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BACKGROUND AND PURPOSE: Gamma-aminobutyric acid and glutamate system disruptions may underlie neonatal brain injury. However, in vivo investigations are challenged by the need for special 1H-MR spectroscopy sequences for the reliable measurement of the neurotransmitters in this population. We used J-edited 1H-MR spectroscopy (Mescher-Garwood point-resolved spectroscopy) to quantify regional in vivo gamma-aminobutyric acid and glutamate concentrations during the early postnatal period in healthy neonates. MATERIALS AND METHODS: We prospectively enrolled healthy neonates and acquired Mescher-Garwood point-resolved spectroscopy spectra on a 3T MR imaging scanner from voxels located in the cerebellum, the right basal ganglia, and the right frontal lobe. CSF-corrected metabolite concentrations were compared for regional variations and cross-sectional temporal trends with advancing age. RESULTS: Fifty-eight neonates with acceptable spectra acquired at postmenstrual age of 39.1 (SD, 1.3) weeks were included for analysis. Gamma-aminobutyric acid (+ macromolecule) (2.56 [SD, 0.1]) i.u., glutamate (3.80 [SD, 0.2]), Cho, and mIns concentrations were highest in the cerebellum, whereas NAA (6.72 [SD, 0.2]), NAA/Cho, Cr/Cho, and Glx/Cho were highest in the basal ganglia. Frontal gamma-aminobutyric acid (1.63 [SD, 0.1]), Glx (4.33 [SD, 0.3]), Cr (3.64 [SD, 0.2]), and Cho concentrations were the lowest among the ROIs. Glx, NAA, and Cr demonstrated a significant adjusted increase with postmenstrual age (ß = 0.2-0.35), whereas gamma-aminobutyric acid and Cho did not. CONCLUSIONS: We report normative regional variations and temporal trends of in vivo gamma-aminobutyric acid and glutamate concentrations reflecting the functional and maturational status of 3 distinct brain regions of the neonate. These measures will serve as important normative values to allow early detection of subtle neurometabolic alterations in high-risk neonates.

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BACKGROUND AND PURPOSE: Early disturbances in systemic and cerebral hemodynamics are thought to mediate prematurity-related brain injury. However, the extent to which CBF is perturbed by preterm birth is unknown. Our aim was to compare global and regional CBF in preterm infants with and without brain injury on conventional MR imaging using arterial spin-labeling during the third trimester of ex utero life and to examine the relationship between clinical risk factors and CBF. MATERIALS AND METHODS: We prospectively enrolled preterm infants younger than 32 weeks' gestational age and <1500 g and performed arterial spin-labeling MR imaging studies. Global and regional CBF in the cerebral cortex, thalami, pons, and cerebellum was quantified. Preterm infants were stratified into those with and without structural brain injury. We further categorized preterm infants by brain injury severity: moderate-severe and mild. RESULTS: We studied 78 preterm infants: 31 without brain injury and 47 with brain injury (29 with mild and 18 with moderate-severe injury). Global CBF showed a borderline significant increase with increasing gestational age at birth (P = .05) and trended lower in preterm infants with brain injury (P = .07). Similarly, regional CBF was significantly lower in the right thalamus and midpons (P < .05) and trended lower in the midtemporal, left thalamus, and anterior vermis regions (P < .1) in preterm infants with brain injury. Regional CBF in preterm infants with moderate-severe brain injury trended lower in the midpons, right cerebellar hemisphere, and dentate nuclei compared with mild brain injury (P < .1). In addition, a significant, lower regional CBF was associated with ventilation, sepsis, and cesarean delivery (P < .05). CONCLUSIONS: We report early disturbances in global and regional CBF in preterm infants following brain injury. Regional cerebral perfusion alterations were evident in the thalamus and pons, suggesting regional vulnerability of the developing cerebro-cerebellar circuitry.

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OBJECTIVE: The purpose of this study is to highlight the relationship between obstructive hydrocephalus, changes in intracranial pressure, and sensorineural hearing loss. METHODS: A case of a 10-month old infant with sensorineural hearing loss secondary to obstructive hydrocephalus is reported. A literature review, with a focus on sensorineural hearing loss in the setting of changes in intracranial pressure, was performed. RESULTS: The authors report the case of a 10-month old infant with metopic and bicoronal craniosynostosis who presented with bilateral moderately severe sensorineural hearing loss after failing newborn hearing screening. Imaging subsequently demonstrated obstructive hydrocephalus, which was treated with the insertion of a VP shunt. The patient had immediate improvement of her hearing post-operatively, with repeat hearing tests showed resolution of her hearing loss. CONCLUSION: Sensorineural hearing loss is a rare complication of hydrocephalus, but changes in intracranial pressure should be considered in the differential diagnosis. We put forth a flow diagram illustrating the hypothesized relationship between intracranial pressures, alterations in the levels of cochlear fluid, and hearing.

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Variations in cerebral venous development can influence the ability to regulate drainage. In cerebral sinovenous thrombosis, these variations can be associated with elevated intracranial pressure. We present a series of pediatric patients with unilateral cerebral sinovenous thrombosis and investigate whether the contralateral venous sinus size increases the risk of developing elevated intracranial pressure. Patients diagnosed with a unilateral cerebral sinovenous thrombosis were identified by querying our institutional radiology data base. The difference in the occurrence of elevated intracranial pressure in patients with cerebral sinovenous thrombosis with and without hypoplastic venous sinuses was studied. Twelve cases of unilateral cerebral sinovenous thrombosis met the inclusion criteria and had sufficient images. Six patients had hypoplastic contralateral venous sinuses. The presence of hypoplastic contralateral venous sinus in the setting of thrombosis of a dominant sinus was associated with elevation of intracranial pressure (83% versus 0%, P = .015). Patients with cerebral sinovenous thrombosis and contralateral hypoplastic venous sinuses are at higher risk of developing elevated ICP and may benefit from screening with an ophthalmologic examination.

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OBJECTIVE: To evaluate the clinical impact of routine term-equivalent magnetic resonance imaging (TE-MRI) for extremely low-birth-weight infants at a regional neonatal intensive care unit. STUDY DESIGN: This is a single-center retrospective study evaluating preterm survivors who underwent TE-MRI. MRI abnormalities were compared between infants with and without cranial ultrasonography (CUS) abnormalities. Cost analysis comparing imaging modalities was also performed. RESULTS: TE-MRI use increased from 17% in 2006 to 76% in 2010. MRI detected new findings in nearly half of infants, whether or not they had known ultrasound abnormalities. MRI detected more cerebellar (18% vs 6%, P=0.04) and moderate white matter injury (12% vs 7%, P<0.001), and altered simulated neurological prognosis across developmental domains. The cost of TE-MRI was $1600, which was comparable to serial CUSs. CONCLUSION: TE-MRI detects new abnormalities and impacts developmental prognosis in the extremely low birth weight, which supports its use despite the added financial cost.

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Elevated cerebral lactate is increasingly detected by magnetic resonance spectroscopy in the human fetus diagnosed with various pathologic conditions. However, the significance of detectable cerebral lactate remains uncertain. We present two cases of fetal cerebral lactate with adverse pregnancy outcomes.

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1. The suction pipette technique was used to examine the effect of a conditioning pre-flash on the saturation time (tsat) of a bright test flash (intensity 10,000-250,000 isomerizations) delivered to intact salamander or toad rod outer segments. The conditioning flash was delivered 0-60 s before the test flash; its intensity was typically between six and sixty times dimmer than the test flash, and it was sufficient by itself to fully saturate the photocurrent. 2. A saturating pre-flash delivered before a saturating test flash reduced the tsat of the test flash. This was equivalent to a reduction in phototransduction gain (psi). 3. The pre-flash had little effect on tau zero the time constant of decay of the rate-limiting species in photoresponse inactivation (activated rhodopsin or the activated G-protein-phosphodiesterase complex). 4. The tsat declined exponentially as the separation time between a fixed intensity pre-flash and test flash was increased. The time constant (tau p) of decline in tsat was approximately 2.4s. The maximum reduction in tsat corresponded to a reduction in the apparent gain of phototransduction to approximately 0.10 of its original level. This exponential decline is consistent with a [Ca2+]i-mediated effect. 5. We conclude that the rate-limiting step in response inactivation and the step responsible for light-induced gain reduction constitute separate and distinct steps of the phototransduction cascade.

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