Use of AAC by a Preshooler with a History of In-Utero Stroke

Introduction Fetal stroke may follow an ischemic (thromboembolic) or hemorrhagic event which occurs between 14 weeks of gestation and the onset of labor resulting in delivery (Ozduman, et al., 2004). In ischemic strokes, cerebral blood flow falls below a level necessary to maintain nerve cell integrity and neurological function. Hemorrhagic strokes occur secondary to intra-cranial bleeding. A perinatal stroke is similar to an ischemic stroke, but it occurs between 28 weeks of gestation and 7 days of age. Poor understanding of etiologies of fetal and perinatal strokes have led to an estimate of 1 in 4,000 live births, with the true incidence probably being higher. Diagnosis usually includes ultrasound measurement of the fetal cranium and, more recently, fetal magnetic resonance imaging (MRI) and computed tomography (CT), which provide better definition of the injury to the fetal cerebrum. Patients often remain undiagnosed, as clinical outcomes of surviving infants may not be present until later in the first year of life (Ozduman, et al., 2004). Reports of in-utero strokes began some 30 years ago, based on autopsy data, and continue to follow a case report format, viewing living brains. An early review of nearly 600 infants examined at autopsy (Barmada, Moossy & Shuman, 1979) indicated the presence of cerebral infarcts (necrosis in an area of brain tissue, caused by an obstruction, usually a thrombosis or an embolism) in about one in twenty (5.4%) instances. Neonates delivered at term were more likely to be brain-damaged than premature infants, where multiple smaller infarcts had occurred. Surprisingly, for the infants who survived, disorders associated with focal neurological deficits were not predominant. Rather, the clinical features tended to include such autonomic disturbances as prolonged apnea and episodic seizures, and, in those infants with less severe complications, hemiplegia, mental and motor retardation, and recurrent seizures. As recently as 25 years ago, few infants surviving stroke were reported in the literature (Ment, Duncan & Ehrenkranz, 1984). Among infants who died during the first months of life, necrotic foci (areas of cell death) were generally located in border zones between vascular territories (Lou, 1983). This suggests that the in-utero brain is fragile, offering the brain poor protection against perfusion pressure, with normal birth causing a decrease in oxygen or mild hypotension sufficient to abolish autoregulation (the process by which organs maintain their own blood supply). Inadequate pressure, caused by reduced blood flow to the brain, can cause ischemia. Neonatal ischemia in surviving infants was seen as decisive in development of atrophic encephalopathy, where brain cells decrease in size, with the resultant clinical picture of motor and cognitive dysfunction. Etiologies of fetal and neonatal strokes are reported both as ischemic (thromboembolic) in "a significant number of these events" (Chalmers, 2005, p. 333) and hemorrhagic, with intracranial hemorrhage occurring in "approximately 40% of infants of less than 32 weeks' gestation" (Huang, Chen, Tseng, Ho, & Chou, 2006, p. 135). One cause of the discrepancy may be the use of ultrasonography (US) for prenatal detection of fetal strokes. The use of MRI to supplement US findings may contribute to diagnostic accuracy and improve prediction of postnatal neurodevelopmental prognosis (Elchalal, et al., 2005). Confirmation of diagnosis by MRI or CT scan has implicated the brain's ventricles, which produce the cerebrospinal fluid (CSF) needed to surround and protect the brain. Periventricular venous infarction may result in a focally enlarged lateral ventricle (Takanashi, Barkovich, Ferriero, Suzuki, & Kohno, 2003; Takanashi, Tada, Barkovich, & Kohno, 2005), or in hydrocephalus following hemorrhage in the choroids plexuses, which manufacture CSF in the ventricles (Huang, et al., 2006). Motor outcomes, after follow-up of more than five years, included leg hemiparesis and spasticity, if the basal ganglia were involved; non-motor disorders associated with cortical involvement included cognitivebehavioral impairments, visual deficits, and epilepsy (Kirton, Deveber, Pontigon, Macgregor, & Shroff, 2008). …