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velopment in the neonatal or early infantile period of life is aided little by tests of tendon and plantar re exes Arm re exes are always rather dif cult to obtain in infants, and a normal neonate may have a few beats of ankle clonus The plantar response tends to be wavering and uncertain in pattern However, a consistent extension of the great toe and fanning of the toes on stroking the side of the foot is abnormal at any age The early detection of cerebral palsy is hampered by the fact that the corticospinal tract is not fully myelinated until 18 months of age, allowing only quasivoluntary movements up to this time For this reason, a congenital hemiparesis may not be evident until many months after birth Even then it is manifest only by subtle signs, such as holding the hand in a sted posture or clumsiness in reaching for objects and in transferring them from one hand to the other Later, the leg is seen to be less active as the infant crawls, steps, and places the foot Early hand dominance should always raise the suspicion of a motor defect on the opposite side In the upper limb, the characteristic catch and yielding resistance of spasticity is most evident in passive abduction of the arm, extension of the elbow, dorsi exion of the wrist, and supination of the forearm; in the leg, the change in tone is best detected by passive exion of the knee However, the time of appearance and degree of spasticity are variable from child to child The stretch re exes are hyperactive, and the plantar re ex may be extensor on the affected side With bilateral hemiplegia, the same abnormalities are detectable, but there is a greater likelihood of pseudobulbar manifestations, with delayed, poorly enunciated speech Later, intelligence is likely to be impaired (in 40 percent of hemiplegias and 70 percent of quadriplegias) In diparesis or diplegia, hypotonia gives way to spasticity and the same delay in motor development except that it predominates in the legs Aside from the hereditary spastic paraplegias, which may become evident in the second and third years, the common causes of weak spastic legs are prematurity and matrix hemorrhages These various forms of cerebral palsy are described in Chap 38 Developmental motor delay and other abnormalities are present in a large proportion of infants with hypotonia When the oppy infant is lifted and its limbs are passively manipulated, there is little muscle reactivity In the supine position, the weakness and laxity result in a frog-leg posture, along with an increased mobility at the ankles and hips Hypotonia, if generalized and accompanied by an absence of tendon re exes, is most often due to Werdnig-Hoffmann disease (an early-life loss of anterior horn cells-spinal muscular atrophy), although the range of possible diagnoses is large and includes diseases of muscle, nerve, and the central nervous system (see Chaps 38 and 52) The other causes of this type of neonatal and infantile hypotonia muscular dystrophies and congenital myopathies, maternal myasthenia gravis, polyneuropathies, Down syndrome, Prader-Willi syndrome, and spinal cord injuries are described in their appropriate chapters Hypotonia that arises in utero may be accompanied by congenital xed contractures of the joints, termed arthrogryposis, as discussed in Chap 52 Infants who will later manifest a central motor defect can sometimes be recognized by the briskness of their tendon re exes and by the postures they assume when lifted In the normal infant, the legs are exed, slightly rotated externally, and associated with vigorous kicking movements The hypotonic infant with a defect of the motor projection pathways may extend the legs or rotate them internally, with dorsi exion of the feet and toes Exception-.

gives Collecting terms and substituting parameters the -Ti*r*204Ti4+r:08

9:

.

(e26)

Q: A:

ally, the legs are rmly exed, but in either instance relatively few movements are made When hypotonia is a forerunner of an extrapyramidal motor disorder (eg, so-called double athetosis, another type of cerebral palsy), the rst hint of abnormality may be an opisthotonic posturing of the head and neck However, involuntary choreic movements usually do not appear in the upper limbs before 5 to 6 months of age and often are so slight as to be overlooked They worsen as the infant matures and by 12 months assume a more athetotic character, often combined with tremor Tone in the affected limbs is by then increased but may be interrupted during passive manipulation When hypotonia is a prelude to a cerebellar motor defect, the ataxia becomes apparent when the infant makes the rst reaching movements Tremulous, irregular movements of the trunk and head are seen when the infant attempts to sit without support Still later, as the infant attempts to stand, there is unsteadiness of the entire body In distinction to the gross de cits in motor development described above, there is a relatively small but distinct group of young children who exhibit only mild abnormalities of muscle tone, clumsiness or unusual postures or rhythmic movements of the hands, tremor, and ataxia ( ne motor de cit ) Such awkwardness in the somewhat older child are referred to as soft signs and have been extensively described by Gubbay and colleagues in what they called the clumsy child Like speech delay and dyslexia, ne motor de cits of this sort are more frequent in males Tirosh found that intranatal problems were more prevalent among children with ne motor de cits (compared to those with gross motor de cits), as were minor physical anomalies and seizures Systemic diseases in infancy pose special problems in evaluation of the motor system The achievement of motor milestones is delayed by illnesses such as congenital heart disease (especially cyanotic forms), cystic brosis, renal and hepatic diseases, infections, and surgical procedures Under such conditions one does well to deal with the immediate illnesses and defer pronouncements about the status of cerebral function The brain proves to be simultaneously affected in 25 percent of patients with serious forms of congenital heart disease and an even higher proportion of patients with rubella and Coxsackie B viral infections In a disease such as cystic brosis, where the brain is not affected, it is advisable to depend more on the analysis of language development than on assessment of motor function, because muscular activity may be generally enfeebled.

Thus, Eq (924)has beentransformed from a differentialequationinto an algebraicequation Equation(926) can now be appliedto eachof the interior nodes:

funduscopy Faulty vision becomes increasingly apparent in older infants when the normal sequences of hand inspection and visuomanual coordination fail to emerge Retention of pupillary light re exes in a sightless child signi es a defect in the geniculocalcarine tracts or occipital lobes conditions that may be con rmed by MRI and testing of visual evoked responses With respect to hearing, again there is the dif culty in evaluating this function in an infant Normally, after a few weeks of life, alert parents notice a brisk startle to loud noises and a response to other sounds A tinkling bell brought from behind the infant usually results in hearkening or head turning and visual searching, but a lack of these responses warns only of the most severe hearing defects The detection of slight degrees of deafness, enough to interfere with auditory learning, requires special testing To make the problem even more dif cult, both a peripheral and a central disorder may be present in some conditions, such as kernicterus Brainstem auditory-evoked responses (BAERs) are particularly helpful in con rming peripheral (cochlear and eighth nerve) abnormalities in the infant and young child After the rst few months, impaired hearing becomes more obvious and interferes with language development, as described further on