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cinal encephalomyelitis in man, in Kies MW, Alvord EC Jr (eds): Allergic Encephalomyelitis Spring eld, IL, Charles C Thomas, 1959, pp 58 129 SIBLEY WA, BAMFORD CRF, CLARK K, et al: A prospective study of physical trauma and multiple sclerosis J Neurol Neurosurg Psychiatry 54:584, 1991 SIMON JH, LULL J, JACOBS LD, RUDICK RA, et al: A longitudinal study of T1 hypointense lesions in relapsing MS: MSCRG trial of interferon beta-1a Multiple Sclerosis Collaborative Research Group Neurology 55: 185, 2000 SLAMOVITIS S, ROSEN CE, CHENG KP, et al: Visual recovery in patients with optic neuritis and visual loss to no light perception Am J Ophthalmol 111:209, 1991 STEWART JM, HOUSER GW, BAKER HL: Magnetic resonance imaging and clinical relationships in multiple sclerosis Mayo Clin Proc 62:174, 1987 STRICKER RD, MILLER RG, KIPROV DO: Role of plasmapheresis in acute disseminated (postinfectious) encephalomyelitis J Clin Apheresis 7:173, 1992 THOMAS PK, WALKER RWH, RUDGE P, et al: Chronic demyelinating peripheral neuropathy associated with multifocal central nervous system demyelination Brain 110:53, 1987 THOMPSON AJ, POLMAN CH, MILLER DH, et al: Primary progressive multiple sclerosis Brain 120:1085, 1997 THYGESSEN P: The Course of Disseminated Sclerosis: A Close-Up of 105 Attacks Copenhagen, Rosenkilde and Bagger, 1953 TIPPET DS, FISHMAN PS, PANITCH HS: Recurrent transverse myelitis Neurology 41:703, 1991 TOURTELLOTTE WW, BOOE IM: Multiple sclerosis: The blood-brain barrier and the measurement of de novo central nervous system IgG synthesis Neurology 28(Suppl):76, 1978 VRETHEM M, MATTSSON E, HEBELKA H, et al: Increased plasma homocysteine levels without signs of vitamin B12 de ciency in patients with multiple sclerosis assessed by blood and cerebrospinal uid homocysteine and methylmalonic acid Mult Scler 9:239, 2003 WAKSMAN BH, ADAMS RD: Studies of the effect of the Schwartzman reaction on the lesions of experimental allergic encephalomyelitis Am J Pathol 33:131, 1957 WEINSHENKER BG, RICE GP, NOSEWORTHY JH, et al: The natural history of multiple sclerosis: A geographically based study: 2 Predictive value of the early clinical course Brain 112:1419, 1989 ZIVADINOV R, RUDICK RA, DE MASI R, et al Effects of IV methylprednisolone on brain atrophy in relapsing-remitting MS Neurology 57:1239, 2001.

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Advances in biochemistry and molecular genetics have led to the discovery of such a large number of metabolic diseases of the nervous system that it taxes the mind just to remember their names Since the causes and mechanisms of the diseases included in this chapter (and in several that follow) are increasingly being expressed in terms of molecular genetics, it seems appropriate, by way of introduction, to consider brie y some basic facts pertaining to the genetics of neurologic disease A complete account of this subject may be found in the four-volume text edited by Scriver and colleagues One must be reminded that the biochemistry of every human organism is unique (ie, never duplicated) and that every person, in some particular way, has an inborn tendency to develop certain diseases This constitutional predisposition, or diathesis, lies in the variations of DNA of the chromosomes of each cell Knowledge of the molecular basis of this constitutional predisposition may ultimately provide the means of diagnosis, prevention, and perhaps treatment of many human diseases The diseases grouped in this chapter and the next represent four particular categories of genetic abnormality: (1) monogenic disorders determined by a single mutant gene that follow a mendelian pattern of inheritance; (2) multifactorial disorders, again following a mendelian pattern of inheritance but in which intrinsic (ie, genetic) factors interact with exogenous environmental ones; (3) nonmendelian chromosomal aberrations, characterized by an excess, a lack, or a structural alteration of one or more of the 23 pairs of chromosomes (these are considered in the next chapter, with the developmental disorders); and (4) mitochondrial transmission of disease in a nonmendelian, mainly maternal pattern As stated in the monograph of Scriver et al, 6 to 8 percent of diseases in hospitalized children are attributable to single gene defects and 04 to 25 percent to a chromosomal abnormality Another 22 to 31 percent have a disease thought to be gene-in uenced In the general population, when multifactorial inheritance of lateonset diseases is included, the latter gure rises to about 60 percent Mitochondrial inheritance of mutations is much less frequent and has unusual patterns of transmission, mostly through maternal lines The nervous system is more frequently affected by a genetic abnormality than any other organ system, probably because of the large number of genes implicated in its development (an estimated one-third of all the genes in the human genome) Approximately one-third of all inherited diseases are neurologic to some extent; if one adds the inherited diseases affecting the musculature, skeleton, eye, and ear, the number rises to 80 to 90 percent Of the almost 6000 entities itemized in the 1998 edition of McKusick s catalogue of inherited diseases, about 500 are identi ed as enzymopathies ie, mendelian disorders with a demonstrated primary enzyme defect The latter constitute only one-third of the known recessive (autosomal and X-linked) disorders Most of the enzymopathies become manifest in infancy and childhood; 797.

FIGURE 10-1

only a few appear as late as adolescence or adult life Many damage the nervous system so severely that survival to adult years and reproduction are impossible, and some cause death in utero As a group, these diseases along with congenital anomalies (Chap 38), birth injuries, epilepsy, disharmonies of development, and learning disabilities (Chap 28) make up the bulk of the clinical problems with which the pediatric neurologist must contend

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