhaskar S 3 Aug 2017 Glasgow Coma Scale Technique and Interpretation Clinics in Surgery Archived from the original on 2020 01 16 Retrieved 2020 01 23 Hellweg Stephanie Johannes Stonke February 2008 Physiotherapy after traumatic brain injury A systematic review of the literature Brain Injury 22 5 365 73 doi 10 1080 02699050801998250 PMID 18415716 S2CID 13374136 a b Watson Martin 2001 Do patients with severe traumatic brain injury benefit from physiotherapy A review of the evidence Physical Therapy Reviews 6 4 233 49 doi 10 1179 ptr 2001 6 4 233 S2CID 71247575 Canning C Shepherd R Carr J Alison J Wade L White A 2003 A randomized controlled trial of the effects of intensive sit to stand training after recent traumatic brain injury on sit to stand performance Clinical Rehabilitation 17 4 355 62 doi 10 1191 0269215503cr620oa PMID 12785242 S2CID 36841611 Wilson D Powell M Gorham J Childers M 2006 Ambulation training with or without partial weightbearing after traumatic brain injury Results of a controlled trial American Journal of Physical Medicine amp Rehabilitation 85 1 68 74 doi 10 1097 01 phm 0000193507 28759 37 PMID 16357551 S2CID 44957954 Turner Stokes Lynne Pick Anton Nair Ajoy Disler Peter B Wade Derick T 2015 12 22 Multi disciplinary rehabilitation for acquired brain injury in adults of working age The Cochrane Database of Systematic Reviews 2015 12 CD004170 doi 10 1002 14651858 CD004170 pub3 ISSN 1469 493X PMC 8629646 PMID 26694853 Barman Apurba Chatterjee Ahana Bhide Rohit 2016 Cognitive Impairment and Rehabilitation Strategies After Traumatic Brain Injury Indian Journal of Psychological Medicine 38 3 172 81 doi 10 4103 0253 7176 183086 ISSN 0253 7176 PMC 4904751 PMID 27335510 Traumatic brain injury Diagnosis and treatment Mayo Clinic Archived from the original on 2023 03 17 Retrieved 2023 03 17 Schmidt Adam T Holland Jessica N 2015 Static and Dynamic Factors Promoting Resilience following Traumatic Brain Injury A Brief Review Neural Plasticity 2015 902802 doi 10 1155 2015 902802 PMC 4539485 PMID 26347352 a b Holtz Pamela 2015 06 09 10 Myths About Traumatic Brain Injury Task amp Purpose Archived from the original on 2016 08 02 Retrieved 2016 12 09 a b Myths amp Facts About TBI CBIRT Archived from the original on 2016 11 27 Retrieved 2016 12 09 Li Linda Liu Jianghong 2013 The effect of pediatric traumatic brain injury on behavioral outcomes a systematic review Developmental Medicine amp Child Neurology 55 1 37 45 doi 10 1111 j 1469 8749 2012 04414 x ISSN 1469 8749 PMC 3593091 PMID 22998525 Haas L F 2001 Phineas Gage and the Science of Brain Localisation Journal of Neurology Neurosurgery and Psychiatry 71 6 761 doi 10 1136 jnnp 71 6 761 PMC 1737620 PMID 11723197 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 Guenther Katja 2013 11 01 The Disappearing Lesion Sigmund Freud Sensory Motor Physiology and the Beginnings of Psychoanalysis Modern Intellectual History 10 3 569 601 doi 10 1017 S147924431300022X ISSN 1479 2443 S2CID 16372696 Further reading editSam Kean 2015 The Tale of the Dueling Neurosurgeons The History of the Human Brain as Revealed by True Stories of Trauma Madness and Recovery Back Bay Books ISBN 978 0316182355 External links edit nbsp Look up brain damage in Wiktionary the free dictionary Brain damage at Curlie Brain injury at Curlie International Brain Injury Association Retrieved from https en wikipedia org w index php title Brain damage amp oldid 1216962534, wikipedia, wiki, book, books, library,

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