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months In the older child, there is evident hyperactivity of tendon re exes and usually a Babinski sign The arm is held exed, adducted, and pronated, and the foot assumes an equinovarus posture Sensory and visual eld defects can be detected in some patients Mental defect may be associated with infantile hemiplegia but is less common and lesser in degree than with cerebral diplegia and much less common than with bilateral hemiplegia There may also be speech delay, regardless of the side of the lesion; when this is present, one should look for mental retardation and expect to nd a bilaterality of motor abnormality Convulsions occur in 35 to 50 percent of children with congenital hemiplegia, and these may persist throughout life They may be generalized but are frequently unilateral and limited to the hemiplegic side (or the contralateral side if the hemiplegia is severe) Often, after a series of seizures, the weakness on the affected side will be increased for several hours or longer (Todd s paralysis) Gastaut and associates have described a hemiconvulsive-hemiplegic syndrome in which the progressive paralysis and cerebral atrophy are attributed to the convulsions As months and years pass, the osseous and muscular growth of the hemiplegic limbs is retarded, leading to an obvious hemiatrophy With respect to the causation of congenital hemiplegia, it is generally agreed that perinatal asphyxia is only one of the possibilities In the series of 681 children with cerebral palsy collected by Hagberg and Hagberg, there were 244 with hemiplegia Of the latter, 189 were full-term babies and 55 preterm Prenatal risk factors were identi ed in only 45 percent, and they were mostly in the infants born prematurely In nearly half of the cases, there was no clue as to the time in the intrauterine period when the cerebral lesion occurred In another group acquired infantile hemiplegia a normal infant or young child, usually between the ages of 3 and 18 months, develops a massive hemiplegia, with or without aphasia, within hours The disorder often begins with seizures, and the hemiplegia may not be recognized until the seizures have subsided In Banker s autopsy series, there was arterial or venous thrombosis in some cases, but instances without vascular occlusions were found Some of the latter cases, in which arteriography had been normal, may have been embolic, possibly of cardiac origin In the recent era, imaging has shown a large area of cerebral infarction, not dissimilar to a stroke in the territory of the middle cerebral artery, acquired during infancy but usually with a normal arteriogram (Fig 38-13) If the stroke occurs at an early age, the recovery of speech may be complete, though reduced scholastic capacity remains The degree of recovery of motor function varies Often, as the de cit recedes, the arm becomes involved by athetotic, tremulous, or ataxic movements; there may be an interval of months or years between the hemiplegia and the athetosis Encephaloclastic (destructive) lesions underlie most of the cases of infantile hemiplegia and some cases of bilateral hemiplegia (as well as many cases of seizures in the rst few days of life) The pathologic change is essentially that of ischemic necrosis In many cases, the lesions must have been acquired in utero Precipitant delivery, fetal distress, and prepartum uterine hemorrhage may have been indications of the process The lesions seemingly re ect those of circulatory insuf ciency (ischemia), the result of hypotension or local circulatory failure What is most notable is that the ischemia tends to affect the tissues lying in arterial cortical border zones; there may also be venous stasis with congestion and hemorrhage occurring particularly in the deep central structures, such as the basal ganglia and periventricular matrix zones If they are purely hypoxic, the lesions should be bilateral Myers has repro-
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Figure 38-13 MRI of an adult with congenital hemiplegia There is severe encephalomalacia mainly in the territory of the right middle cerebral artery
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duced such lesions in the neonatal monkey by reducing the maternal circulation for several hours As the lesions heal, the monkeys develop the same sclerotic changes in the cortex and white matter of the cerebrum (lobar sclerosis) and the marbling (etat marbre) that characterizes the brains of patients with spastic diplegia and double athetosis (see below) The quadriplegic state differs from bilateral hemiplegias in that the bulbar musculature is often involved in the latter and mental retardation is more severe The condition is relatively rare and is usually due to a bilateral cerebral lesion However, one should also be alert to the possibility of a high cervical cord lesion In the infant, this is usually the result of a fracture dislocation of the cervical spine incurred during a dif cult breech delivery Similarly, in paraplegia, with weakness or paralysis limited to the legs, the lesion may be either a cerebral or a spinal one Sphincteric disturbances and a loss of somatic sensation below a certain level on the trunk always point to a spinal localization Congenital cysts, tumors, and diastematomyelia are more frequently causes of paraplegia than of quadriplegia Another recognized cause of infantile paraplegia is spinal cord infarction from thrombotic complications of umbilical artery catheterization Extrapyramidal Syndromes The spastic cerebral diplegias discussed above shade almost imperceptibly into the congenital extrapyramidal syndromes Patients with the latter syndromes are found in every cerebral palsy clinic, and ultimately they reach adult neurology clinics as well Corticospinal tract signs may be completely absent, and the student, familiar only with the syndrome of pure spastic diplegia, is always puzzled as to their classi cation Some cases of extrapyramidal type are undoubtedly attributable to severe perinatal hypoxia and others to diseases such as erythroblastosis fetalis with kernicterus In order to state the probable path-
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