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I/O Resource Manager gives you the ability to provision the I/O bandwidth from the Exadata Storage Server to the database grid by consumer group, database, and category In doing so, I/O Resource Manager, or IORM, delivers the most precious quality of performance consistency Remember that there are really two definitions of performance The definition used by IT personnel has to do with actual timings of discrete or aggregate operations The more important definition comes from users, who have an expectation of performance that trumps the more mundane measurement A SQL query that takes 5 seconds to return results could be seen either as slow if the query was expected to return in 2 seconds or blazingly fast if the expectation was for results in 20 seconds By dividing up the overall bandwidth for a database or cell, IORM lets you ensure that there will be sufficient resources to meet customer expectations IORM, like other resource plan aspects, does not start to limit I/O resources until those resources are oversubscribed, which means that this feature will not waste bandwidth by limiting access when there is enough to spare Instead, IORM guarantees that a particular group of sessions will always get at least a particular percentage of I/O bandwidth The actual implementation of IORM plans gives you a great deal of flexibility, as the next section details

The hallmark of all the hereditary metabolic diseases is psychosensorimotor regression However, those that have their onset in the rst year of life pose extraordinary problems in neurologic diagnosis If the onset is in the rst postnatal months, before the infant has had time to develop the normal complex repertoire of behavior, the rst signs of disease may take the form of subtle delays in maturation rather than of psychomotor regression Departures from normalcy include a lack of interest in the surroundings, a lack of visual engagement, poor head control, an inability to sit up at the usual time, poor hand-eye coordination, and persistence of infantile automatisms Of course, embryologic maldevelopment of the brain may have similar effects, and systemic diseases and other visceral malformations such as cystic brosis, renal disease, biliary atresia and congenital heart disease, chronic infection, malnutrition, and seizures (with drug therapy) may appear to impede psychomotor development Diagnosis becomes somewhat easier in the second half of the rst year, especially if development in the rst half had proceeded normally Then an observant mother, usually one with older children, can perceive a loss of certain early acquisitions, attesting to the progressive nature of a disease The most distinctive members of this category of neurologic disease are the leukodystrophies and the so-called lysosomal storage diseases The leukodystrophies are a group of inherited metabolic diseases of the nervous system characterized by progressive, symmetrical, and usually massive destruction of the white matter of the brain and sometimes of the spinal cord; each type of leukodystrophy is distinguished by a particular abnormal product of degeneration of myelinated bers In the lysosomal storage diseases, there is a genetic de ciency of the enzymes (usually one or more of the acid hydrolases) necessary for the degradation of speci c glycosidic or of peptide linkages in the intracytoplasmic lysosomes, causing nerve cells to become engorged with material that they would ordinarily degrade These metabolites eventually damage the nerve cell or its myelin sheath Most of these diseases are classed as sphingolipidoses It was Brady in 1966 who made the observation that in each of these disorders an increased quantity of sphingolipid accumulated in the brain and other tissues The sphingolipids are a class of intracellular lipids that all have ceramide as their basic structure, but each has a different attached oligosaccharide or phosphorylcholine The rate.

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FIGURE 10-7

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of synthesis of the sphingolipids is normal and their accumulation results from a defect of a speci c lysosomal enzyme that normally degrades each of the glycoproteins, glycolipids, and mucopolysaccharides by removing a monosaccharide or sulfate moiety It is the type of enzyme de ciency and accumulated metabolite, as well as the tissue distribution of the undegradable substrate, that impart a distinctive biochemical and clinical character to each of the diseases in this category The concept of lysosomal storage diseases, introduced by Hers in 1965, excited great interest among neurologists at the time because it provided the potential for prenatal diagnosis and the detection of carriers The diagnosis of this group of diseases has also been facilitated by the use of CT scanning, MRI, and evoked response techniques, which con rm the existence of leukodystrophies, and by the electron microscopic examination of skin, rectal, or conjunctival biopsies, circulating lymphocytes, and cultured amniotic uid cells, which discloses the lysosomal storage material in nonneural cells The activity of most lysosomal enzymes can be determined by exposing them to arti cial chromogenic or uorogenic substrates There are now more than 40 lysosomal storage diseases in which the biochemical abnormalities have been determined They are listed in Table 37-3, which was adapted originally from the review of Kolodny and Cable and recently updated by our colleague E Kolodny In addition to the sphingolipidoses, which are the lysosomal storage diseases most likely to be encountered in the rst year of life, the table includes the storage diseases that may not appear clinically until a later age (in childhood and adolescence) to be considered later in this chapter The frequency of each of the various types as detected in a comprehensive study of the Australian population is given by Meikle and colleagues and generally accords with the ordering below A broad perspective on the frequency of the lysosomal disorders can be appreciated from the report of the Australian national referral laboratory There were 545 cases (75 detected prenatally) over a 16-year period, a calculated frequency of 1 case per 7700 live births This is close to the estimate in the United States, which is approximately 1 per 5000 births The more frequent types of lysosomal storage diseases are as follows: 1 2 3 4 5 6 7 8 9 10 11 Tay-Sachs disease (GM2 gangliosidosis) and variants such as Sandhoff disease Infantile Gaucher disease Infantile Niemann-Pick disease Infantile GM1 generalized gangliosidosis Krabbe globoid-body leukodystrophy Farber lipogranulomatosis Pelizaeus-Merzbacher and other sudanophilic leukodystrophies Spongy degeneration (Canavan-van Bogaert-Bertrand disease) Alexander disease Zellweger encephalopathy Lowe oculorenal-cerebral disease.

In the following descriptions, we have summarized the clinical and pathologic features of each of the diseases listed above and have italicized the characteristic clinical signs and corroborative laboratory tests Leigh disease, which may appear in this age group,

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