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THE INHERITED METABOLIC DISEASES OF THE NERVOUS SYSTEM
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basis of this and related gene mutations, apparent milder forms of Alexander disease have been reported in juveniles and adults They differed clinically in lacking the cerebral leukoencephalopathy Instead, after a long period of constipation, sleep disorder, and orthostatic hypotension during adolescence, bulbar symptoms (dysarthria, dysphonia, and dysphagia), seizures, and in some cases ataxia gradually emerged during adult years The myelin changes and atrophy of the medulla seen in MRI were con rmed by postmortem examination and the Rosenthal bers; GFAP bers were present in two autopsied cases Stumpf and colleagues advanced the idea that the glial and GFAP changes relate the cases in the large kindred they studied to a variant of Alexander disease Alpers Disease This is a progressive disease of the cerebral gray matter, known also as progressive cerebral poliodystrophy or diffuse cerebral degeneration in infancy A familial form (probably autosomal recessive) as well many sporadic cases has been reported In both groups there is a certain uniformity of clinical features loss of smile and disinterest in the surroundings, sweating attacks, seizures and diffuse myoclonic jerks beginning in early infancy and followed by incoordination of movements; progressive spasticity of limb, trunk, and cranial muscles; blindness and optic atrophy; growth retardation and increasing microcephaly; and nally virtual decortication In some instances, the late onset of jaundice and fatty degeneration or cirrhosis of the liver have been described (Alpers-Huttenlocher syndrome); the hepatic changes are distinctive and probably not related to the use of anticonvulsant drugs, as had been hypothesized (Harding et al) By the age of 4 years, these patients are hypotonic, anemic, and thrombopenic They also show hair changes (trichorrhexis) The nature of this combined hepatic-cerebral degeneration remains unexplained, but some instances have been connected to the mitochondrial disorders, as noted below EEG abnormalities, progressive atrophy (particularly occipital) on the CT scan, loss of visual evoked potentials, and abnormal liver function tests are diagnostically useful Neuropathologic examination shows marked atrophy of the cerebral convolutions and cerebellar cortex, with loss of nerve cells and brous gliosis ( walnut brain ) The cerebral white matter and basal ganglia are relatively preserved In some cases, the spongiform vacuolization of the gray matter of the brain resembles that seen in Creutzfeldt-Jakob disease Hypoglycemic, hypoxic, and hypotensive encephalopathies must always be considered in the diagnosis but can usually be eliminated by knowledge of the clinical circumstances at the onset of the illness A number of biochemical abnormalities have been identi ed in patients with Alpers disease, including pyruvate dehydrogenase de ciency, decreased pyruvate utilization, dysfunction of the citric acid cycle, and decreased cytochromes a and aa3 The biochemical and pathologic changes suggest a relationship to Leigh encephalomyelopathy and a mitochondrial transmission Many authoritative texts classify it with the mitochondrial diseases, but its nosologic status is in our opinion still uncertain (see Shaffner and Wallace)
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Figure 37-3 Spongy degeneration of infancy (Canavan-van Bogaert-Bertrand disease) T2-weighted axial MRI from an infant with a positive urine assay for N-acetyl-L-aspartic acid The abnormal white matter appears hyperintense and extends to the cortex without sparing of the arcuate ber (Reproduced by permission from Lee SH, Rao K, Zimmerman RA: Cranial MRI and CT, 3rd ed New York, McGraw-Hill, 1992)
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type II astrocytes throughout the cerebral cortex and basal ganglia Adachi and coworkers have demonstrated an abnormal vacuolar accumulation of uid in astrocytes and between split myelin lamellae; they have suggested that the loss of myelin is secondary to these changes The enlargement of the brain in this disease must be distinguished clinically from GM2 gangliosidosis, Alexander disease, Krabbe disease, and nonprogressive megalocephaly and pathologically from a variety of disorders characterized by vacuolation of nervous tissue There is no treatment
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