generate barcode c# .net THE INHERITED METABOLIC DISEASES OF THE NERVOUS SYSTEM in Microsoft Office

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THE INHERITED METABOLIC DISEASES OF THE NERVOUS SYSTEM
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TELLEZ-NAGEL I, RAPIN I, IWAMOTO T, et al: Mucolipidosis IV Arch Neurol 33:828, 1976 TENNISON MB, BOULDIN TW, WHALEY RA: Mineralization of the basal ganglia detected by CT in Hallervorden-Spatz syndrome Neurology 38: 155, 1988 THOMAS PK, ABRAMS JD, SWALLOW D, STEWART G: Sialidosis type I: Cherry-red spot-myoclonus syndrome with sialidase de ciency and altered electrophoretic mobilities of some enzymes known to be glycoproteins J Neurol Neurosurg Psychiatry 42:873, 1979 TROBE JD, SHARPE JA, HIRSCH DK, GEBARSKI SS: Nystagmus of Pelizaeus-Merzbacher disease: A magnetic search-coil study Arch Neurol 48:87, 1991 TSAIRIS P, ENGEL WK, KARK P: Familial myoclonic epilepsy syndrome associated with skeletal muscle abnormalities Neurology 23:408, 1973 TSUJI S, CHOUDARY PV, MARTIN BM, et al: A mutation in the human glucocerebrosidase gene in neuronopathic Gaucher s disease N Engl J Med 311:570, 1987 TSUJI S, YAMADA T, TSUTSUMI A, MIYATAKE T: Neuraminidase de ciency and accumulation of sialic acid in lymphocytes in adult type sialidosis with partial -galactosidase de ciency Ann Neurol 11:541, 1982 TURPIN JC, BAUMANN N: Man estations psychiatriques ou cognitves inaugurales dans les neurolipidoses de l adulte Rev Neurol 159:637, 2003 VAKILI S, DREW AL, VON SCHUCHING S, et al: Hallervorden-Spatz syndrome Arch Neurol 34:729, 1977 VAN BOGAERT L: Contribution clinique et anatomique a l etude de la paralysie agitante juvenile primitive Rev Neurol 2:315, 1930 VAN BOGAERT L: Le cadre des xanthomatoses et leurs differents types: Xanthomatoses secondaires Rev Med 17:433, 1962 VAN BOGAERT L, BERTRAND I: Sur une idiotie famaliale avec degener escence spongieuse du neuraxe Acta Neurol Belg 49:572, 1949 VAN GEEL MB, ASSIES J, WANDERS RJ, BARTH P G: X linked adrenoleukodystrophy: Clinical presentation, diagnosis and therapy J Neurol Neurosurg Psychiatry 63:4, 1997
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VOGT C, VOGT O: Zur Lehre der Erkrankungen des striaren Systems J Psychol Neurol 25:627, 1920 WALSH PJ: Adrenoleukodystrophy Arch Neurol 37:448, 1980 WILLIAMS FJB, WALSHE JM: Wilson s disease: An analysis of the cranial computerized tomographic experiences found in 60 patients and the changes in response to treatment with chelating agents Brain 104:735, 1981 WILLIAMS RS, MARSHALL PC, LOTT IT, et al: The cellular pathology of Menkes steely hair syndrome Neurology 28:575, 1978 WILLVONSEDER R, GOLDSTEIN NP, MCCALL JT, et al: A hereditary disorder with dementia, spastic dysarthria, vertical eye movement paresis, gait disturbance, splenomegaly, and abnormal copper metabolism Neurology 23:1039, 1973 WILNER JP, GRABOWSKI GA, GORDON RF, et al: Chronic GM2 gangliosidosis masquerading as atypical Friedreich s ataxia: Clinical, morphologic, and biochemical studies of nine cases Neurology 31:787, 1981 WILSON SAK: Progressive lenticular degeneration: A familial nervous disease associated with cirrhosis of the liver Brain 34:295, 1912 WINKELMAN MD, BANKER BQ, VICTOR M, MOSER HW: Non-infantile neuronopathic Gaucher s disease: A clinico-pathologic study Neurology 33:994, 1983 WISNIEWSKI KE, ZHONG N, PHILLIPART M: Pheno/genotypic correlations of neuronal ceroid lipofuscinosis Neurology 57:576, 2001 YOKOI S, NAKAYAMA H, NEGESHI T: Biochemical studies on tissues from a patient with Lafora disease Clin Chim Acta 62:415, 1975 YOUNG RR, KLEINMAN G, OJEMANN RG, et al: Compressive myelopathy in Maroteaux-Lamy syndrome: Clinical and pathological ndings Ann Neurol 8:336, 1980 ZEMAN W, DONAHUE S, DYKEN P, GREEN J: The neuronal ceroid-lipofuscinoses (Batten-Vogt syndrome), in Vinken PJ, Bruyn GW (eds): Handbook of Clinical Neurology Vol 10 Amsterdam, North-Holland, 1970, pp 588 679
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DEVELOPMENTAL DISEASES OF THE NERVOUS SYSTEM
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Subsumed under this broad heading is a diversity of both developmental malformations and diseases acquired during the intrauterine period of life They number in the hundreds, according to the tabulation of Dyken and Krawiecki, although many are very rare Taxonomically they make up two broad categories The rst includes many unrelated genetic pathologic processes: some stem from germplasm abnormalities; others are associated with triplication, deletion, and translocations of chromosomes; and probably some are inherited on a polygenic basis A remarkable accomplishment has been the identi cation in the past several years of speci c gene defects that give rise to malformations of the brain The second category is composed of the effects of a variety of noxious agents acting at different times on the immature nervous system, ie, during the embryonal, fetal, and paranatal periods of life It would be intellectually satisfying if all the states that originate in the intrauterine period could be separated strictly into genetic (hereditary) or nongenetic forms, but in many instances the biologic information and the pathologic changes in the brain at this early age do not allow such a division For example, among the many diseases in which the neural tube fails to close (rachischisis), more than one member of a family may be affected; but it cannot be stated whether a genetic factor is operative or an exogenous factor, such as folic acid de ciency, has acted on several members during a succession of pregnancies of one mother Even what appears to be an outright malformation of the brain may be no more than a re ection of the timing of an exogenous process that has affected the nervous system and other organs early in the embryonal period, derailing later processes of development Teratology, the scienti c study of neurosomatic malformations, is replete with such examples Several points should be noted regarding the frequency of developmental disorders Smith (see K L Jones) points out that a single malformation, usually of no clinical signi cance, occurs in 14 percent of newborns Two malformations appear in 08 percent, and in this group, a major defect is ve times more frequent than in the normal population Three or more malformations are found in 05 percent of newborns, and in this latter group, more than 90 percent have one or more major abnormalities (de ned as structural abnormalities of prenatal origin that seriously interfere with viability or physical well-being) The gures for major congenital malformations, compiled by Kalter and Warkany, are somewhat higher What is most important for the neurologist is the fact that the nervous system is involved in most of these infants with major malformations In fact, about 40 percent of deaths during the rst postnatal year are in some manner related to prenatal malformations of the central nervous system (CNS) A perusal of the following pages makes it evident that there is a great variety of structural defects of the nervous system in early life; in fact, every part of the brain, spinal cord, nerves, and musculature may be affected Furthermore, certain principles are applicable to the entire group of developmental brain disorders First, the abnormality of the nervous system is frequently accompanied by an abnormality of some other structure or organ (eye, nose, 850
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cranium, spine, ear, and heart), which relates them chronologically to a certain period of embryogenesis Conversely, the presence of these malformations of nonnervous tissues suggests that an associated abnormality of the nervous system is developmental in nature This principle is not inviolable; in certain maldevelopments of the brain, which must have originated in the embryonal period, all other organs are normal One can only assume that in this instance the brain was more vulnerable than any other organ to prenatal as well as natal in uences Perhaps this occurs because the nervous system, of all organ systems, requires the longest time for its development and maturation, during which it is susceptible to disease Second, a maldevelopment of whatever cause should be present at birth and remain stable thereafter, ie, be nonprogressive (in contrast to the majority of metabolic diseases of infancy discussed in the preceding chapter) Again, this principle requires quali cation the abnormality may have affected parts of the brain that are not functional at birth, so that an interval of time must elapse postnatally before the defect can express itself Third, for an abnormality to be characterized as developmental, birth should have been nontraumatic and the pregnancy uncomplicated by infection or other injurious event Conversely, the occurrence of a traumatic birth is not proof of a causative relationship between the injury (or infection) and the abnormality, because a defective nervous system may itself interfere with the birth or the gestational process Fourth, if the congenital abnormality has occurred in other members of the family of the same or previous generations, it is usually genetic although, as noted above, this does not exclude the possible adverse effects of exogenous agents Fifth, many of the teratologic conditions that cause birth defects pass unrecognized because they end in spontaneous abortions For example, defects due to chromosomal abnormalities occur in about 06 percent of live births, but such defects are found in more than 5 percent of spontaneous abortions at 5 to 12 weeks gestational age Sixth, low birth weight and gestational age, indicative of premature birth, increase the risk of mental subnormality, seizures, cerebral palsy, and death Regarding etiology, which is really the crux of the problem of birth defects, some order and classi cation have emerged In general, malformations may be subdivided into four groups: (1) one in which a single mutant gene is responsible (225 per 1000 live births); (2) one in which birth defects are associated with chromosomal aberrations (duplication, breakage); (3) a group comprising defects attributable solely to exogenous factors (a virus or other infectious agent, irradiation, or toxin); and (4) the largest group of all, 60 percent of cases, in which no cause can be identi ed It has been stated that true malformations are due to fundamental endogenous disturbances of cytogenesis and histogenesis occurring in the rst half of gestation and that exogenous factors, which destroy brain tissue but do not cause malformations, operate in the second half The potential fallacy of this division is obvious An exogenous lesion occurring during the embryonal period may not only destroy tissue but also derail the neuronal migrations of normal development
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