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Stroke Pathophysiology Case Study

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Stroke Pathophysiology Case Study
Stroke Pathophysiology
Sid Shah, MD

Pathophysiology of Stroke Sid Shah, MD

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Stroke Pathophysiology
Introduction The two major mechanisms causing brain damage in stroke are, ischemia and hemorrhage. In ischemic stroke, which represents about 80% of all strokes, decreased or absent circulating blood deprives neurons of necessary substrates. The effects of ischemia are fairly rapid because the brain does not store glucose, the chief energy substrate and is incapable of anaerobic metabolism.1 Non-traumatic intracerebral hemorrhage represents approximately 10% to 15% of all strokes. Intracerebral hemorrhage originates from deep penetrating vessels and causes injury to brain tissue by disrupting connecting pathways and causing
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Jones TH, Morawetz RB, Crowell RM, et al. Thresholds of focal ischemia in awake monkeys. J Neurosurg. 1981; 54:773-782. 2. Wass CT, Lanier WL,. Glucose modulation of ischemic brain injury: review and clinical recommendations. Mayo Clin Proc. 1996;71:801-812. 3. Bruno A, Biller J, Adams HP Jr, et al. Acute blood glucose level and outcome from ischemic stroke. Neurology. 1999;52:280-284. 4. Reith J, Jorgensen HS, Pedersen PM, et al. Body temperature in acute stroke: relation to stroke severity, infarct size, mortality, and outcome. Lancet. 1996;347:422-425. 5. Schwab S, Spranger M, Aschoff A, et al. Brain temperature monitoring and modulation in patients with severe MCA infarction. Neurology. 1997;48:762-767. 6. Pulsinelli WA. The ischemic penumbra in stroke. Sci Med. 1995;1:16-25. 7. Hakim AM. Ischemic penumbra, the therapeutic window. Neurology. 1998;51(Suppl 3):S44-S46. 8. Astrup J, Seisjo BK, Symon L. Thresholds in cerebral ischemia – the ischemic penumbra. Stroke. 1981;12:723-725. 9. Zivin JA, Choi DW. Stroke therapy. Sci Med. 1991;265:56-53. 10. Wise RJ, Bernardi S, Frackowiak RS, Legg NJ, Jones T. Serial observations on the pathophysiology of acute stroke: the transition form ischaemia to infarction as reflected in regional oxygen extraction. Brain. 1983;106 (Pt 1):197-222. 11. Heros R. Stroke: early pathophysiology and treatment. Stroke. 1994;25:1877-1881. 12. Garcia JH, Liu K, Yoshida Y et al. Brain mictrovessels:factors altering their patency after …show more content…
Answer e. Several studies have shown that hypothermia is actually beneficial in attenuating effects of brain ischemia. 2. Answer b. A common site of a watershed infarction is the border zone between the anterior and middle cerebral arteries that extends over the frontomotor homunculi at approximately the level of the cortical representation of the arm. The resulting clinical syndrome consists of paralysis and sensory loss, predominantly involving the arm. Face is not affected and speech is spared. The watershed infarct involving the anterior, middle and posterior cerebral arteries occurs in parietal occipital region causing homonymous hemianopia with visual agnosia, disorientation in space, apraxia, dysgraphia and dyslexia. Speech difficulties are more commonly seen with a stroke involving the vascular territory of middle cerebral artery. 3. Answer d. Cerebral blood flow in the ischemic penumbra (IP) is approximately 25% to 50% of normal. Cellular integrity and function are preserved in this area of limited ischemia for variable periods of time. This makes IP a potentially salvageable area. 4. Answer c. The hemorrhagic transformation of an ischemic infarct - the so-called reperfusion hemorrhage is a complex phenomenon. The three main factors associated with this include the size of the infarct, richness of collateral circulation, and the use of anticoagulants and thrombolytic agents. Interestingly hypertension is not considered to a risk factor for reperfusion

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