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)

Paediatric neurosurgical procedures request special considerations for the anaesthetic management. Due to patients age and diagnostic findings certain therapeutic procedures are performed under anaesthetic care. Main reasons for craniotomy are hydrocephalus, intracranial tumors and craniofacial synostosis. Neurosurgical therapy of newborn children is related mostly to hereditary spinal dysraphism. In spinal surgery and specific intracranial procedures for monitoring reasons sensory and/or motor evoked potentials (SEP, MEP) are used to improve surgical outcome. Due to sensibility for anaesthetic drugs these techniques request sound knowledge of physiologic and pharmacologic interaction. Cerebrovascular malformations are today usually treated using radiologic interventional procedures. Operative access will be performed for selected cases additionally to embolization, but is associated with risk of massive bleeding. Severe traumatic craniocerebral injury leads to compromised cerebral blood flow and hypoxic ischemia. The article imparts funded knowledge of surgical as well as anaesthetic rationale and techniques in neuropaediatric therapies.
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PMID:[Paediatric anaesthesia for neurosurgical procedures]. 1760 14

Chronic hydrocephalus (CH) is a neurological disease characterized by increased cerebrospinal fluid volume and pressure that is often associated with impaired cognitive function. By and large, CH is a complex and heterogeneous cerebrospinal fluid (CSF) disorder where the exact site of brain insult is uncertain. Several mechanisms including neural compression, fiber stretch, and local or global hypoxia have been implicated in the underlying pathophysiology of CH. Specifically, the hippocampus, which plays a significant role in memory processing and is in direct contact with expanding CSF ventricles, may be involved. Using our model of chronic hydrocephalus, we quantified the density of vascular endothelial growth factor receptor 2 (VEGFR-2(+)) neurons, glial, endothelial cells, and blood vessels in hippocampal regions CA1, CA2-3, dentate gyrus and hilus using immunohistochemical and stereological methods. Density and %VEGFR-2(+) cell populations were estimated for CH animals (2-3 weeks vs. 12-16 weeks) and surgical controls (SC). Overall, we found approximately six- to eightfold increase in the cellular density of VEGFR-2(+) and more than double blood vessel density (BVd) in the hippocampus of CH compared with SC. There were no significant regional differences in VEGFR-2(+) cellular and BVd expression in the CH group. VEGFR-2(+) and BVds were significantly related to changes in CSF volume (P<or=0.05), and not intracranial pressure (ICP). The %VEGFR-2(+) was significantly greater in CH than SC (P<or=0.05), and was significantly correlated with BVd (P<or=0.05). These results showed that CH elicited a profound increase in VEGFR-2(+) in hippocampus that corresponded to increased BVd. It was unclear whether increased VEGFR-2(+) and blood vessel expression was related to focal compression alone or in combination with global ischemia/hypoxia conditions as previously described. These findings suggest that VEGFR-2 may play an adaptive role in angiogenesis after CH-induced hypoxia. Modulation of vascular endothelial growth factor/VEGFR-2(+) may be important in developing treatments for hypoxic conditions including hydrocephalus and other forms of cerebral ischemia.
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PMID:Chronic hydrocephalus-induced hypoxia: increased expression of VEGFR-2+ and blood vessel density in hippocampus. 1826 64

Sarcoidosis is a multisystem disease of uncertain etiology characterized by multifocal areas of discrete and confluent granulomatous inflammation that may rarely be responsible for sudden and unexpected death. Two cases are reported to demonstrate disparate pathological features in fatal cases, one involving cardiac sarcoidosis, and the other neurosarcoidosis with hypothalamic infiltration. Sarcoidosis in individuals dying suddenly may be completely unrelated to the death, contributory or causal. Cardiovascular causes of sudden death in sarcoidosis include arrhythmias associated with cardiomyopathy and ischemia, ventricular rupture, and cor pulmonale due to pulmonary hypertension; respiratory causes include hemorrhage and upper airway obstruction; central nervous system causes include arrhythmias from infiltration of autonomic centers, epilepsy, and obstructive hydrocephalus from brainstem involvement; and gastrointestinal deaths may be due to hemorrhage from esophageal varices associated with portal hypertension. The diagnosis relies on the demonstration of typical noncaseating granulomas and the exclusion of other infective and environmental diseases with similar histopathological findings.
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PMID:Sarcoidosis and mechanisms of unexpected death. 1836 80

Petroclival meningiomas are technically challenging lesions. They have a tendency to grow slowly, involve cranial nerves and compress the brainstem and basilar artery, pushing them to the opposite side. Their natural history is marked by clinical deterioration and fatal outcome. They were once considered inoperable lesions; decades ago, mortality rates were higher than 50%. The authors describe 15 petroclival meningiomas treated surgically between 1995 and 2007. The main approaches used were combined anterior petrosectomy and retrosigmoid (3 cases), retrosigmoid (8 cases), and pre-sigmoid and subtemporal (4 cases). The mortality rate was 13.5% due to surgical bed hematoma and brain ischemia. The post-operative complications were hydrocephalus in 2 cases, cerebrospinal fluid leak in 2 cases and infection of surgical flap in one case. Limiting factors for surgical removal are tumor consistency, encasement of brainstem perforators and pre-operative clinical status.
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PMID:Petroclival meningiomas: surgical management and common complications. 1931 54

Surrogate markers have enormous potential for contributing to the diagnosis, prognosis, and therapeutic evaluation of acute brain damage, but extensive prior study of individual candidates has not yielded a biomarker in widespread clinical practice. We hypothesize that a panel of neuron-enriched proteins measurable in cerebrospinal fluid (CSF) and blood should vastly improve clinical evaluation and therapeutic management of acute brain injuries. Previously, we developed such a panel based initially on the study of protein release from degenerating cultured neurons, and subsequently on rodent models of traumatic brain injury (TBI) and ischemia, consisting of 14-3-3beta, 14-3-3zeta, three distinct phosphoforms of neurofilament H, ubiquitin hydrolase L1, neuron-specific enolase, alpha-spectrin, and three calpain- and caspase-derived fragments of alpha-spectrin. In the present study, this panel of 11 proteins was evaluated as CSF and serum biomarkers for severe TBI in humans. By quantitative Western blotting and sandwich immunoassays, the CSF protein levels were near or below the limit of detection in pre-surgical and most normal pressure hydrocephalus (NPH) controls, but following TBI nine of the 11 were routinely elevated in CSF. Whereas different markers peaked coordinately, the time to peak varied across TBI cases from 24-96 h post-injury. In serum, TBI increased all four members of the marker panel for which sandwich immunoassays are currently available: a calpain-derived NH(2)-terminal alpha-spectrin fragment and the three neurofilament H phosphoforms. Our results identify neuron-enriched proteins that may serve as a panel of CSF and blood surrogate markers for the minimally invasive detection, management, mechanistic, and therapeutic evaluation of human TBI.
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PMID:A panel of neuron-enriched proteins as markers for traumatic brain injury in humans. 1981 Oct 94

It is hypothesized that in all traumatic brain injury (TBI) patients with a clinical history of closed or penetrating head injury, the initial head trauma is associated with a vibratory sensation and noise exposure, with resultant alteration in vascular supply to the structures and contents of the fluid compartments of brain and ear (i.e., the fluid dynamics vascular theory of brain-inner-ear function [FDVTBE]). The primary etiology-head trauma-results in an initial fluctuation, interference, or interaction in the normal fluid dynamics between brain and labyrinth of the inner ear, with a resultant clinical diversity of complaints varying in time of onset and severity. Normal function of the brain and ear is a reflection of a normal state of homeostasis between the fluid compartments in the brain of cerebrospinal fluid and perilymph-endolymph in the labyrinth of the ear. The normal homeostasis in the structures and contents between the two fluid compartment systems--intracerebral and intralabyrinthine--is controlled by mechanisms involved in the maintenance of normal pressures, water and electrolyte content, and neurotransmitter activities. The initial pathophysiology (a reflection of an alteration in the vascular supply to the brain-ear) is hypothesized to be an initial acute inflammatory response, persistence of which results in ischemia and an irreversible alteration in the involved neural substrates of brain-ear. Clinically, a chronic multisymptom complex becomes manifest. The multisymptom complex, individual for each TBI patient regardless of the diagnostic TBI category (i.e., mild, moderate, or severe), initially reflects processes of inflammation and ischemia which, in brain, result in brain volume loss identified as neurodegeneration and hydrocephalus ex vacuo or an alteration in cerebrospinal fluid production (i.e., pseudotumor cerebri) and, in ear, secondary endolymphatic hydrops with associated cochleovestibular complaints of hearing loss, tinnitus, vertigo, ear blockage, and hyperacusis. The FDVTBE integrates and translates a neurovascular hypothesis for Alzheimer's disease to TBI. This study presents an FDVTBE hypothesis of TBI to explain the clinical association of head trauma (TBI) and central nervous system neurodegeneration with multisensory complaints, highlighted by and focusing on cochleovestibular complaints. A clinical case report, previously published for demonstration of the cerebrovascular medical significance of a particular type of tinnitus, and evidence-based basic science and clinical medicine are cited to provide objective evidence in support and demonstration of the FDVTBE.
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PMID:Fluid dynamics vascular theory of brain and inner-ear function in traumatic brain injury: a translational hypothesis for diagnosis and treatment. 2042 Mar 35

Intraventricular hemorrhage during pregnancy is usually followed by a poor recovery. When caused by moyamoya disease, ischemic or hemorrhagic episodes may complicate the management of high intracranial pressure. A 26-year-old Caucasian woman presented with generalized seizures and a Glasgow Coma Score (GCS) of 3 during the 36th week of pregnancy. The fetus was delivered by caesarean section. The brain CT in the mother revealed bilateral intraventricular hemorrhage, a callosal hematoma, hydrocephalus and right frontal ischemia. Refractory high intracranial pressure developed and required bilateral ventricular drainage and intensive care treatment with barbiturates and hypothermia. Magnetic resonance imaging and cerebral angiography revealed a moyamoya syndrome with rupture of the abnormal collateral vascular network as the cause of the hemorrhage. Intracranial pressure could only be controlled after the surgical removal of the clots after a large opening of the right ventricle. Despite an initially low GCS, this patient made a good functional recovery at one year follow-up. Management of refractory high intracranial pressure following moyamoya related intraventricular bleeding should require optimal removal of ventricular clots and appropriate control of cerebral hemodynamics to avoid ischemic or hemorrhagic complications.
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PMID:Refractory High Intracranial Pressure following Intraventricular Hemorrhage due to Moyamoya Disease in a Pregnant Caucasian Woman. 2050 23

The ultrastructural pathology of cerebral cortex in human hydrocephalus is reviewed and compared with experimental hydrocephalus. Nerve cells show moderate and severe swelling. The neighboring neuropil exhibits notable enlargement of extracellular space, synaptic plasticity and degeneration, damage of myelinated axons, and myelination delay. The astrocytes display edematous changes and phagocytic activity. Glycogen rich- and glycogen-depleted astrocytes are observed. Some oligodendroglial cells exhibit normal morphology, and other exhibit hydropic changes. The capillary wall shows signs of blood-brain barrier dysfunction. The role of ischemia, oxidative stress, increased calcium concentration, activation of NMDA receptors, and disturbance of ion homeostasis are discussed in relationship with the fine structural alterations of hydrocephalic brain parenchyma.
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PMID:Submicroscopic pathology of human and experimental hydrocephalic cerebral cortex. 2092

Tuberculous meningitis (TBM) is the most lethal form of tuberculosis; mortality is high and survivors are often left neurologically disabled. Several factors contribute to this poor outcome, including cerebrovascular involvement with ensuing brain ischemia, hydrocephalus and raised intracranial pressure, direct parenchymal injury, hyponatremia, and seizures. However, there is little standardisation of management with respect to these aspects of care across different centers, largely because the evidence base for much of the supportive treatment of patients with TBM is poor, leading to substantial differences in management protocols. This review emphasizes some of the uncertainties and controversies pertinent to the surgical treatment of hydrocephalus in TBM and the medical supportive management of the patient during the acute phase of the illness, with the aims of raising awareness and stimulating debate. The focus is on the management of hyponatremia, cerebral hemodynamics and intracranial pressure, medical and surgical treatment for hydrocephalus, and the intensive care management of patients in the acute severe stage of the illness. Very little data are available to address these issues with good evidence and so institutional preferences are common; this is perhaps most notable for the management of hydrocephalus, and so in this the review highlights our personal practice. The brain needs protection while the source of the illness is addressed. Without attention to these aspects of management there will always be a limit to the effectiveness of antimicrobial therapy in TBM, so there is a strong imperative for the controversies to be resolved and the limitations of our current care to be addressed. Existing protocols should be rigorously examined and novel strategies to protect the brain should be explored. To this end, a prospective, multi-disciplinary and multi-centered approach may yield answers to the questions raised in this review.
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PMID:The neurosurgical and acute care management of tuberculous meningitis: evidence and current practice. 2097 Mar 81

Cerebral sinovenous thrombosis in neonatal period may cause neurological impairment, epilepsy, and lead to stroke. It is caused primarily by coagulopathy of numerous reasons, occasionally perinatal asphyxia, traumatic delivery and hyperhomocysteinemia. Dandy-Walker malformation is characterized by agenesis or hypoplasia of the cerebellar vermis, cystic dilatation of the fourth ventricle, and enlargement of the posterior fossa. Dandy-Walker malformation, variant, and mega cisterna magna represent a spectrum of developmental anomalies. Insults to developing cerebellar hemispheres and the fourth ventricle are believed to be the cause of malformation. Our patient was born from noncomplicated pregnancy, noncomplicated nontraumatic vaginal delivery at term, excellent Apgar scores, without peculiarities in clinical status. She was brest-fed by the 42nd hour of life when she had rightsided seizures during sleep that repeated for five times in next 24 hours. Brain Ultrasound (US) revealed clot in left lateral ventricle, slight dilatation of left ventricle, both sided periventricular echodensity, ischemia, slight enlargement of forth ventricle and a bit smaller cerebellum. There was no visible flow through left transverse, superior sagittal and straight sinus. Magnetic Resonance (MRI) confirmed the finding and showed thrombosis of left and right transverse venous sinuses and confluence of sinuses. Electroencephalogram (EEG) showed leftsided focal changes. The newborn was treated with phenobarbiton for 8 days and had no convulsions during that period. All coagulation parameters, homocistein, lipoproteins (a) and D-dimers were normal. There were no mutations on FV R506Q, PT 20210A, MTHFR 677C/T. No antiphospholipides were found. Heart US showed no structural anomalies. No other patology or risk factors were present at the time. Before discharge, US showed hydrocephalus. Flow in affected sinuses was visible with color Doppler. MRI showed recanalization of affected sinuses, also hydrocephalus and presentation of Dandy Walker On EEG there was borderline finding. Due to progression of hydrocephalus ventriculo-peritoneal shunt was placed. In age of 1 year EEG was slower for age but without focus. Neurological development was normal for age. The question is whether this child had intrauterine insult and inception of Dandy Walker with further postnatal progress of thrombosis and evolution to full picture of Dandy Walker with hydrocephalus OR thrombosis that led to development of hydrocephalus and Dandy Walker malformation in this child were accidental coexistance.
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PMID:Coexistance of cerebral sinovenous thrombosis and Dandy Walker malformation in newborn. 2164 52


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