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This is an autosomal recessive disease without ethnic predominance, rst described by Gaucher in 1882 The onset of the neuronopathic form is usually before 6 months and frequently before 3 months The clinical course is more rapid than that of Tay-Sachs disease (most patients with infantile Gaucher disease do not survive beyond 1 year and 90 percent not beyond 2 years) Oculomotor apraxia and bilateral strabismus are early signs and are accompanied by rapid loss of head control, of ability to roll over and sit, and of purposeful movements of the limbs along with apathy, irritability, frequent crying, and dif culty in sucking and swallowing In some cases progression is slower, with acquisition of single words by the rst year, bilateral corticospinal signs (Babinski signs and hyperactive tendon re exes), persistent retro exion of the neck, and strabismus Laryngeal stridor and trismus, diminished reaction to stimuli, smallness of the head, rare seizures, normal optic fundi, enlarged spleen and slightly enlarged liver, poor nutrition, yellowish skin and scleral pigmentation, osteoporosis, vertebral collapse and kyphoscoliosis, and sometimes lymphadenopathy complete the clinical picture The CSF is normal; the EEG is abnormal but nonspeci cally so The important laboratory ndings are an increase in serum acid phosphatase and characteristic histiocytes (Gaucher cells) in marrow smears and liver and spleen biopsies A de ciency of glucocerebrosidase in leukocytes and hepatocytes is diagnostic; glucocerebroside accumulates in the involved tissues The characteristic pathologic feature is the Gaucher cell, 20 to 60 m in diameter, with a wrinkled appearance of the cytoplasm and eccentricity of the nucleus These cells are found in the marrow, lungs, and other viscera; neuronal storage is seldom evident In the brain, the main abnormality is a loss of nerve cells particularly in the bulbar nuclei but also in the basal ganglia, cortex, and cerebellum and a reactive gliosis that extends into the white matter In contrast to the type II form described above, type I Gaucher disease is a nonneuronopathic and relatively benign form A less frequent type III Gaucher disease is neuronopathic It expresses itself in late childhood or adolescence by a slowly progressive mental decline, seizures, and ataxia, and, later, by spastic weakness and splenomegaly Vision and retinae remain normal Highly diagnostic is the defect in voluntary lateral gaze, with full movements on the oculocephalic ( doll s-head ) maneuver These signs help to differentiate Gaucher from Niemann-Pick disease, in which vertical eye movements are lost (see below) The nucleotide sequence of the cloned glucocerebrosidase of type I Gaucher disease was found by Tsuji and associates to be different from that of types II and III There is no treatment for the latter types.

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is jaundice and ascites Cerebral abnormalities are de nite by the end of the rst year, often earlier The usual manifestations are loss of spontaneous movements, lack of interest in the environment, axial hypotonia with bilateral corticospinal signs, blindness and amaurotic nystagmus, and a macular cherry-red spot (in about onequarter of the patients) Seizures may occur but are relatively late There is no acoustic-induced startle or myoclonus, and head size is normal or slightly reduced Loss of tendon re exes and slowed conduction in peripheral nerves have been recorded but are rare Protuberant eyes, mild hypertelorism, slight yellowish pigmentation of oral mucosa, and dysplasia of dental enamel have also been reported but are rare Most patients succumb to an intercurrent infection by the end of the second year Vacuolated histiocytes ( foam cells ) in the bone marrow and vacuolated blood lymphocytes are the important laboratory ndings A de ciency of sphingomyelinase in leukocytes, cultured broblasts, and hepatocytes is diagnostic Pathologic examination reveals a decrease in the number of neurons; many of the remaining ones are pale and ballooned and have a granular cytoplasm The most prominent neuronal changes are seen in the midbrain, spinal cord, and cerebellum The white matter is little affected The retinal nerve cell changes are similar to those in the brain The foamy histiocytes (Niemann-Pick cells) that ll the viscera contain sphingomyelin and cholesterol; the distended nerve cells contain mainly sphingomyelin There are also less severe late infantile and juvenile forms of Niemann-Pick disease types C and D These are discussed in a later section of this chapter

Infantile Generalized GM1 Gangliosidosis (Type I, -Galactosidase De ciency, Pseudo-Hurler Disease)

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This is probably an autosomal recessive disease without ethnic predominance The infants appear abnormal at birth They have dysmorphic facial features, like those of the mucopolysaccharidoses: depressed and wide nasal bridge, frontal bossing, hypertelorism, puffy eyelids, long upper lip, gingival and alveolar hypertrophy, macroglossia, and low-set ears These features, with the bone changes mentioned below, account for the term pseudo-Hurler Other indications of the disease are the onset of impaired awareness and reduced responsivity in the rst days or weeks of life; lack of psychomotor development after 3 to 6 months; hypotonia, and later hypertonia with lively tendon re exes and Babinski signs Seizures are frequent The head size is variable (microcephaly more often than macrocephaly) Loss of vision, coarse nystagmus and strabismus, macular cherry-red spots (in half the cases), exion pseudocontractures of elbows and knees, kyphoscoliosis, and enlarged liver and sometimes enlarged spleen are the other important clinical ndings Radiographic abnormalities include subperiosteal bone formation, midshaft widening and demineralization of long bones, and hypoplasia and beaking of the thoracolumbar vertebrae Vacuoles are seen in 10 to 80 percent of blood lymphocytes and foam cells in the urinary sediment A partial or complete de ciency of -galactosidase and accumulation of GM1 ganglioside in the viscera and in neurons and glial cells throughout the CNS are the speci c biochemical abnormalities In addition, the epithelial cells of renal glomeruli, histiocytes of the spleen, and liver cells contain a modi ed keratan sulfate and a galactose-containing oligosaccharide The changes in the bone are also like those in the Hurler form of mucopolysac-

Infantile Niemann-Pick Disease (Sphingomyelinase De ciency)

This is also an autosomal recessive disease Two-thirds of the affected infants have been of Ashkenazi Jewish parentage The onset of symptoms in the usual type A disease is between 3 and 9 months of age, frequently beginning with marked enlargement of liver, spleen, and lymph nodes and in ltration of the lungs; rarely there

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charidosis The disease should be suspected in an infant having the facial features of mucopolysaccharidosis and severe early-onset neurologic abnormalities A remarkably benign variant, also inherited as an autosomal recessive trait, begins later in childhood but may advance so slowly as to allow attainment of adult life Dystonia, myoclonus, seizures, visual impairment, and macular red spots were features of the two cases described by Goldman and coworkers

Globoid Cell Leukodystrophy (Krabbe Disease, Galactocerebrosidase De ciency)

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