Brain injury

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Brain injury
Other namesBrain damage, neurotrauma
Traumaticbraininjury2010.jpg
A CT of the head years after a traumatic brain injury showing an empty space where the damage occurred, marked by the arrow
Specialty Neurology
Symptoms Depending on brain area injured
Types Acquired brain injury (ABI), traumatic brain injury (TBI), focal or diffuse, primary and secondary

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.

Contents

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 ]

Impaired function of affected areas can be compensated through neuroplasticity by forming new neural connections.

Signs and symptoms

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

Mild brain injuries

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

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

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

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

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

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

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. Coup injury.jpg
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

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

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

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

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

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

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

Acute

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

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

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

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

Related Research Articles

<span class="mw-page-title-main">Aphasia</span> Inability to comprehend or formulate language

In aphasia, a person may be unable to comprehend or unable to formulate language because of damage to specific brain regions. The major causes are stroke and head trauma; prevalence is hard to determine but aphasia due to stroke is estimated to be 0.1–0.4% in the Global North. Aphasia can also be the result of brain tumors, epilepsy, autoimmune neurological diseases, brain infections, or neurodegenerative diseases.

<span class="mw-page-title-main">Expressive aphasia</span> Language disorder involving inability to produce language

Expressive aphasia is a type of aphasia characterized by partial loss of the ability to produce language, although comprehension generally remains intact. A person with expressive aphasia will exhibit effortful speech. Speech generally includes important content words but leaves out function words that have more grammatical significance than physical meaning, such as prepositions and articles. This is known as "telegraphic speech". The person's intended message may still be understood, but their sentence will not be grammatically correct. In very severe forms of expressive aphasia, a person may only speak using single word utterances. Typically, comprehension is mildly to moderately impaired in expressive aphasia due to difficulty understanding complex grammar.

<span class="mw-page-title-main">Language center</span> Speech processing areas of the brain

In neuroscience and psychology, the term language center refers collectively to the areas of the brain which serve a particular function for speech processing and production. Language is a core system that gives humans the capacity to solve difficult problems and provides them with a unique type of social interaction. Language allows individuals to attribute symbols to specific concepts, and utilize them through sentences and phrases that follow proper grammatical rules. Finally, speech is the mechanism by which language is orally expressed.

<span class="mw-page-title-main">Receptive aphasia</span> Language disorder involving inability to understand language

Wernicke's aphasia, also known as receptive aphasia, sensory aphasia, fluent aphasia, or posterior aphasia, is a type of aphasia in which individuals have difficulty understanding written and spoken language. Patients with Wernicke's aphasia demonstrate fluent speech, which is characterized by typical speech rate, intact syntactic abilities and effortless speech output. Writing often reflects speech in that it tends to lack content or meaning. In most cases, motor deficits do not occur in individuals with Wernicke's aphasia. Therefore, they may produce a large amount of speech without much meaning. Individuals with Wernicke's aphasia are typically unaware of their errors in speech and do not realize their speech may lack meaning. They typically remain unaware of even their most profound language deficits.

<span class="mw-page-title-main">Head injury</span> Serious trauma to the cranium

A head injury is any injury that results in trauma to the skull or brain. The terms traumatic brain injury and head injury are often used interchangeably in the medical literature. Because head injuries cover such a broad scope of injuries, there are many causes—including accidents, falls, physical assault, or traffic accidents—that can cause head injuries.

Aphasiology is the study of language impairment usually resulting from brain damage, due to neurovascular accident—hemorrhage, stroke—or associated with a variety of neurodegenerative diseases, including different types of dementia. These specific language deficits, termed aphasias, may be defined as impairments of language production or comprehension that cannot be attributed to trivial causes such as deafness or oral paralysis. A number of aphasias have been described, but two are best known: expressive aphasia and receptive aphasia.

<span class="mw-page-title-main">Anomic aphasia</span> Medical condition

Anomic aphasia is a mild, fluent type of aphasia where individuals have word retrieval failures and cannot express the words they want to say. By contrast, anomia is a deficit of expressive language, and a symptom of all forms of aphasia, but patients whose primary deficit is word retrieval are diagnosed with anomic aphasia. Individuals with aphasia who display anomia can often describe an object in detail and maybe even use hand gestures to demonstrate how the object is used, but cannot find the appropriate word to name the object. Patients with anomic aphasia have relatively preserved speech fluency, repetition, comprehension, and grammatical speech.

<span class="mw-page-title-main">Wernicke encephalopathy</span> Medical condition

Wernicke encephalopathy (WE), also Wernicke's encephalopathy, or wet brain is the presence of neurological symptoms caused by biochemical lesions of the central nervous system after exhaustion of B-vitamin reserves, in particular thiamine (vitamin B1). The condition is part of a larger group of thiamine deficiency disorders that includes beriberi, in all its forms, and alcoholic Korsakoff syndrome. When it occurs simultaneously with alcoholic Korsakoff syndrome it is known as Wernicke–Korsakoff syndrome.

<span class="mw-page-title-main">Wernicke's area</span> Speech comprehension region in the dominant hemisphere of the hominid brain

Wernicke's area, also called Wernicke's speech area, is one of the two parts of the cerebral cortex that are linked to speech, the other being Broca's area. It is involved in the comprehension of written and spoken language, in contrast to Broca's area, which is primarily involved in the production of language. It is traditionally thought to reside in Brodmann area 22, which is located in the superior temporal gyrus in the dominant cerebral hemisphere, which is the left hemisphere in about 95% of right-handed individuals and 70% of left-handed individuals.

<span class="mw-page-title-main">Conduction aphasia</span> Medical condition

Conduction aphasia, also called associative aphasia, is an uncommon form of difficulty in speaking (aphasia). It is caused by damage to the parietal lobe of the brain. An acquired language disorder, it is characterised by intact auditory comprehension, coherent speech production, but poor speech repetition. Affected people are fully capable of understanding what they are hearing, but fail to encode phonological information for production. This deficit is load-sensitive as the person shows significant difficulty repeating phrases, particularly as the phrases increase in length and complexity and as they stumble over words they are attempting to pronounce. People have frequent errors during spontaneous speech, such as substituting or transposing sounds. They are also aware of their errors and will show significant difficulty correcting them.

<span class="mw-page-title-main">Carl Wernicke</span> German physician and neuropathologist (1848–1905)

CarlWernicke was a German physician, anatomist, psychiatrist and neuropathologist. He is known for his influential research into the pathological effects of specific forms of encephalopathy and also the study of receptive aphasia, both of which are commonly associated with Wernicke's name and referred to as Wernicke encephalopathy and Wernicke's aphasia, respectively. His research, along with that of Paul Broca, led to groundbreaking realizations of the localization of brain function, specifically in speech. As such, Wernicke's area has been named after the scientist.

<span class="mw-page-title-main">Global aphasia</span> Medical condition

Global aphasia is a severe form of nonfluent aphasia, caused by damage to the left side of the brain, that affects receptive and expressive language skills as well as auditory and visual comprehension. Acquired impairments of communicative abilities are present across all language modalities, impacting language production, comprehension, and repetition. Patients with global aphasia may be able to verbalize a few short utterances and use non-word neologisms, but their overall production ability is limited. Their ability to repeat words, utterances, or phrases is also affected. Due to the preservation of the right hemisphere, an individual with global aphasia may still be able to express themselves through facial expressions, gestures, and intonation. This type of aphasia often results from a large lesion of the left perisylvian cortex. The lesion is caused by an occlusion of the left middle cerebral artery and is associated with damage to Broca's area, Wernicke's area, and insular regions which are associated with aspects of language.

<span class="mw-page-title-main">Traumatic brain injury</span> Injury of the brain from an external source

A traumatic brain injury (TBI), also known as an intracranial injury, is an injury to the brain caused by an external force. TBI can be classified based on severity ranging from mild traumatic brain injury (mTBI/concussion) to severe traumatic brain injury. TBI can also be characterized based on mechanism or other features. Head injury is a broader category that may involve damage to other structures such as the scalp and skull. TBI can result in physical, cognitive, social, emotional and behavioral symptoms, and outcomes can range from complete recovery to permanent disability or death.

Transcortical sensory aphasia (TSA) is a kind of aphasia that involves damage to specific areas of the temporal lobe of the brain, resulting in symptoms such as poor auditory comprehension, relatively intact repetition, and fluent speech with semantic paraphasias present. TSA is a fluent aphasia similar to Wernicke's aphasia, with the exception of a strong ability to repeat words and phrases. The person may repeat questions rather than answer them ("echolalia").

<span class="mw-page-title-main">Mixed transcortical aphasia</span>

Mixed transcortical aphasia is the least common of the three transcortical aphasias. This type of aphasia can also be referred to as "Isolation Aphasia". This type of aphasia is a result of damage that isolates the language areas from other brain regions. Broca's, Wernicke's, and the arcuate fasiculus are left intact; however, they are isolated from other brain regions.

Memory disorders are the result of damage to neuroanatomical structures that hinders the storage, retention and recollection of memories. Memory disorders can be progressive, including Alzheimer's disease, or they can be immediate including disorders resulting from head injury.

Language disorders or language impairments are disorders that involve the processing of linguistic information. Problems that may be experienced can involve grammar, semantics (meaning), or other aspects of language. These problems may be receptive, expressive, or a combination of both. Examples include specific language impairment, better defined as developmental language disorder, or DLD, and aphasia, among others. Language disorders can affect both spoken and written language, and can also affect sign language; typically, all forms of language will be impaired.

Post-traumatic amnesia (PTA) is a state of confusion that occurs immediately following a traumatic brain injury (TBI) in which the injured person is disoriented and unable to remember events that occur after the injury. The person may be unable to state their name, where they are, and what time it is. When continuous memory returns, PTA is considered to have resolved. While PTA lasts, new events cannot be stored in the memory. About a third of patients with mild head injury are reported to have "islands of memory", in which the patient can recall only some events. During PTA, the patient's consciousness is "clouded". Because PTA involves confusion in addition to the memory loss typical of amnesia, the term "post-traumatic confusional state" has been proposed as an alternative.

Traumatic brain injury can cause a variety of complications, health effects that are not TBI themselves but that result from it. The risk of complications increases with the severity of the trauma; however even mild traumatic brain injury can result in disabilities that interfere with social interactions, employment, and everyday living. TBI can cause a variety of problems including physical, cognitive, emotional, and behavioral complications.

Sleep disorder is a common repercussion of traumatic brain injury (TBI). It occurs in 30%-70% of patients with TBI. TBI can be distinguished into two categories, primary and secondary damage. Primary damage includes injuries of white matter, focal contusion, cerebral edema and hematomas, mostly occurring at the moment of the trauma. Secondary damage involves the damage of neurotransmitter release, inflammatory responses, mitochondrial dysfunctions and gene activation, occurring minutes to days following the trauma. Patients with sleeping disorders following TBI specifically develop insomnia, sleep apnea, narcolepsy, periodic limb movement disorder and hypersomnia. Furthermore, circadian sleep-wake disorders can occur after TBI.

References

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