A 4-day-old male newborn has an incidental head ultrasound finding.Born to a 22-year-old gravida 2, para 1 White womanAntenatal serologic testing unremarkableNormal prenatal ultrasound scansNo history of consanguinityEstimated gestational age 36 weeksSpontaneous vaginal delivery, rupture of membranes 1 hour before deliveryApgar score: 9 and 10 at 1 and 5 minutes, respectivelyA male newborn is admitted to the NICU on day 2 after birth due to respiratory distress and was noted to have a sparse petechial rash; these symptoms resolved within 24 hours. A sepsis evaluation was completed and was negative. He remained hospitalized for 12 days due to feeding difficulties that improved over time.Heart rate: 152 beats/minRespiratory rate: 34 breaths/minBlood pressure: 75/56 mm Hg (mean 63 mm Hg)Oxygen saturation: 100% (in room air)Temperature: 98°F (36.6°C)Birthweight 2,635 kg (42nd percentile), length 46.5 cm (39th percentile), head circumference 33.0 cm (59th percentile)Weight 2,420 kgHead: Normocephalic; normal, open, flat fontanelles; symmetric facies; patent nares; intact palate; no neck mass or crepitus; nondysmorphicOral cavity: Pink mucosae, intact palate, no lymphadenopathy, normal suck and rooting reflexLungs: Clear, equal breath sounds; no respiratory distressCardiovascular: Normal S1, S2; regular rate and rhythm; no murmurs or gallopsAbdomen: Not distended; no organomegaly; no apparent discomfort on abdominal palpationGenitourinary: Normal male genitalia; patent anusSkeletal: Spine appears normalSkin: No icterus, birthmarks, or other rashesNeurologic: Symmetric Moro reflex, normal strength and toneComplete blood cell count with differential: NormalC-reactive protein: <0.29 mg/dL (<2.9 mg/L)Blood culture: SterileAt 4 days of age, head ultrasonography was performed in accordance with unit protocol for late preterm infants (Fig 1A and 1B).For a 4-day old late preterm newborn with an incidental finding on cranial ultrasonography, differential diagnostic considerations include: Hypoxic-ischemic encephalopathyCongenital infection (cytomegalovirus [CMV], toxoplasmosis, HIV, syphilis, rubella)Intracranial hemorrhageStrokeCongenital CMV infection.The ultrasound findings consist of thick hyperechogenic linear streaks in the thalami and basal ganglia (Figs 2A and 2B), without any signs of hemorrhage or stroke. These are consistent with stage 3 lenticulostriate vasculopathy (LSV). Antenatal serologic tests were reviewed: the mother was not tested for CMV during pregnancy. A CMV polymerase chain reaction (PCR) urinary screen was performed on day 8, with positive result.The infant had a normal hearing screen. Liver enzymes, bilirubin concentration, and renal function were also normal. He was discharged from the hospital at 12 days of age with a recommendation for follow-up in the neonatology outpatient clinic. He is currently 4 months old, has remained asymptomatic, and his neurodevelopment, vision, and hearing are all normal. Currently, he is not receiving any therapy.Given the risk of sensorineural deafness and ophthalmologic, neurologic, and neurodevelopmental disorders associated with CMV, this child will follow up with a multidisciplinary team with periodic developmental assessments.LSV is an ultrasonographic finding that is characterized by increased echogenicity in the lenticulostriate arteries at the basal ganglia and/or thalamus. The pathogenesis is unclear. (1) The diagnosis of LSV is operator-dependent; to reduce interrater variability, Sisman et al proposed a classification system that categorizes LSV into 4 stages, according to vessel thickness and hyperechogenicity (2): Stage 0: Lenticulostriate vessels are not visibleStage 1: Lenticulostriate vessels are thin and faintly seenStage 2: Lenticulostriate vessels are thin, but hyperechogenicStage 3: Lenticulostriate vessels are thick and hyperechogenic (echogenicity similar to sylvian fissure)LSV can be associated with many conditions, infectious and noninfectious, including Toxoplasma gondii, other agents, rubella, CMV, and herpes simplex virus (TORCH) infections, chromosomal disorders, and asphyxia. LSV can also be a nonspecific finding in 19% of cases and it is most commonly associated with hypoxic-ischemic conditions. (3) It is detected in 0.4% to 5.8% of head ultrasound scans obtained in neonates. (4) A more accurate classification by stages and the assessment of progression may be useful in the future to reduce the range of differential diagnoses. (2)The most common congenital infection associated with LSV is CMV; the greater the severity of the LSV, the more likely the infant has CMV. (5) In addition, when LSV is associated with other structural abnormalities in the brain, CMV infection is even more likely and associated with worse outcomes. (5) Routine CMV assessment in the presence of isolated LSV is controversial; in this scenario, it is reasonable to perform urine CMV PCR screening, keeping in mind that this is an inexpensive and noninvasive test. (1)(6) Amir et al suggest that LSV is a possible marker of high risk for sensorineural loss in both symptomatic and asymptomatic CMV congenital infection. (4) The prognostic value of LSV has been challenged by other authors who believe that more extensive neuroimaging anomalies have greater prognostic value. (7) The clinical significance of asymptomatic LSV on long-term neurodevelopmental outcome is not clear. (1)Several cranial ultrasound signs are suggestive of congenital infections; these include ventriculomegaly; calcifications; subependymal, periventricular, or germinolytic cysts; and brain atrophy. (7)(8) Maternal serologies can help to exclude HIV, syphilis, and rubella.Hypoxic-ischemic encephalopathy in the newborn may also present with focal brain injury in the thalamic and basal ganglia regions. Ultrasound findings include focal or diffuse hyperechogenicity in the thalamus, basal ganglia, and perirolandic cortex, and signs of cerebral edema, such as loss of grey-white matter differentiation and obliteration of the cerebrospinal fluid–containing spaces. (8) Magnetic resonance imaging is more specific and sensitive than ultrasonography to diagnose hypoxic-ischemic encephalopathy. In the case presented, this etiology was less likely because there was no prenatal sentinel event, there were no signs of fetal distress or need for resuscitation, the infant’s Apgar scores were normal, and the infant had normal neurologic findings.A thalamic stroke or hemorrhage can also present with hyperechogenicity on cranial ultrasonography. However, it usually has a curved well-delineated configuration as opposed to the linear streaks in LSV and is mostly unilateral. The clinical signs associated with these conditions include seizures, apnea, and hypotonia, among other neurologic deficits.LSV is often a nonspecific ultrasonographic finding but it can be associated with congenital infections or other etiologies.Although controversial, if LSV stage 3 is identified on head ultrasonography, testing for CMV should be considered.Early detection can have an impact on prognosis because of the possibility of close follow-up and initiation of potential therapies in cases of LSV that are associated with congenital CMV.