Original articleLinear hyperechogenicity within the basal ganglia and thalamus of preterm infants
Introduction
Linear hyperechogenicity (LHE) involving the blood vessels contiguous with the basal ganglia and thalamus is an uncommon sonographic finding occurring more often in term infants and usually identified at birth [1], [2], [3], [4], [5], [6], [7], [8], [9]. The most frequently associated conditions include intrauterine infection [1], [2], [3], [4], [5] (e.g., cytomegalovirus [CMV]) and chromosomal abnormalities (e.g., trisomy 13 and trisomy 21) [1], [4], [6], [7], [8]. LHE has also been observed in the preterm infant and usually evolves later during a prolonged hospitalization [9]. The neuropathologic correlate of LHE appears to be a vasculopathy [4], [9]. The etiology of this lesion is unclear. However, during development, the basal ganglia and thalamus are selectively vulnerable to hypoxia-ischemia. This vulnerability is in part the result of a border zone blood supply to this region, which increases the risk of injury during episodes of hypoxia-ischemia [10]. Such injury may be further exacerbated secondary to a transient dense expression of glutamate receptors within the basal ganglia [11], [12], [13]. Infants with apnea and bradycardia or chronic lung disease would appear to be more vulnerable to the development of LHE as a consequence of recurrent episodes of hypoxia or ischemia.
The long-term clinical significance of LHE in preterm infants has not been fully evaluated. Because the basal ganglia and thalamus are integrated centers controlling movement, cognition, emotion, and behavior [14], [15], we hypothesized that preterm infants with LHE involving the blood vessels supplying this region would be at increased risk of abnormal neurodevelopmental outcome involving fine motor, cognitive, and behavioral performance compared with infants without such abnormalities. The objectives of this study were to determine the clinical characteristics and neurodevelopmental outcome and, more specifically, the cognitive and behavioral performance in sick preterm infants who develop LHE during hospitalization.
Section snippets
Cranial ultrasound imaging
Serial cranial ultrasound scans of preterm infants with a birth weight less than 1,250 gm who were admitted to the Neonatal Intensive Care Unit at Parkland Memorial Hospital between January 1995 and December 1996 were reviewed, and infants with LHE were identified. At our institution, preterm infants who weighed less than 1,250 gm are routinely scheduled for cranial ultrasound scans on days 3-5, 10-14, and 28 after birth and before discharge. Scans of coronal and parasagittal images are
Results
LHE was observed in 10 (5.1%) of 193 infants with a birth weight of less than 1,250 gm who were admitted during the study period. The mean ± S.D. birth weight of the 10 infants was 907 ± 224 gm and the gestation age was 28.0 ± 1.4 weeks, similar to the birth weight and gestation age of the 20 control infants (859 ± 108 gm and 27.2 ± 1.1 weeks, respectively).
Discussion
The data in this report describe the evolution, associated clinical characteristics, and outcome of preterm infants with LHE. LHE was observed in approximately 5% of preterm infants with a birth weight of less than 1,250 gm, which is slightly more common than the reported 3% incidence of cystic periventricular leukomalacia in our institution [18]. In contrast to the early appearance of LHE in term infants, this lesion evolved slowly, with a mean age at diagnosis of 1 month. The lesion was
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2008, Seminars in PerinatologyCitation Excerpt :Although the authors noted that injury could be detected by MRI, CT, or CUS, CUS findings were transient in some cases. Several groups have reported on the ability to recognize basal ganglia and thalamic hyperechogenicity by serial CUS,11,55,56 but the association of this particular finding with adverse neurodevelopmental outcome is variable. MRI may demonstrate basal ganglia injury more clearly and frequently than CUS, but MRI studies have also suggested a strong relationship of these lesions with other types of brain injury.57,58