Infarction cerebral

Other nootropic agents in some stage of clinical development include nebracetam (9), nefinacetam (10), and BMY 21502 (11). Nebracetam, an aminomethyl pyrrolidinone derivative, is expected to be approved in Japan in 1994 (73). In clinical studies involving patients having cerebrovascular or senile dementia of the Alzheimer s type, clinical symptoms such as spontaneous or emotional expression were enhanced in up to 71% of cases. Long-term treatment using nebracetam in patients with cerebral infarction also afforded marked improvement in most cases with few side effects (74). A review of this compound has beenpubUshed (75). 

Horowitz SH, Zito XL, Donnarumma R, Patel M, Alvir X. Computed tomographic-angiographic findings within the first five hours of cerebral infarction. Stroke 1991 22 1245-1253. 

Zorzon M, Mase G, Pozzi-MuceUi F, Biasutti E, Antonutti L, Iona L, Cazzato G. Increased density in the middle cerebral artery by nonenhanced computed tomography. Prognostic value in acute cerebral infarction. Eur Neurol 1993 33 256-259. 

Wardlaw JM, Dorman PJ, Lewis SC, Sandercock PAG. Can stroke physicians and neuroradiologists identify signs of early cerebral infarction on CT J Neurol Neurosurg Psychiatry 1999 67 651-653. 

Ischemic stroke has numerous causes. Cerebral infarction may result from large artery atherosclerosis, cardiac embolism, small artery lipohyalinosis, cryptogenic embolism, or, more rarely, from other diverse conditions such as arterial dissection, infective endocarditis, and sickle cell disease. Arterial occlusion is the cause of at least 80% of acute cerebral infarctions. " ... 

Del Zoppo GJ, Copeland BR, Anderchek K, Hacke W, Koziol JA. Hemorrhagic transformation following tissue plasminogen activator in experimental cerebral infarction. Stroke. 1990 21 596-601. 

Fiorelli M, Bastianello S, von Kummer R, del Zoppo GJ, Larrue V, Lesaffre E, Ringleb AP, Lorenzano S, Manelfe C, Bozzao L. Hemorrhagic transformation within 36 hours of a cerebral infarct Relationships with early clinical deterioration and 3-month outcome in the european cooperative acute stroke study i (ECASS i) cohort. Stroke. 1999 30 2280-2284. 

Badr AE, Yin W, Mychaskiw G, Zhang JH. Dual effect of hbo on cerebral infarction in mcao rats. Am J Physiol Regul Integr Comp Physiol 2001 280 R766-R770. 

Burt JT, Kapp JP, Smith RR. Hyperbaric oxygen and cerebral infarction in the gerbil. Surg Neurol 1987 28 265-268. 

Elynn EP, Auer RN. Eubaric hyperoxemia and experimental cerebral infarction. Ann Neurol 2002 52 566-572. 

Subramaniam S, Hill MD. Massive cerebral infarction. Neurologist 2005 11 150-160. 

Robertson SC, Lennarson P, Hasan DM, Traynelis VC. Clinical course and surgical management of massive cerebral infarction. Neurosurgery 2004 55 55-61 [discussion 61-52]. 

Camerlingo M, Salvi P, Belloni G, Gamba T, Mario Cesana B, Mamoli A. Intravenous heparin started within the first 3 hours after onset of symptoms as a treatment for acute nonlacunar hemispheric cerebral infarctions. Stroke 2005 36 2415-2420. 

Tris-hydroxymethyl-aminomethane (THAM) has been evaluated in ischemic stroke to reduce mass effect and ICP. It acts as a bulfer, neutralizing acidosis on a local level, including in the brain parenchyma. It has been studied in animal models of stroke, showing an effect in reducing the size of and swelling from cerebral infarction. To date, however, THAM has not been studied in a controlled fashion in humans with ischemic stroke. 

Corticosteroids have been evaluated in several types of cerebral injury, including cerebral infarction. Corticosteroids reduce vasogenic edema, such as that associated with neoplasms, but not cytotoxic edema, the type associated with ischemic stroke. A large meta-analysis found no benefit to the use of corticosteroids in ischemic stroke (or intracerebral hemorrhage), and their use is not recommended, except to treat concomitant conditions that mandate it (e.g., COPD flare). 

TABLE 8.6 Guidelines for the Management of Cerebral Edema in Patients with Massive Hemispheric Cerebral Infarction. 

Patients with massive cerebral infarction may require ICP monitoring, as this may help to guide therapy and predict outcome. Schwab et al. ° evaluated 48 patients with massive hemispheric infarctions and clinical signs of elevated ICP. They found that ICP measurements correlated well with the patient s clinical status, CT findings and outcome, although they did not find a significant effect of their therapies for elevated ICP on patient outcomes. Multiple methods of monitoring ICP are avail-... 

Meyer JS, Teraura T, Marx P, Hashi K, Sakamoto K. Brain swelling due to experimental cerebral infarction changes in vasomotor capacitance and effects of intravenous glycerol. Brain 1972 95(4) 833-852. 

Uhl E, Kreth EW, Elias B, Goldammer A, Hempelmann RG, Liefner M, Nowak G, Oertel M, Schmieder K, Schneider GH. Outcome and prognostic factors of hemicraniectomy for space occup3nng cerebral infarction. J Neurol Neurosurg Psychiatry 2004 75(2) 270-274. 

Saatci I, Baskan O, Cekirge HS, Besim A. Comparison of MR sequences in early cerebral infarction at 0.5 T. Acta Radiol 2000 41(6) 553-558. 

Nadeau SE, Jordan JE, Mishra SK, Haerer AE. Stroke rates in patients with lacunar and large vessel cerebral infarction. J Neurol Sci 1993 114 128-137. 

Anderson CS, Taylor BV, Hankey GJ, Stewart-Wynne EG, Jamrozik KD. Validation of a clinical classification for subtypes of acute cerebral infarction. J Neurol Neurosurgery Psychiatry 1994 57 1175-1179. 

Bamford J, Sandercock P, Dennis M, Bum J, Warlow C. Classification and natural history of clinical identifiable subt)fpes of cerebral infarction. Lancet 1991 337 1521-1526. 

Epidemiological data on carotenoids and cerebral infarcts or strokes indicate a protective effect of P-carotene and lycopene. Indeed, the Basel prospective study, the Kuopio Ischaemic Heart Disease Risk Factor study, and the Physicians Health Study " have shown an inverse correlation between carotenoid plasma level and risk of stroke. In the same way, Hirvonen et al. demonstrated, in findings from the ATBC cancer prevention stndy, an inverse association between P-carotene dietary intake and stroke. However, clinical data on carotenoids and stroke are nonexistent and they are needed to confirm this possible protective effect of carotenoids on stroke. 

Understand the types of cerebrovascular disease including transient ischemic attack, cerebral infarction, and cerebral hemorrhage. 

Ischemic stroke is the abrupt development of a focal neurologic deficit that occurs due to inadequate blood supply to an area of the brain. Most often, this is due to a thrombotic or embolic arterial occlusion leading to cerebral infarction. 

There are two main classifications of cerebral ischemic events transient ischemic attacks and cerebral infarction. 

Ischemic stroke is the abrupt development of a focal neurologic deficit that occurs due to inadequate blood supply to an area of the brain. Most often, this is due to a thrombotic or embolic arterial occlusion leading to cerebral infarction. A thrombotic occlusion occurs when a thrombus forms inside an artery in the brain. An embolism refers to a clot originating outside of the brain in which a piece of the clot breaks loose and is carried to the brain. 

Alzheimer s disease Cerebral infarction Cerebral tumors Closed head injury Cushing s syndrome Hemodialysis Hepatic encephalopathy Huntington s disease Hyperthyroidism Ictal or post-ictal mania Multiple sclerosis Neurosyphilis... 

There have been many sporadic reports that lipo-PGEj is effective in fulminant hepatitis, neuralgia associated with herpes zoster, multiple spinal canal stenosis, cerebral infarction, myocardial infarction, chronic renal failure, and bed sores as well as for its registered indications. 

Baird, A. E., Austin, M. C., McKay, W. J. and Donnan, G. A. Sensitivity and specificity of 99mTc-HMPAO SPECT cerebral perfusion measurements during the first 48 hours for the localization of cerebral infarction. Stroke 28 976-980,1997. 

It is interesting to note that the nitrosyl moieties of S N P and Roussin s salts exhibit significant N0+ character and they are also excellent NO donors. In particular, S N P is used widely to induce hypotension during surgery [14,15]. It significantly reduces the cerebral infarct size [16,17] and also inhibits platelet aggregation [18]. Transurethral administration of SNP can also induce an erectile response in cats without much side effects [19]. 

In addition to coronary sclerosis, evidence is accumulating that high Lp(a) levels may be important in the development of cerebrovascular and peripheral arterial disease, as well (J6, T8, U2). Lp(a) levels not only correlated well with clinical endpoints such as transient ischemic attack and cerebral infarction, but also were associated with the extent and severity of carotid atherosclerosis, as assessed by bidirectional Doppler ultrasound (K23, M33, Z2). 

M33. Murai, A., Miyahara, T., Fujimoto, M., and Kameyama, M., Lp(a)liprotein as a risk factor for coronary heart disease and cerebral infarction. Atherosclerosis (Shannon. Irel.) 59, 199 (1985). 

Babikian VL, Wolfe N, Lin R, Knoefel JE, Albert ML. (1990). Cognitive changes in patients with multiple cerebral infarcts. Stroke. 21 1013-18. 

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