Brain injury

"Brain damage" redirects here. For other uses, see Brain damage (disambiguation).

For the scientific journal on brain injuries, see Brain Injury (journal).

Brain injury, also known as brain damage or neurotrauma, is the destruction or degeneration of brain cells. It may result from external trauma, such as accidents or falls, or internal factors, such as strokes, infections, or metabolic disorders.

Brain injury
Other names	Brain damage, neurotrauma
A CT of the head years after a traumatic brain injury showing an empty space where the damage occurred, marked by the yellow arrow in the bottom left
Specialty	Neurology, Psychiatry
Symptoms	Depending on brain area injured
Types	Acquired brain injury (ABI), traumatic brain injury (TBI), focal and diffuse brain injury, primary and secondary

Traumatic brain injury (TBI), the most common type of brain injury, is typically caused by external physical trauma to the head.^[1] Acquired brain injuries occur after birth, in contrast to genetic or congenital brain injuries that patients are born with.^[2]

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.^[3]

Because of neuroplasticity, the brain can partially recover function by forming new neural connections to compensate for damaged areas. Patients may regain adaptive skills such as movement and speech, especially if they undergo therapy and practice.^[1]

Signs and symptoms

Symptoms of brain injuries vary based on the severity of the injury, the area of the brain injured, and how much of the brain was affected. The three categories used for classifying the severity of brain injuries are mild, moderate, or severe.^[4]

Severity of injuries

Mild brain injuries

Symptoms of a mild brain injury include headaches, confusions, tinnitus, fatigue and changes in sleep patterns, mood or behavior. Other symptoms include trouble with memory, concentration, attention or thinking.^[5] Because mental fatigue can be attributed to many disorders, patients may not realise the connection between a minor brain injury and fatigue.

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 wake from sleep, weakness in extremities and a loss of coordination.^[5]

Symptoms in children

Children may not be able to communicate their emotions or thought processes, so their behaviours must be observed to discern symptoms. Signs may include changes in eating habits, persistent anger, sadness, attention loss, losing interest in activities they used to enjoy, or sleep problems.^[5]

Association between location of injury and symptoms

Symptoms can depend on the location of the brain that was damaged, and certain types of impairments can be attributed to damage to certain areas of the brain. Larger lesions tend to cause worse symptoms and more complicated recoveries.^[6]

Peope who suffer severe brain injuries have a high chance of incurring severe disabilities, 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.^[7]

Brain lesions are correlated with language, speech and category-specific disorders. Wernicke's aphasia is associated with word retrieval deficits, unknowingly making up words (neologisms), and problems with language comprehension. The symptoms of Wernicke's aphasia are caused by damage to the posterior section of the superior temporal gyrus.^[8][9]

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.^[10]

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.^[11]

Lesions to the fusiform gyrus often result in prosopagnosia, the inability to distinguish faces and other complex objects from each other.^[12] 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.^[13]

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.^[14] Lesions to V4 can cause color-blindness,^[15] 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.^[16]

Physiological and cognitive effects

Physiological and cognitive complications of a brain injury, caused by damage to the neurons, nerve tracts or sections of the brain, can occur immediately or at varying times after the injury. The immediate response can take many forms. Initially, there may be symptoms such as swelling, pain, bruising, or loss of consciousness.^[17] Post-traumatic amnesia, and issues with both long- and short-term memory,^[18] are common with brain damage, as is temporary aphasia, or impairment of language.^[19]

Complications tend to become clearer as time progresses. Tissue damage and loss of blood flow caused by the injury may cause amnesia and aphasia (impairment in speech) to become permanent. Apraxia, the impairment of motor coordination and movement, has been documented in patients. ^[20][21] Headaches, occasional dizziness, and fatigue—all temporary symptoms of brain trauma—may become permanent, or may not disappear for a long time. Brain damage predisposes patients to seizures, Parkinson's disease, dementia and hormone-secreting gland disorders; monitoring is essential for detecting the development of these diseases and treating them promptly.^[22]

Psychological effects

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.^[23] Individuals may experience sudden, severe mood swings that subside quickly.^[23] Emotional changes, which may not be triggered by a specific event, can cause distress to the injured party and their family and friends.^[24] Brain injuries increase the risk of developing depression and aggression.^[25] Often, counseling in either a one-on-one or group setting is suggested for those who experience emotional dysfunction after their injury.

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.

• trauma; multiple traumatic injuries can lead to chronic traumatic encephalopathy
• coup-contrecoup injury
• head injury^[26]
  • open head injury like depressed skull fracture and skull fractures associated with epidural hematoma, subdural hematoma, intracerebral hematoma
  • closed head injury
  • penetrating: a sharp object enters the brain, causing a large damage area. Penetrating injuries caused by bullets have a 91 percent mortality rate.
  • blast injury^[27]
• deceleration injuries
• poisoning, such as from heavy metals, including mercury and compounds of lead
• genetic disorder
• hypoxia, including birth hypoxia^[28]
• brain tumors
• infections
• stroke leading to infarct, which may follow thrombosis, embolisms, angiomas, aneurysms, and large artery arteriosclerosis^[29]
• neurological illness or disorders, such as cerebral palsy, Parkinson's disease, and similar diseases
• neurosurgery
• substance use disorder
• neurotoxins – pollution exposure or biological exposure
• suicide attempt such as hanging, falling off from height, and even on rare occasion getting shot by a firearm

Chemotherapy

Chemotherapy can cause brain damage to the neural stem cells and oligodendrocyte cells that produce myelin. This is commonly known as "Chemo Brain". The 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.^[30][31]

Wernicke–Korsakoff syndrome

Wernicke–Korsakoff syndrome, caused by a vitamin B1 (thiamine) deficiency, can result in brain damage.^[32][33] 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.^[32]

Korsakoff psychosis typically follows after the symptoms of Wernicke's decrease.^[32][33] 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.^[32]

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.^[34]

Diffuse axonal

Diffuse axonal injury is caused by shearing forces on the brain leading to lesions in the white matter tracts of the brain.^[35] 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.^[36]

Diagnosis

The Glasgow Coma Scale (GCS) is the most widely used scoring system to assess the severity of a brain injury. The scale is based on three traits: whether the person can open his or her eyes, whether he or she can speak coherently and whether he or she can follow a command to move.^[37] Eye opening is worth 4 points, speech is worth 5 and motor ability is worth 6. Severe brain injuries score 3–8, moderate brain injuries score 9–12 and mild brain injuries score 13–15.^[37]

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 widely used techniques and are the most effective. CT scans can show brain haemorrhages, fractures of the skull and fluid buildup in the brain that will lead to increased cranial pressure.^[38]

MRI scans are better at detecting smaller injuries, injuries inside of the brain, diffuse axonal injuries, injuries to the brainstem, injuries to the posterior fossa and injuries to the subtemporal and subfrontal regions. However, patients with pacemakers, metallic implants or other metal within their bodies cannot undergo MRI scans. Typically the other imaging techniques are not used in clinical settings because they are costly and not as widely available.^[39]

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. Early intervention to maintain oxygen and normal blood pressure can reduce further brain damage and improve recovery outcomes.^[40]

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.^{[medical citation needed]}

In the case of brain damage from traumatic brain injury, dexamethasone or mannitol may be used.^[41]

Monitoring intracranial pressure is recommended to guide treatment decisions.^[42]

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.^[43]

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.^[44] Sensory stimulation refers to regaining sensory perception through the use of modalities. There is no evidence to support the efficacy of this intervention.^[45] 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.^[45]

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).^[46][47] Overall, studies suggest that patients with TBIs who participate in more intense rehabilitation programs will see greater benefits in functional skills.^[48] More research is required to better understand the efficacy of the treatments mentioned above.^[49]

Other treatments for brain injury can include medication, psychotherapy, neuropsychological rehabilitation, neurotherapy and/or surgery.^[50]

Prognosis

Further information: Traumatic brain injury, Focal and diffuse brain injury, and Primary and secondary brain injury

The prognosis of a brain injury depends on its presentation, cause and location. It is difficult to predict the outcome of a brain injury, as victims of minor injuries may experience severe symptoms and complications; even a mild concussion can have long-term effects that may not resolve.^[51][52] A common misconception is that people who experience brain damage cannot fully recover. Though not every patient returns to pre-injury levels of cognitive functioning, it is not impossible.^[52] 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.^[53]

Adults aged 60 or older tend to experience more severe outcomes, including greater psychosocial limitations, longer periods of coma, increased complications, and slower recovery, even when the initial injury is equivalent in severity to that of a younger individual. This is because older individuals experience age-related changes in brain structure and function, and have reduced physiological reserves.^[54] As children's brains are still developing, outcomes of pediatric brain injuries are more difficult to predict than adults'.^[55] 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.^[56]

History

The connection between brain injuries and functional impairments was first documented in the 16th century BC, in the Edwin Smith Papyrus of Ancient Egypt. The manuscript stated, for the first time in recorded history, that injuries to the meninges resulted in stiffness of the neck, that lesions of the cerebrum resulted in paralysis and that temporal lobe damage resulted in aphasia. It recommended that head injuries be treated by rubbing grease across the site of the injury, dressing open wounds if there was not a skull fracture and ensuring that the patient sat upright.^[57][58] In Ancient Greece in the 1st millennium BC, the physicians Hippocrates, Celsus and Galen remarked that traumatic brain injuries were often followed by a loss of consciousness. ^[59]

In the 16th century AD, Jacopo Berengario da Carpi wrote in his treatise De Fractura Calvae sive Craniei that brain injuries resulted in vomiting, haemorrhages, aphasia and vertigo.^[60] In 1825, French physician Jean-Baptiste Bouillaud, inspired by other scientists' case reports and experiments, first proposed that lesions of the frontal lobe were responsible for disturbances in speech, though he did not discover that the localisation was left-sided.^[61]

In 1848, a railroad construction foreman named Phineas Gage was paving way for a new railroad line when an explosion sent a tamping iron through his frontal lobe. Gage retained his functional abilities but reportedly became rude, inconsiderate and indecisive after the accident; John Martyn Harlow, the physician who treated Gage, stated that Gage had previously been friendly and respectful.^[62][63] Gage's case was written about in almost 60% of psychology textbooks published between 1983 and 1998 and is, according to neuroscientist Malcolm Macmillan, "the most famous case of personality change after brain damage".^[62]

Broca's area (blue) and Wernicke's area (green)

In the 1860s, Paul Broca examined two patients exhibiting impaired speech. Broca's first patient, Louis Victor Leborgne,^[64] lacked productive speech and could utter only the syllable "tan". Broca, who met Leborgne in 1861,^[64] saw Leborgne's case as an opportunity to address Bouillaud's theory that language skills were localised to the frontal lobe. After Leborgne died the same year, an autopsy revealed that he did, in fact, have a lesion in his left frontal lobe. The second patient, Lazare Lelong, who had suffered a stroke the year before Broca met him, was similarly aphasic, able to utter only five words (two of which were mispronunciations). Lelong's autopsy showed that he also had a left frontal lobe lesion. 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.^[65]

In 1874, a German neuroscientist, Carl Wernicke, published a case report on a stroke patient who experienced neither speech nor hearing impairments, but had lost his ability to comprehend spoken and written language.^[66] After the patient's death, an autopsy found a lesion located in the left temporal region. This area became known as Wernicke's area and the condition as Wernicke's aphasia. Wernicke later hypothesized that there was a relationship between Wernicke's area and Broca's area, which was later proved correct.^[67]

In 1928, pathologist Harrison Martland reported upon a phenomenon of what he called "punch drunk", in which boxers who suffered many blows to the head during their careers went on to develop dementia, Parkinsonian symptoms and other cognitive disorders. He recorded 23 examples (5 of whom he personally examined) and theorised that repeated head trauma causes glial cells in the brain to proliferate, leading to neurological dysfunction and encephalitis. Physicians previously did not believe that complications of head trauma could appear long after the injury had occurred.^[68] In 1940, psychiatrists Abram Blau and Karl Murdoch Bowman described the case of a 28-year-old boxer with a history of cognitive impairment and psychosis, and coined the term "chronic traumatic encephalopathy" to replace "punch drunk".^[69]

Epidemiology

Traumatic brain injuries

Further information: Traumatic_brain_injury § Epidemiology

On average, 1,691,481 people (576.8 per 100,000) were hospitalised in the United States for traumatic brain injuries between 2002 and 2006. The vast majority (465.4 per 100,000) of these patients were released shortly after being admitted and treated; 275.146 (93.8 per 100,000) were hospitalised but survived, and 51,538 (17.6 per 100,000) died. In 1991, about 1.5 million people out of 46,761 households sustained nonfatal brain injuries, 25% of whom sought no treatment.^[70]

70% to 95% of traumatic brain injuries are mild. A study of adults undergoing inpatient rehabilitation for head trauma showed that 19.2% had severe trauma, and 10.3% moderate trauma. The ratio of moderate and severe trauma to mild trauma tends to be inflated, as people often do not go to the hospital for mild TBIs.^[70]

Traumatic brain injuries are consistently found to occur more often, and to be more severe, in males than in females across all age groups. The average annual TBI rate for men is 998,176, whereas the female rate is 693,329. 17% of men who suffer TBIs are hospitalised and 4% die; 15% of women who suffer TBIs are hospitalised and less than 2% die.^[70]

Children between the ages of 0 and 4 and adolescents between the ages of 15 and 19 are the age groups most commonly afflicted by TBIs. However, older adults 75 or older also have a high rate of TBIs, and are 3 times as likely than the average TBI patient to die and 3.5 times as likely to be hospitalised.^[70]

There is a correlation between alcohol consumption and traumatic brain injuries; between 56% and 72% of people presenting to the hospital with a TBI have a positive blood alcohol concentration. Someone who has previously had a TBI is likely to have another; people who experience one TBI are 2.3 to 3 times more likely than the general population to experience a second, and people who experience a second TBI are 7.8 to 9 times more likely to experience a third. Repeated TBIs are associated with alcohol use.^[70]

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.^[71] 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.^[72]

See also

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• Psychology portal

• Cerebral palsy – Movement disorders that appear in early childhood
• Encephalopathy – Disorders or diseases 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 source