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plications, cyanotic congenital heart disease, and shock from many causes The essential pathologic change in DIC is the occurrence of widespread brin thrombi in small vessels, resulting in numerous small infarctions of many organs, including the brain Sometimes DIC is manifest by a hemorrhagic diathesis in which petechial hemorrhages are situated around small penetrating vessels In some cases cerebral hemorrhage is quite extensive, similar to a primary hypertensive hemorrhage The main reason for the hemorrhage is the consumption of platelets and various clotting factors that occurs during brin formation; in addition, brin degradation products have anticoagulant properties of their own The diffuse nature of the neurologic damage may suggest a metabolic rather than a vascular disorder of the brain In the absence of a clear metabolic, infective, or neoplastic cause of an encephalopathy, the onset of acute and uctuating focal neurologic abnormalities or a generalized and sometimes terminal neurologic deterioration during the course of a severe illness should arouse suspicion of DIC, and coagulation factors and brin split products should be measured Platelet counts are invariably depressed and there is evidence of consumption of brinogen and other clotting factors, indicated by prolonged prothrombin and partial thromboplastin times In the related illness abbreviated as HELLP mentioned previously, women with eclampsia develop liver failure and thrombocytopenia; the contribution of this limited form of DIC to the eclamptic effects on the nervous system have not been established (see earlier discussion of eclampsia)

critical is identifying and isolating your high-risk products and separating them in your mind from the diversi ed portfolio When your objective is to place your portfolio risk somewhere centered on the ef cient frontier, you have high- and low-risk components to that objective If the high-risk components have a risk reversal, sell-buy-sell, or short option premium built around the position, you can raise the ef ciency of your risk Of the many spread strategies we discuss, the best tools for management of risk are the simple option spreads selling premium or using short delta to offset risk You can be an excellent portfolio manager by following some simple rules about markets and using options: Options are a fantastic independent investment and addition to any portfolio Options create opportunity to manage risk or capitalize on movement with decreased risk The keys discussed throughout this book are that you watch your volatility and use some other people s money to pay for your positions by selling premium Don t overanalyze We all overanalyze everything in nancial markets We nd unnecessary reasons for growth where growth is natural Setbacks in growth and periods of negativity are also natural It has happened several times before and will happen again Use your option strategies wisely The worst thing to watch is a trader who will spend 90 percent of his option investment adjusting and protecting an option trade until there is no way to win If you re wrong the market, be wrong and learn from it Risk controls should be hard objectives even if you cannot place

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sequential biopsy of numerous sites (fat pad, kidney, liver) Also, if the sural nerve is severely depopulated of nerve bers, the amount of congophilic staining and the characteristic birefringence may be meager and yield a spuriously negative result It is also critical to assure the accuracy of congophilic staining by comparison with positive and negative control tissue from the same laboratory The CSF has a normal or mildly elevated protein concentration but this does not distinguish the neuropathic process from many others Lachmann and colleagues have emphasized that 10 percent of patients who appear by all the usual criteria to have primary amyloidosis will turn out in the end to have a genetic type However, only a small proportion of the latter group has a monoclonal gammopathy and it tends to be of low concentration (estimated to occur in one quarter of familial cases but we have not encountered it) This difference and the rapid progression of the primary acquired form assist in distinguishing it from the genetic type In addition to the more slowly evolving familial types, the differential diagnosis of acquired amyloid neuropathy includes the myelomatous varieties, toxic and nutritional small- ber neuropathies, paraneoplastic polyneuropathy, Sjogren disease, and an idi opathic small- ber sensory neuropathy, all of which can cause pain and which we have encountered more frequently than amyloidosis The hereditary amyloid polyneuropathies are discussed further on (page 1160) Treatment The prognosis is dismal and attempts at immunomodulation, immunosuppression (which may help the renal disease), or removal of amyloid by plasma exchange have been marginally effective The most recent approach has been bone marrow suppression with high doses of melphalan followed by stem-cell replacement (harvested from the patient) Several such patients have survived for years with marked improvement in the neuropathy Pain is a serious problem that may be treated with transcutaneous fentanyl patches or with oral narcotic medications Orthostatic hypotension responds to the use of leg stockings and mineralocorticoids as well as sleeping with the bed elevated at the head so that the patient s entire body is angled down toward the feet Chronic In ammatory Demyelinating Polyradiculoneuropathy This form of polyneuropathy was separated from acute in ammatory polyradiculopathy, or GBS, by Austin in 1958 on the basis of a prolonged and relapsing course, enlargement of nerves, and responsiveness to corticosteroids Excluding the duration of evolution, there are numerous clinical similarities between the acute and chronic forms Both are widespread polyradiculoneuropathies, usually with cytoalbuminologic dissociation of the CSF (raised protein concentration with fewer or no cells); both exhibit nerve conduction abnormalities characteristic of a demyelinating neuropathy (reduced conduction velocity and partial conduction block in motor nerves), and pathologically, both show similar multifocal perivenous in ammatory in ltrates But there are also important differences, the most evident of which are the mode of evolution and prognosis As a rule, CIDP begins insidiously and evolves slowly, either in a steadily progressive or stepwise manner, attaining its maximum severity after several months or longer From the beginning it may be asymmetrical or involve the arms predominantly However, in a small proportion of patients (16 percent in the series of McCombe et al, and a smaller proportion in our own series) the disease at rst emerges from a mild or moderate case of GBS In.

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