The Temporal Genesis of Primary and Secondary Brain Damage in Experimental and Clinical Head Injury

  • Donald P. Becker
Part of the NATO ASI Series book series (NSSA, volume 115)


Head injury in both the clinical and laboratory setting is a complex and multifactorial process which may involve many interactive primary and secondary insults. Not only is direct mechanical injury a factor but ischemia/hypoxia, brain swelling and edema, arterial and intracranial hypertension, subarachnoid hemorrhage, to name but a few, are frequently involved. Studies from our head injury center during the past ten years have attempted to identify and document primary and secondary factors, examine their temporal relationships and study their interaction in the pathophysiology of traumatic brain injury. It will be the purpose of this presentation to summarize the data from our head injury center regarding some of these factors. This will include both clinical and laboratory studies aimed at distinguishing between primary and secondary effects and their temporal sequence. It is our fundamental hypothesis that much of the damage incurred in head trauma is due to secondary effects and that areas of brain tissue which are rendered marginally dysfunctional can recover if the proper milieu is provided. Clinical and laboratory studies will be presented in the order of occurrence following trauma.


Head Injury Severe Head Injury Secondary Brain Damage Fluid Percussion Injury Head Injury Center 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. 1.
    Rosner MJ, Newsome HH, and Becker DP, Mechanical brain injury: The sympathoadrenal response, J Neurol Surg (in press).Google Scholar
  2. 2.
    Hayes RL, Kulkarni P, Galinat BJ, and Becker DP, Effects of naloxone on systemic and cerebral responses to experimental concussive injury in the cat, J Neurosurg 58: 720 (1983).CrossRefGoogle Scholar
  3. 3.
    Millen JE, Glauser FL, and Zimmerman M, Physiological effects of controlled concussive brain trauma, J Applied Physiol 49: 856 (1980).Google Scholar
  4. 4.
    Katayama Y, Glisson JD, Becker DP, and Hayes RL, Concussive head injury producing suppression of sensory transmission within the lumbar spinal cord in cats, J Neurosurg 63: 97 (1985).CrossRefGoogle Scholar
  5. 5.
    Hayes RL, Pechura CM, Katayama Y, Povlishock JT, Giebel ML, and Becker DP, Activation of pontine cholinergic sites implicated in unconsciousness following cerebral concussion in the cat, Science 223: 301 (1984).CrossRefGoogle Scholar
  6. 6.
    Hayes RL, Katayama Y, Hellgeth MC, and Becker DP, Behavioral suppression produced by carbachol microinjections into the rostral pons of the cat: Antagonism by naloxone and thyrotropin-releasing hormone (in preparation).Google Scholar
  7. 7.
    Lewelt W, Jenkins LW, and Miller JD, Autoregulation of cerebral blood flow after experimental fluid-percussion injury of the brain, J Neurosurg 53: 500 (1980).CrossRefGoogle Scholar
  8. 8.
    Lewelt W, Jenkins LW, and Miller JD, Effects of experimental fluid percussion injury of the brain on cerebrovascular reactivity to hypoxia and to hypercapnia, J Neurosurg 56: 332 (1982).CrossRefGoogle Scholar
  9. 9.
    DeWitt DS, Jenkins LW, Lutz H, Wei EP, Kontos HA, Miller JD, and Becker DP, Regional cerebral blood flow following fluid percussion injury, J Cereb Blood Flow Metabol 1, Suppl. 1: 579 (1981).Google Scholar
  10. 10.
    Povlishock JT, Becker DP, Sullivan HG, and Miller JD, Vasculature permeability alterations to horseredish peroxidase in experimental brain injury, Brain Res 152: 223 (1978).CrossRefGoogle Scholar
  11. 11.
    Miller JD, and Corales RL, Brain edema as a result of head injury: Fact or Fallacy? in: “Brain Edema,” de Vlieger M, deLange S, and Beks JWF, eds., John Wiley and Sons, New York (1981).Google Scholar
  12. 12.
    Povlishock JT, and Kontos HA, The pathophysiology of pial and intra-parenchymal vascular dysfunction, in: “Head injury: Basic and clinical aspects”, Grossmann RS, and Gildenberg PL, eds., Raven Press, New York (1982).Google Scholar
  13. 13.
    Povlishock JT, Kontos HA, Wei EP, Rosenblum WI, and Becker DP, Changes in the cerebral vasculature after hypertension and trauma: A combined scanning and transmission electron microscopic analysis, in: “The cerebral microvasculature”, Eisenberg HM, and Suddith RL, eds., Plenum, New York (1980).Google Scholar
  14. 14.
    Wei EP, Dietrich WD, Povlishock JT, Navari RM, and Patterson JL, Functional, morphological and metabolic abnormalities of the cerebral microcirculation after concussive brain injury in cats, Circ Res 46: 37 (1980).Google Scholar
  15. 15.
    Wei EP, Kontos HA, Dietrich WD, Povlishock JT, and Ellis EF, Inhibition by free radical scavengers and by cyclooxygenase inhibitors of pial arteriolar abnormalities from concussive brain injury in cats, Circ Res 48: 95 (1981).Google Scholar
  16. 16.
    Wei EP, Christman CW, Kontos HA, and Povlishock JT, Effects of oxygen radicals on cerebral arterioles, Am J Physiol (In press).Google Scholar
  17. 17.
    Graham DI, and Adams JH, Ischemic brain damage in fatal head injuries, Lancet 1: 265 (1971).CrossRefGoogle Scholar
  18. 18.
    Overgaard J, Mosdal C, and Tweed WA, Cerebral circulation after head injury. Part 3: Does reduced regional cerebral blood flow determine recovery of brain function after blunt head injury? J Neurosurg 55: 63 (1981).CrossRefGoogle Scholar
  19. 19.
    Jones TH, Morawetz RB, Crowell RM, Marcoux FW, FitzGibbon SJ, DeGirolami U, and Ojemann RG, Thresholds of focal cerebral ischemia in awake monkeys, J Neurosurg 54: 77 (1981).Google Scholar
  20. 20.
    Muizelaar JP, Wei EP, Kontos HA, and Becker DP, Mannitol causes compensatory cerebral vasoconstriction and vasodilation in response to viscosity changes, J Neurosurg 59: 822 (1983).CrossRefGoogle Scholar
  21. 21.
    DeWitt DS, Becker DP, and Hayes RL, A technique for the simultaneous, quantitative measurement of blood flow and glucose utilization within tissue samples from the feline brain, (in preparation).Google Scholar
  22. 22.
    Becker DP, Miller JD, Ward JD, Greenberg RP, Young HF, and Sakalas R, The outcome from severe head injury with early diagnosis and intensive management, J Neurosurg 47: 491 (1977).CrossRefGoogle Scholar
  23. 23.
    Marshall LF, Smith RW, Shapiro HM, The outcome with aggresive treatment in severe head injuries. I. The significance of intracranial pressure monitoring, J Neurosurg 50: 20 (1979).CrossRefGoogle Scholar
  24. 24.
    Tornheim PA, McLaurin RL, and Thorpe JF, The edema of cerebral contusion, Surg Neurol 5: 171 (1976).Google Scholar
  25. 25.
    Corales RL, Miller JD, and Becker DP, Intracranial pressure and brain water content in acute graded experimental cerebral trauma, in: “Intracranial pressure, IV”, Shulman K, Marmarou A, Miller JD, Hochwald G, Becker DP, and Brock M, eds., Springer Verlag, Berlin (1980).Google Scholar
  26. 26.
    Siesjö BK, Cell damage in the brain: A speculative synthesis, J Cereb Blood Flow Metabol 1: 155 (1981).CrossRefGoogle Scholar
  27. 27.
    Rehncrona S, Rosen I, Siesjö BK, Brain lactic acidosis and ischemic cell damage. 1. Biochemistry and neurophysiology, J Cereb Blood Flow Metabol 1: 297 (1981).CrossRefGoogle Scholar
  28. 28.
    Enevoldsen EM, and Jensen FT, Cerebrospinal fluid lactate and pH in patients with acute severe head injury, Clin Neurol Neurosurg 80: 213 (1977).CrossRefGoogle Scholar
  29. 29.
    Povlishock JT, Becker DP, Cheng CLY, and Vaughan GW, Axonal change in minor head injury, J Neuropath Exp Neurol 42: 255 (1983).CrossRefGoogle Scholar
  30. 30.
    Gennarelli TA, Jane J, Thibault LE, and Steward O, Axonal damage in mild head injury demonstrated by the Nauta method, in: “Advances in neurotraumatology”, Villani R, Papo I, Giovanelli M, Gaini SM, and Tomei G, eds., Excerpta Medica, Amsterdam (1982).Google Scholar
  31. 31.
    Adams JH, Mitchell DE, Graham DI, and Doyle D, Diffuse brain damage of an immediate impact type, Brain 200: 489 (1977).CrossRefGoogle Scholar
  32. 32.
    Strich SJ, Shearing of nerve fibers as a cause of brain damage due to head injury, Lancet 2: 443 (1961).CrossRefGoogle Scholar
  33. 33.
    Gennarelli TA, Thibault LE, Adams JH, Graham DI, Thompson CJ, and Marcincin RP, Diffuse axonal injury and traumatic coma in the primate, Ann Neurol 12: 564 (1982).CrossRefGoogle Scholar
  34. 34.
    Povlishock JT, Becker DP, Miller JD, Jenkins LW, and Dietrich WD, The morphopathologic substrates of concussion, Acta Neuropath 47: 1 (1979).CrossRefGoogle Scholar
  35. 35.
    Povlishock JT, Becker DP, Kontos HA, and Jenkins LW, Neural and vascular alterations in brain injury, in: “Neural trauma - seminars in neurological surgery”, Popp AJ, Bourke RS, Nelson LR, and Kimelberg HK, eds., Raven Press, New York (1979).Google Scholar
  36. 36.
    Povlishock JT, The fine structure of axons and growth cones of the human fetal cerebral cortex, Brain Res 114: 379 (1976).CrossRefGoogle Scholar
  37. 37.
    Guth L, Barrett CP, Dontai EJ, Deshipande SS, and Albuquerque EX, Histopathological reactions and axonal regeneration in the transsected spinal cord of hibernating squirrels, J Comp Neurol 203: 297 (1981).CrossRefGoogle Scholar
  38. 38.
    Barrow KD, Dentinger MP, Nelson LR, and Miney JE, Ultrastructure of axonal reaction in red nucleus of cats, J Neuropath Exp Neurol 34: 222 (1975).CrossRefGoogle Scholar

Copyright information

© Plenum Press, New York 1986

Authors and Affiliations

  • Donald P. Becker
    • 1
  1. 1.Division of Neurological SurgeryMedical College of VirginiaRichmondUSA

Personalised recommendations