Brain damage

For other uses, see Brain damage (disambiguation).
See also: Brain injury
Brain damage
Classification and external resources
ICD-10 Xxx.x
ICD-9-CM xxx

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. 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 due to a disorder or congenital malady.[1]

In general, brain damage refers to significant, undiscriminating trauma-induced damage, while neurotoxicity typically refers to selective, chemically induced neuron damage.


The foundation for understanding human behavior and brain injury can be attributed to Phineas Gage injury and Paul Broca’s milestone discoveries of leisons in the frontal lobe. In 1848, Phineas Gage encountered a tamping iron that destroyed his frontal lobe. Gage was observed to be intellectually unaffected by the serious injury but exemplified postinjury behavioral deficits. Phineas Gage’s injury is one of the most astonishing brain injuries in history.[2] Ten years later, Paul Broca examined two patients that acquired brain injuries to their frontal lobes affecting their speech. His first case assessed language localization. His second case confirmed his findings. His findings led to a vital confirmation of the relationship between speech and left cerebral hemisphere. This later became known as what we know today as Broca’s Area and the deficit known as Broca’s Aphasia.[3]

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.[4]

Mild Brain Injuries

Symptoms of a mild brain injury include headaches, confusions, ringing ears, fatigue, changes in sleep patterns, mood or behavior. Trouble with memory, concentration, attention or thinking.[5]

Moderate/Severe Brain Injuries

The physical symptoms include headaches that do not go away or worsen, vomiting or nausea, convulsions, abnormal dilation of the eyes, inability to awaken from sleep, weakness in extremities and loss of coordination. Cognitive symptoms include confusion, aggressive, abnormal behavior, slurred speech and coma or other disorders of consciousness.[5]

Symptoms in Children

Since young children lack the ability to properly communicate symptoms similar to adults. Symptoms observed in children include changes in eating habits, persistent irritability or sadness, changes in attention, disrupted sleeping habits, or loss of interest in toys.[5]

Symptoms of brain injuries can also be influenced by the location of the injury.

Brain injuries often create impairment or disability that can vary greatly in severity. In cases of serious 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 will 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.

Mental fatigue is a common debilitating experience and may not be linked by the patient to the original (minor) incident. Narcolepsy and sleep disorders are common misdiagnoses.

Studies show there is a correlation between brain lesion and language, speech, and category-specific disorders. However, lesions in Broca's and Wernicke's areas are not found to alter language comprehension.

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

Lesions to the visual cortex have different effects depending on the sub-area effected. Lesions to V1, for example, can cause blindness in different areas of the brain depending on the size of the lesion and location relative to the calcarine fissure. Lesions to V4 can cause color-blindness, and bilateral lesions to MT/V5 can cause the loss of the ability to perceive motion.

Lesion in 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.

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.[6]

Lesion size is correlated with severity, recovery, and comprehension.

In the Wisconsin Card Sorting Test with unilateral frontal or nonfrontal lesions, patients with left frontal lesions did more poorly but had high perseverative error scores. In right frontal and nonfrontal lesions are impaired but due to differences in patients. As a result, medial frontal lesions are associated with poor performance.

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 suffering from 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 pure alexics can still write, speak, and even transcribe letters without understanding their meaning.[7]


Brain injuries occur due to a very wide range of conditions, illnesses, and injuries. Possible causes of widespread brain damage include birth hypoxia,[8] prolonged hypoxia (shortage of oxygen), poisoning by teratogens (including alcohol), infection, and neurological illness. Brain tumors increase intracranial pressure, causing brain damage. 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.[9][10]

Brain injuries can result from a number of conditions including open head injury, closed head injury, deceleration injuries, exposure to toxic chemicals, lack of oxygen, tumors, infections, stroke.[11]

Wernicke-Korsakoff Syndrome can cause brain damage and results from a Vitamin B deficiency. This syndrome presents with two conditions, Wernicke’s encephalopathy and Korsakoff psychosis. Typically Wernicke’s encephalopathy proceeds symptoms of Korsakoff psychosis. Wernicke’s encephalopathy causes bleeding in the thalamus or hypothalamus, which controls the nervous and endocrine system. Due to the bleeding, brain damage occurs causing problems with vision, coordination and balance. Korsakoff psychosis typically follow after the symptoms of Wernicke’s decrease and result from chronic brain damage.[12] Korsakoff psychosis affect memory. Wernicke-Korsakoff Syndrome is typically caused by chronic alcohol abuse or by conditions that affect nutritional absorption, including colon cancer, eating disorders and gastric bypass.[13]

Common causes of focal or localized brain damage are physical trauma (traumatic brain injury, stroke, aneurysm, surgery, other neurological disorder), and poisoning from heavy metals including mercury and its compounds of lead. Vascular disorders of the brain disrupt the flow of blood to the brain, resulting in a lesion called an infarct. Vascular disorders of the brain include thrombosis, embolisms, angiomas, aneurysms, and cerebral arteriosclerosis.

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.[14]


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.[15]

The Eye Opening

  1. None
  2. To pain
  3. To Voice
  4. Spontaneous

Verbal Response

  1. None
  2. No words, only sounds
  3. Words, not coherent
  4. Disoriented conversation
  5. Normal conversation

Motor Response

  1. None
  2. Decorticate: abnormal posture characterized by clenched fists, legs straight, arms bent toward chest
  3. Decerebrate: abnormal posture in which the arms and legs are held straight out, toes pointed downward and the chin angled up.
  4. Withdraws to pain
  5. Localized to pain
  6. Normal

Based on the Glasgow Coma Scale severity is classifed as follows, severe brain injuries score 3-8, moderate brain injuries score 9-12 and mild score 13-15.[15]

Imaging Techniques

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) and magnetic resonance spectroscopy (MRS), positron emission tomography (PET), single-photon emission tomography (SPECT). CT scans and MRI are the two techniques widely used and are most effective. CT scans can show brain bleeds, fractures of the skull, fluid build up in the brain that will lead to increased cranial pressure. MRI is able to better to detect smaller injuries, detect damage within the brain, diffuse axonal injury, injuries to the brainstem, posterior fossa, and subtemporal and subfrontal regions. However patients with pacemakers, metallic implants, or other metal within their bodies are unable to have an MRI done. Typically the other imaging techniques are not used in a clinical setting because of the cost, lack of availability.[16]


Various professions may be involved in the medical care and rehabilitation of someone suffering 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.

Physiotherapists also play a significant role in rehabilitation after a brain injury. In the case of a traumatic brain injury (TBIs), physiotherapy treatment during the post-acute phase may include: sensory stimulation, serial casting and splinting, fitness and aerobic training, and functional training.[17] Sensory stimulation refers to regaining sensory perception through the use of modalities. There is no evidence to support the efficacy of this intervention.[18] 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.[18] Studies also report that fitness and aerobic training will increase cardiovascular fitness; however the benefits will not be transferred to the functional level.[19] 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).[20][21] Overall, studies suggest that patients with TBIs who participate in more intense rehabilitation programs will see greater benefits in functional skills.[19] More research is required to better understand the efficacy of the treatments mentioned above.

Other treatments for brain injury include medication, psychotherapy, neuropsychological rehabilitation, snoezelen, surgery, or physical implants such as deep brain stimulation.

In the case of brain damage from traumatic brain injury, dexamethasone and/or Mannitol may be used. [22]


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. Not everyone fully heals from brain damage, but it is possible to have a full recovery. People with minor brain damage can have debilitating side effects. The side effects of a brain injury depend on location and the body’s response to injury.[23] Even a mild concussion can have long term effects that may not resolve.[24] 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.[24]


Prognosis, or the likely progress of a disorder, depends on the nature, location, and cause of the brain damage (see Traumatic 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.

It is a common misconception that a brain injury sustained during childhood always has a better chance of successful recovery than similar injury acquired in adult life. However, the consequences of childhood injury may simply be more difficult to detect in the short term. 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.

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 symptoms such as swelling, pain, bruising, or loss of consciousness.[25] Post-traumatic amnesia is also common with brain damage, as is temporary aphasia, or impairment of language.[26]

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.[27] 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.[28] Headaches, occasional dizziness, or 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 swings often caused by damage to the various parts of the brain that control human emotions and behavior.[29] Some who have experience emotional changes related to brain damage may have emotions that come very quickly and are very intense, but have very little lasting effect.[29] Emotional changes may not be triggered by a specific event, and can be a cause of stress to the injured party and their family or friends.[30] Often, counseling is suggested for those who experience this effect after their injury, and may be available as an individual or group session. It may also be covered by insurance, or offered at a discounted price, or for free. See local resource centers near you for more information.

It is important to note that 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. Different types and degrees of trauma will cause different effects, and if any concerning symptoms, signs, or changes to behaviors are occurring, a healthcare provider should be consulted.

Body's Response to Brain Injury

Cytokines are known to be induced in response to brain injury.[31] 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.[32]

See also


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  2. Haas, L. F. "Phineas Gage and the Science of Brain Localisation." Journal of Neurology, Neurosurgery, and Psychiatry 71.6 (2001): 761. Web. 31 Oct. 2016.
  3. 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 Neurology130.5 (2007): 1432-441. Web. 31 Oct. 2016.
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  5. 1 2 3 "Traumatic brain injury Symptoms - Mayo Clinic". Retrieved 2016-11-15.
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  7. More Brain Lesions, Kathleen V. Wilkes
  8. "Birth Hypoxia and Brain Damage to Newborns". Michael E. Duffy. Retrieved 2013-07-27.
  9. Prevention, Cancer Resources from OncoLink | Treatment, Research, Coping, Clinical Trials,. "Possible Side Effects of Radiation Treatment for Brain Tumors | OncoLink". Retrieved 2016-09-22.
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  13. "Wernicke-Korsakoff Syndrome". Healthline. Retrieved 2016-11-15.
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  15. 1 2 "What Is the Glasgow Coma Scale?". Retrieved 2016-11-15.
  16. Watanabe, Thomas; Marino, Michael. Current Diagnosis & Treatment: Physical Medicine & Rehabilitation. McGraw-Hill Education. ISBN 978-0-07-179329-2 via Access Medicine.
  17. Hellweg, Stephanie; Johannes, Stonke (February 2008). "Physiotherapy after traumatic brain injury: A systematic review of the literature". Brain Injury. 22 (5): 365–373. doi:10.1080/02699050801998250. PMID 18415716.
  18. 1 2 Watson, Martin (2001). "Do patients with severe traumatic brain injury benefit from physiotherapy? A review of the evidence". Physical Therapy Reviews. 6: 233–249. doi:10.1179/ptr.2001.6.4.233. Retrieved May 8, 2012.
  19. 1 2 Turner-Stokes, L; Disler, P.; Nair, A.; Wade, T. (2005). "Multidisciplinary rehabilitation for acquired brain injury in adults of working age". Cochrane Database of Systematic Reviews. 3: 1–45. doi:10.1002/14651858.CD004170.pub2. PMID 16034923.
  20. 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" (PDF). Clinical Rehabilitation. 17 (4): 355–362. doi:10.1191/0269215503cr620oa. Retrieved May 8, 2012.
  21. 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 and Rehabilitation. 85: 68–74. doi:10.1097/01.phm.0000193507.28759.37. Retrieved May 8, 2012.
  22. "Corticosteroids in acute traumatic brain injury: systematic review of randomised controlled trials". BMJ. Retrieved 2012-07-29.
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  24. 1 2 "Myths & Facts About TBI". Retrieved 2016-11-14.
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  26. "Aphasia Definitions - National Aphasia Association". National Aphasia Association. Retrieved 2016-11-12.
  27. "Definition of AMNESIA". Retrieved 2016-11-12.
  28. Baumard, Josselin; Osiurak, François; Lesourd, Mathieu; Le Gall, Didier (2014-01-01). "Tool use disorders after left brain damage". Cognition. 5: 473. doi:10.3389/fpsyg.2014.00473. PMC 4033127Freely accessible. PMID 24904487.
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  30. Währborg, Peter (1991). Assessment & Management of Emotional Reactions to Brain Damage & Aphasia. Far Communications Ltd.
  31. 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 3657129Freely accessible. PMID 19026332.
  32. 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 2785020Freely accessible. PMID 17426506.

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