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states of intellectual development in the child, but Piaget s theory has been criticized as being too anecdotal and lacking the quantitative validation that could be derived only from studies of a large normal population Further, it does not take into account the individual s special abilities, which do not develop and reach their maximum at the same time as the more general intellectual capacities Further details can be found on page 501 One would suppose that in neurology, where one is exposed to so many diseases affecting the cerebrum, it might be possible to verify one of these several theories of intelligence and to determine its anatomy Presumably the g factor of intelligence would be maximally impaired by diffuse lesions, in proportion to the mass of brain involved (expressed by Lashley as the mass-action principle ) Indeed, according to Chapman and Wolff, there is a correlation between the volume of tissue lost and a general de cit of cerebral function Others have disagreed, claiming that no universal psychologic de cit has been linked to lesions affecting particular parts of the brain Probably the truth lies between these two divergent points of view According to Tomlinson and colleagues, who studied the effects of vascular lesions in the aging brain, lesions that involve more than 50 mL of tissue cause some general reduction in performance, especially in speed and capacity to solve problems Piercy, on the other hand, found correlations only between speci c intellectual de cits and lesions of particular parts of the left and right hemispheres These are discussed in Chap 22 It is surprising that lesions of the frontal lobes, and particularly the prefrontal regions, which so profoundly disorder planning and executive functions, do not measurably affect IQ except in subtests speci c to these skills The authors conclude from personal experience and from evidence provided by neurologic studies that intelligence is a gestalt of multiple primary abilities, each of which seems to be inherited and each of which has a separate but as yet poorly delineated anatomy Yet we would disagree with Thurstone and with Gardner that these special abilities are of equivalent rank with regard to what is generally considered as intelligence We would attach a disproportionate importance to some of them (linguistic and mathematical and perhaps spatial-dimensional abilities) These last abilities are integral to ideation and problem solving and are largely absent in the mentally retarded and lost early in dementing diseases To the extent that facility with general mental performance (that requiring the manipulation of abstract symbols and thoughts) marks an individual as intelligent and that these correlate with each other, we nd Spearman s g factor to be a credible but not completely satisfying explanation for intelligence Neurologic data certainly do not exclude the possibility of a g factor one that is unavoidably measured in many different tests of cerebral functions It is expressed in thinking and abstract reasoning and is operative only if the connections between the frontal lobes and other parts of the brain are intact Attention, drive, and motivation are noncognitive psychologic attributes of fundamental importance, the precise anatomy and physiology of which remain to be identi ed A current account of the subject of IQ and intelligence can be found in the monograph by Mackintosh Also, we would insist that retentive memory and capacity to learn constitute a separate cognitive entity, with its own neuroanatomic localization The relationships of some of these special abilities have been thoughtfully analyzed by Luria (see the section on frontal lobes in Chap 22) An even more complex problem arises in the neurologic analysis of the highest human achievement and the method of human.

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advancement, namely creativity In some ways, creativity is tied to special skills along the lines of Gardner s modality-based intelligence, particularly as it relates to artistic work, but the brain structures involved in aesthetics and abstraction are entirely obscure, as Zeki points out Some insight is gained from the fact that intelligence and problem-solving ability are innately but only roughly tied to creativity and that there are congenital absences and de ciencies of appreciation of visual, artistic, or mathematical skills As pointed out in the following chapter, traits such as creativity almost certainly do not reside in a particular lobe or structure of the brain but may depend on the overdevelopment of certain associative areas as well as on frontal lobe drive and, of course, are fully manifest only by educational exposure

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Dementia is a syndrome consisting of a loss of several separable but overlapping intellectual abilities and presents in a number of different combinations These varied constellations of intellectual de cits constitute the pre-eminent clinical abnormalities in several cerebral diseases and are sometimes (eg, in Alzheimer disease) virtually the only abnormalities, in which case the syndrome is virtually equivalent to the disease The most common types of dementing diseases and their relative frequency are listed in Table 21-1 What is noteworthy about the gures in this table is the apparently high level of accuracy of diagnosis Rather consistently, postmortem examination con rms the accuracy of the clinical diagnosis of Alzheimer disease is in excess of 80 percent when more rigid research criteria are used (Table 21-2) In many cases, the degenerative diseases can be differentiated by one or two characteristic clinical features, but these distinctions may be dif cult to Table 21-1 The common types of dementing diseases and their approximate frequencies (See also Table 21-2)

RELATIVE DEMENTING DISEASE FREQUENCY,

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Cerebral atrophy, mainly Alzheimer but including Lewy-body, Parkinson, frontotemporal, and Pick disease Multi-infarct dementia Alcoholic dementia Intracranial tumors Normal-pressure hydrocephalus Huntington chorea Chronic drug intoxications Miscellaneous diseases (hepatic failure; pernicious anemia; hypo- or hyperthyroidism; dementias with amyotrophic lateral sclerosis, cerebellar atrophy; neurosyphilis; Cushing syndrome, Creutzfeldt-Jakob disease; multiple sclerosis; epilepsy) Cerebral trauma AIDS dementia Pseudodementias (depression, hypomania, schizophrenia, hysteria, undiagnosed)

This parameter is used to specify whether to display an export dialog This parameter is used to specify the format of the paper: DIN A4 (DINA4) Letter (LETTER) Ledger 11 x 17 Inch (LEDGER) Invoice 55 x 85 Inch (INVOICE) Executive 725 x 105 Inch (EXECUTIVE) A5 128 x 210 mm (DINA5) A4-0 1682 x 2378 mm (DINA40) A3 297 x 420 mm (DINA3) A2-0 1189 x 1682 mm (DINA20) A2 420 x 594 mm (DINA2) A1 594 x 841 mm (DINA1) A0 814 x 1189 mm (DINA0) Broadsheet 17 x 22 Inch (BROADSHEET)

SOURCE:

We can use the option chain in Figure 88 to construct our condor spread The options listed are $250 per point, and we would typically be looking at an option spread that is much wider than what is displayed so as to allow the market signi cant trading room, but we can get down the basics of the spread We consider selling the May options because of the accelerated time decay and decreased time for the market to break outside the trading range Assume a sale of the May 855 call option at 3510 and the purchase of the May 865 call at 3060 while selling the May 825 put for 4050 and buying the May 815 put for 3650 On the call side we net a credit of 450, and on the put side we net a credit of 400 for a total credit of 850 Our maximum risk is the distance between the two strike prices on either side of the market minus the premium captured, so in this case our maximum risk is 150 $250 or $375 plus costs of trading four option positions The maximum pro t in this example is 850 $250 or $2,125 The risk-to-reward ratio on this condor is exceptional Let s look at a model of the iron condor for pro t and loss in Figure 89 The model shows the maximum risk on both sides of the spread if the price was out of the range of the purchased option strike prices

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Table 21-2 Neuropathologic diagnoses for 261 cases with a clinical diagnosis of Alzheimer disease: Data from the Massachusetts ADRC Brain Registry, 1984 1993a

Alzheimer disease Parkinson and Alzheimer diseases Lewy-body disease Pick disease Multiple infarcts Binswanger disease Corticobasal ganglionic degeneration Mixed dementia Other Total

218 16 8 6 5 1 1 1 5 261

835 61 31 23 19 04 04 04 19 100

This parameter is used to specify the page orientation for the export format: Portrait (PORTRAIT) Landscape (LANDSCAPE)

ber of factors have been identi ed as associated with a progression of a state to indisputable dementia These include elevated blood pressure, signal changes in the cerebral white matter on MRI, and perhaps not surprisingly certain biologic markers that are connected to Alzheimer disease At the moment, the clinician must simply counsel caution and reassurance in advising patients with mild memory impairment and exclude treatable causes Nonetheless, if the symptoms are progressive or interefere in any consistent way with other mental functions or with the performance of daily activities, a dementing illness is likely

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