Brain damage

For other uses, see Brain Damage (disambiguation).
See also: Brain injury

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.

Signs and symptoms

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.

Brain injury whether from stroke, alcohol abuse, traumatic brain injury, or vitamin B deficiency can sometimes result in Korsakoff's Psychosis, where the individual engages in confabulations. Confabulations involve the inability to separate daydream memory from real memory and the filling in of memory lapses with daydreams. Like all other symptoms of brain injuries, Korsakoff's Psychosis is often mis-diagnosed, in this case as schizophrenia.

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.[2]

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.[3]

Causes

Brain injuries occur due to a very wide range of conditions, illnesses, and injuries. Possible causes of widespread brain damage include birth hypoxia,[4] 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. 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.[5]

Management

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.[6] Sensory stimulation refers to regaining sensory perception through the use of modalities. There is no evidence to support the efficacy of this intervention.[7] 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.[7] Studies also report that fitness and aerobic training will increase cardiovascular fitness; however the benefits will not be transferred to the functional level.[8] 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).[9][10] Overall, studies suggest that patients with TBIs who participate in more intense rehabilitation programs will see greater benefits in functional skills.[8] 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. [11]

Prognosis

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.

Body's response to brain injury

Cytokines are known to be induced in response to brain injury. 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.

See also

References

  1. ↑ Headway Brain Injury Services and Support
  2. ↑ Denny-Brown, D., and Betty Q. Banker. "Amorphosynthesis from Left Parietal Lesion". A.M.A. Archives of Neurology and Psychiatry 71, no. 3 (March 1954): 302–13.
  3. ↑ More Brain Lesions, Kathleen V. Wilkes
  4. ↑ "Birth Hypoxia and Brain Damage to Newborns". Michael E. Duffy. Retrieved 2013-07-27.
  5. ↑ Glenn, Lehmann, Mumby, Woodside. "Differential Fos Expression Following Aspiration, Electrolytic, or Excitotoxic Lesions of the Perirhinal Cortex in Rats"
  6. ↑ 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.
  7. 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.
  8. 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.
  9. ↑ 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.
  10. ↑ 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.
  11. ↑ "Corticosteroids in acute traumatic brain injury: systematic review of randomised controlled trials". BMJ. Retrieved 2012-07-29.

External links

This article is issued from Wikipedia - version of the Thursday, March 10, 2016. The text is available under the Creative Commons Attribution/Share Alike but additional terms may apply for the media files.