Recovery of Brain Function Following Ischemia

  • Lindsay Symon
Conference paper
Part of the Acta Neurochirurgica book series (NEUROCHIRURGICA, volume 57)


Experimental evidence conveys clear suggestions that early reperfusion following at least focal cerebral ischemia in the primate is accompanied by a return of function demonstrably suspended during the ischemic period.

Complete and permanent arrest of the cerebral circulation has been known within seconds to lead to depression of brain electrical activity, and within minutes to gross disruption of the normal energy metabolism with failure of ionic homeostatic mechanisms. There is irreversible cell change and death within 5 to 10 minutes.

Very much more protracted periods of ischemia have been shown more recently to be associated with potential viability of neuronal function, and in clinical neurosurgery we have known for years that patients with established cerebral vascular occlusion and a dense neurological deficit may show quite evident improvement over months or years. In these protracted recoveries, the potential for relearning in nervous circuits may play a part, but in more acute circumstances, for example in the progressive recovery from vasospasm, re-learning is clearly not a factor, and this demonstrates quite evidently that neurons at one moment apparently non-functioning, can again within a few minutes recover function even after hours of apparent suppression.

The experimental evidence is fairly well known. In this symposium and elsewhere we have presented a model of experimental occlusion of the middle cerebral artery in primates demonstrating irreversible recovery of electrical function after some 20 minutes of middle cerebral artery occlusion, and reversible recovery of ionic homeostasis after periods of up to an hour. Measurements of regional blood flow has established thresholds for electrical function of around 16 ml/100 g × min and for ionic homeostasis of around 10 ml/100 g × min.

Interestingly, pH changes appear to occur in the region of the higher flow threshold for electrical failure, and the same applies to the early movements of water as assessed by accumulation in tissue.

Many of the biochemical experiments from Hossmann–s group demonstrate disintegration of biochemical aspects, such as protein synthesis during ischemia and the question of free radical generation remains uncertain.

This paper addresses a number of cases of careful monitoring during aneurysm surgery or during the recovery from sub-arachnoid hemorrhage associated with vasospasm in which protracted periods of dysfunction with definable occlusion as assessed by either direct operative observation, angiography, or bedside blood flow measurements with transcranial Doppler. The studies have shown unequivocal recovery in a time scale, which attests to the validity of the experimentally generated hypotheses in man.


Focal cerebral ischemia ischemic flow thresholds recovery from ischemia 


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. 1.
    Ames A III, Gurian BS (1963)Effects of glucose and oxygen deprivation on function of isolated mammalianretina. J Neurophysiol 26: 617–634PubMedGoogle Scholar
  2. 2.
    Astrup J, Symon L, Branston NM, Lassen NA (1977)Cortical evoked potential and extracellular K+ and H+ atcritical levels of brain ischaemia. Stroke 8: 51–57PubMedCrossRefGoogle Scholar
  3. 3.
    Branston NM, Strong AJ, Symon L(1977) Extracel lular potassium activity, evoked potential and tissue bloodflow, relationship during progessive ischaemia in baboon cerebral cortex. J Neurol Sci 32: 305–321PubMedCrossRefGoogle Scholar
  4. 4.
    Branston NM, Symon L, Crockard HA,Pasztor E (1974) Relationship between the cortical evoked potential and localcortical blood flow following acute middle cerebral artery occlusion in thebaboon. Exp Neurol 45: 195–208PubMedCrossRefGoogle Scholar
  5. 5.
    Collewijn H, van Harreveld A (1966)Intracellular recording of spinal motoneurones during acute asphyxia. J Physiol185: 1–14PubMedGoogle Scholar
  6. 6.
    Collewijn H, van Harrevald A (1966)Membrane potential of cerebral cortical cells during spreading depression andasphyxia. Exp Neurol 15: 425–436PubMedCrossRefGoogle Scholar
  7. 7.
    Dennis C, Kabat H (1939) Behaviourof dogs after complete temporary arrest of the cephalic circulation. Proc SocExper BiolMed 40: 559–561Google Scholar
  8. 8.
    Grenell RG (1946) Central nervoussystem resistance. I. The effects of temporary arrest of cerebral circulationfor a period of two to ten minutes. J Neuropath Exper Neurol 5: 131–154CrossRefGoogle Scholar
  9. 9.
    Harris RJ, Symon L, Branston NM,Bayhan M (1981) Changes in extracellular calcium activity in cerebralischaemia. J Cereb Blood Flow Metabol 1: 203–209CrossRefGoogle Scholar
  10. 10.
    Harris RJ, Richards PG, Symon L, Habib A-HA, Rosenstein J (1987)pH, K+ and PO2 of the extracellular space during ischaemia ofprimate cerebral cortex. J Cereb Blood Flow Metabol 7: 599–604CrossRefGoogle Scholar
  11. 11.
    Harvey J,Rasmussen T (1951) Occlusion of the middle cerebral artery. Arch Neurol 66:20–29Google Scholar
  12. 12.
    Hass WK (1981) Beyond cerebralblood flow, metabolism and ischaemic thresholds: an examination of the role ofcalcium in the initiation of cerebral infarction. In: Meyer JS (eds) Cerebral vasculardisease 3. Excerpta Medica, Amsterdam, pp 3–17Google Scholar
  13. 13.
    Hossmann KA, Sato K (1970) The effect of ischemia on sensorimotorcortex of cat. Z Neurol 198: 33–45PubMedCrossRefGoogle Scholar
  14. 14.
    Hossmann KA, Schuier FJ (1979) Metabolic (cytotoxic) type ofbrain oedema following middle cerebral artery occlusion in cats. In: Price T,Nelson E (eds) Cerebrovascular diseases. Raven, New York, pp 141–165Google Scholar
  15. 15.
    Hossmann KA, Takagi S (1976) Osmolality of brain in cerebral ischaemia.Exp Neurol 51: 124–131CrossRefGoogle Scholar
  16. 16.
    Kaplan HA, Ford DH (1966) The BrainVascular System. Elsevier, LondonGoogle Scholar
  17. 17.
    Lassen NA (1966) The luxury-perfusion syndrome and its possiblerelation to acute metabolic acidosis localized within the brain. Lancet 2:113–115Google Scholar
  18. 18.
    LazorthesG, Campan L (1964) La cirulation cerebrale. Editions Sandoz, ParisGoogle Scholar
  19. 19.
    Pasztor E, Symon L, Dorsch NWC,Branston NM (1973) The hydrogen clearance method in assessment of blood flow incortex, white matter and deep nuclei of baboons. Stroke 4: 556–567PubMedCrossRefGoogle Scholar
  20. 20.
    Przybylski A (1971) Activitypattern of visceral cortex neurons during asphyxia. Exp Neurol 32: 12–21PubMedCrossRefGoogle Scholar
  21. 21.
    Strong L, Tomlinson B, Venables G,Gibson G, Hardy J (1983) The cortical ischaemic penumbra associated withocclusion of the middle cerebral artery in the cat. 2. Studies ofhistopathology, water contents, in vitroneurotransmitter uptake. JCereb Blood Flow Metabol 3: 97–108CrossRefGoogle Scholar
  22. 22.
    Symon L, Branston NM, Chikovani O(1979) Ischaemic brain oedema following middle cerebral artery occlusion inbaboons. Relationship between regional cerebral water content and blood flow at12 hours. Stroke 10: 184–191PubMedCrossRefGoogle Scholar
  23. 23.
    Symon L, Branston NM, Strong AJ,Hope TD (1977) The concepts of thresholds of ischaemia in relation to brainstructure and function. J Clin Path 30 [Suppl 111: 149–154CrossRefGoogle Scholar
  24. 24.
    Symon L, Dorsch NWC,Crockard HA (1975) The production and clinical features of a chronic strokemodel in experimental primates. Stroke 6: 476–481PubMedCrossRefGoogle Scholar
  25. 25.
    Symon L, Pasztor E, Branston NM(1974) The distribution and density of reduced cerebral blood flow followingacute middle cerebral artery occlusion: an experimental study by the techniqueof hydrogen clearance in baboons. Stroke 5: 355–364PubMedCrossRefGoogle Scholar
  26. 26.
    Waltz AG (1969) Red venous blood:occurrence and significance in ischaemic and non-ischaemic cerebral cortex. JNeurosurg 31: 141–148CrossRefGoogle Scholar
  27. 27.
    Zwetnow NN (1970) Effects ofincreased cerebrospinal fluid pressure on the blood flow and on the energymetabolism of the brain. Acta Physiol Scand Suppl 339: 1–31Google Scholar

Copyright information

© Springer-Verlag 1993

Authors and Affiliations

  • Lindsay Symon
    • 1
  1. 1.Gough-Cooper Department of Neurological SurgeryInstitute of NeurologyLondonUK

Personalised recommendations