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Regional cerebral blood flow and its autoregulation after intravenous glycerol infusion have been studied in eight patients in the acute phase of cerebral infarction. Glycerol seems to improve the cerebral blood flow in the damaged region but does not seem to restore autoregulation.
Four cases of homonymous hemianopia due to cerebral infarction in the posterior cerebral artery territory showed loss of pupillomotor sensitivity within the hemianopic defects, using small threshold-stimuli under perimetric conditions. Sensory and pupillographic profiles paralleled each other. The recordings were done with a portable pupillograph measuring the infrared light reflected from the iris. A Tübinger perimeter served as stimulator.
BACKGROUND AND PURPOSE: Superoxide anion radicals (O2*-) are implicated in ischemia/reperfusion injury, although a direct relationship has not been elucidated. Recently, a specific method of hydroethidine (HEt) oxidation by O2*- was developed to detect O2*- production in a variety of experimental brain injury models. To clarify the role of O2*- in the mechanism of ischemia/reperfusion, we investigated O2*- production after ischemia/reperfusion and ischemia/reperfusion injury in mutant mice deficient in mitochondrial manganese superoxide dismutase (MnSOD) and in wild-type littermates. METHODS: Ischemia/reperfusion was performed for 60 minutes using intraluminal suture blockade of the middle cerebral artery in the mutant or wild-type mice. We evaluated fluorescent kinetics of HEt or ethidium, the oxidized form of HEt, in brains after an intravenous injection of HEt, followed by measurement of cellular O2*- production using specific HEt oxidation by O2*- before and after ischemia/reperfusion. Furthermore, we compared O2*- production and subsequent infarct volume in the mice using triphenyltetrazolium chloride after ischemia/reperfusion. RESULTS: HEt oxidation to ethidium is primarily a result of mitochondrially produced O2*- under physiological conditions. Cerebral ischemia/reperfusion produced O2*- prominently in neurons shortly after reperfusion, followed by a delayed increase in endothelial cells. A deficiency in MnSOD in mutant mice increased mitochondrial O2*- production and exacerbated cerebral infarction, worsening neurological deficits after ischemia/reperfusion. CONCLUSION: These results suggest that mitochondrial O2*- production may be a critical step underlying the mechanism of ischemia/reperfusion injury and that MnSOD may protect against ongoing oxidative cell death after ischemia/reperfusion.
The effect of FK 506, an immunosuppressant which is widely used in the transplantation of liver, kidney and bone marrow, on cerebral infarction volume in transient focal ischemia was investigated. Focal cerebral ischemia was produced by 2 h occlusion of the left middle cerebral artery in rats. FK 506 (0.3 mg/kg body weight) and vehicle were administered intravenously immediately after induction of cerebral ischemia. After 24 h reperfusion the rats were sacrificed and brain infarct volume and edema volume were determined. The FK 506 treatment group showed a significantly reduced infarct volume in the cerebral cortex when it was compared with the vehicle treatment group, but infarct volume was not significantly reduced in the striatum which was the ischemic core in this focal ischemia model. However, FK 506 did not reduce the edema volume significantly. These results suggest that the reduction of infarct volume is a result of the neuroprotective effect of FK 506. This immunosuppressant may be useful in the treatment of cerebral infarction.
BACKGROUND: Massive cerebral infarcts cause brain edema with midline shifts and impingement on vital structures producing coma and death. The mortality rate is estimated at 80% with standard medical treatment. Surgical decompression with hemicraniectomy has proved to be life saving, but the impact on functional outcomes is largely unknown. The focus of this review is to discuss the treatment options for massive cerebral infarcts. REVIEW SUMMARY: Neurologic deterioration following massive cerebral infarct needs to be recognized early enough for medical and surgical interventions. Medical management includes monitoring in a neurologic intensive care unit, hyperosmolar agents, and hyperventilation. Surgical management includes decompressive hemicraniectomy and duraplasty with resection of infarcted tissue in some instances. CONCLUSION: Hemicraniectomy is emerging as a promising treatment of patients with massive cerebral infarcts, but only select patients benefit from this procedure. Further information from randomized controlled trials is required to elucidate the best treatment options for this kind of stroke.
A cerebral infarction occurred in a 37-year-old man following wasp stings. Computerized axial tomography documented the neurologic lesion.
The present study investigates the neuroprotective effects of midkine (MK) and retinoic acid (RA) against ischemia in the CNS. Primary cortical neurons, derived from rat E15 embryos (DIV9), were treated with 9-cis-RA (9cRA), all-trans-RA (atRA) or vehicle. Using quantitative PCR, the level of MK mRNA was significantly increased at 4h after 9cRA application. The protective effect of RA and MK was also investigated in adult Sprague-Dawley rats. 9cRA, atRA, MK, or vehicle was injected into the lateral ventricle prior to a 60-min-MCA ligation. Pretreatment with 9cRA or MK attenuated cerebral infarction in stroke animals. Application of a similar dose of atRA did not reduce the size of infarction. In conclusion, our data suggest that 9cRA has neuroprotective effects against ischemia-related brain injury which may involve upregulation of midkine.
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For an early and definitive diagnosis of acute cerebral infarction by computed tomography (CT), we retrospectively analyzed the initial CT findings of 14 patients with proven acute middle cerebral artery (MCA) infarction within 4 hours after stroke onset. The following results were obtained: (a) abnormal CT findings could be recognized quite early in 13 patients (92.9%), (b) the most common and earliest finding was loss of defination of the gray-white interface at the lateral margins of the insula. This sign was recognized in 12 patients (85.7%) and could be detected as early as 1 hour after stroke onset, (c) the next common finding was narrowing or blurring of the Sylvian fissure in 10 patients (71.4%) and could be detected 1.5 hours after stroke onset, (d) an obscured outline or partial disappearance of the lentiform nucleus was recognized in 7 patients (50%) and could be detected 1.5 hours after stroke onset, (e) effacement of the cerebral sulci was found in 6 patients (42.9%) and could be detected 2.5 hours after stroke onset, (f) increased density in MCA or its major branches was not seen in our patients.
A 38-year-old man was admitted to our hospital with headache, dysarthria and paraparesis. Brain CT and diffusion MRI disclosed cerebral infarction at bilateral anterior cerebral artery (ACA) territories. His symptoms and signs deteriorated in several days despite intensive antithrombotic therapy, resulting in right hemiparesis, akinetic mutism, memory disturbance, change of personality, urinary incontinence, forced grasping, and starting delay of speech and motion. Cerebral angiography demonstrated occlusion with contrast pooling at the right ACA A2 portion. Stenosis and dilatation were found at left ACA A2 portion. An intimal flap was also demonstrated on serial angiography. This case was diagnosed as cerebral infarction caused by dissection of bilateral ACA. Although no definite primary arteriopathy was demonstrated, bilateral dissection could be occurred simultaneously.