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the nervous system may escape postnatal damage The effective use of these measures has practically eradicated this dreaded disease Both kernicterus and ischemic etat marbre must be differen tiated clinically from hereditary choreoathetosis, the Lesch-Nyhan syndrome, and later in life from ataxia-telangiectasia and Friedreich ataxia Congenital and Neonatal Ataxias In these patients, dif culty in standing and walking cannot be attributed to spasticity or paralysis Again, hypotonia and poverty of movement are the initial motor abnormalities; the cerebellar de cit becomes manifest only later, when the patient begins to sit, stand, and walk There may or may not be a delay in reaching the normal motor milestones Attempts to attain sitting balance will rst reveal an unsteadiness that is not soon overcome, even with practice Reaching for a proffered toy is accomplished by jerky, incoordinated movements The rst steps are unsteady, as would be expected, with many tumbles, but the gait remains clumsy Instability of the trunk may be accompanied by similar, more or less rhythmic bobbing movements of the head, so-called titubation Despite the severity of the ataxia, the muscles are of normal size, and voluntary movements, though weak in some patients, are possible in all the limbs The tendon re exes are present, and the plantar re exes are either exor or extensor In some cases, the ataxia is later associated with spasticity rather than hypotonia (spastic-ataxic diplegia) Relative improvement may occur in later years In the older child, a cerebellar gait, ataxia of limb movements, nystagmus, and uneven articulation of words are readily distinguished from myoclonus, chorea, athetosis, dystonia, and tremor We have seen cases of a cerebellar-like tremor in adults that had been attributed to neonatal injury; the MRI did not show cerebellar atrophy In only a few cases have the pathologic changes been studied Aplasia or hypoplasia of the cerebellum has been observed, but sclerotic lesions of the cerebellum are more common The CT scan or MRI veri es the cerebellar atrophy A cerebral and cerebellar lesion may coexist in patients with congenital ataxia, which is the reason for the term cerebrocerebellar diplegia Several risk factors have been identi ed in the congenital ataxias Most importantly, cerebellar ataxia may be the most prominent or sole effect of neonatal ischemia-hypoxia A genetic factor is operative in some cases (Hagberg and Hagberg) Radiation of the maternal abdomen during the rst trimester of pregnancy is said to have resulted in cerebellar hypoplasia Mercury poisoning in utero is another cause of congenital ataxia Many cases remain unexplained in our experience Pontocerebellar Hypoplasias Aside from the congenital ataxia described above, there are several rare familial forms in which a failure of cerebellar development is associated with mental retardation Joubert reported a family in which there was dysgenesis of the vermis of the cerebellum; mental retardation; episodic hyperpnea; irregular, jerky eye movements; and unsteady gait The syndrome appeared in four of six siblings In other reports, choroidalretinal colobomas, polydactyly, cryptorchidism, and prognathism have been mentioned Detailed examination of the cerebra of such individuals has been lacking In the Gillespie syndrome, a combination of aniridia, cerebellar ataxia, and mental retardation are the denominating features In the Paine syndrome, a familial disorder with developmental delay and mental retardation, there is microcephaly, spasticity, optic hypoplasia, and myoclonic ataxia, the last presumably related to the cerebellar hypoplasia These dysgeneses
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and the disequilibrium syndrome reported from Sweden are uni ed by the cerebellar ataxia; in the past, they fell into the group of ataxic cerebral palsies Imaging studies demonstrate the cerebellocerebral abnormality Genetic factors are operative in some, but matters pertaining to etiology remain obscure (see Harding for details) One form of a pure congenital cerebellar hypoplasia has been mapped to a gene locus on chromosome Xq The ataxia was inherited as an X-linked recessive trait and was nonprogressive beyond early childhood Differential Diagnosis of the Congenital Ataxias The congenital ataxias must be distinguished from the progressive hereditary ataxias The latter are likely to begin at a later age than the congenital ones Some hereditary ataxias are intermittent or episodic, one of which is responsive to acetazolamide, as pointed out on page 827 Several forms of childhood ataxia are neither congenital nor hereditary; they have an acute onset and may persist during childhood, adolescence, and adult life Also to be distinguished from the ataxias of congenital and neonatal origin is an acute cerebellar ataxia of childhood, which can usually be traced to a viral infection or a postinfectious encephalitis, particularly after chickenpox The opsoclonus-myoclonus ( dancing eyes ) syndrome of Kinsbourne is another postinfectious disease peculiar to childhood (see pages 239 and 641) The cerebellar ataxia in this disease may be overshadowed by polymyoclonus, which mars every attempted movement With improvement, under the in uence of corticosteroids, a cerebellar disorder of speech and movement becomes evident A majority of the patients in which the disease became chronic (16 of the 26 cases followed by Marshall et al) were found later to be mentally backward The cause of the disease has never been established An occult neuroblastoma or other tumor is uncovered occasionally In the differential diagnosis of these acute forms of cerebellar ataxia, one must not overlook intoxication with phenytoin, barbiturates, or similar drugs The Flaccid Paralyses and the Floppy Infant (Table 38-5; See also pages 946 and 1198) The rare cerebral form of generalized accidity, rst described by Foerster and called cerebral atonic diplegia, has already been mentioned It can usually be distinguished from the paralysis of spinal and peripheral nerve origin and congenTable 38-5 Causes of congenital hypotonia the oppy infant syndrome (see also Chap 52) I Cerebral A Cerebral atonic diplegia (Foerster) B Prader-Willi syndrome C Idiopathic slackness II Spinal A Werdnig-Hoffman spinal muscular atrophy B Spinal cord natal injury III Myopathic A Polymyopathies central core, nemaline, rod-body, myotubular, ber-type disproportion B Infantile muscular dystrophy C Myotonic dystrophy D Polymyositis IV Neuropathic A In ammatory demyelinating neuropathy
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