Acute Neuronal Injury: The Role of Excitotoxic Programmed by PDF
Denson G. Fujikawa 2+ within the early Eighties it was once famous that over the top Ca inflow, possibly via 2+ 2+ voltage-gated Ca channels, with a resultant bring up in intracellular Ca, was once linked to neuronal loss of life from cerebral ischemia, hypoglycemia, and standing epilepticus (Siejo 1981). Calcium activation of phospholipases, with arachidonic acid accumulation and its oxidation, producing loose radicals, was once considered a possible mechanism during which neuronal harm happens. In cerebral ischemia and a pair of+ hypoglycemia, power failure used to be considered the cause of over the top Ca inflow, while in prestige epilepticus it was once suggestion that repetitive depolarizations have been in charge (Siejo 1981). in the meantime, John Olney chanced on that monosodium glutamate, the nutrients additive, while given to immature rats, used to be linked to neuronal degeneration within the arcuate nucleus of the hypothalamus, which lacks a blood-brain barrier (Olney 1969). He up this statement with a chain of observations within the Nineteen Seventies that management of kainic acid, which we now comprehend prompts the GluR5-7 subtypes of glutamate receptor, and different glutamate analogues, triggered not just post-synaptic cytoplasmic swelling, but additionally dark-cell degeneration of neurons, while considered by way of electron microscopy (Olney 1971; Olney et al. 1974).
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Denson G. Fujikawa 2+ within the early Nineteen Eighties it used to be famous that over the top Ca inflow, most likely via 2+ 2+ voltage-gated Ca channels, with a resultant raise in intracellular Ca, was once linked to neuronal loss of life from cerebral ischemia, hypoglycemia, and standing epilepticus (Siejo 1981). Calcium activation of phospholipases, with arachidonic acid accumulation and its oxidation, producing unfastened radicals, was once considered a possible mechanism wherein neuronal harm happens.
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They tried to uncover the relevance of anemia, polyneuropathy and treatment with epoetin alfa in connection with end-stage renal disease. Fifty-five patients (mean duration of dialysis 37 months) receiving either hemodialysis (n = 34) or continuous ambulatory peritoneal dialysis (n = 21) were assessed: 22 patients had RLS (40%, diagnostic criteria not mentioned). RLS was related to duration of dialysis (long vs. 01). Patients with RLS had a lower hemoglobin than those who did not (82 vs. 03). There was no relation between the presence of RLS and clinical evidence of peripheral neuropathy, or its severity, as assessed clinically by grading of vibration sense and tendon jerks in the legs and feet.
An MRI study in five patients with RLS demonstrated a decreased iron concentration in the putamen and in the substantia nigra in patients with RLS34. As iron is a co-factor for the dopamine-producing enzyme thyrosine hydroxylase, there is a possible link between iron deficit and a dopaminergic deficit. Lower dopamine concentrations could be the result of low iron levels. Moreover, iron is important for the functioning of dopamine D2 receptors, so that iron deficiency could also induce an impairment of the normal receptor function35.
Ulfberg J, Nyström B, Carter N, Edling C. Restless legs syndrome among men aged 18 to 64 years: An association with somatic disease and neuropsychiatric symptoms. Mov Disord 2001;16:1159–63 7. Rothdach AJ, Trenkwalder C, Haberstock J, et al. Prevalence and risk factors of RLS in an elderly population. The MEMO study. Neurology 2000;54:1064–8 34 EPIDEMIOLOGY 8. Montplaisir J, Boucher S, Poirier G, et al. Clinical, polysomnographic, and genetic characteristics of restless legs syndrome: a study of 133 patients diagnosed with the new standard criteria.
Acute Neuronal Injury: The Role of Excitotoxic Programmed Cell Death Mechanisms