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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Spontaneous subarachnoid hemorrhage is usually caused by a ruptured cerebral aneurysm. Aneurysmal rupture classically presents with sudden severe headache, often accompanied by an altered mental status. Diagnosis is made with computed tomography or lumbar puncture. Patients with ruptured cerebral aneurysms are at risk for rebleeding, cerebral artery vasospasm (and subsequent ischemia or stroke), and hydrocephalus. Early surgical clipping of the aneurysm under the microscope is usually the initial treatment of choice. This surgery prevents rebleeding and allows for safe use of pressors in the event that clinical vasospasm develops. Factors that would favor delayed surgery, "coiling" procedures, or conservative management include poor patient condition, basilar artery aneurysms, and unusually large or irregular aneurysms. Patients with ruptured aneurysms are treated with nimodipine, a calcium-channel blocker, to help prevent vasospasm-related ischemia. The degree of vasospasm that develops in the first 2 wks after aneurysmal rupture is assessed by transcranial Doppler sonography and cerebral angiography, in addition to the clinical examination. Patients with symptomatic vasospasm are kept well hydrated and treated with pressors (provided the aneurysm has been successfully clipped).
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PMID:Surgical management of subarachnoid hemorrhage. 943 90

Moyamoya syndrome is a vaso-occlusive disease involving the intracranial vessels of the circle of Willis which is accompanied by an intense compensatory recruitment of new vessels. Angiogenic substances such as basic fibroblast growth factor (bFGF) present in the cerebrospinal fluid (CSF) have been proposed as possible mediators of the neovascular response. We analyzed CSF samples collected intraoperatively from predominantly pediatric patients with moyamoya and other conditions such as Chiari malformation (Ch), tethered cord (TC), arteriovenous malformation (AVM), brain tumor (BT) and hydrocephalus (HCP). We found that CSF bFGF was significantly elevated in patients with moyamoya (141 pg/ml, n = 37), Ch (56.7 pg/ml, n = 22), TC (55.1 pg/ml, n = 23), AVM (354 pg/ml, n = 5), and BT (208 pg/ml, n = 5) compared to patients with HCP (5.5 pg/ml, n = 7) and controls (1.6 pg/ml, n = 25; p < 0.05). There was no dependence of CSF bFGF on patient age or gender. Although CSF bFGF in the moyamoya group showed no correlation with the Suzuki radiographic stage at either pre- or post-operative (1-year follow-up) angiography, it showed a trend with the Matsushima angiographic score with increasing collateral vascularization from the synangiosis developing at higher levels of CSF bFGF. Our findings suggest that CSF bFGF may be playing a wide-ranging role in a number of central nervous system conditions associated with ischemia and hypervascularity. Although not a specific marker for moyamoya, elevated CSF bFGF may serve as a weak predictor of the extent of angiogenesis to be expected in indirect revascularization procedures.
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PMID:Elevation of cerebrospinal fluid levels of basic fibroblast growth factor in moyamoya and central nervous system disorders. 957 71

The pathophysiology of elevated intracranial pressure (ICP) is assessed from a three cerebral compartment model and from brain compliance. The mechanisms leading to elevated ICP (expanding process, cerebral edema, brain swelling, hydrocephalus) and their consequences (brain herniation, ischemia-anoxia phenomenon, Cushing reaction and neurogenic pulmonary edema) are overviewed. The causes of elevated ICP in children are reported with emphasis on traumatology. Diagnostic procedures include clinical assessment, fundoscopy, cerebral computerized tomography scan and specific problems of cerebrospinal fluid investigation. Methods and results of intracranial pressure monitoring are reported. The treatment of elevated ICP is based upon clinical follow-up and monitoring of ICP. General therapeutic rules consist of adequate position, suppression of any neck, skull and abdominal compression, stimuli limitation and fluid restriction. Specific treatments include mechanical ventilation, sedation and analgesia, barbiturates, anticonvulsant drugs, mannitol, corticosteroids, hypothermia, enteral nutrition, and antibiotics.
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PMID:[Intracranial hypertension in the infant: from its physiopathology to its therapeutic management]. 975 78

Medical treatment of subarachnoid haemorrhage, is focused on the prevention of rebleeding and vasospasm, of damages of oxitading products, and on the improvement of general conditions of the patient. Some authors consider use of antifibrinolytic usefull to reduce the risk of rebleeding, but the percentage of hydrocephalus and ischemia are increased. In our Centre combination of nimodipine-cloricromene and hemodilution is used for the prevention of vasospasm. We report conclusions about 216 patients in I-II-III grade of Hunt-Hess scale, treated before 48 hours from SAH. We obtained only 8% postspasm ischemias, with no neurological deficit, and only 23% of increased cerebral blood flow revealed by transcranial Doppler. Cloricromene is used only after aneurysm is occlused. It presents different action mechanisms. It is an inhibitor of platelet activation and aggregation, of cyclooxygenase and lipooxygenase activity, so reducing thromboxanes ratio. Phospholipase A2 inhibition it's possible but not demonstrated. It also interferes with phosphoinositoles path and so with proteinkinase C activity, and reduces hemostatic thrombotic balance activation and leukocyte endothelial adhesion and activation. It reduces, finally, the release of free radicals, cytokines inflammation amplyfing. The reduced damage to the endothelium allows the releasing of vasodilatatory agents like NO.
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PMID:[Pharmacologic therapy of subarachnoid hemorrhage]. 977 63

The alterations induced by ischemia and anoxia upon smooth endoplasmic membranes are studied in 38 patients with congenital malformations, brain tumours and brain trauma. The effects of vasogenic and cytotoxic brain edema are examined in the Golgi apparatus of nerve and endothelial cells. Samples of cortical biopsies were conventionally processed for transmission electron microscopy. Cortical biopsies were performed according to the basic principles of Helsinki declaration. Slices of 2 to 5 mm were immediately fixed in the surgical room in 4% glutaraldehyde-0.1 M sodium phosphate buffer, pH 7.4 at 4 degrees C, and postfixed in 1% osmium tetroxide in similar buffer. The pathological alterations of the Golgi complex were studied in samples with moderate and severe brain edema. Moderate edema was mainly found in congenital malformations and severe edema in brain trauma and tumours. In some severely edematous neurons, observed in hydrocephalus associated to Arnold-Chiari malformation, small vesicular type Golgi complexes and atrophic ones were observed, characterized mainly by partial or total disappearance of stacked Golgi cisternae and presence of congregated vesicular profiles. In brain trauma and tumours the Golgi complex showed enlargement and fragmentation of the stacked cis- medial- and trans-Golgi cisternae and vacuolization of trans-Golgi network. In addition, an increased formation of Golgi and coated vesicles was observed in the cis- and trans-Golgi regions. Most Golgi and clathrin coated vesicles were observed throughout the cytoplasm suggesting an increased vesicular transport. In severe edema the nerve cell plasma membranes appeared fragmented, presumably due to an interference of the protein insertion process into the plasma membrane. In brain trauma, a hypertrophic Golgi complex was observed in some nerve cells and endothelial cells of cortical capillaries, with increased formation of Golgi and coated vesicles. The ischemia and anoxia associated to the vasogenic and cytotoxic brain edema induced enlargement, fragmentation and disappearance of stacked Golgi cisternae.
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PMID:Ultrastructural pathology of Golgi apparatus of nerve cells in human brain edema associated to brain congenital malformations, tumours and trauma. 1045 6

Paget's disease of bone is associated with involvement of the central and peripheral nervous system. The brain, spinal cord, cauda equina, spinal roots, and cranial nerves can be affected in Paget's disease due to their anatomic relationship to bone. Neurologic syndromes are uncommon but include headache, dementia, brain stem and cerebellar dysfunction, cranial neuropathies, myelopathy, cauda equina syndrome, and radiculopathies. The central complications result from pagetic involvement of the skull. Expansion of diseased bone can result in compression of cranial nerves as they exit their bony foramina. Softening of the skull leads to basilar invagination with compression of the brain stem, cerebellum, and lower cranial nerves. Brain stem compression can cause hydrocephalus. Rarely, there is direct compression of the brain from acute epidural hematoma or hypertrophy of the calvarium. Myelopathy, cauda equina syndrome, and radiculopathies most commonly result from hypertrophy of the spine with direct compression. Spinal stenosis can also result from ossification of extradural structures or pathologic fractures. Ischemia from vascular compression or a steal syndrome has also been described. Neurologic complications rarely occur due to sarcomatous transformation of pagetic bone. Magnetic resonance imaging (MRI), computerized tomography (CT)-myelography, and bone X-rays are helpful to localize the lesion and direct therapy. Treatment options include surgical decompression, ventricular shunt placement, and medical management with calcitonin and/or the bisphosphonates. The selection of treatment will vary depending upon the rate of progression and the severity of the neurologic deficit.
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PMID:The neurologic complications of Paget's disease. 1051 Feb 21

Pediatric neuroimaging plays an important role in the timely diagnosis of postnatal central nervous system (CNS) infections, and in some patients the imaging findings are sufficiently specific to suggest a cause. The sequela of CNS infection, including hydrocephalus, subdural collections, ischemia/infarction, cerebral abscess, demyelination, and vascular thrombosis, can be accurately depicted and serially followed with current imaging techniques. The purpose of this review is to describe the spectrum of pediatric postnatal CNS infections, emphasizing key pathological and neuroimaging features, and to outline the strengths, weaknesses, and applications of current neuroimaging technology. The prenatal and perinatal infections falling under the designation of TORCH (toxoplasmosis, other [e.g., syphilis, HIV], rubella, cytomegalovirus, and herpes simplex II) are not covered.
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PMID:Neuroimaging of postnatal pediatric central nervous system infections. 1064 38

Precocious puberty and amenorrhea have been associated with hydrocephalus, but the pathogenesis has not been determined. Approximately 22 cases of amenorrhea, and a few cases of precocious puberty, have been reported in hydrocephalic patients. Shunt treatment leads to initiation and maintenance of normal reproductive cycles in most cases. An underlying mechanism responsible for reproductive dysfunction may involve the role of gonadotrophin releasing hormone (GnRH). The exact pathway by which hydrocephalus disrupts the hypothalamic GnRH system is unknown. However, compressive forces, ischemia, and impairment of neurotransmitter feedback loops are likely candidates.
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PMID:A brief review of the effects of chronic hydrocephalus on the gonadotropin releasing hormone system: implications for amenorrhea and precocious puberty. 1067 90

Hydrocephalus is a pathological dilatation of the cerebrospinal fluid (CSF)-containing ventricles of the brain. Damage to periventricular white matter is multifactorial with contributions by chronic ischemia and gradual physical distortion. Acute ischemic and traumatic brain injuries are associated with calcium-dependent activation of proteolytic enzymes. We hypothesized that hydrocephalus is associated with calcium ion accumulation and proteolytic enzyme activation in cerebral white matter. Hydrocephalus was induced in immature and adult rats by injection of kaolin into the cisterna magna and several different experimental approaches were used. Using the glyoxal bis (2-hydroxyanil) method, free calcium ion was detected in periventricular white matter at sites of histological injury. Western blot determinations showed accumulation of calpain I (mu-calpain) and immunoreactivity for calpain I was increased in periventricular axons of young hydrocephalic rats. Proteolytic cleavage of a fluorogenic calpain substrate was demonstrated in white matter. Immunoreactivity for spectrin breakdown products was detected in scattered callosal axons of young hydrocephalic rats. The findings support the hypothesis that periventricular white matter damage associated with experimental hydrocephalus is due, at least in part, to calcium-activated proteolytic processes. This may have implications for supplemental drug treatments of this disorder.
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PMID:Calcium-mediated proteolytic damage in white matter of hydrocephalic rats? 1108 72

Hereditary hemorrhagic telangiectasia (HHT) is an autosomal dominant disorder because of mutations in the genes coding for endoglin (HHT1) or ALK-1 (HHT2). The disease is associated with haploinsufficiency and a murine model was obtained by engineering mice that express a single Endoglin allele. Of a total of 171 mice that were observed for 1 year, 50 developed clinical signs of HHT. Disease prevalence was high in 129/Ola strain (72%), intermediate in the intercrosses (36%), and low in C57BL/6 backcrosses (7%). Most mice first presented with an ear telangiectasia and/or recurrent external hemorrhage. One-third of mice with HHT showed severe vascular abnormalities such as dilated vessels, hemorrhages, liver and lung congestion, and/or brain and heart ischemia. Disease sequelae included stroke, hydrocephalus, fatal hemorrhage, and congestive heart failure. Thus the murine model reproduces the multiorgan manifestations of the human disease. Levels of circulating latent transforming growth factor (TGF)-beta1 were significantly lower in the 129/Ola than in the C57BL/6 strain. Intercrosses and 129/Ola mice expressing reduced endoglin also showed lower plasma TGF-beta1 levels than control. These data suggest that modifier genes involved in the regulation of TGF-beta1 expression act in combination with a single functional copy of endoglin in the development of HHT.
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PMID:Potential role of modifier genes influencing transforming growth factor-beta1 levels in the development of vascular defects in endoglin heterozygous mice with hereditary hemorrhagic telangiectasia. 1139 79


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