C A R E G I V I N G I N H O S P I TA L S 2 7 in .NET

Include qrcode in .NET C A R E G I V I N G I N H O S P I TA L S 2 7

i = R(pr , pi ) R(po , pi ) + (c trr c tro ) + + Nro (8.123) i hi xro + + Nro (8.124)
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altemative,called the Neumannboundary condition, is the case where the derivative is given. We can use the heatedrod introducedearlierin this chapterto demonstrate how a derivative boundaryconditioncan be incorporated into the finite-difference approach: 0: d2T _ +/r'(f\-f)
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Fig. 33-1
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-
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