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Tratamento do acidente vascular cerebral agudo

Treatment of acute stroke

Resumos

Avanços tecnológicos recentes beneficiaram o diagnóstico do acidente vascular cerebral (AVC), reduziram os riscos e aumentaram a freqüência de estudos acerca dos mecanismos do AVC. Projetos baseados em bancos de dados computadorizados trouxeram novas luzes quanto à freqüência de subtipos de AVC e aos riscos de sua progressão e recorrência. Elevada freqüência de AVC devidos a infarto continua sem explicação, apesar de exaustiva investigação laboratorial. Esses infartos de causa não determinada apresentam índices de recorrência quase tão elevados como no embolismo cardiogênico, forçando rápida decisão terapêutica, mesmo na ausência de causa demonstrada para eles. AVC devido a aterosclerose é menos comum do que se acreditava, mas traz consigo maior risco de piora e de recorrência precoce, obrigando a adoção de tratamento precoce na tentativa de evitar sua progressão. Os métodos Doppler duplex e transcraniano de imagem de vasos e fluxo tornaram possível atualmente seguir de modo não invasivo a evolução de estenose ateromatosa, embolismo e recanalização, desenvolvimento de circulação colateral e, ainda, ocorrência de vasospasmo em aneurismas rotos e malformações arteriovenosas. Doença ateromatosa extracraniana pode progredir rapidamente, passando a estenose de discreta a severa, podendo, no entanto, estabilizar-se em qualquer ponto da evolução. O grau de estenose extracraniana não permite pressupor aquele de circulação colateral intracraniana. Recanalização ocorre precocemente no embolismo cerebral. Vasospasmo após hemorragia sub-aracnóidea é comum e, por vezes, severo. Sempre que possível deve ser dada preferência à ressonância magnética, em lugar da tomografia computadorizada, para o diagnóstico de qualquer tipo de AVC. inclusive hemorrágico.


Recent advances in technology have improved stroke diagnosis, reduced the risks and increased the frequency of studies of stroke mechanism. Computer-assisted stroke data bank projects have provided new insights into the frequencies of stroke subtypes and the risks for progression and recurrence. A high frequency of strokes due to infarction remain unexplained despite thorough laboratory investigation. These infarcts of undetermined cause suffer recurrence rates almost as high as cardiogenic embolism, forcing a therapeutic decision even in the absence of a demonstrated cause. Stroke from atherosclerosis is far less common than formerly believed but carries the highest risk of worsening and early recurrence, prompting early treatment to attempt to avoid progression. Duplex and transcranial doppler methods of imaging blood vessels and insonating flow have now made it possible non-invasively to follow the course of atheromatous stenosis, embolism and recanalization, development of collateral flow, and vasospasm in ruptured aneurysms and arteriovenous malformations. Extracranial atheromatous disease may progress rapidly from mild to severe stenosis, stabilize at any point; intracranial collateral is not predicted by the degree of extracranial stenosis. Recanalization of cerebral embolism occurs early. Vasospasm after subarachnoid hemorrhage is common and often severe. Where available, magnetic resonance imaging is preferred to CT scanning for the diagnosis of every form of stroke including hemorrhage.


J. P. MohrI; V. OliveiraII

ISciarra Professor of Clinical Neurology - The New York Neurological Institute (NYNI), Columbia-Presbyterian Medical Center, New York City

IIResearch Fellow at NYNI, Interno de Neurologia do Hospital Santa Maria, Lisboa - The New York Neurological Institute (NYNI), Columbia-Presbyterian Medical Center, New York City

RESUMO

Avanços tecnológicos recentes beneficiaram o diagnóstico do acidente vascular cerebral (AVC), reduziram os riscos e aumentaram a freqüência de estudos acerca dos mecanismos do AVC. Projetos baseados em bancos de dados computadorizados trouxeram novas luzes quanto à freqüência de subtipos de AVC e aos riscos de sua progressão e recorrência. Elevada freqüência de AVC devidos a infarto continua sem explicação, apesar de exaustiva investigação laboratorial. Esses infartos de causa não determinada apresentam índices de recorrência quase tão elevados como no embolismo cardiogênico, forçando rápida decisão terapêutica, mesmo na ausência de causa demonstrada para eles. AVC devido a aterosclerose é menos comum do que se acreditava, mas traz consigo maior risco de piora e de recorrência precoce, obrigando a adoção de tratamento precoce na tentativa de evitar sua progressão. Os métodos Doppler duplex e transcraniano de imagem de vasos e fluxo tornaram possível atualmente seguir de modo não invasivo a evolução de estenose ateromatosa, embolismo e recanalização, desenvolvimento de circulação colateral e, ainda, ocorrência de vasospasmo em aneurismas rotos e malformações arteriovenosas. Doença ateromatosa extracraniana pode progredir rapidamente, passando a estenose de discreta a severa, podendo, no entanto, estabilizar-se em qualquer ponto da evolução. O grau de estenose extracraniana não permite pressupor aquele de circulação colateral intracraniana. Recanalização ocorre precocemente no embolismo cerebral. Vasospasmo após hemorragia sub-aracnóidea é comum e, por vezes, severo. Sempre que possível deve ser dada preferência à ressonância magnética, em lugar da tomografia computadorizada, para o diagnóstico de qualquer tipo de AVC. inclusive hemorrágico.

SUMMARY

Recent advances in technology have improved stroke diagnosis, reduced the risks and increased the frequency of studies of stroke mechanism. Computer-assisted stroke data bank projects have provided new insights into the frequencies of stroke subtypes and the risks for progression and recurrence. A high frequency of strokes due to infarction remain unexplained despite thorough laboratory investigation. These infarcts of undetermined cause suffer recurrence rates almost as high as cardiogenic embolism, forcing a therapeutic decision even in the absence of a demonstrated cause. Stroke from atherosclerosis is far less common than formerly believed but carries the highest risk of worsening and early recurrence, prompting early treatment to attempt to avoid progression. Duplex and transcranial doppler methods of imaging blood vessels and insonating flow have now made it possible non-invasively to follow the course of atheromatous stenosis, embolism and recanalization, development of collateral flow, and vasospasm in ruptured aneurysms and arteriovenous malformations. Extracranial atheromatous disease may progress rapidly from mild to severe stenosis, stabilize at any point; intracranial collateral is not predicted by the degree of extracranial stenosis. Recanalization of cerebral embolism occurs early. Vasospasm after subarachnoid hemorrhage is common and often severe. Where available, magnetic resonance imaging is preferred to CT scanning for the diagnosis of every form of stroke including hemorrhage.

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  • 1. Aaslid R - Transcranial Doppler Sonography. Springer, New York, 1986.
  • 2. Aaslid R, Markwalde T-M, Nornes H - Noninvasive transcranial Doppler ultrasound recording of blood flow in basal cerebral arteries. J Neurosurg 57: 769, 1982.
  • 3. Arders A - Neurosurgical Applications of Transcranial Doppler Sonography. Springer, New York, 1986.
  • 4. Awad AI, Carter LP, Spetzler RF, et al - Clinical vasospasm after subharacnoid hemorrhage: response to hypervolemic hemodilution and arterial hypertension. Stroke 18: 365, 1986.
  • 5. Barnett HJM, Mohr JP, Stein BM, Yatsu FM - Stroke: Pathophysiology, Diagnosis and Management. Churchill Livingstone, New York, 1968.
  • 6. Baron JC, Bousser MG, Rey, et al - Reversal of focal «misery perfusion syndrome» by extra-intracranial arterial bypass in hemodynamic cerebral ischemia. Stroke 12:454, 1981.
  • 7. Bradley WG Jr, Schmidt PG - Effects of methemoglobin formation on the MR appearance of subarachnoid hemorrhage. Radiology 156: 99, 1985.
  • 8. Brass LR, Prohovnik I, Pavlakis S, Möhr JP - Transcranial Doppler examination of middle cerebral artery velocity versus xenon rCBF: two measures of cerebral blood flow. Neurology 37 (suppl): 85, 1987.
  • 9. Comerota AJ, Cranley JJ, Cook SE - Real-time B-mode carotid imaging in diagnosis of cerebrovascular disease. Surgery 6: 718, 1981.
  • 10. Damasio H - A computed tomographic guide to the identification of cerebral vascular territories. Arch Neurol 40: 138, 1985.
  • 11. Delal PM, Shah PM, Aiyar RR - Arteriographic study of cerebral embolism. Lancet 2: 358, 1965.
  • 12. Demeurisse M, Verhas M, Capon A, Paternot J - Lack of evolution of the cerebral blood flow during clinical recovery of a stroke. Stroke 14: 77, 1983.
  • 13. Donaldson RM, Emanuel RW, Eearl CJ - The role of two-dimensional echocardiography in the detection of potentially embolic intracardiac masses in patients with cerebral ischemia. J Neurol Neurosurg Psychiat 44: 803, 1981.
  • 14. Fisher CM, Gore I, Okabe N, White PD - Atherosclerosis of the carotid and vertebral arteries-extraeranial and intracranial. J Neuropath Exp Neurol 24: 455, 1965.
  • 15. Fisher CM, Ojemann RG - A clinico-pathologic study of carotid endarterectomy plaques. Rev Neurol (Paris) 142: 573, 1986.
  • 16. Gilles C, Brucher JM, Khoubesserian P, et al - Cerebral amyloid angiopathy as a cause of multiple intracerebral hemorrhage. Neurology 34: 730, 1984,
  • 17. Gomori JM, Grossman RI, Goldberg HI, et al - Intracranial hematomas: imaging by high-field MR. Radiology 157: 87, 1985.
  • 18. Gray F, Dubas F, Roullet E, Escourolle R - Deukoencephalopathy in diffuse hemorrhagic cerebral amyloid angiopathy. Ann Neurol 18: 54, 1985.
  • 19. Gross CR, Kase CS, Mohr JP, Cunningham SC - Stroke, in south Alabama: incidence and diagnostic features. Stroke 15: 249, 1984.
  • 20. Härders A, Gilsbach J - Time course of blood velocity changes related to vasospasm in the circle of Willis measured by transcranial Doppler. J Neurosurg 66: 718, 1987.
  • 21. Harvey JR, Teague SM, Anderson JL, et al - Clinically silent atrial septal defects with evidence for cerebral embolization. Ann Int Med 105: 695, 1986.
  • 22. Heiss W-D (ed): Functional Mapping of the Brain in Vascular Disorders. Springer, Berlin, 1985.
  • 23. Heiss W-D, Herholz K, Boecher-Schwarz HG, et al: PET, CT, and MR imaging in cerebrovascular disease. J Comp Tomogr 10: 903, 1986.
  • 24. Hilal SK, Maudsley AA, Simon HE, et al - In vivo imaging of sodium-23 in the human head. J Comput Asst Tomog 9: 1, 1985.
  • 25. Hinton RC, Kistler JP, Fallon JT, et al - Influence of etiology of atrial fibrillation on incidence of systemic embolism. Am J Cardiol 40: 509, 1977.
  • 26. Hinton RC, Mohr JP, Ackerman RA, et al - Symptomatic middle cerebral artery stenosis. Ann Neurol 5: 152, 1979.
  • 27. Irino T, Tandea M, Minami T - Angiographic manifestations in posrecanalized cerebral infarction. Neurology 27: 471, 1977.
  • 28. Jacobson HG (ed) - Fundamentals of magnetic resonance imaging. JAMA 258: 3417, 1987.
  • 29. Kase CS, Williams JP, Mohr JP - Lobar intracerebral hematomas. Neurology 32: 1146, 1982.
  • 30. Kelcz F, Hilal SK, Hartwell P, Joseph PM - CT measurement of the xenon blood-brain partition coefficient and implications for rCBF: a preliminary report. Radiology 127: 385, 1978.
  • 31. Kroener JM, Dorn PL, Shoor PM, et al - Prognosis of asymptomatic ulcerating carotid lesions. Arch Surg 115: 1387, 1980.
  • 32. Kunitz S, Gross CR, Heyman A, et al - The pilot stroke data bank: definition, design, data. Stroke 15: 740, 1984.
  • 33. Lassen N, Ingvar DH, SKinhoj EL - Brain function and blood flow. Scientific American 239: 62, 1978.
  • 34. Lennihan L, Kupsky WJ, Mohr JP, et al - Lack of association between carotid plaque hematoma and ipsilateral cerebral symptoms. Stroke 18: 879, 1987.
  • 35. Levy DE, Scherer PB, Lapinski RH, et al - Predicting recovery from acute ischemic stroke using multiple clinical variables. In Plum F, Pulsinelli W (eds): Cerebrovascular Disorders, Raven Press, New York, 1985, pg 69.
  • 36. Maudsley A, Hilal SK, Perman W, Simon H - Spatially resolved high resolution spectroscopy by «four dimensional» NMR. J Magn Reson 51: 147, 1983.
  • 37. Melamed N, Satya-Murit S - Cerebellar hemorrhage. Arch Neurol 39: 425, 1984.
  • 38. Mohr JP - Neurologic complications of cardiac valvular disease and cardiac surgery. In Vinken PJ, Bruyn GW (eds): Handbook of Clinical Neurology, Vol. 34, Medical Conditions. North Holland, Amsterdam, 1979, pg 143.
  • 39. Mohr JP - Asymptomatic carotid artery disease. Stroke 13: 431, 1982.
  • 40. Mohr JP - Lacunes. Neurol Clin N Amer 1: 201, 1983.
  • 41. Möohr JP, Caplan LR, Melski JW, et al - The Harvard cooperative stroke registry: a prospective registry of cases hospitalized with stroke. Neurology 28: 754, 1978.
  • 42. Mohr JP, Rubenstein L, Edelstein SZ, et al - Approaches to pathophysiology of stroke through the NINCDS Data Bank. In Plum F, Pulsinelli W (eds): Cerebrovascular Disorders, Raven Press, New York, 1985, pg 63.
  • 43. Mokri B, Sundt TM Jr, Houser OW, Piepgras DG - Spontaneous dissection of the cervical internal carotid artery. Ann Neurol 19: 126, 1986.
  • 44. Norrving B, Nilsson B, Olsson J - Progression of carotid disease after endarterectomy: a Doppler ultrasound study. Ann Neurol 12: 548, 1982.
  • 45. Pessin MS, Duncan GW, Mohr JP, Poskanzer DC - Carotid artery territory transient ischemic attacks. N Eng J Med 296: 358, 1977.
  • 46. Pessin MS, Hinton RC, Davis KR, et al - Mechanisms of acute carotid stroke. Ann Neurol 6: 245, 1979.
  • 47. Petty GW, Lennihan L, Mohr JP, et al - Complications of long term anticoagulation. Ann Neurol 20: 157, 1986.
  • 48. Powers WJ, Press GA, Grubb R, et al - The effect of hemodynamically significant carotid artery disease on the hemodynamic status of the cerebral circulation. Ann Int Med 106: 27, 1987.
  • 49. Reuten GM - Ultrasonic Diagnosis of Cerebrovascular Diseases. Martinus Nijhoff, Dordrecht, 1987.
  • 50. Roger DR, Cho E-S, Kempin J, Posner JB - Cerebral infarction from non-bacterial thrombotic endocarditis: clinical and pathological study including the effects of anticoagulation. Am J Med 83: 746, 1987.
  • 51. Säcco RL, Mohr JP, Tatemichi T'K, et al - Reclassification of acute stroke with nondiagnostic computed tomography and angiogram: infarction of undetermined cause in the NINCDS Stroke Data Bank. Ann Neurol 20: 156, 1986.
  • 52. Sacco RL, Owen J, Tatemichi TK, Mohr JP - Protein S deficiency and intracranial vascular occlusion. Ann Neurol 22: 115, 1987 (Abtr).
  • 53. Sandercock P, Warlow C, Bamford J, et al - Is a controlled trial of long-term oral anticoagulants in patients with stroke and non-rheumatic atrial fibrillation worthwhile? Lancet 1: 788, 1986.
  • 54. Schwartz A, Hennerici M - Noninvasive transcranial doppler ultrasound in intracranial angiomas. Neurology 36: 626, 1986.
  • 55. Sipponen JT, Kaste M, Sepponen RE, et al - Nuclear magnetic resonance imaging in reversible cerebral ischaemia. Lancet 1: 294, 1983.
  • 56. Weaver RG Jr, Howard G, McKinney WM, et al - Comparison of Doppler ultrasonography with arteriography of the carotid bifurcation. Stroke 4: 402, 1980.
  • 57. Yatsu FM, Mohr JP - Anticoagulation therapy for cardiogenic emboli to brain. Neurology 32: 274, 1982.
  • 58. Zwiebel WJ - Vascular Ultrasonography. Ed 2. Grune & Stratton. New York, 1986.
  • Tratamento do acidente vascular cerebral agudo

    Treatment of acute stroke
  • Datas de Publicação

    • Publicação nesta coleção
      21 Jun 2011
    • Data do Fascículo
      Jun 1988
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