Neurologic survival

The primary objective of CPR is to obtain neurologic survival. Since this is often unobtainable, many health care professionals are... 

Fatal hereditary disorder that typically presents in the neonatal period. Clinical features include an array of hepatic, renal and neurological dysfunctions. Patients with Zellweger syndrome rarely survive the first year of life. The disease is caused by mutations in the Pex proteins leading to an defective import of peroxisomal matrix proteins and consequently to a loss of most peroxisomal metabolic pathways. 

In addition to the role of chemokines/chemokine receptors in viral infection, transmission, and pathogenesis, chemokines also play important roles in cellular trafficking and survival pathways. The role of chemokines and their receptors are of particular importance in the development of neurologic complications of AIDS, involving mechanisms discussed in the following sections. 

Bacellar H, Munoz A et al (1994) Temporal trends in the incidence of HIV-l-related neurologic diseases Multicenter AIDS Cohort Study, 1985-1992. Neurology 44(10) 1892-1900 Banki K, Hutter E et al (1998) Molecular ordering in HIV-induced apoptosis. Oxidative stress, activation of caspases, and cell survival are regulated by transaldolase. . J Biol Chem 273(19) 11944-11953... 

With modest impairment of blood flow, this mechanism allows for preservation of oxidative metabolism without alteration in electrical function. However, when CPP and therefore CBF are sufficiently low, OEF reaches a maximum and cannot increase further. Brain tissue ceases to function electrically, resulting in a neurologic deficit. Microvascular collapse occurs, and CBV falls. If the oxygen supply falls low enough, the tissue dies. Of critical clinical importance is the observation that the amount of time it takes for tissue to suffer irreversible damage is inversely related to the severity of the ischemic insult. Tissue that is completely deprived of blood will die within a few minutes, but less severely hypoperfused tissue may survive for many hours, and may be saved by timely thrombolysis that restores perfusion, or perhaps by another therapeutic intervention. 

Bushnell CD, Phillips-Bute BG, Laskowitz DT, Lynch JR, Chilukuri V, Borel CO. Survival and outcome after endotracheal intubation for acute stroke. Neurology 1999 52(7) 1374-1381. 

Hereditary triose phosphate isomerase (TPI) deficiency is an autosomal recessive disorder that has the most severe clinical manifestations of the erythroenzy-mopathies, including hemolytic anemia, neurological dysfunction, sudden cardiac death, and increased susceptibility to infection. Since the first description by Schneider et al. (S10), more than 25 unrelated families have been reported (Fll). Cases of decreased TPI activities associated with cat cry syndrome and pancytopenia were reported, whereas the correlation between TPI deficiency and these disorders was not clear. Although the degree of anemia is variable, most patients require blood transfusions. Neurological involvement, such as paraparesis, weakness, and hypotonia, is progressive in most cases. No specific therapy is available for the neuropathic manifestations of the disease, and most severely affected children fail to survive beyond the age of 5 years. 

Mohs RC, Doody RS, Morris JC, Ieni JR, Rogers SL, Perdomo CA and Pratt RD (2001). A 1-year, placebo-controlled preservation of function survival study of donepezil in AD patients. Neurology, 57, 481-488. 

Intrauterine seizures may occur. The electroencephalogram often displays a hypsarrhythmia or a burst-suppression pattern. Patients display myoclonic jerks, hiccuping and a profound hypotonia. The few patients who survive past the first week usually sustain profound mental retardation and neurological disability. Brain imaging shows atrophy and a loss of myelin. Rarely, patients present later in life with psychomotor retardation and growth failure. Others have had initial normal development followed by a progressive loss of developmental milestones. Some patients have manifested spinocerebellar degeneration and other symptoms of motor dysfunction [27],... 

Barth, P. G., Majoie, C. B., Gootjes, J. et al. Neuroimaging of peroxisome biogenesis disorders (Zellweger spectrum) with prolonged survival. Neurology 62 439-444, 2004. 

The use of glucocorticoids for tuberculous meningitis remains controversial. The administration of steroids such as oral prednisone, 60 to 80 mg/ day (1 to 2 mg/kg/day in children), or 0.2 mg/kg/day of IV dexametha-sone, tapered over 4 to 8 weeks, improves neurologic sequelae and survival in adults and decrease mortality, long-term neurologic complications, and permanent sequelae in children. 

Colledge NR, Wilson 1A, Macintyre CC et al. (1994) The prevalence and characteristics of dizziness in an elderly community. Age Ageing 23(2) 117-120 The Consensus Committee of the American Autonomic Society and the American Academy of Neurology. (1996) Consensus statement on the definition of orthostatic hypotension, pure autonomic failure, and multiple system atrophy. Neurology 46(5) 1470 Cooper C, Atkinson El, lacobsen SI et al. (1993) Population-based study of survival after osteoporotic fractures. Am 1 Epidemiol 137(9) 1001-1005 Cummings SR and Melton LI (2002) Epidemiology and outcomes of osteoporotic fractures. Lancet 359(9319) 1761-1767... 

GB interferes with neural synapses. It causes overstimulation of the nervous system, which in turn causes over-reactivity in the muscles and malfunctioning of various body organs. Exposure to GB will result in massive congestion of enzymes and fluids in all the major organs, throughout the nervous system, and within the brain. Those who survive exposure may suffer permanent neurological damage.1... 

Effect of Dose and Duration of Exposure on Toxicity. The severity of neurological effects in humans and animals after acute oral exposure to cyanide is dose-related (Chen and Rose 1952 Lasch and El Shawa 1981). Central nervous system effects have been observed following acute-duration exposures (Levine and Stypulkowski 1959a) and chronic-duration exposures (Hertting et al. 1960), via the inhalation and oral routes. Necrosis is the most prevalent central nervous system effect following acute-duration exposure to high concentrations of cyanide, whereas demyelination is observed in animals that survive repeated exposure protocols (Bass 1968 Ibrahim et al. 1963). 

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