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Brain injury

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

Brain injury

Brain damage, neurotrauma

Depending on brain area injured

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.


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

Trauma

open head injury

Deceleration injuries

; for example, from heavy metals including mercury and compounds of lead

Poisoning

Genetic disorder

including birth hypoxia[23]

Hypoxia

Tumors

Infections

leading to infarct, which may follow thrombosis, embolisms, angiomas, aneurysms, and cerebral arteriosclerosis.[24]

Stroke

or disorders such as cerebral palsy, Parkinson's disease, etc.

Neurological illness

Surgery

Substance use disorder

- pollution exposure or biological exposure (Annonaceae, rotenone,[25] Aspergillus spores, West Nile fever, Viral meningitis)

Neurotoxins

such as hanging, falling off from height, and even on rare occasion getting shot by a firearm, etc.

Suicide attempt

Acute total or sleep deprivation lasting longer than a day[26]

REM

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. Mouse NGF has been licensed in China since 2003 and is used to promote neurological recovery in a range of brain injuries, including intracerebral hemorrhage.[38]


In the case of brain damage from traumatic brain injury, dexamethasone and/or Mannitol may be used. [39]

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.[40]


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.[41] Sensory stimulation refers to regaining sensory perception through the use of modalities. There is no evidence to support the efficacy of this intervention.[42] 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.[42]


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).[43][44] Overall, studies suggest that patients with TBIs who participate in more intense rehabilitation programs will see greater benefits in functional skills.[45] More research is required to better understand the efficacy of the treatments mentioned above.[46]


Other treatments for brain injury can include medication, psychotherapy, neuropsychological rehabilitation, and/or surgery.[47]

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.[52]


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.[53]


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.[54]

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.  978-0316182355.

ISBN

at Curlie

Brain injury

at Curlie

Brain injury

International Brain Injury Association