Once the motor features of cerebral palsy have been established, assistive devices, physical therapy, and conventional orthopedic measures for joint stabilization and relief of spasticity are all useful. Injection of botulinum toxin for the relief of spasticity has gained wide favor and is now used early in the child’s life to preempt deformities. Most published trials of either of these approaches have been too small, however, to allow firm conclusions to be drawn about the long-term durability of treatment. In experienced hands, selective and partial section of dorsal spinal roots has had a beneficial effect on regional spasticity. Hyperbaric oxygen treatment of children with cerebral palsy was ineffective in a randomized trial conducted by Collet and colleagues, despite periodic claims to the contrary.
In summary, it can be said that all these forms of disabling motor abnormalities rank high as important issues in neuropediatrics. In attempts at prevention, steps have been taken in most hospitals to identify and eliminate risk factors. Indeed, better prenatal care, reduction in premature births, and control of respiratory problems in critical care wards has reduced their incidence and prevalence. Physical and mental therapeutic measures appear to be helpful, but many of the methods have been difficult to evaluate in a nervous system undergoing maturation and development. The neurologist can contribute most by segregating groups of cases of identical pattern and etiology and in differentiating the congenital groups of delayed expressivity from the treatable acquired diseases of this age period. Woefully lacking are critical neuropathologic studies.
Throughout the intrauterine period the embryo and fetus are subject to particular infections. Because the infective agent must reach the fetus through the placenta, it is evident that the permeability of the latter at different stages of gestation and the immune status of the maternal organism are determinative. We include a discussion of these intrauterine infections here because some of them may lead to malformations or destructive lesions of the brain and, later in life, must be distinguished from developmental abnormalities.
Until the third to fourth month of gestation, the large microbial organisms—such as bacteria, spirochetes, protozoa, and fungi—cannot invade the embryo, even if the mother harbors the infection. Viruses, however, may do so, specifically rubella, CMV, HIV, and possibly others. The rubella virus enters embryonal tissues during the first trimester, Treponema pallidum in the fourth to fifth postconceptional months, and Toxoplasma after that period. Bacterial meningitis (except for that caused by Listeria monocytogenes, described below) is essentially a perinatal infection contracted during or immediately after parturition. Neonatal herpes simplex encephalitis, as a result of the type 2 (genital) virus, is also usually acquired by passage through an infected birth canal. Some cases of HIV infection may be acquired during delivery, but most are a result of transplacental transmission.
The main neonatal infections—toxoplasmosis, rubella, CMV, and herpes—have been commonly designated by the acronym TORCH (toxoplasmosis, other infections, rubella, cytomegalovirus, and herpes simplex). With the persistence of Listeria, the rise of AIDS infections, and a marked reduction in rubella infections, the mnemonic LATCH, which includes Listeria and HIV, might be more appropriate. There has been recent interest in maternal Zika virus infection during the first trimester and microcephaly with developmental delay in infants, discussed below.