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drome of delirium and extreme hyperthermia More interesting are the strokes that arise during and just after cocaine use Here, as emphasized by Levine and colleagues (1991), a clear distinction should be made between the complications of cocaine hydrochloride (the usual form of ingestable cocaine) and the alkaloid form, or crack cocaine The former, when injected intravenously more so than when used intranasally, is prone to cause cerebral hemorrhage as a result of acute hypertension, similar to the bleeding that may be precipitated by other sympathomimetic drugs such as amphetamine and phenylpropanolamine Both subarachnoid and intracerebral hemorrhage may result Or, the features of hypertensive encephalopathy are precipitated, including changes in the posterior white matter of the cerebral hemispheres that are so striking on imaging studies The strokes with crack cocaine, however, are more often ischemic, typically involving the territory of a large vessel Some ambiguity attends the vasculopathy induced by crack cocaine, less often by cocaine hydrochloride, and by the amphetamines There are undoubted instances of a true cerebral in ammatory vasculitis, perhaps of a hypersensitivity type such as those reported with biopsy veri cation by Krendel and colleagues and by Merkel and associates and others What is confusing about these cases is the normal angiographic appearance in many instances and large-vessel occlusions in others, in contrast to the pathologic changes, which are concentrated in small cortical vessels Furthermore, many cases seem to be of an entirely different type, displaying long segments of vascular attenuation in the angiogram and no evidence of an in ammatory process in biopsy or autopsy material The correct treatment, aside from lowering the blood pressure, is uncertain Crack cocaine may also cause a choreiform disorder ( crack dancing ), not unlike that associated with antiphospholipid antibody but generalized rather than focal (see further on); usually there are small infarctions in the basal ganglia, but an immune mechanism has also been suggested Another type of small-vessel arteritis occurs as a hypersensitivity phenomenon Often it is associated with an allergic skin lesion (Stevens-Johnson vasculopathy or a leukocytoclastic vasculitis) The clinical picture does not resemble that of polyarteritis nodosa, but the central or peripheral nervous system is affected in rare instances The response to corticosteroids is excellent Yet another ill-de ned form of vasculitis has been described by Susac and colleagues (Susac syndrome) This is a microangiopathy affecting mainly the brain and retina Psychiatric symptoms, dementia, sensorineural deafness, and impairments of vision are the clinical manifestations Funduscopy (multiple retinal artery branch occlusions) and arteriography manifest evidence of the vasculopathy The patients seem to respond to steroid therapy Only biopsy material has been examined Mixed essential cryoglobulinemia, a vasculitic disorder that more often affects the peripheral than the central nervous system, may nonetheless produce an encephalopathy Behcet Disease This disorder may suitably be considered here, since it is essentially a chronic, recurrent vasculitis, involving small vessels, with prominent neurologic manifestations It is most common in Turkey, where it was rst described, in other Near Eastern countries, and in Japan, but it occurs throughout Europe and North America, affecting men more often than women The disease was originally distinguished by the triad of relapsing iridocyclitis and recurrent oral and genital ulcers, but it is now recognized to be a systemic disease with a much wider range of symptoms, including.

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erythema nodosum, thrombophlebitis, polyarthritis, ulcerative colitis, and a number of neurologic manifestations, some of them encephalitic or meningitic in nature The most reliable diagnostic criteria, according to the International Study Group that assembled data on 914 cases from 12 medical centers in 7 countries, were recurrent aphthous or herpetiform oral ulceration, recurrent genital ulceration, anterior or posterior uveitis, cells in the vitreous or retinal vasculitis, and erythema nodosum or papulopustular lesions The nervous system is affected in about 30 percent of patients with Behcet disease (Chajek and Fainaru); the manifestations are: recurrent meningoencephalitis, cranial nerve (particularly abducens) palsies, cerebellar ataxia, and corticospinal tract signs There may be episodes of diencephalic and brainstem dysfunction resembling minor strokes A few postmortem examinations have related these small foci of necrosis to a vasculitis, including perivascular and meningeal in ltration of lymphocytes There may also be cerebral venous thrombosis The neurologic symptoms usually have an abrupt onset and are accompanied by a brisk spinal uid pleocytosis (lymphocytes or neutrophils may predominate), along with elevated protein but normal glucose values (in one of our patients, 3000 neutrophils per cubic millimeter were found at the onset of an acute meningitis) As a rule, neurologic symptoms clear completely in several weeks, but they have a tendency to recur, and some patients are left with persistent neurologic de cits Rarely, the clinical picture is that of a progressive confusional state or dementia (see the reviews of Alema and of Lehner and Barnes for detailed accounts) The cause of Behcet disease is unknown We have been unable to detect virus particles in the margins of an ulcerative mouth lesion A pathergy skin test the formation of a sterile pustule at the site of a needle prick is listed as an important diagnostic test by the International Study Group, but on the basis of admittedly limited US expeirence, we and our colleagues have found it to be of questionable value Administration of corticosteroids has been the usual treatment, on the assumption of an autoimmune etiology Since the episodes of disease naturally subside and recur, evaluation of treatment is dif cult.

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nothing The short call is very critical to ensuring that you are not burning up pro ts on premium Managing risk on sector components or sector indices can be handled in much the same fashion selling calls and buying puts This may sound like a broken record, but it is a strategy that works Consider if you were able to capture a 5 percent index premium selling an at-the-money call premium every quarter When we discuss spreads, we talk at length about the covered call, but apply the idea to portfolio management Capturing 5, 10, or 15% annually in call premium against held positions in broad indices or individual components adds a great deal to the bottom line in the long run Offset your put premium costs with short call premium as much as possible, unless you are able to buy puts in a at or negative volatility curve If you are able to place a oor under the market with a low implied volatility put, there is usually a reason why the put options are cheap A small number of people think that this particular security is going down soon This does not mean that you should not buy the put option; it just means that you will get it at a better price and that you should be cautious on the short call premium In our option strategy and spread discussion we talk about managing risk on individual components, so we won t be redundant here The risk to individual component management, especially with options, is micromanagement Diversi cation will take care of a portion of individual risk when the portfolio is viewed as a whole High-risk components are the best candidates for individual management, but you should avoid micromanaging Even the best portfolio managers fall victim to micromanaging from time to time, which is one of the reasons why the indexed funds outperform managed funds at times Micromanagement of a portfolio is costly trading commissions, missed opportunities from being out of a market, and missed objectives from overtrading What is most.