Brain injury

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In medicine, brain injuries are "acute and chronic injuries to the brain, including the cerebral hemispheres, cerebellum, and brain stem. Clinical manifestations depend on the nature of injury. Diffuse trauma to the brain is frequently associated with diffuse axonal injury or coma, post-traumatic. Localized injuries may be associated with neurobehavioral manifestations; hemiparesis, or other focal neurologic deficits.."[1]

Types of brain injury include:

Injury Effects

Primary Brain Injury

Secondary Brain Injury

Secondary effects of a brain injury are those that follow from the body’s compensatory and reactionary mechanisms in response to the injury, both at the organ and cellular level. These effects can permanently damage the patient if not managed properly. They include cerebral swelling, brain tissue ischemia, excitotoxicity, oxidative stress and eventually apoptosis, also referred to as programmed cell death. Theoretically, these effects are both preventable and reversible. [9]

Ischemia

Ischemia is defined as a period of time during which a tissue’s blood supply is temporarily stopped. Therefore, brain tissue ischemia is a period of time where the brain tissue lacks sufficient blood flow, which in turn prevents proper tissue oxygenation which is required for cells to remain alive and healthy. If this period of ischemia persists for too long, permanent brain damage may occur. Cerebral swelling, a cellular response to injury, increases intracranial pressure (ICP), which in turn leads to intracranial hypertension, the direct cause of the ischemia. Ischemic episodes in the brain can have very detrimental effects, with consequences that include cognitive damage and motor impairment.[10]

Excitotoxicity

Excitotoxicity results from excessive release of excitatory neurotransmitters such as glutamate. Excitatory neurotransmitters increase cytosolic calcium ion (Ca2+) levels inside neurons, while inhibitory neurotransmitters maintain low cytosolic Ca2+ levels. When exposed to an abnormally high amount of excitatory neurotransmitter, a post-synaptic neuron becomes hyperactive. In a brain injury, the hyperactive neurons are those cells that have been injured. As Ca2+ is a potent modulator of many active processes, this high degree of activity will activate a higher than normal quantity of degradative enzymes, which will in turn mediate the apoptosis resulting from an excitotoxic condition.[11]

Diagnosis

Imaging

X-ray computed tomography of the head should be considered, especially if the patient fulfills any criteria from the New Orleans Criteria clinical prediction rule:[12]

"headache, vomiting, an age over 60 years, drug or alcohol intoxication, deficits in short-term memory, physical evidence of trauma above the clavicles, and seizure"

X-ray of the cervical spine should be considered, especially if the patient fulfills criteria from the Canadian C-Spine Rule clinical prediction rule for neck injury: [13]

  • Age 65 years or more
  • Paresthesias in extremities
  • Dangerous fall ("elevation >=3 ft or 5 stairs; an axial load to the head (e.g., diving); a motor vehicle collision at high speed (>100 km/hr) or with rollover or ejection; a collision involving a motorized recreational vehicle; or a bicycle collision")
  • Inability to rotate the neck 45° to the right and left
    • Only test if "simple rear-end motor vehicle collision, sitting position in ED, ambulatory at any time since injury, delayed onset of neck pain, or absence of midline C-spine tenderness"[14]
  • Glasgow Coma Scale less than 15 (the Canadian C-Spine Rule was only designed for alert patients)

Biochemical Analyses

When patients enter the hospital with brain trauma, bodily fluids such as urine, cerebrospinal fluid (CSF), and blood are obtained in the assessment and treatment procedure.[15] In many cases, these fluids are tested for certain chemicals that indicate the severity of injury.[16]

Among the things tested for are cytokines, special proteins that are secreted by damaged cells and cells surrounding the injured site. These proteins participate in either a protective or damaging manner. Cytokines that result in neuroprotection will attenuate the body’s immune response against damaged cells, while cytokines that result in neurodegeneration will exacerbate or initiate the body’s immune response against damaged cells.[17][18]

Interleukins (ILs) are a large class of proteins that participate in immune responses, both protectively and degeneratively. For example, IL-6 and nerve growth factor (NGF) respond neuroprotectively in a mutually dependent manner in response to brain injury [19], while IL-18 responds neurodegradatively in response to brain injury. children with severe traumatic brain injury. Journal of Neurotrauma, 2008. 25(3): p. 225-234.</ref>[20] Many other cytokines are synthesized in response to brain injury. Although the exact mechanisms of neuroprotection or neurodegradation resulting from the secretion of cytokines have yet to be entirely elucidated, the knowledge that these mechanisms exist is one of the first steps toward determining the most effective way to utilize this information in a clinical treatment context.[21][22]

Another indicator of injury severity is if a change in the amount of oxidation that is occurring is detected. For example, lipid peroxidation is one form of oxidation that occurs at a higher rate in response to brain injury. Thiobarbituric acid reactive species (TBARS) are metabolic byproducts of the peroxidation of lipid membranes. Therefore, the amount of TBARS detected can be used to indicate if oxidation has indeed been occurring in response to a brain injury. However, one drawback to this method for detecting the quantity of oxidation that has been occurring is that actual brain tissue is required, meaning that this procedure can only be used in experimental investigations.[23]

Treatment

Mild injury may not benefit from multidisciplinary[24] or rehabilitation[25] treatment.

References

  1. ↑ Anonymous (2024), Brain injury (English). Medical Subject Headings. U.S. National Library of Medicine.
  2. ↑ Brown CV, Zada G, Salim A, Inaba K, Kasotakis G, Hadjizacharia P et al. (2007). "Indications for routine repeat head computed tomography (CT) stratified by severity of traumatic brain injury.". J Trauma 62 (6): 1339-44; discussion 1344-5. DOI:10.1097/TA.0b013e318054e25a. PMID 17563645. Research Blogging.
  3. ↑ Smith JS, Chang EF, Rosenthal G, Meeker M, von Koch C, Manley GT et al. (2007). "The role of early follow-up computed tomography imaging in the management of traumatic brain injury patients with intracranial hemorrhage.". J Trauma 63 (1): 75-82. DOI:10.1097/01.ta.0000245991.42871.87. PMID 17622872. Research Blogging.
  4. ↑ Sifri ZC, Homnick AT, Vaynman A, Lavery R, Liao W, Mohr A et al. (2006). "A prospective evaluation of the value of repeat cranial computed tomography in patients with minimal head injury and an intracranial bleed.". J Trauma 61 (4): 862-7. DOI:10.1097/01.ta.0000224225.54982.90. PMID 17033552. Research Blogging.
  5. ↑ Velmahos GC, Gervasini A, Petrovick L, Dorer DJ, Doran ME, Spaniolas K et al. (2006). "Routine repeat head CT for minimal head injury is unnecessary.". J Trauma 60 (3): 494-9; discussion 499-501. DOI:10.1097/01.ta.0000203546.14824.0d. PMID 16531845. Research Blogging.
  6. ↑ Brown CV, Weng J, Oh D, Salim A, Kasotakis G, Demetriades D et al. (2004). "Does routine serial computed tomography of the head influence management of traumatic brain injury? A prospective evaluation.". J Trauma 57 (5): 939-43. PMID 15580014.
  7. ↑ Kaups KL, Davis JW, Parks SN (2004). "Routinely repeated computed tomography after blunt head trauma: does it benefit patients?". J Trauma 56 (3): 475-80; discussion 480-1. PMID 15128116.
  8. ↑ 8.0 8.1 Bee TK, Magnotti LJ, Croce MA, Maish GO, Minard G, Schroeppel TJ et al. (2009). "Necessity of repeat head CT and ICU monitoring in patients with minimal brain injury.". J Trauma 66 (4): 1015-8. DOI:10.1097/TA.0b013e31819adbc8. PMID 19359908. Research Blogging.
  9. ↑ Bayir, H., P.M. Kochanek, and R.S.B. Clark, Traumatic brain injury in infants and children - Mechanisms of secondary damage and treatment in the intensive care unit. Critical Care Clinics, 2003. 19(3): p. 529-+.
  10. ↑ Bayir, H., P.M. Kochanek, and R.S.B. Clark, Traumatic brain injury in infants and children - Mechanisms of secondary damage and treatment in the intensive care unit. Critical Care Clinics, 2003. 19(3): p. 529-+.
  11. ↑ Bayir, H., P.M. Kochanek, and R.S.B. Clark, Traumatic brain injury in infants and children - Mechanisms of secondary damage and treatment in the intensive care unit. Critical Care Clinics, 2003. 19(3): p. 529-+.
  12. ↑ Haydel MJ, Preston CA, Mills TJ, Luber S, Blaudeau E, DeBlieux PM (July 2000). "Indications for computed tomography in patients with minor head injury". N. Engl. J. Med. 343 (2): 100–5. PMID 10891517. [e]
  13. ↑ Stiell IG, Clement CM, McKnight RD, et al (December 2003). "The Canadian C-spine rule versus the NEXUS low-risk criteria in patients with trauma". N. Engl. J. Med. 349 (26): 2510–8. DOI:10.1056/NEJMoa031375. PMID 14695411. Research Blogging.
  14. ↑ Stiell IG, Wells GA, Vandemheen KL, et al (October 2001). "The Canadian C-spine rule for radiography in alert and stable trauma patients". JAMA 286 (15): 1841–8. PMID 11597285. [e]
  15. ↑ Ates, O., et al., Post-traumatic early epilepsy in pediatric age group with emphasis on influential factors. Childs Nervous System, 2006. 22(3): p. 279-284.
  16. ↑ Ozdemir, D., et al., Effect of melatonin on brain oxidative damage induced by traumatic brain injury in immature rats. Physiological Research, 2005. 54(6): p. 631-637.
  17. ↑ Chiaretti, A., et al., Interleukin-6 and nerve growth factor upregulation correlates with improved outcome in children with severe traumatic brain injury. Journal of Neurotrauma, 2008. 25(3): p. 225-234.
  18. ↑ Dinarello, C.A., Interleukin 1 and interleukin 18 as mediators of inflammation and the aging process. American Journal of Clinical Nutrition, 2006. 83(2): p. 447S-455S.
  19. ↑ Chiaretti, A., et al., Interleukin-6 and nerve growth factor upregulation correlates with improved outcome in children with severe traumatic brain injury. Journal of Neurotrauma, 2008. 25(3): p. 225-234.
  20. ↑ Dinarello, C.A., Interleukin 1 and interleukin 18 as mediators of inflammation and the aging process. American Journal of Clinical Nutrition, 2006. 83(2): p. 447S-455S.
  21. ↑ Chiaretti, A., et al., Interleukin-6 and nerve growth factor upregulation correlates with improved outcome in children with severe traumatic brain injury. Journal of Neurotrauma, 2008. 25(3): p. 225-234.
  22. ↑ Dinarello, C.A., Interleukin 1 and interleukin 18 as mediators of inflammation and the aging process. American Journal of Clinical Nutrition, 2006. 83(2): p. 447S-455S.
  23. ↑ Ozdemir, D., et al., Effect of melatonin on brain oxidative damage induced by traumatic brain injury in immature rats. Physiological Research, 2005. 54(6): p. 631-637.
  24. ↑ Ghaffar O, McCullagh S, Ouchterlony D, Feinstein A (August 2006). "Randomized treatment trial in mild traumatic brain injury". J Psychosom Res 61 (2): 153–60. DOI:10.1016/j.jpsychores.2005.07.018. PMID 16880017. Research Blogging.
  25. ↑ Elgmark Andersson E, Emanuelson I, Björklund R, Stålhammar DA (February 2007). "Mild traumatic brain injuries: the impact of early intervention on late sequelae. A randomized controlled trial". Acta Neurochir (Wien) 149 (2): 151–9; discussion 160. DOI:10.1007/s00701-006-1082-0. PMID 17252176. Research Blogging.
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