Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Within a six-year period (1988-1993), we diagnosed and treated 143 cases of fetal hydrocephalus. We investigated the relationship between the degree of dilatation of the cerebral ventricles, the thickness of the pallium, and blood flow velocities in cerebral arteries. The assumption that progressive dilatation of the fetal ventricles leads to increasing resistance of the cerebral blood flow and disrupted cerebral perfusion was confirmed. Applying the postnatal pediatric principle of indication for shunt implantation based on Doppler sonographic diagnosis, delivery was instituted immediately in cases with pathologically increased pulsatility indices (PI). In all cases, this indication and the need for immediate shunt implantation were confirmed by postnatal pediatric ultrasonography. Cerebral Doppler velocimetry enables timely identification of fetuses at risk for pressure- or ischemia-induced cerebral tissue damage. The timing of delivery and subsequent neurosurgical therapy can thus be optimized.
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PMID:[Cerebral Doppler ultrasound in fetal hydrocephalus]. 772 66

The neonatal cat model of kaolin-induced hydrocephalus is associated with progressive and severe ventriculomegaly. In this experiment we studied the evolution of the histopathological changes in hydrocephalic (n = 23) cats from 5-168 days after the induction of hydrocephalus along with age-matched controls (n = 10). In the periventricular white matter, extracellular edema and axonal damage were present within days of the onset of hydrocephalus. This was followed by reactive gliosis, white matter atrophy, and in some animals gross cavitation of the white matter. Even in the chronic, apparently compensated state there was ongoing glial cell death. Six cats were shunted an average of 23.6 +/- 6.5 days after the induction of hydrocephalus because they were no longer able to feed independently. In spite of clinical improvement the white matter changes persisted. Overt cortical changes were minimal except where areas of white matter destruction encroached upon the deep layers. The white matter changes are very similar to those seen in periventricular leukomalacia and suggest that ischemia plays a role in neonatal brain injury caused by hydrocephalus.
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PMID:Acute and chronic cerebral white matter damage in neonatal hydrocephalus. 787 13

In this prospective study, a series of 89 patients with subarachnoid hemorrhage (SAH), most of whom had a "good" neurological outcome, were assessed with a range of tests of memory and cognition as inpatients and at 10 weeks and 12 months after SAH. On tests of verbal cognition and memory, most patients had scores in the normal range 12 months after SAH. However, a significant number of patients still showed impairment on tests of visuospatial construction and memory, mental flexibility, and psychomotor speed at the 12-month assessment. Statistical analyses were carried out for each test score to see whether aneurysm site, location of blood on the admission computed tomographic scan, vasospasm, ischemia, hydrocephalus, grades at admission to and at discharge from hospital, and Glasgow Outcome Scale score at follow-up were associated with test scores. Aneurysm site was not shown to be associated with performance on any test at any time, and the other complications of SAH had only minimal predictive value. The grade at discharge proved to be the best predictor of impairment of cognition and memory at both follow-up assessments. Older subjects did not recover to the same extent as younger subjects by the 12-month assessment. The authors conclude that the diffuse effects of SAH are more important than focal neuropathology in relation to cognitive impairment in this group of patients.
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PMID:A prospective study of impairment of cognition and memory and recovery after subarachnoid hemorrhage. 823 96

A patient undergoing surgery within 24 hours of aneurysm rupture was administered recombinant tissue plasminogen activator (rt-PA) directly into the basal subarachnoid cisterns after aneurysm clipping. Preoperatively, the patient had diffuse thick subarachnoid blood clots on CT. The rt-PA was given as a single injection of 10 mg. Postoperatively the patient was evaluated by serial CT scans and daily transcranial Doppler (TCD) examinations. An almost complete clot clearance was demonstrated on CT scans carried out on day 2 and day 4 after surgery. TCD studies failed to show any acceleration of blood flow velocity indicative of vasospasm. The postoperative curse was uneventful, without any clinical indication of delayed ischemia and no evidence of progressive hydrocephalus. Considering the data of the literature, as well as our initial experience, it appears that intracisternal thrombolysis with rt-PA can be achieved with relative safety and is effective for large-volume subarachnoid blood collections removal and vasospasm prevention. Results from open trials recently published suggest that a substantial advance in the management of an important subgroup of patients with aneurysmal subarachnoid hemorrhage (SAH) may be in the offing. However, randomized, placebo-controlled trials are still needed to confirm that there is a well-definite clinical benefit from the use of rt-PA. These considerations now call for a nation-wide multicentric italian trial which should be also addressed to evaluate other dose regimens and modalities of application.
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PMID:Intracisternal rt-PA during early surgery for aneurysmal subarachnoid hemorrhage: an Italian report. 830 73

Over a period of 12 years, 80 patients underwent ventricular shunting for normal pressure hydrocephalus. Three developed sixth cranial nerve palsy in the first two weeks after surgery. This uncommon complication is usually transitory following the same pattern of abducens palsy after lumbar puncture or spinal anesthesia. Traction on the nerve with local ischemia has been involved as the responsible mechanism in both instances.
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PMID:Abducens palsy following shunting for hydrocephalus. 833 73

Cerebrovascular disease is one of the most common causes of epilepsy in the elderly. Most of the studies published relate to cortical infarction, subarachnoid, and intracranial hemorrhage, whereas the incidence of epilepsy from subcortical ischemia, i.e. deep lacunar infarctions and diffuse white matter lesions, is obscure. Therefore, we prospectively examined 18 patients with the precisely defined diagnosis of subcortical vascular encephalopathy (SVE), who were admitted to our hospital due to epileptic seizures (group A), and compared them to a similarly selected group matched for age, sex, risk factors, and neurological deficits with an equivalent severity of SVE but without seizures (group B). Subcortical lacunar infarctions were significantly more frequent in group A than group B (15/18 versus 4/18, p < 0.001), whereas neither the extension, degree, distribution of periventricular white matter changes, nor the presence of internal hydrocephalus, focal or diffuse cortical atrophy showed any statistical significance. However, a temporal constant theta or delta EEG focus was present in 10/18 patients in group A but only in 1/18 patients from group B (p < 0.005). 10/18 patients developed epilepsy with further seizures during follow-up. The association of SVE, multiple subcortical lacunas, and temporal EEG abnormalities are suggestive for an increased risk for epileptic seizures, which is particularly important for the treatment of patients with SVE if uncertain paroxysmal episodes occur, e.g. transient ischemic attacks, seizures, or cardiac syncope.
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PMID:Epileptic seizures in subcortical vascular encephalopathy. 858 82

The rupture of a cerebral aneurysm is the main cause of a spontaneous subarachnoid hemorrhage. Complications after the initial hemorrhage are recurrent bleeds, hydrocephalus and ischemia. Main symptom of a subarachnoid hemorrhage is the sudden, intense headache, often followed by loss of consciousness. The diagnosis is made by CT. If the CT is negative, lumbar puncture has to be performed, because in 5% of patients the blood may not be seen on the CT. If the diagnosis is confirmed, the patients has to be transferred as an emergency to a neurosurgical center. If his condition is satisfactory, the aim of the treatment is to occlude the ruptured aneurysm by microsurgical technique within the first three days after the hemorrhage. In patients with high surgical risk or bad general condition, the aneurysm can also be treated by the interventional neuroradiologist with endovascular techniques.
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PMID:[Subarachnoid hemorrhage]. 871 34

The authors investigated functional neuronal changes in experimental hydrocephalus using immunohistochemical techniques for glutamic acid decarboxylase (GAD) and two neuronal calcium-binding proteins: parvalbumin (PV) and calbindin D28K (CaBP). Hydrocephalus was induced in 16 adult Wistar rats by intracisternal injection of a kaolin solution, which was confirmed microscopically via atlantooccipital dural puncture. Four control rats received the same volume of sterile saline. Immunohistochemical staining for GAD, PV, and CaBP, and Nissl staining were performed at 1, 2, 3, and 4 weeks after the injection. Hydrocephalus occurred in 90% of kaolin-injected animals with various degrees of ventricular dilation. In the cerebral cortex, GAD-, PV-, and CaBP-immunoreactive (IR) interneurons initially lost their stained processes together with a concomitant loss of homogeneous neuropil staining, followed by the reduction of their total number. With progressive ventricular dilation, GAD- and PV-IR axon terminals on the cortical pyramidal cells disappeared, whereas the number of CaBP-IR pyramidal cells decreased, and ultimately in the most severe cases of hydrocephalus, GAD, PV, and CaBP immunoreactivity were almost entirely diminished. In the hippocampus, GAD-, PV-, and CaBP-IR interneurons demonstrated a reduction of their processes and terminals surrounding the pyramidal cells, with secondary reduction of CaBP-IR pyramidal and granular cells. On the other hand, Nissl staining revealed almost no morphological changes induced by ischemia or neuronal degeneration even in the most severe cases of hydrocephalus. Hydrocephalus results in the progressive functional impairment of GAD-, PV-, and CaBP-IR neuronal systems in the cerebral cortex and hippocampus, often before there is evidence of morphological injury. The initial injury of cortical and hippocampal interneurons suggests that the functional deafferentation from intrinsic projection fibers may be the initial neuronal event in hydrocephalic brain injury. Although the mechanism of this impairment is still speculative, these findings emphasize the importance of investigating the neuronal pathophysiology in hydrocephalus.
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PMID:Progressive loss of glutamic acid decarboxylase, parvalbumin, and calbindin D28K immunoreactive neurons in the cerebral cortex and hippocampus of adult rat with experimental hydrocephalus. 901 Apr 28

Arteriovenous malformation of the vein of Galen (VGM) is a unique vascular anomaly in children. Its extra parenchymal location allows for aggressive endovascular treatment. Depending on the age of the child, the clinical presentation of VGM varies from congestive heart failure to hydrocephalus. The deleterious consequences to the brain depend on many factors, the most important of which is the volume of blood shunting through the malformation and away from the brain parenchyma ("steal" phenomenon). High flow in a fetus with a developing brain will lead not only to brain ischemia but also to multiple organ failure. At the other end of the spectrum, a small malformation can be well tolerated. Treatment should be tailored to each individual case.
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PMID:Arteriovenous malformation of the vein of Galen in children. 917 22

Although hydrocephalus is a multifactorial disorder, the processes responsible for neurologic impairment can be classified into primary and secondary mechanisms. Primary mechanisms include mechanical compression and stretching of brain parenchyma, ischemia and anoxia, cerebral edema, and blood brain barrier dysfunction. These processes lead to secondary mechanisms, which include cytologic and cytoarchitectural alterations of neurons, reduced size and numbers of cerebral microvessels, axonal degeneration and demyelination, and so on. Shunting studies suggest that neuronal cell death may not play a major role until severe stages of hydrocephalus and that some impairments in connectivity can be reversed. Relatively early shunting may alleviate many of the pathologic features of hydrocephalus, but residual impairments in neurotransmitter levels and dependence on anaerobic respiration leave the treated hydrocephalic brain vulnerable to subsequent insults.
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PMID:Neonatal hydrocephalus. Mechanisms and consequences. 940 66


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