Hi,
Thank you for your concern. This is Phil's wife Pamela. I am very concerned about this also although the Dr. said they are confident that it is this single pill that is causing this and is just taking a long to get out of his system. With Phil's impaired Kidney function things are probably taking longer than usual.
Phil had a Brain MRI and EEG and the neurologist said there was no brain damage that he could see. Everything looked good. If things don't completely clear up we will of course go in for a second opinion. He also was tested for a stroke amongst many other things and everything else was fine also.
The pill was taken within 5 to 15 minutes before the incident so it is most likely the definite cause. He had never taken one before that. For the first 27 hours that Phil was in the Hospital he was not able to communicate with us to tell us that he had taken the pill so you can imagine how frightful this was. The thing that kept me going is that he did show gradual improvement every few hours.
I want to let everyone know that he is fine and resting. If anyone got any strange texts or emails I apologize he is trying but is still not 100%. He is back home though and back online and is going in for a follow up tomorrow.
I appreciate everyone's concerns. This happened Sunday night and this has been an extremely difficult time for us.
Thank you,
Pamela Hernon
Oxidative Stress in Brain Ischemia - Love - 2006 - Brain Pathology - Wiley Online Library
Brain ischemia initiates a complex cascade of metabolic events, several of which involve the generation of nitrogen and oxygen free radicals. These free radicals and related reactive chemical species mediate much of damage that occurs after transient brain ischemia, and in the penumbral region of infarcts caused by permanent ischemia. Nitric oxide, a water- and lipid-soluble free radical, is generated by the action of nitric oxide synthases. Ischemia causes a surge in nitric oxide synthase 1 (NOS 1) activity in neurons and, possibly, glia, increased NOS 3 activity in vascular endothelium, and later an increase in NOS 2 activity in a range of cells including infiltrating neutrophils and macrophages, activated microglia and astrocytes. The effects of ischemia on the activity of NOS 1, a Ca2+-dependent enzyme, are thought to be secondary to reversal of glutamate reuptake at synapses, activation of NMDA receptors, and resulting elevation of intracellular Ca2+. The up-regulation of NOS 2 activity is mediated by transcriptional inducers. In the context of brain ischemia, the activity of NOS 1 and NOS 2 is broadly deleterious, and their inhibition or inactivation is neuroprotective. However, the production of nitric oxide in blood vessels by NOS 3, which, like NOS 1, is Ca2+-dependent, causes vasodilatation and improves blood flow in the penumbral region of brain infarcts. In addition to causing the synthesis of nitric oxide, brain ischemia leads to the generation of superoxide, through the action of nitric oxide synthases, xanthine oxidase, leakage from the mito-chondrial electron transport chain, and other mechanisms. Nitric oxide and superoxide are themselves highly reactive but can also combine to form a highly toxic an ion, peroxynitrite. The toxicity of the free radicals and peroxynitrite results from their modification of macromolecules, especially DNA, and from the resulting induction of apoptotic and necrotic pathways. The mode of cell death that prevails probably depends on the severity and precise nature of the ischemie injury. Recent studies have emphasized the role of peroxynitrite in causing singlestand breaks in DNA, which activate the DNA repair protein poly(ADP-ribose) polymerase (PARP). This catalyzes the cleavage and thereby the consumption of NAD+, the source of energy for many vital cellular processes. Over-activation of PARP, with resulting depletion of NAD+, has been shown to make a major contribution to brain damage after transient focal ischemia in experimental animals. Neuronal accumulation of poly(ADP-ribose), the end-product of PARP activity has been demonstrated after brain ischemia in man. Several therapeutic strategies have been used to try to prevent oxidative damage and its consequences after brain ischemia in man. Although some of the drugs used in early studies were ineffective or had unacceptable side effects, other trials with antioxidant drugs have proven highly encouraging. The findings in recent animal studies are likely to lead to a range of further pharmacological strategies to limit brain injury in stroke patients.
Brain ischemia, also known as cerebral ischemia, is a condition in which there is insufficient blood flow to the brain to meet metabolic demand.[1] This leads to poor oxygen supply or cerebral hypoxia and thus to the death of brain tissue or cerebral infarction / ischemic stroke.[2] It is a sub-type of stroke along with subarachnoid hemorrhage and intracerebral hemorrhage.[3]
Ischemia leads to alterations in brain metabolism, reduction in metabolic rates, and energy crisis.[4]
There are two types of ischemia: focal ischemia, which is confined to a specific region of the brain; and global ischemia, which encompasses wide areas of brain tissue.
The main symptoms involve impairments in vision, body movement, and speaking. The causes of brain ischemia vary from sickle cell anemia to congenital heart defects. Symptoms of brain ischemia can include unconsciousness, blindness, problems with coordination, and weakness in the body. Other effects that may result from brain ischemia are stroke, cardiorespiratory arrest, and irreversible brain damage
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