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ADULT FORMS OF INHERITED METABOLIC DISEASES
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The increasing range and precision of biochemical and cytologic tests has brought to light a number of inherited metabolic diseases that sometimes have their onset in adult life Such disorders, while uncommon, nevertheless are important because they must be considered in the differential diagnosis of degenerative diseases and cerebral atrophies, for which explanations are beginning to be found Also to be considered in the differential diagnosis is an array of mitochondrial disorders, to be discussed further on in this chapter In the last decade or two, the authors have personally observed or have otherwise come to know of examples of the following metabolic diseases, the onset of which was in late adolescence or adult life: 1 2 3 4 5 6 7 8 9 10 11 12 Metachromatic leukoencephalopathy Adrenoleukodystrophy Globoid body leukodystrophy (Krabbe disease) Kufs form of neuronal ceroid lippofuscinosis GM2 gangliosidosis Wilson disease Leigh disease Gaucher disease Niemann-Pick disease Mucopolysaccharide encephalopathy Mucolipidosis type I Polyneuropathies (Andrade disease, Fabry disease, porphyria, Refsum disease) 13 Mitochondrial diseases, particularly progressive external ophthalmoplegia and Leigh disease In the encephalopathic forms of the metabolic and mitochondrial diseases, the diagnosis is usually made only after symptoms have been present for months or years, the disease having been
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mistaken for some other condition, particularly depression or a degenerative dementia Even a manifest psychosis may have occurred in relation to some of these disorders, but such occurrences are admittedly rare For example, one of our patients with metachromatic leukodystrophy, a 30-year-old man, began failing in college years and was later unsuccessful in holding a job because of carelessness and mistakes in his work and indifference to criticism, irritability, and stubbornness (clearly traceable to a mild dementia) Only when Babinski signs and loss of tendon re exes in the legs were detected was the correct diagnosis entertained for the rst time By then he had been ill for nearly 10 years Bosch and Hart described a patient with the onset of dementia at 62 years of age and drew attention to 27 other similar cases of adult-onset metachromatic leukoencephalopathy (see also the seven cases of Turpin and Baumann) Overt signs of neuropathy are usually lacking in these adult-onset cases, but EMG and sural nerve biopsy will disclose the characteristic abnormalities One of our adult patients with Wilson disease had been committed to a psychiatric hospital because of his paranoid tendencies and ghting with his family; the presence of a tremor and mild rigidity of the limbs had been attributed at rst to phenothiazine drugs In some of Grif n s cases of adrenomyeloneuropathy, a spastic weakness of the legs and sensory ataxia progressing over several years were the main clinical manifestations; a spinocerebellar degeneration was suspected One of our patients with Kufs lipid storage disease began to deteriorate mentally in early adult life and only much later showed an increasing rigidity, with athetotic posturing of limbs and dif culty in walking; he succumbed to his disease after more than a decade of symptoms Another recent patient with Kufs disease presented at age 51 with vague visual dif culty, which was followed by spasticity of the legs, behavioral disinhibition, and dementia spanning 6 years Josephs and colleagues describe two patients of ve with adult-onset type C Niemann-Pick disease who had a psychosis beginning at ages 61 and 27, respectively We have observed cerebellar ataxia, polymyoclonus, and progressive blindness in adolescents and adults with a variant of GM2 gangliosidosis; cherry-red macular spots provided the clue to diagnosis Several such cases have been reported in the last decade, particularly among the Japanese (Miyatake et al) Notable also are nine cases of a spinocerebellar ataxia from four Ashkenazic Jewish families with dementia or psychosis of adult onset described by Wilner and colleagues Also on our services have been two adult patients with progressive spinal muscular atrophy who proved to have this same GM2 hexosaminidase de ciency; the process was clinically almost indistinguishable from a very slowly progressive lower motor neuron form of motor neuron disease (such as Kugelberg-Welander disease in adolescents), but they had no macular changes and displayed the additional features of ataxia and an intermittent and atypical psychosis Dementia, optic atrophy, mild cerebellar ataxia, and corticospinal signs have been features of several personally observed patients with Leigh disease who survived in a relatively helpless state for nearly 20 years Kalimo and associates have reported a similar family An asymmetrical corticospinal syndrome with are exia had advanced so slowly in one of our cases of Krabbe disease that she became disabled only in her sixties Another of our patients, an adolescent with severe diffuse myoclonus and seizures and slight intellectual deterioration, was found after several years to have one of the rare variants of Gaucher disease Another with dementia, rigidity, choreoathetosis, slight cerebellar ataxia, and Babinski signs had a variant of Niemann-
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