Year 2007 Vol. 15 No 4

MODERN DIAGNOSTICS AND THERAPY

LUKOMSKY I.V., PASHKOV A.A., PASHKOVA I.A., ULASCHIK V.S., ZENKOV A.A.

NEUROLOGICAL ASPECTS OF RECONSTRUCTIVE OPERATIONS ON THE CEREBRAL ARTERIES

Application of surgical treatment methods in the patients with stenosis and occlusions of carotic and vertebral arteries extra-cranial sections has revealed a number of organizational, ethical and clinical problems. Organizational problems are linked with the regulation of the system, revealing the patients who need the reconstructive operative interventions on the cerebral arteries as well as the procedure regulation of their detailed examination and postoperative dispensary observation. Interconnected ethical and clinical problems touch on the problem of patients’ selection criteria for performing various surgical interventions as well as possible complications and expected results predicting. The literature data analysis on the given problems, the observation results of the patients, operated on the own clinical basis, are presented in the article. The theoretical and practical aspects of the neurological perioperative complications treatment and prophylaxis are studied in the article. The material of the publication is addressed to angiosurgeons, neurologists, general practitioners who deal with the problems of cerebral vascular diseases diagnostics, treatment and prophylaxis.

Keywords: arteries, reconstructive operations, neurological aspects.
p. 70 - 80 of the original issue
References
  1. Êëèíè÷åñêàÿ àíãèîëîãèÿ: â 2 ò. / ïîä ðåä. À.Â.Ïîêðîâñêîãî. – Ì.: Ìåäèöèíà, 2004. – Ò. 1. – 888 ñ.
  2. Áîëåçíè íåðâíîé ñèñòåìû: â 2 ò. / ïîä ðåä. Í. Í. ßõíî, Ä. Ð. Øòóëüìàíà. – Ì.: Ìåäèöèíà, 2001. – Ò. 2: Íàðóøåíèå êðîâîîáðàùåíèÿ â ãîëîâíîì è ñïèííîì ìîçãå / È. Â. Äîìóëèí [è äð.]. – 2001. – Ñ. 231-302.
  3. Ðóêîâîäñòâî ïî ïðîôèëàêòèêå èíñóëüòà ó ïàöèåíòîâ ñ èøåìè÷åñêèì èíñóëüòîì è òðàíçèòîðíîé èøåìè÷åñêîé àòàêîé: Áþëëåòåíü Àìåðèêàíñêîé àññîöèàöèè ñåðäöà (American Heart Association) ÀÍÍÀ/ Ñîâåò ïî èíñóëüòó Àìåðèêàíñêîé àññîöèàöèè ïî ïðîáëåìå èíñóëüòà (American Stroke Association) äëÿ ñïåöèàëèñòîâ â ñôåðå çäðàâîîõðàíåíèÿ [Ýëåêòðîííûé ðåñóðñ]. – 2006. – Ðåæèì äîñòóïà: http://stroke.ahajournals.org/cgi/content/full/37/2/577. – Äàòà äîñòóïà: 25.01.2006.
  4. Beneficil effect of carotid endarterectomi in sym-ptomatic patients with high-grade stenosis: Nort American Symptomatic Carotid Endarterectomy Trial Collaborators//N. Engl. J. Med. – 1991. – N 325. – P. 445-453.
  5. MRS Europen Carotid Surgery Trial: interim results for symptomatic patients with severe (70-99%) or with mild (0-29%) carotid stenosis: Europen Carotid Surgery Trialists Collaborative Group // Lancet. – 1991. – N 337. – P. 1235–1243.
  6. Benefit of carotid endarterectomi in patients wirt symptomatic moderate or severe stenosis: Nort American Symptomatic Carotid Endarterectomy Trial Collaborators / Y.J. Barnett [et al.] // N. Engl. J. Med. – 1998. – N 339. – P. 1415–1425.
  7. Randomised trial of endarterectomi for recently carotid stenosis: final results of the NRC Europen Carotid Surgery Trial (ECST) // Lancet. – 1998. – N 351. – P. 1379–1387.
  8. Carotid Endarterectomy Trialists Collaborators. Carotid endarterectomi for symptomatic carotid stenosis in relation to clinical subgroups and timing of surgery / P. M. Rothwell [et al.] // Lancet. – 2004. – N 363. – P. 915–924.
  9. 9.Guidelines for Carotid Endarterectomy / W. S. Moore [et al.] // Stroke. – 1995. – N 26(1) .– P. 188–201.
  10. Ðåêîíñòðóêòèâíàÿ õèðóðãèÿ ìàãèñòðàëüíûõ àðòåðèé ãîëîâû ïðè öåðåáðàëüíîé èøåìèè / Í. Â. Äîáæàíñêèé [è äð.] // Î÷åðêè àíãèîíåâðîëîãèè / Í. Â. Âåðåùàãèí [è äð.]; ïîä ðåä. Ç. À. Ñóñëèíîé. – Ì.: Àòìîñôåðà, 2005. – Ãë. 17. – Ñ. 231-249.
  11. Èíñóëüò: êëèíè÷åñêîå ðóêîâîäñòâî / Ä. Î. Âèáåðñ [è äð.]. – Ì.: ÁÈÍÎÌ, 2005. – 607 ñ.
  12. Ðåêîíñòðóêòèâíûå îïåðàöèè íà ñîííûõ àðòåðèÿõ – âçãëÿä íåâðîëîãà / È. À. Ïàøêîâà [è äð.] // Ñîâðåìåííûå àñïåêòû ïðîôèëàêòèêè, äèàãíîñòèêè è ëå÷åíèÿ àðòåðèàëüíîé ãèïåðòåíçèè: ìàòåðèàëû IV Ìåæäóíàð. íàó÷.-ïðàêòè÷. êîíô. – Âèòåáñê: ÂÃÌÓ, 2007. – Ñ. 158 – 162.
  13. 13.Carotid angioplasty and stenting in highrisk patients / G. P. Teitelbaum [et al.] // Surg. Neurol. – 1998. – N 50. – P. 300–312.
  14. Elective stenting of the extracranial carotid arteries / J. S. Yadav [et al.] // Circulation. – 1997. – N 95. – P. 376–381.
  15. Percutaneous transluminal angioplasty of the symptomatic atherosclerotic carotid arteries: results, complications, and followup / A. Gil-Peralta [et al.] // Stroke. – 1996. – N 27. – P. 2271–2273.
  16. Cerebral ischemia. II. The no-reflow phenomenon / A. Ames [et al.] // Am. J. Pathol. – 1968. –N 52(2). – P. 437–453.
  17. Correlation of cerebral blood flow and electro-encephalographic changes during carotid endarterectomy / T. M. Sundt [et al.] // Mayo Clin. Proc. – 1981. – N 56. – P. 533–543.
  18. Brain edema after carotid surgery / J. C. Breen [et al.] // Neurology. – 1996. – N 46. – P. 175–181.
  19. Carotid angioplasty and stenting: will periprocedural transcranial Doppler monitoring be important? / H. J. Benichou [et al.] // Endovasc. Surg. – 1996. – N 3. –P. 217–223.
  20. Wayne M, Clark. Reperfusion Injury in Stroke / ClarkWayne M. [Ýëåêòðîííûé ðåñóðñ]. – 2000. – Ðåæèì äîñòóïà: http://www.emedicine.com. – Äàòà äîñòóïà: 05.03.2007.
  21. Cerebral hyperperfusion syndrome: a cause of neurologic dysfunction after carotid endarterectoniy / M. M. Reigel [et al.] // J. Vasc. Stirg. – 1987. – N 5. – P. 628-634.
  22. Postcarotid endarterectomy hyperperfusion or reperfusion syndrolme / T. Karapanayiotides [et al.] // Stroke. – 2005. – N 36. – P. 21–26.
  23. Perfusion-weighted magnetic resonance imaging in patients with carotid artery disease before and after carotid endarterectomy / A. Doerfler [et al.] // J. Vasc. Surg. – 2001 – N 34. – P. 587–593.
  24. Hypertensive emergencies / C. J. Vaughan [et al.] // Lancet. – 2000. – N 356 . – P. 411-417.
  25. Ëèòâèöêèé, Ï. Ô. Àäàïòèâíûå è ïàòîãåííûå ýôôåêòû ðåïåðôóçèè è ðåîêñèãåíàöèè ìèîêàðäà / Ï. Ô. Ëèòâèöêèé, Â. À. Ñàíäðèêîâ, Å. À. Äåìóðîâ. – Ì.: Ìåäèöèíà, 1994. – 320 ñ.
  26. Peripheral administration of Interleukin-1 Receptor antagonist inhibits brain damage after focal cerebral ischemia in the rat / J. K. Relton // Exp. Neurol. – 1996. – N 138(2). – P. 206–213.
  27. Tumor necrosis factor alpha serum levels and inflammatory response in acute ischemic stroke patients / D. Intiso [et al.] // Neurol. Sci. – 2004. – N 24(6). – P. 390–396.
  28. Plasmatic level of neuroinflammatory markers predict the extent of diffusion-weighted image lesions in hyperacute stroke / J. Montaner [et al.] // J. Cereb. Blood Flow Metab. – 2003. – N 23(12). – P. 1403–1407.
  29. The release of tumor necrosis factor-alpha is associated with ischemic tolerance in human stroke / J. Castillo [et al.] // Ann. Neurol. – 2003. – N 54(6). – P. 811–819.
  30. Proliferation of astrocytes in vitro in response to cytokines. A primary role for tumor necrosis factor / K. W. Selmaj [et al.] // J. Immunol. – 1990. – N 144(1). – P. 129–135.
  31. Proinflammatory cytokines in serum of patients with acute cerebral ischemia: kinetics of secretion and relation to the extent of brain damage and outcome of disease / K. Fassbender [et al.] // J. Neurol. Sci. – 1994. – N 122(2). – P. 135–139.
  32. Circulating selectin- and immunoglobulin-type adhesion molecules in acute ischemic stroke / K. Fassbender [et al.] // Stroke. – 1995. – N 26(8). – P. 1361–1364.
  33. Reduction of central nervous system ischemic injury by monoclonal antibody to intercellular adhesion molecule / W. M. Clark [et al.] // J. Neurosurg. – 1991. –N 75(4). – P. 623–627.
  34. Anti-CD11b monoclonal antibody reduces ischemic cell damage after transient focal cerebral ischemia in rat / H. Chen [et al.] // Ann. Neurol. – 1994. – N 35(4). – P. 458–463.
  35. Role of cell adhesion molecules in brain injury after transient middle cerebral artery occlusion in the rat / Y. Matsuo [et al.] // Brain Res. – 1994. – N 656(2). – P. 344–352.
  36. Monoclonal leukocyte antibody does not decrease the injury of transient focal cerebral ischemia in cats / R. Takeshima [et al.] // Stroke. – 1992. – N 23(2). – P. 247–252.
  37. Cytokine and superoxide production in clinical stroke / W. M. Clark [et al.] // J. Stroke Cerebrovasc. Dis. – 1995. – N 5. – P. 166–171.
  38. Anti-ICAM-1 antibody reduces ischemic cell damage after transient middle cerebral artery occlusion in the rat / R. L. Zhang [et al.] // Neurology. – 1994. – N 44(9). – P. 1747–1751.
  39. Time course of ICAM-1 expression and leukocyte subset infiltration in rat forebrain ischemia / W. M. Clark [et al.] // Mol. Chem. Neuropathol. – 1995. – N 26(3). – P. 213–230.
  40. Reduction of central nervous system reperfusion injury in rabbits using doxycycline treatment / W. M. Clark [et al.] // Stroke. – 1994. – N 25(7). – P. 1411–1415.
  41. Monoclonal antibody to the ICAM-1 adhesion site reduces neurological damage in a rabbit cerebral embolism stroke model / M. P. Bowes [et al.] // Exp. Neurol. – 1993. – N 119(2). – P. 215–219.
  42. Effects of a selective CD11b/CD18 antagonist and recombinant human tissue plasminogen activator treatment alone and in combination in a rat embolic model of stroke / L. Zhang [et al.] // Stroke. – 2003. – N 34(7). – P. 1790–1795.
  43. Ñðàâíèòåëüíàÿ õàðàêòåðèñòèêà èñïîëüçîâàíèÿ âûñîêî- è íèçêîìîëåêóëÿðíîãî ãåïàðèíîâ ïðè íàðóøåíèÿõ ìîçãîâîãî êðîâîîáðàùåíèÿ â ýêñïåðèìåíòå / Í. Å. Ìàêñèìîâè÷ [è äð.] // Îò÷åò ïî ÍÈÈÐ / Ãðîäíåíñêèé ãîñ. ìåä. óí.-ò. [Ýëåêòðîííûé ðåñóðñ]. – 2006. – Ðåæèì äîñòóïà: http://.www.med.by/dn00/St19_3.htm. – Äàòà äîñòóïà: 02.02.2006.
  44. Îêîâèòûé, Ñ. Â. Êëèíè÷åñêàÿ ôàðìàêîëîãèÿ àíòèîêñèäàíòîâ / Ñ. Â. Îêîâèòûé // ÔÀÐÌèíäåêñ-Ïðàêòèê. – 2003. – Âûï. 5. – Ñ. 85-111.
  45. Ìåäèöèíñêàÿ ðåàáèëèòàöèÿ áîëüíûõ ìîçãîâûì èíñóëüòîì / Ë. Ñ. Ãèòêèíà [è äð.]; ïîä îáù. ðåä. Ë. Ñ. Ãèòêèíîé. – Ìèíñê, 1998. – 60 ñ.
  46. Ëå÷åáíûå ôèçè÷åñêèå ôàêòîðû â ðåàáèëèòàöèè áîëüíûõ öåðåáðàëüíûìè èíñóëüòàìè / À. Â. Êî÷åòêîâ [è äð.] // Âåñòíèê ïðàêòè÷åñêîé íåâðîëîãèè. – 1999. – ¹ 5. – Ñ. 21–24.
  47. Therapeutic use transcranial magnetic stimulation of ischemic stroke patients / O. V. Kisten [et. al.] // European Journal of Neurology. – 2004. – Vol. 11. – P. 149.
  48. Ãåìîäèíàìè÷åñêèå ýôôåêòû òðàíñöåðåáðàëüíîé ýëåêòðî- è ýëåêòðîìàãíèòîòåðàïèè áîëüíûõ èíñóëüòîì / À. Â. Êî÷åòêîâ [è äð.] // Âîïð. êóðîðòîëîãèè. – 1999. – ¹ 4. – Ñ. 17–21.
  49. 49.Òðàíñêðàíèàëüíàÿ ìàãíèòíàÿ ñòèìóëÿöèÿ êàê ëå÷åáíûé ôàêòîð / Â. Â. Åâñòèãíååâ [è äð.] // Çäðàâîîõðàíåíèå. – 2004. – ¹ 9. – Ñ. 32-38.
  50. Ñîâðåìåííûå òåõíîëîãèè ìàãíèòîòåðàïèè / Â. Ñ. Óëàùèê // Çäðàâîîõðàíåíèå. – 2006. – ¹ 12. – Ñ. 30-36.
Contacts | ©Vitebsk State Medical University, 2007-2023