Corticosteroids vasogenic edema

Eyes Verbal Motor Does not open eyes Makes no noise (1) No motor response to pain Opens eyes to painful stimuli  Moans, makes unintelligible noises  (2) Extensor response (decerebrate)   Opens eyes upon loud verbal command  Talks but nonsensical   (3) Flexor response (decorticate)   Opens eyes spontaneously Seems confused and disoriented  (4) Moves parts of body but does not remove noxious stimuli    Alert and oriented (5) Moves away from noxious stimuli      (6) Follows simple motor commands Treatment and Prognosis Patients with head trauma need to be referred to an emergency department, and a neurosurgical consultation is important. All patients known to be unconscious for more than 10 to 15 minutes, or with a skull fracture or a neurologic abnormality, require hospital admission and observation, because the possibility exists of delayed deterioration from expanding mass lesions (Gennarelli and Kotapa 1992).

Q. what is "pulmonary edema" and what are the risks? my Dr. told me I'm in a risk group for pulmonary edema, he tried to explain what it is but i didn't understand fully...if someone may give me a brief explanation- I'll appreciate it! A. pulmonary edema occurs when, lets say, your heart left ventricle stops working properly and your right ventricle works fine. that means your lungs getting lets presume- 1 liter of blood -but your left ventricle can pump out of it only 990 ml. that means you have high blood pressure in your lungs and fluid comes out of blood vessels and fills your lungs, making it harder and harder breathing.

The effectiveness of WBRT has been examined mainly in retrospective studies (Table 3).[13-20,25] Interpreting the data from these studies, however, is difficult because different criteria were used to measure response rates.[23] The response criteria used in the older studies were often based on symptomatic improvement rather than on objective measurements of tumor size on radiographic studies. In addition, many of the patients included in these studies were also treated with chemotherapy, either concurrently with radiation or shortly thereafter. Finally, the chemotherapy regimens varied widely from study to study.

Genetic loss on chromosomes 1p/19q (co-deletion or loss of heterozygosity [LOH] 1p/19q) is a consequence of a chromosomal translocation and describes a distinct tumour entity characterised by a prolonged natural history irrespective of treatment, and increased sensitivity both to radiotherapy (RT) and to chemotherapy ( Jenkins 2006) . LOH 1p/19q should be evaluated to support a diagnosis of oligodendroglioma.
The incidence of either 1p or 19q chromosomal deletions in OD is approximately 75%, the combined loss of 1p and 19q is observed in 25% to 48% of all ODs ( van den Bent 2013b; Cairncross 2013) . Additional chromosomal deletions, such as loss of heterozygosity for 9p, deletion of CDKN2A gene, deletions on chromosome 10 and chromosome 7 amplification, occur less frequently in anaplastic OD ( Bigner 1999; Jeuken 1999) . Oligodendroglial tumours with a classical histological appearance (perinuclear halo, chicken-wire vascular pattern) show 1p/19q co-deletions, whereas in tumours with an atypical appearance, other chromosomal abnormalities are often found (., TP53 mutations) ( Sasaki 2002; van den Bent 2003) . In AOD both the loss of 10q and the amplification of EGFR were found inversely related to 1p/19q loss, and were associated with poor chemosensitivity and short survival ( Hoang-Xuan 2001) . The mutually exclusive occurrence of 1p/19q loss and TP53 mutations, EGFR amplification, 10q loss, or PTEN mutations suggests that these tumours are in fact derived from different precursor cells. This hypothesis is supported by the marked differences in outcome and prognosis.
Recent genome sequencing of high-grade gliomas has identified mutations of the isocitrate dehydrogenase gene (IDH) as an early event in glioma genesis ( Yan 2009) . IDH1 mutations are present in 55% to 80% of grade III oligodendrogliomas and astrocytomas ( Sanson 2009) . Less frequently, glial tumours show mutations of the IDH2.
The presence of IDH 1 or 2 mutations is characteristic of a high-grade glioma developing from a lower grade precursor lesion ( Sturm 2012; Hartmann 2013) .
MGMT promoter methylation is highly associated with LOH 1p/19q and IDH mutations ( Sanson 2009) . Conversely, IDH1 was correlated with an absence of EGFR, absence of chromosome 7 polisomy, or absence of loss of chromosome 10.

Initial effects of bubbles are mechanical-they cause mass effect in tissues, obstruct venous outflow, and occlude arteries. In addition to causing damage at the final resting place, bubbles injure the vascular endothelium while in transit. Secondary biochemical effects include activation of leukocytes, platelets, complement, and the clotting cascade. In addition, attachment of polymorphonuclear cells and granulocyte- mediated reperfusion injury may occur. An increase of vascular permeability leads to hemoconcentration. In the brain, microvascular flow, cerebral perfusion, and autoregulation are disturbed; breakdown of the blood-brain barrier, and extension of the ischemic penumbra can occur (1, 11 ,30).

Corticosteroids vasogenic edema

corticosteroids vasogenic edema

Genetic loss on chromosomes 1p/19q (co-deletion or loss of heterozygosity [LOH] 1p/19q) is a consequence of a chromosomal translocation and describes a distinct tumour entity characterised by a prolonged natural history irrespective of treatment, and increased sensitivity both to radiotherapy (RT) and to chemotherapy ( Jenkins 2006) . LOH 1p/19q should be evaluated to support a diagnosis of oligodendroglioma.
The incidence of either 1p or 19q chromosomal deletions in OD is approximately 75%, the combined loss of 1p and 19q is observed in 25% to 48% of all ODs ( van den Bent 2013b; Cairncross 2013) . Additional chromosomal deletions, such as loss of heterozygosity for 9p, deletion of CDKN2A gene, deletions on chromosome 10 and chromosome 7 amplification, occur less frequently in anaplastic OD ( Bigner 1999; Jeuken 1999) . Oligodendroglial tumours with a classical histological appearance (perinuclear halo, chicken-wire vascular pattern) show 1p/19q co-deletions, whereas in tumours with an atypical appearance, other chromosomal abnormalities are often found (., TP53 mutations) ( Sasaki 2002; van den Bent 2003) . In AOD both the loss of 10q and the amplification of EGFR were found inversely related to 1p/19q loss, and were associated with poor chemosensitivity and short survival ( Hoang-Xuan 2001) . The mutually exclusive occurrence of 1p/19q loss and TP53 mutations, EGFR amplification, 10q loss, or PTEN mutations suggests that these tumours are in fact derived from different precursor cells. This hypothesis is supported by the marked differences in outcome and prognosis.
Recent genome sequencing of high-grade gliomas has identified mutations of the isocitrate dehydrogenase gene (IDH) as an early event in glioma genesis ( Yan 2009) . IDH1 mutations are present in 55% to 80% of grade III oligodendrogliomas and astrocytomas ( Sanson 2009) . Less frequently, glial tumours show mutations of the IDH2.
The presence of IDH 1 or 2 mutations is characteristic of a high-grade glioma developing from a lower grade precursor lesion ( Sturm 2012; Hartmann 2013) .
MGMT promoter methylation is highly associated with LOH 1p/19q and IDH mutations ( Sanson 2009) . Conversely, IDH1 was correlated with an absence of EGFR, absence of chromosome 7 polisomy, or absence of loss of chromosome 10.

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