In both clinical observation and animal models, infants have experienced seizures a period of hours after an initial asphyxia event, the effect that these seizures have in terms of neural damage however, is not known. Meldrum (1999) seizures as the sudden simultaneous firing of cells in a particular part of the brain. This is shown as high amplitude/high frequency EEG waves; and could cause physical convulsions of the body. The effect to the brain is a lot more wide spread with consequences that occur both during and for some time after the seizure activity. A paper by Fernandes, Dube, Boyet, Marescaux and Nehlig (1999) explained that knowing how the brain would react to an epileptic event after a period of asphyxia at one point in development,
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Fernandes et al (1999) performed a study on 10 day old, 21-day old and adult rats to determine whether there was a relationship between neuronal damage and hyper metabolism during an induced epileptic event. They found an increase in metabolic rate in the P10 and P21 rats which was mostly isolated to the fore rain and cortical regions and did not extend into the hypothalamus or brainstem regions however, the P21 group did show a varying degree of damage among subjects therefore indicating that some did experience neuronal damage. The P10 rats did not show any neuronal damage caused by the seizure activity. Fernandes et al (1999) explained that these two populations did not support the relationship between neuronal damage and hyper metabolism. However, the adult rats showed both a metabolic increase as well as neuronal damage that diffused from cortical regions into the thalamic, brainstem and hypothalamic regions of the brain also. Therefore, immature rats appear to be able to experience a sustained duration of increased metabolic rate caused by epileptic activity with little chance of leading to brain …show more content…
They explained the developing brain appeared to have some protective ability towards ischemic and anoxic events but why is this, was not known. The rats in this experiment were exposed to 100percent nitrogen that was bubbled through water and delivered in gas form at 37degrees Celsius to produce anoxia. Duffy et al (1975) found an inverse correlation between survival time of the subjects and age, with the term foetuses surviving significantly longer than adults, 7-day old rats and 1-day old rats. They also found that energy consumption was significantly smaller in the immature rats compared to the adult rats in proportion to their typical metabolic rates. Another study by Vasconcelos, Farrandon and Nehlig (2002) also looked at the cerebral metabolic and its effect by seizures, as well as looking at the cerebral blood flow to the affected region. They wanted to determine whether it were a combination of a depletion of cerebral blood supply and hyper metabolism which caused neural damaged induced by seizures. Vasconcelos et al (2002) found in the P21 rats there was an increase in the metabolic demand which was not matched with an increase in cerebral blood flow, these results were not as significant as in the adult rat population however. In the P10 rats there was also a mismatch between blood flow to the area and
Fernandes et al (1999) performed a study on 10 day old, 21-day old and adult rats to determine whether there was a relationship between neuronal damage and hyper metabolism during an induced epileptic event. They found an increase in metabolic rate in the P10 and P21 rats which was mostly isolated to the fore rain and cortical regions and did not extend into the hypothalamus or brainstem regions however, the P21 group did show a varying degree of damage among subjects therefore indicating that some did experience neuronal damage. The P10 rats did not show any neuronal damage caused by the seizure activity. Fernandes et al (1999) explained that these two populations did not support the relationship between neuronal damage and hyper metabolism. However, the adult rats showed both a metabolic increase as well as neuronal damage that diffused from cortical regions into the thalamic, brainstem and hypothalamic regions of the brain also. Therefore, immature rats appear to be able to experience a sustained duration of increased metabolic rate caused by epileptic activity with little chance of leading to brain …show more content…
They explained the developing brain appeared to have some protective ability towards ischemic and anoxic events but why is this, was not known. The rats in this experiment were exposed to 100percent nitrogen that was bubbled through water and delivered in gas form at 37degrees Celsius to produce anoxia. Duffy et al (1975) found an inverse correlation between survival time of the subjects and age, with the term foetuses surviving significantly longer than adults, 7-day old rats and 1-day old rats. They also found that energy consumption was significantly smaller in the immature rats compared to the adult rats in proportion to their typical metabolic rates. Another study by Vasconcelos, Farrandon and Nehlig (2002) also looked at the cerebral metabolic and its effect by seizures, as well as looking at the cerebral blood flow to the affected region. They wanted to determine whether it were a combination of a depletion of cerebral blood supply and hyper metabolism which caused neural damaged induced by seizures. Vasconcelos et al (2002) found in the P21 rats there was an increase in the metabolic demand which was not matched with an increase in cerebral blood flow, these results were not as significant as in the adult rat population however. In the P10 rats there was also a mismatch between blood flow to the area and