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aseptic venous occlusion, is still of uncertain value, but it is usually administered as well (see Chap 34) Septic Cavernous Sinus Thrombophlebitis This condition is usually secondary to infections of the ethmoid, sphenoid, or maxillary sinuses or the skin around the eyes and nose, sometimes originating in a seemingly innocuous lesion Occasionally, no antecedent infection can be recognized In addition to headache, high uctuating fever, and signs of systemic toxicity, there are characteristic local effects Obstruction of the ophthalmic veins leads to chemosis, proptosis, and edema of the ipsilateral eyelids, forehead, and nose The retinal veins become engorged, and this may be followed by retinal hemorrhages and papilledema More often, however, vision in the affected eye is lost by a yet unde ned type of optic neuropathy as noted below, without visible alterations in the fundus Involvement of the third, fourth, sixth, and ophthalmic division of the fth cranial nerves, which lie in the lateral wall of the cavernous sinus (Fig 34-32), leads to ptosis, varying degrees of ocular palsy, pain around the eye, and sensory loss over the forehead Within a few days, spread through the circular sinus to the opposite cavernous sinus results in bilateral symptoms The posterior part of the cavernous sinus may become infected via the superior and inferior petrosal veins without the occurrence of orbital edema or ophthalmoplegia but usually with abducens and facial paralysis The CSF is usually normal unless there is an associated meningitis or subdural empyema The only effective therapy in the fulminant variety, associated with thrombosis of the anterior portion of the sinus, is the administration of high doses of antibiotics aimed at coagulase-positive staphylococci and probably gram-negative pathogens as well As with septic lateral sinus phlebitis, anticoagulants have been used, but their value has not been proved In our cases, the cranial nerve palsies have resolved to a large extent, but visual loss, if it occurs, tends to remain, with ndings suggestive of infarction of the retroorbital part of the optic nerve; the mechanism of this complication is not clear Cavernous sinus thrombosis must be differentiated from mucormycosis infection of the sinuses and orbital cellulitis, which usually occur in patients with uncontrolled diabetes, and from other fungus infections (notably Aspergillus), carcinomatous invasion of the sphenoid bone, and sphenoid wing meningioma Septic Thrombosis of the Superior Sagittal (Longitudinal) Sinus This may be asymptomatic, but more often there is a clinical syndrome of headache, unilateral convulsions, and motor weakness, rst on one side of the body, then on the other, due to extension of the thrombophlebitis into the superior cerebral veins Papilledema and increased intracranial pressure almost always accompany these signs Severe generalized and vertex headache is a typical complaint in the awake patient Because of the localization of function in the cortex that is drained by the sinus, the weakness may take the form of a crural (lower limb) monoplegia or, less often, of a paraplegia A corticosensory loss may occur in the same distribution Homonymous hemianopia or quadrantanopia, aphasia, paralysis of conjugate gaze, and urinary incontinence (in bilateral cases) have also been observed As in the case of aseptic thrombosis, loss of the ow void in the superior sagittal sinus in the MRI is diagnostic, and the clot may be visualized if the correct imaging sequences are used A similar change can be seen on axial images of the contrastenhanced CT scan by altering the viewing windows so as to show the clot within the posterior portion of the sagittal sinus The CT.

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The goal of buying a call option is to gain the right to a long position in the underlying asset at a particular price with limited risk This can be either an independent investment or an enhancement of risk control to another position The advantage is that the call option is obtaining a long position with only the premium paid for the option at risk Let s look at an example of a call purchase using an at-the-money call on Home Depot common stock and the breakeven scenario for the purchase In Figure 41 we show the purchase of one May $2000 call option for Home Depot, Inc In the trade column, 1 represents the purchase quantity This gives the buyer the right to purchase 100 shares of Home Depot common stock at $2000 per share The last column shows the purchase price of $233 per share In the Acutals row at the top of the gure, you can see that the price of the underlying market at the time of this purchase was $2071 With the call strike price at $2000 and the underlying Home Depot stock at $2071, the call option has an intrinsic value of $071

with the chronic use of disul ram in the treatment of alcoholism Its neurotoxic effects have been attributed to the action of carbon disul de, which is produced during the metabolism of the drug, and is known to cause polyneuropathy and sometimes an optic neuropathy in workers in the viscose rayon industry Pathologic data, though scant, tend to discredit this notion, insofar as disul ram evokes a wallerian type of axonal degeneration, whereas carbon disul de neuropathy is characterized by swollen (giant) axons that are lled with neuro laments (Bouldin et al) Other Pharmaceutical Agents Causing Polyneuropathy Some patients who have taken phenytoin for decades may show an absence of ankle and patellar re exes, a mild distal symmetrical impairment of sensation, reduced conduction velocity in the peripheral nerves of the legs, and, rarely, weakness of the distal musculature The mechanism and frequency of this complication are not clear The cholesterol lowering statin drugs have been implicated in a painful, paresthetic distal axonal polyneuropathy, often, it has been stated, with retained re exes (Geist et al) More often the problem with statins is one of a toxic myopathy The frequency of polyneuropathy is very low but, if no other explanation is identi ed, it may be advisable to discontinue the drug Colchicine has long been known to cause a myopathy, but a few cases of predominantly axonal sensory neuropathy have also been reported Thalidomide, which can produce sensory polyneuropathy, had been withdrawn from the market but is now being used again experimentally for graft-versus-host disease and for drug-resistant erythema nodosum, leprous eruptions, and apthous stomatitis, particularly in AIDS patients also as an experimental antineoplastic agent for vascular tumors The thalidomide polyneuropathy is dosedependent and can be anticipated at certain levels of administration Severe botulinum poisoning and the prolonged use of neuromuscular blocking agents is said to leave some patients with a distal axonopathy, but this must be rare Residual effects of polyneuropathy were seen in patients with the toxic eosinophilia-myalgia syndrome; the problem was traced to the ingestion of adulterated L-tryptophan which had been used in nonprescription drugs for insomnia (page 1211) One patient under our care suffered permanent are exic quadriplegia There may be an eosinophilic in ltrate in nerves, but the neuropathy is probably the result of a direct toxic mechanism A sensory neuropathy resulting from excessive pyridoxine ingestion, alluded to earlier, is still seen among individuals who take huge doses of vitamin supplements Amitriptyline is capable of producing paresthesias, but the effect seems to be idiosyncratic and infrequent The anesthetic agent trichloroethylene, as with the aforementioned stilbamidine, has a predilection for cranial nerves, particularly the fth The neurotoxicity is apparently due to dichloroacetylene, formed as a decomposition product of trichloroethylene The neuropathic potential of nitrous oxide has already been mentioned.

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