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premiums in agriculture and energy were especially affected through most of this period The major consideration to the in ated premium is the elevated risk to option traders As we discuss option strategies, it is important to understand that the increased volatility can work in favor of the option trader, but also represent a signi cant element of risk Also, volatility does not necessarily result in higher pricing; it is the indicator of dramatic swings in price Increased market volatility is often caused by increased interest on the part of speculators and large institutional traders regardless of the current direction of market prices If a market is demonstrating volatility, then high-risk traders are more attracted to short-term trading opportunities This perpetuates the cycle and further increases short-term volatility More money moving means more volatile price swings In this way volatility becomes a self-ful lling prophecy as one form of volatility attracts another As markets experience decreasing assets from negative market information, volatility can increase as traders and investors see downward trends develop and begin running for the door Volatility is also not a directional indicator in that as markets peak or bottom, volatility can decrease until a new direction is established Volatility also builds into news events, earnings reports, and other known but unpredictable market events After the event, volatility tends to reduce somewhat quickly, reverting back to preevent levels There is a tendency to see increases in volatility as markets rise and decrease as markets fall This is an aftereffect and not necessarily a leading indication The explanation for increasing volatility in uptrending markets may be more psychological than anything else, in that many traders do not understand short-trading the market, so money ows more freely into uptrends creating increasing

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The preceding illustration shows the initial color setting In the next illustration, the colors for the marker are adjusted so that we can show a circle with some depth to it We have adjusted the primary and secondary colors

onstration of electrocerebral silence ( at or, more accurately, isoelectric EEG, shown rst by Schwab), which is considered to be present if there is no electrical potential of more than 2 mV during a 30-min recording (except for artifacts created by the ventilator, ECG, or surrounding electrical devices) We still follow this practice in almost all cases There are cases on record in which a patient with an isoelectric EEG has had preserved brainstem re exes It must also be emphasized that cerebral unresponsivity and a at EEG do not always signify brain death; both may occur and may be reversible in states of profound hypothermia or intoxication with sedative-hypnotic drugs and immediately following cardiac arrest For this reason, it has been recommended that the diagnosis of brain death not be entertained until several hours have passed from the time of initial observation If the examination is performed at least 6 h after the ictus and there is prima facie evidence of overwhelming brain injury from trauma, anoxia, or massive cerebral hemorrhage (the most common conditions causing brain death), there is no need for serial testing If cardiac arrest was the antecedent event, or the cause of neurologic damage is unclear, or drug or alcohol intoxication could reasonably have played a role in suppressing the brainstem s re exes, it is advisable to wait about 24 h before pronouncing the patient dead Toxicologic screening of the serum or urine is requisite in the latter circumstances Evoked potentials show interesting but variable abnormalities in brain-dead patients but are not of primary value in the diagnosis Some centers use nuclide brain scanning or cerebral angiography to demonstrate an absence of blood ow to the brain, equating this with brain death; but there are technical pitfalls in the use of these methods, and it is preferable to keep the diagnosis of death primarily clinical The same can be said for transcranial Doppler sonography, which in brain death shows a to-and-fro pendel uss blood- ow pattern in the basal vessels In our experience, the main dif culties that arise in relation to brain death are not the technical issues but those involving the sensitive conversations and relationships with the family of the patient and, to a lesser extent, with other medical professionals These tasks often fall to the neurologist From our experience, it is best not to embark on clinical or EEG testing for brain death unless there is a clear intention on the part of the physician to remove the ventilator or request organ donation at the end of the process The process and its intended outcome should be explained to the family The family s desires regarding organ transplantation should be sought after adequate time has passed for them to absorb the shock of the circumstances Neurologists must, of course, resist pressures from diverse sources that might lead them to the premature designation of a state of brain death At the same time, it should be clari ed that while brain death is an operational state that allows transplantation to proceed and mandates withdrawal of ventilation and blood pressure support, patients with overwhelming brain injuries need not ful ll these absolute criteria in order for medical support to be withdrawn A task force for the determination of brain death in children has recommended the adoption of essentially the same criteria as for adults Because of the great dif culty in evaluating the status of nervous function in relation to perinatal insults, they have suggested that a diagnosis of brain death not be made before the seventh postnatal day and that the period of observation be extended to 48 h As with adults, the possibility of reversible brain dysfunction from toxins, drugs, hypothermia, and hypotension must always be considered.

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