[Differential diagnosis brain neoplasms--brain infarct. Angiographic problems in the differentiation of a cerebro-vascular attack due to an intracranial tumor].
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Adult↗
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Regional cerebral blood flow in patients with brain infarcts. A study with the 85Kr clearance technique.
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Aged↗
Induction of reproducible brain infarction by photochemically initiated thrombosis.
We have used a photochemical reaction in vivo to induce reproducible thrombosis leading to cerebral infarction in rats. After the intravenous injection of rose bengal, a potent photosensitizing dye, an ischemic lesion was formed by irradiating the left parietal convexity of the exposed skull for 20 minutes with green light (560 nm) from a filtered xenon arc lamp. Animals were allowed to survive from 30 minutes to 15 days after irradiation. Early microscopic alterations within the irradiated zone included the formation of thrombotic plugs and adjacent red blood cell stasis within pial and parenchymal vessels. Scanning electron microscopy revealed frequent platelet aggregates adhering to the vascular endothelium, often resulting in vascular occlusion. Carbon-black brain perfusion demonstrated that occlusion of vascular channels progressed after irradiation and was complete within 4 hours. Histopathological examination at 1, 5, and 15 days revealed that the associated infarct evolved reproducibly through several characteristic stages, including a phase of massive macrophage infiltration. Although cerebral infarction in this model is initiated by thrombosis of small blood vessels, the fact that the main pathological features of stroke are consistently reproduced should permit its use in assessing treatment regimens. Further, the capability of producing infarction in preselected cortical regions may facilitate the study of behavioral, functional, and structural consequences of acute and chronic stroke.
Animals↗
Relation of hyperglycemia early in ischemic brain infarction to cerebral anatomy, metabolism, and clinical outcome.
We studied the relation of serum glucose level measured in the first 12 hours of symptoms to the clinical findings, results of computed tomography (CT), and patterns of cerebral metabolism in 39 patients who had acute ischemic cerebral infarction. Structural damage was assessed by CT. Metabolic disruption was assessed using 18F-fluorodeoxyglucose and positron emission tomography (PET). Median initial serum glucose concentration was 155 mg/dl (6.7 mM). Clinical recovery was significantly poorer in patients with initial serum glucose levels higher than the median (p less than 0.05, chi square). PET tended to show normal results or minor abnormalities in patients with initial glucose levels less than the median, as opposed to lobar or multilobe abnormalities in patients with levels that were higher than the median (p less than 0.05, Kendall's Tau b). The severity of hypometabolism in the ischemic region, expressed as the percent asymmetry of local cerebral glucose metabolism between homologous brain regions, was greater in patients with initial glycemia concentrations higher than the median (p less than 0.001, t test). Relationships of serum glucose level with metabolic derangement and structural damage, but not outcome, held true in patients without a history of diabetes mellitus.
Aged↗
FK419, a nonpeptide platelet glycoprotein IIb/IIIa antagonist, ameliorates brain infarction associated with thrombotic focal cerebral ischemia in monkeys: comparison with tissue plasminogen activator.
The binding of platelet glycoprotein (GP) IIb/IIIa to fibrinogen is the final common pathway in platelet aggregation, a process known to play a key role in the pathogenesis of ischemic brain damage. We compared the effects of FK419, a novel nonpeptide GPIIb/IIIa antagonist, with recombinant tissue plasminogen activator (rt-PA) on middle cerebral artery (MCA) patency and ischemic brain damage in a thrombotic stroke model in squirrel monkeys. FK419 not only inhibited in vitro platelet aggregation (IC50: 88 nmol/L), but also showed disaggregatory activity to aggregated platelet (EC50: 286 nmol/L). FK419 dose-dependently reduced the time to first reperfusion and total occlusion time of MCA blood flow when administered immediately after the termination of photoirradiation. FK419 reduced cerebral infarction and ameliorated neurologic deficits with similar dose-dependency. Although rt-PA reduced the time to first reperfusion, total occlusion time, and cerebral infarction, it did not significantly ameliorate neurologic deficits and induced petechial intracerebral hemorrhages. These results indicate: (1) FK419 restored cerebral blood flow after thrombotic occlusion of MCA, (2) FK419 reduced ischemic brain injury by its thrombolytic actions in a non-human primate stroke model, and (3) FK419 has superior antithrombotic efficacy and is safer than rt-PA.
Animals↗
Survival of fetal neocortical grafts implanted in brain infarcts of adult rats: the influence of postlesion time and age of donor tissue.
We have previously found that fetal cortex taken from 16- to 18-day-old donors survives grafting to the infarcted cortex 5-7 days after middle cerebral artery occlusion. The present study was undertaken to examine the effect on graft survival of varying the age of the fetal donor tissue and the time between vessel occlusion and graft implantation. First, a cell suspension of neocortical tissue was grafted from fetuses aged 15, 17, or 20 gestational days to the infarcted cortex of hypertensive rats which had undergone arterial occlusion 5-7 days earlier. There were no significant differences in the mean size or general morphology assessed in Nissl- and acetylcholinesterase-stained sections between the groups. Second, neocortical tissue was grafted from fetuses aged 15 gestational days to the infarcted cortex at different times following arterial occlusion. When surgery was delayed until 5-7 days, 3 weeks, or 8 weeks postocclusion, graft survival was significantly better than when implanted 1 day postocclusion. Implantation after 3 weeks yielded grafts that also were significantly larger than those in rats grafted 5-7 days after cortical infarction. The results indicate that there is no crucial upper donor age limit for dissociated fetal neocortical grafts in terms of graft survival and volume. Furthermore, a delay between lesion and transplantation is desirable in this stroke model. The host brain environment seems to be most hospitable around 3 weeks after arterial occlusion.
Acetylcholinesterase↗
Effect of a novel free radical scavenger, edaravone (MCI-186), on acute brain infarction. Randomized, placebo-controlled, double-blind study at multicenters.
Edaravone, a novel free radical scavenger, demonstrates neuroprotective effects by inhibiting vascular endothelial cell injury and ameliorating neuronal damage in ischemic brain models. The present study was undertaken to verify its therapeutic efficacy following acute ischemic stroke. We performed a multicenter, randomized, placebo-controlled, double-blind study on acute ischemic stroke patients commencing within 72 h of onset. Edaravone was infused at a dose of 30 mg, twice a day, for 14 days. At discharge within 3 months or at 3 months after onset, the functional outcome was evaluated using the modified Rankin Scale. Two hundred and fifty-two patients were initially enrolled. Of these, 125 were allocated to the edaravone group and 125 to the placebo group for analysis. Two patients were excluded because of subarachnoid hemorrhage and disseminated intravascular coagulation. A significant improvement in functional outcome was observed in the edaravone group as evaluated by the modified Rankin Scale (p = 0.0382). Edaravone represents a neuroprotective agent which is potentially useful for treating acute ischemic stroke, since it can exert significant effects on functional outcome as compared with placebo.
Acute Disease↗
Effect of nicardipine and magnesiumon cerebral infarction - brain surface perfusion technique.
The protective effect of pre- and postischemia treatment of the brain by surface perfusion with nicardipine (Nic) and/or magnesium (Mg) was evaluated in a rat focal cerebral ischemia model. Artificial cerebrospinal fluid was perfused into the subarachnoid space of rats, containing Nic or Nic/Mg prior to vessel occlusion and Nic/Mg after occlusion. Reductions in the total amount of glutamate in the microdialysis perfusate and the volume of infarction tissue stained with 2,3,5-triphenyltetrazolium chloride were significant in all treated groups, even in rats treated after ischemia. An additive effect of Mg was also observed. These results suggest that this method may have clinical applications in patients suffering from ischemic insult.
Administration, Topical↗
Visual and spectral EEG analysis in the evaluation of the outcome in patients with ischemic brain infarction.
Serial EEGs were recorded in 15 patients with acute cerebral infarctions in order to study clinical and prognostic correlations. The EEG was recorded within 48 h from the first symptoms and thereafter weekly for 4 weeks. The EEGs were analyzed both visually and with a computerized spectral analysis. Eight of the patients recovered fully and seven had permanent neurological deficits. On admission, 87% of the patients had an abnormal EEG by visual analysis. The spectral parameters correlated well with visual findings, especially the delta and alpha bands. The spectral analysis was superior to visual in predicting the correct laterality of the lesion. It showed the correct side of the lesion in 87%, while the visual did it in only 54% of the cases. The first EEG records reliably predicted the outcome of the patients. The degree of background abnormality was most important in visual EEG analysis. In spectral analysis, parameters from single derivations were superior to the average of all derivations. A high proportion of delta or low proportion of alpha power were reliable indicators of poor outcome.
Adult↗
The importance of brain infarct size and location in predicting outcome after stroke.
Fifty-six consecutive elderly ( > or = 65 years) patients, admitted for acute stroke to a geriatric department were included in the study and underwent CT scanning. Functional status was graded according to the modified Rankin scale. Three patients had primary intra-cerebral haemorrhage, 22 deep hemispheric infarct, 17 had anterior circulation cortical infarcts, five had posterior circulation infarcts and in nine the CT scan was normal. Stroke risk factors were equally distributed among the different CT scan groups, and all three larger groups had similar rates of non-neurological major complications including death (41%). However, independence in ADL (Rankin 0-2) was observed in 72% of deep infarct survivors, but only 15% of the cortical infarct group (p = 0.00018). For the normal scan group, functional recovery was intermediate. In the cortical infarct group patients with an infarct of > or = 50 mm mean diameter (five cases) should worse functional recovery than did eight patients with small infarcts. The mean difference between pre- and post-stroke Rankin score (DR) was 3.4 for the larger infarct patients and 1.9 for the smaller infarct group (p = 0.027). Pearson correlation revealed a direct relationship between the infarction size and DR (p = 0.039). Such a relationship was not observed for the deep hemispheric group.
Activities of Daily Living↗
The Circle of Willis--the incidence of developmental abnormalities in normal and infarcted brains.
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Cerebral Arteries↗
[Multiple brain infarcts in zoster infection].
The clinical, CSF, CCT and PET findings in a 14-year-old female patient are reported. CCT and PET investigations demonstrated multiple cerebral infarctions; CSF examinations revealed inflammatory changes. Zoster antibodies were synthesized intrathecally, as detected by an ELISA after adjusting serum and CSF to identical IgG concentrations. Therefore the diagnosis of a cerebral zoster angiitis was made. Diagnostic and therapeutic problems of inflammatory vascular lesions are discussed.
Adolescent↗
Experimental brain infarcts in cats. I. Pathophysiological observations.
In 48 cases the left middle cerebral artery was occluded under light barbiturate anaesthesia using a transorbital approach. The animals were kept alive for 1, 2, and 4 hours after vascular occlusion. Regional cerebral blood flow was measured by the intracardiac microsphere injection technique before ischemia, 15 min after the onset of ischemia, and at the end of experiments. The density of regional ischemia was correlated with EEG changes and with the electrolyte, water and metabolite content of the same tissue samples in which blood flow was assessed. In the territory of the occluded middle cerebral artery, cortical blood flow decreased from 41.4 +/- 3.8 to 21.3 +/- 4.0 ml/100 g/min (means +/- SE), the actual flow rate depending on the individual efficacy of collateral blood supply. At flow rates below 10--15 ml/100 g/min, ischemia involved more than 50% of the middle cerebral artery territory, water and electrolyte homeostasis was severely disturbed and ischemic brain edema developed. Adenosine triphosphate decreased to about 60% of the control value at flow rates below 40 ml/100 g/min, but it remained at this level down to flow rates as low as 5 ml/100 g/min. EEG intensity -- but not EEG frequency -- decreased in parallel with blood flow, indicating that with increasing density of ischemia an increasing portion of the excitable neuropil was inhibited. The development of ischemic brain edema determined the further progression of ischemia. When blood flow decreased below the threshold for water and ion disturbance, ischemia was progressive (critical ischemia), but an amelioration of flow occurred in animals in which flow remained above this level (non-critical ischemia). In the contralateral hemisphere the EEG, blood flow, water and electrolyte content did not change significantly during the initial few hours of ischemia. Diaschisis, in consequence, was not a prominent feature during the early phase of infarct development.
Adenosine Triphosphate↗
Brain infarction risk factors in black New York City stroke patients.
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Adult↗
Do transient ischemic attacks with diffusion-weighted imaging abnormalities correspond to brain infarctions?
BACKGROUND AND PURPOSE: Our aim was to determine whether diffusion-weighted imaging (DWI) changes associated with transient ischemic attack (TIA) are reversible or correspond to permanent tissue injury. METHODS: Among 103 consecutive patients admitted for TIA, 36 (34.9%) had abnormalities on initial DWI (delay from TIA = 30 +/- 33 hours [mean +/- SD]). Thirty-three patients (59 DWI lesions) had an MR imaging follow-up (delay from TIA = 10.6 +/- 5 months) including fluid-attenuated inversion recovery, T2, DWI, and 3D T1-weighted sequences. For each lesion, we recorded the quantitative parameters on initial DWI (volume, apparent diffusion coefficient [ADC]) and performed a comparison between reversible and irreversible lesions. RESULTS: MR imaging failed to detect any permanent injury in 7 patients and identified subsequent infarct in regions corresponding to the original DWI abnormalities in 26 patients (79%). Of the 59 lesions initially identified on DWI, 45 (76.3%) were associated with permanent injury on follow-up MR imaging. The DWI volume was significantly larger (0.91 +/- 1.7 versus 0.21 +/- 0.21 cm(3), P = .003) and the ADC ratio values lower (79 +/- 15% versus 91 +/- 9%, P = .001) in lesions with subsequent infarct than in those that were fully reversible. CONCLUSION: By showing that most patients with DWI-positive TIAs share the same imaging outcome as stroke patients, our data provide additional support for the redefinition of TIA, which considers that all cases of transient deficit with characteristic neuroimaging abnormalities should be diagnosed as a stroke.
Adult↗
Cerebral blood volume in acute brain infarction: A combined study with dynamic susceptibility contrast MRI and 99mTc-HMPAO-SPECT.
BACKGROUND AND PURPOSE: The aim of this study was to correlate the abnormality in cerebral blood volume (CBV) measured by dynamic susceptibility contrast-enhanced MRI with that in cerebral blood flow (CBF) estimated by single-photon emission CT with [99mTc]hexamethylpropylenamine-oxime in patients with acute ischemic stroke. METHODS: Nine patients with unilateral occlusion of either the middle cerebral artery or the internal carotid artery (4 men and 5 women; mean+/-SD age, 74.4+/-11.6 years) were studied within 6 hours after stroke onset. The relative CBV (relCBV) and CBF (relCBF) in the lesions were defined relative to the contralateral mirror regions. RESULTS: In the brain regions with mild (relCBF >/=0.60), moderate (0.40</=relCBF<0.60), and severe (relCBF <0.40) hypoperfusion, the mean relCBV values were 1.29+/-0.31, 0.94+/-0.49, and 0.30+/-0.22, respectively. The relCBV was significantly elevated in the brain areas with mild hypoperfusion (P<0.001) and significantly reduced in the brain areas with severe hypoperfusion (P<0.001). The relCBF was significantly better than the relCBV in predicting the evolution of infarction (P<0.02). The probability of evolving infarction for the hypervolemic (relCBV >1.0) regions was significantly lower than that for hypovolemic (relCBV <1.0) regions in the relCBF range between 0.40 and 0.50 (P<0.02). CONCLUSIONS: In acute ischemic stroke within 6 hours of onset the CBV can be either increased, normal, or decreased, depending on the severity of hypoperfusion. The increased CBV has a protective effect on evolving infarction. Although the CBF is a better predictor of tissue outcome, the CBV measurement may help detect potentially salvageable brain tissue in the penumbra with compromised blood flow.
Acute Disease↗
Brain infarction in young adults: etiology and imaging findings.
The causes of stroke in young adults differ substantially from those in older adults. In many instances, the diagnosis can be made by taking a clinical history and performing laboratory studies (e.g., in patients who have multiple thromboses associated with anti-phospholipid antibodies). In other circumstances, clues to the diagnosis can be found on routine CT and MR studies. However, in many circumstances, imaging tailored to a specific diagnosis is important (e.g., MR imaging of the neck in patients with suspected arterial dissection). In yet other cases, additional studies (e.g., echocardiography in suspected cardiogenic embolism) are important to establish the cause.
Adult↗
Inhibition of neutrophil migration by a protein kinase inhibitor for the treatment of ischemic brain infarction.
This study investigated the therapeutic potential of agents that inhibited neutrophil infiltration in cerebral ischemic infarction. The migration of neutrophils elicited by N-formyl-methionyl-leucyl-phenylalanine, tumor necrosis factor, C5a or platelet-activating factor was potently inhibited by fasudil, an inhibitor of protein kinases including rho kinase, protein kinase C and myosin light chain kinase, and hydroxy fasudil, a metabolite of fasudil, in vitro. In a microembolism model in rats, myeloperoxidase-quantified neutrophil accumulation in the ischemic brain was observed 24 hr after embolization. Intravenous administration of fasudil prevented the accumulation of neutrophils. In rats given fasudil, myeloperoxidase activity in the ipsilateral hemisphere (0.04+/-0.01 unit/g wet tissue) was significantly lower than that in ischemic rats (0.11+/-0.02 unit/g wet tissue). Fasudil also significantly reduced the size of the infarct area and improved neurological functions. These results suggest that neutrophil infiltration into the ischemic brain is involved in the pathogenesis of ischemic injury and that inhibiting neutrophil infiltration may provide an effective therapeutic intervention to reduce ischemic injury.
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗