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Using the incomplete cerebral hemisphere infarction model in dogs, observations were made on the effect of 20% mannitol on brain swelling in groups of experimental animals following recirculation. In dogs undergoing 2-hour occlusion, mannitol clearly suppresses subsequent swelling; but after 6-hour occlusion, it was found that mannitol alone had little positive effect.
During Food and Drug Administration phase II and III clinical trials for gadolinium DTPA, the paramagnetic agent was used to study 11 patients with 20 subacute and chronic cerebral infarcts. Five patients had numerous periventricular and deep white-matter lesions, probably due to chronic ischemic disease. Magnetic resonance (MR) imaging was performed 4-30 days after the ictus, preceded by computed tomography (CT) in all but one case. In most cases, the nonenhanced spin-echo (SE) images, obtained at 500-msec repetition times and 30-msec echo times, failed to demonstrate the infarct, and in general the gadolinium-enhanced SE 500/30 images matched the contrast material-enhanced CT scans in pattern. Periventricular lesions and small, deep, white-matter infarcts that were chronic and asymptomatic were not enhanced by gadolinium MR. However, three small, symptomatic capsular and brain-stem infarcts showed definite enhancement. Usually the enhancement was visible at 3 minutes, increasing to a peak at 30 minutes. At 55 minutes, the enhancement increased in the medium-aged infarcts (8-14 days), while it decreased in the late infarcts (15-30 days). The T2 relaxation time-weighted pulse sequences were most sensitive for demonstrating all infarcts, but without the aid of a contrast agent, they were frequently poor in specificity.
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BACKGROUND: Neonatal asphyxia causes long-term neurological and behavioural impairment in the developing brain. Concurrent administration of xenon and hypothermia synergistically reduces long-term damage in a rat model of neonatal asphyxia. This study sought to investigate whether asynchronous administration of xenon and hypothermia is capable of combining synergistically to provide neuroprotection. METHODS: Seven-day-old rats were subjected to right common carotid artery occlusion followed by 90 min hypoxia with 8% oxygen. After a 1 h recovery period, rats received asynchronous administration of mild hypothermia (35 degrees C) and xenon (20%) with a 1 or 5 h gap between interventions, xenon (20%) alone, or mild hypothermia (35 degrees C) alone. Infarct volume in the brain was measured 4 days after injury. RESULTS: Administration of hypothermia or xenon alone, 1 and 6 h after the hypoxic ischaemic insult, respectively, provided no neuroprotection. Asynchronous administration of xenon and hypothermia at a 1 h interval produced a significant reduction in infarct volume [93 (7) vs 74 (8); P < 0.05]. Reduction in infarct volume was also present when hypothermia and xenon were asynchronously administered with an intervening gap of 5 h [97 (5) vs 83 (3); P < 0.05]. CONCLUSIONS: This finding provides a rationale for investigating the combined use of hypothermia and xenon in a progressive manner for the management of neonatal asphyxia. Thus, hypothermia can be administrated at the site of delivery and xenon can be administered later.
Extravasated endogenous serum albumin and fibrinogen were identified immunohistochemically in coronal brain sections from normotensive Wistar Kyoto (WKY) rats and spontaneously hypertensive rats (SHR) after permanent ligation of the right middle cerebral artery. Infarcts were seen in all the SHR but only in 6 out of 14 WKY. Six hours after ligation, extravasated proteins were located primarily within the borders of the infarcts whereas after 24 h and later there was an increasing spread in the white matter. After 7 days, a protein immunoreactivity was seen far outside the infarcted areas, mainly in the white matter and occasionally extending somewhat into the contralateral side. Three weeks after permanent ligation, the immunoreactivity for plasma proteins had a similar extension but was less intense than after 7 days. A gliosis was noted within the protein-positive regions. From 72 h and onwards the immunoreactivity for albumin but not for fibrinogen extended via the white matter into the ipsilateral thalamic nuclei, where marked, mainly cytolytic nerve cell damage and gliosis was found. The close spatial correlation with albumin immunopositivity and the histological features of the thalamic lesions indicate that the propagation of extravasated plasma constituents or degradation products from the infarct may influence the character, timing and extent of remote tissue changes after cerebral infarction.
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We report the case of a 65-year-old woman who presented with severe neurologic complications after envenomation by a viper snake. A computed tomography (CE) scan revealed multiple brain hemorrhagic infarcts. Conservative treatment in this case proved to be sufficient and repetitive CT scans displayed a complete resolution of the radiologic findings. Possible mechanisms for the cerebral infarctions are discussed. The mechanism of infarctions in this case was believed to be the vasomotor and coagulation disorders caused by the toxins present in the snake's venom and was one of the reasons that led to conservative treatment.
The significance of NMR water diffusion measurements performed at short diffusion times (< 10 ms) for brain tissue is examined. An apparent restriction to diffusion for both healthy and cytotoxically edematous tissue is shown: cytotoxic edema lengthens the diffusion time at which this phenomenon is visible. The dramatic reduction in apparent diffusion coefficient (ADC) observed in the core of cytotoxic edema is explained in terms of the enclosure of extracellular water in non-contiguous pockets in conjunction with the shift of water from the extra-to the intracellular space. The model presented provides an explanation for the ADC reduction without recourse to changes in the cell membrane permeability to water, or unrealistic values for the extra- and intracellular diffusion coefficients.
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OBJECTIVE: We describe the CT and MR imaging findings of the brain in patients who inadvertently poisoned themselves with concentrated hydrogen peroxide. Thirty-five percent hydrogen peroxide is commercially available as an oxidant and disinfectant. This solution is currently sold and promoted in health food stores in the United States as a means of "improving oxygenation" in people with coronary artery disease and other health problems. CONCLUSION: Our findings show the high toxicity of concentrated hydrogen peroxide. CNS damage and death are likely consequences after ingestion of this agent.
This study characterized morphological changes in the cortex and hippocampus of Sprague-Dawley rats following photothrombotic infarction and epileptogenesis with emphasis on the distribution of neuropeptide Y (NPY) expression. Animals were lesioned in the left sensorimotor cortex and compared with age-matched naive and sham-operated controls by immunohistochemical techniques at 1, 3, 7, and 180 days post-lesioning (DPL). NPY immunostaining was assessed by light microscopy and quantified by the optical fractionator technique using unbiased stereological methods. At 1, 3, and 7 DPL, the number of NPY-positive somata in the lesioned cortex was increased significantly compared to controls and the contralateral cortex. At 180 DPL, lesioned epileptic animals with frequent seizure activity demonstrated significant increases of NPY expression in the cortex, CA1, CA3, hilar interneurons, and granule cells of the dentate gyrus. In addition to NPY immunostaining, neuronal degeneration, cell death/cell loss, and astroglial response were assessed with cell-specific markers. Nissl and NeuN staining showed reproducible infarctions at each investigated time point. FJB-positive somata were most abundant in the infarct core at 1 DPL, decreased markedly at 3 DPL, and virtually absent by 7 DPL. Activated astroglia were detected in the cortex and hippocampus following lesioning and the development of seizure activity. In summary, NPY protein expression and morphological changes following cortical photothrombosis were time-, region-, and pathologic state-dependent. Alterations in NPY expression may reflect reactive or compensatory responses of the rat brain to acute infarction and to the development and expression of epileptic seizures.
The vascularization of neural grafts in ischemic brain was studied in spontaneously hypertensive rats grafted with a suspension of fetal neocortical tissue into the infarcted area five to six days after ligation of the middle cerebral artery. The brain vasculature was examined by scanning electron microscopy of corrosion vascular casts and the cortical microvasculature was stereologically quantified in light microscopy three months after the occlusion. Patent anastomoses were present between the middle cerebral artery distal to occlusion and the proximal part, as well as to the anterior and posterior cerebral arteries, in both grafted and non-grafted rats. A vascular plexus covering the infarct cavities and the grafts contained leptomeningeal vessels intermingled with a thin capillary network which is not normally found on the brain surface. The graft vessels were derived from this vascular plexus. The regular pattern of arterioles and venules penetrating from the cortical surface in normal neocortex was absent in the grafts but the capillary morphology was similar in both types of tissue. The grafts had a lower capillary density than normal tissue and lacked the laminar distribution of capillaries characteristic of normal neocortex. The results demonstrate the plasticity of the vascular system where remodeling of the vascular tree after an ischemic insult provides suitable conditions for the vascularization of neocortical grafts.
A 63-year-old woman was admitted to our hospital because of fever and altered mentality. Brain magnetic resonance imaging showed multiple infarctions at the basal ganglia, cerebellum, and subcortical white matter with petechial hemorrhage, which was more easily seen on gradient echo images. Erysipelothrix rhusiopathiae was cultured from her blood, and echocardiography showed septic vegetations in the mitral valve. She recovered fully after 6 weeks of appropriate antibiotic treatment.
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