create 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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in some cases Metachromatic material is found in the urinary sediment Pathologically, in addition to metachromasia of degenerating white matter in cerebrum and peripheral nerve, there may be storage material (sulfated glycolipids), like that found in the gangliosidoses in neurons as well as in liver, gallbladder, and kidney Granules are demonstrable in neutrophilic leukocytes There has also been described a state of arylsulfatase pseudode ciency, which exists as a polymorphism in about 7 percent of Europeans and makes the point that low enzyme levels alone are insuf cient to be expressed as a phenotype of metachromatic leukodystrophy Forms of metachromatic leukodystrophy developing in adult years are discussed further on
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such as palsies of horizontal gaze, diffuse myoclonus, generalized seizures, and a chronic course (Winkelman et al) The diagnosis is established by the nding of splenomegaly, Gaucher cells, glucocerebroside storage, and de cient activity of glucocerebrosidase in leukocytes or cultured broblasts
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Late Infantile Early Childhood Niemann-Pick Disease
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A number of cases of subacute or chronic neurovisceral storage diseases with early signs of hepatosplenomegaly and later signs (2 to 4 years) of neurologic involvement have been described Crocker and Farber classi ed them as types III and IV Niemann-Pick disease Others have classi ed them as types C and D, although it is now generally agreed that they are best considered a single entity The neurologic disorder consists of progressive dementia, dysarthria, ataxia, rarely extrapyramidal signs (choreoathetosis), and paralysis of horizontal and vertical gaze, the latter being a distinguishing feature On attempting to look to the side, some of the patients make head-thrusting movements of the same type that one observes in ataxia-telangiectasia and the oculomotor apraxia of Cogan (page 873) Lateral eye movements are full on passive movement of the head (oculocephalic maneuver) Convergence is also de cient A special syndrome called juvenile dystonic lipidosis is characterized by extrapyramidal symptoms and paralysis of vertical eye movements The syndrome of the sea-blue histiocyte (liver, spleen, and bone marrow contain histiocytes with sea-blue granules) in which there is retardation in mental and motor development, grayish macular degeneration, and, in one of our cases, posterior column and pyramidal degeneration may be another variant The diagnosis is made by bone marrow biopsy, which discloses vacuolated macrophages and sea-blue histiocytes, and by measuring the defect in cholesterol esteri cation in cultured broblasts
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Neuroaxonal Dystrophy (Degeneration)
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This is a rare disease, inherited as an autosomal recessive trait In the largest group of cases (77 collected by Aicardi and Castelein), the onset was near the beginning of the second year in 50 patients and before the third year in all instances The clinical constellation comprised psychomotor deterioration (loss of ability to sit, stand, and speak), marked hypotonia but brisk re exes and Babinski signs, and progressive blindness with optic atrophy but normal retinae Seizures, myoclonus, and extrapyramidal signs were rare Loss of sensation was found later in some cases Terminally, bulbar signs, spasticity, and decerebrate rigidity often supervened The course was relentlessly progressive, with fatal issue in a decorticate state in 3 to 8 years There were no abnormalities of the liver and spleen and no facial or skeletal changes Pathologic examination reveals eosinophilic spheroids of swollen axoplasm in the posterior columns and nuclei of Goll and Burdach and in Clarke s column, substantia nigra, subthalamic nuclei, central nuclei of brainstem, and cerebral cortex There is cerebellar atrophy, affecting the granule cell layer predominantly, and increased iron-containing pigment in the basal ganglia (like that observed in Hallervorden-Spatz disease) The CT scans and CSF are normal, and there are no biochemical or blood cell abnormalities After the age of 2 years, however, the EEG shows characteristic high-amplitude fast rhythms (16 to 22 Hz) Evoked responses may be abnormal Nerve conduction velocities are normal despite EMG evidence of denervation The diagnosis can be reliably established during life by electron microscopic examination of skin and conjunctival nerves, which show the characteristic spheroids within axons There is a later-onset form of the disease in which the course is more protracted and the neurologic manifestations (rigidity and spasticity, cerebellar ataxia, and myoclonus) are more pronounced In these cases the mental regression is slow Vision may be retained, but retinal degeneration has been documented Some of the late-onset cases are indistinguishable from Hallervorden-Spatz disease (page 832) The primary mutation in most cases is unknown In early infantile forms there is a mutation in a lysosomal hydrolase
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