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and development, has resulted in rapid amelioration of symptoms but must be started early Retinoids given orally improve the skin lesions Neonatal tyrosinemia can cause liver failure and early death This disease can be distinguished from the Cross syndrome (albinism with mental retardation, growth impairment, spastic weakness, and alkalosis) and from the Waardenberg ocular albinism syndrome (white forelock, hypertelorism, deafness) For a detailed discussion of the albinism syndromes, see the article by Oetting and King Tyrosine Hydroxylase De ciency This relatively recently described disease causes a progressive infantile encephalopathy; it is of special interest because tyrosine is the precursor of L-dopa and the other catecholamines Levels of these chemical substances in the brain are greatly reduced As a result, the encephalopathy takes the form mainly of uctuating extrapyramidal signs in combination with ocular and vegetative symptoms L-Dopa causes some improvement in the motor symptoms (see Hoffmann et al) This disease has implications for juvenile dopa-responsive dystonia, which is exquisitely sensitive to L-dopa treatment (as discussed on page 930) and is contrasted with the de ciency of L-amino decarboxylase, described above, which also causes low levels of catecholamines and a movement disorder Hartnup Disease This amino acid disorder, named after the family in which it was rst observed, is probably transmitted in an autosomal recessive pattern Women carrying this trait deliver babies who are normal at birth The onset of symptoms is in late infancy or early childhood The clinical features consist of an intermittent red, scaly rash over the face, neck, hands, and legs, resembling that of pellagra It is often combined with an episodic personality disorder in the form of emotional lability, uncontrolled temper, and confusional-hallucinatory psychosis; episodic cerebellar ataxia (unsteady gait, intention tremor, and dysarthria); and occasionally spasticity, vertigo, nystagmus, ptosis, and diplopia Attacks of disease are triggered by exposure to sunlight, emotional stress, and sulfonamide drugs and last for about 2 weeks, followed by variable periods of relative normalcy The frequency of attacks diminishes with maturation, but some children suffer retarded growth and development with a mild persistent mental retardation The metabolic faults are due to a transport error of neutral amino acids across renal tubules, with excretion of greatly increased amounts of these amino acids in the urine and feces In particular, there is the excretion of large amounts of indicans, mainly indoxyl sulfate, particularly after oral L-tryptophan loading, and an abnormally high excretion of nonhydroxylated indole metabolites Impaired intestinal transport of tryptophan and loss in the urine reduces its availability for the synthesis of niacin and accounts for the pellagrous skin changes The pathologic basis of the disease is undetermined It must be differentiated from the large number of intermittent and progressive cerebellar ataxias of childhood, described below Treatment consists of avoiding exposure to sunlight and to sulfonamide drugs Because of the similarities between pellagra and Hartnup disease, the usual practice is to give nicotinamide in doses of 50 to 300 mg daily The skin lesions disappear and there are reports of subsidence of ataxia and psychotic behavior However, the results of treatment are inconsistent Possibly a better response is obtained by the administration of L-tryptophan ethyl ester in doses of 20 mg/kg thrice daily.

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Other Metabolic Diseases with Episodic or Persistent Ataxia, Seizures, and Mental Retardation In addition to Hartnup disease, a number of other metabolic diseases give rise to intermittent episodes of ataxia during early childhood These are (1) mild forms of maple syrup urine disease and the congenital hyperammonemias (type II hyperammonemia, citrullinemia, argininosuccinic aciduria, hyperornithinemia), described in an earlier part of the chapter; (2) necrotizing encephalomyelopathy (Leigh disease), described further on; (3) hyperalaninemia and hyperpyruvic acidemia (Lonsdale et al, Blass et al); and (4) autosomal dominant, acetazolamideresponsive ataxia that may have its onset in childhood but usually appears later (page 827) In all these conditions the ataxia, which is of cerebellar type, is highly variable from time to time and may follow a burst of seizures (such as occur in argininosuccinic aciduria) The seizures are treated with anticonvulsant drugs, which may at rst be held responsible for the ataxia In time, however, it becomes apparent that the ataxia lasts a week or two and bears no relation to the anticonvulsant therapy Indeed, seizures and ataxia are both due to the common biochemical abnormality Between attacks, in all the intermittent ataxias, the patient s movements are relatively normal, but most of the affected children are slow in learning and remain backward mentally to a varying degree

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The differentiation of the childhood ataxias is dif cult The problem is twofold rst, to be certain that ataxia exists, and, second, to differentiate cerebellar ataxia from the sensory ataxia of peripheral nerve disease and from generalized tremor and polymyoclonus Since cerebellar ataxia is more a disorder of voluntary than of postural movements, its presence usually cannot be determined with certainty until intentional (projected) movements become part of the child s repertoire of motor activity As indicated in Chap 28, the earliest signs become manifest in the arms when the infant reaches for an object and brings it to his mouth or transfers it from hand to hand A jerky, wavering, tremulous movement then appears; in sitting, a titubation of the head and a tremor of the trunk may be apparent Once walking begins, apart from the usual clumsiness of the toddler, there is a similar incoordination of movement Sensory ataxia is always dif cult to distinguish but is rare at this age and usually accompanied by weakness and absence of tendon re exes By the fourth or fth year, when more detailed sensory testing becomes possible, the presence or absence of a proprioceptive disturbance and a Romberg sign can be demonstrated The group of persistent and progressive cerebellar ataxias is heterogeneous and of varied etiology; some of them merge with Friedreich ataxia, Levy-Roussy neuropathy, and other adolescentadult degenerative hereditary ataxias These disorders are discussed in Chap 39 on degenerative diseases, since, apart from their hereditary nature, neither their cause nor their pathogenesis is known There are many other childhood ataxias that probably belong in the category of degenerative disease, some in which cerebellar ataxia is the most prominent disorder and in which other neurologic abnormalities are more prominent To describe each in detail would be impractical in a book on the principles of neurology; therefore, the non-Friedreich ataxias are only tabulated here 1 The disequilibrium and dyssynergia syndrome of Hagberg.

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