[Early assessment of severe hypoxic-ischemic encephalopathy in neonates by diffusion-weighted magnetic resonance imaging techniques and its significance].
OBJECTIVE
Hypoxic-ischemic encephalopathy (HIE) is an important cause of morbidity and mortality in the neonates. Early and accurate diagnosis is helpful not only for assessing prognosis but also for making treatment decisions. The aim of this study was to explore the value of early assessment of HIE by applying the diffusion-weighted imaging (DWI) in acute (within 72 hours), subacute or chronic stages of HIE in comparison to conventional magnetic resonance imaging (MRI) in clinical practice.


METHODS
Images and clinical charts of fourteen term neonates with clinically diagnosed severe hypoxic-ischemic encephalopathy treated in the NICU from January 2006 to February 2007 were retrospectively reviewed. Inclusion criteria were: term infant (37 approximately 42 weeks) and high clinical suspicion of severe HIE (low Apgar scores, need for resuscitation, metabolic acidosis, acute encephalopathy (eg, hypotonia, coma, seizures). All examinations were performed on a 3.0-T MRI system (Philips Intera Acheva Magnetom Vision) with echo-planar imaging capability with the use of a standard protocol. The imaging protocol for all the patients contained diffuse weighted images (EPI-SE, TR = 2144 ms, TE = 56 ms), T1-weighted images (TR = 389 ms; TE = 15 ms; slice thickness = 4 mm) as well as T2-weighted images (TR = 3035 ms; TE = 100 ms; slice thickness = 4 mm). The studies were first performed within 72 hours of life in these 14 consecutive patients, including both standard T1, T2-weighted image and DWI; follow-up MR studies were performed for 4 patients at the ages of 7 days, for 4 at 14 days, for another 3 at ages of both 21 days and 8 months.


RESULTS
First inspection (on an average of 48 hours after birth): routine T1, T2-weighted images showed normal images in all patients, while diffusion images showed symmetric high intensity signal in the lateral thalami and posterior limbs of internal capsules (PLIC). Following up: on day 7, routine MRI showed both symmetric T1 prolongation and T2 slightly shortening in lateral thalami, DWI showed abnormal high signal intensity in bilateral basal ganglion (mainly in the back site of lentiform nuclei, putamen) and the cortex around central sulcus, but the previous hyperintensity in lateral thalami and PLIC disappeared. On day 14, routine MRI showed symmetric T1 prolongation, T2 shortening in bilateral thalami, lentiform nuclei and cortex around central sulus. On day 21, routine MRI showed T1 prolongation, T2 shortening in bilateral thalami and basal ganglion while previously obvious PLIC disappeared, whereas DWI showed normal images. Eight months later, deeper cerebral sulus, dilation of ventricles and widening of extracerebral space were shown.


CONCLUSIONS
Diffusion-weighted imaging has proved more sensitive than conventional MR imaging sequences in detecting acute cerebral infarction in adult subjects. DWI is proposed as a method for early detection of hypoxic-ischemic brain injury. In this study, DWI showed the same focus (lateral thalami and PLIC) and similar extent of the injury in these severe HIE patients in the early stage after birth (in 72 hours). The sites which showed hyperintensive signals in DWI were consistent with the foci in subsequent follow-up by routine MRI. Thus, DWI is supposed to be a technique for early assessment of the extent of hypoxic-ischemic brain injury and the prognosis in clinic. Though DWI is superior to the other imaging modalities in detecting ischemia, diffusion restriction is not necessarily indicative of permanent damage. The abnormal image on DWI may not last long. However, in chronic stage, the follow-up conventional MRI may compensate the inadequacy of DWI.
Fu
Jian-hua
JH
Department of Pediatrics, Shengjing Hospital of China Medical University, Shenyang 110004, China.
Xue
Xin-dong
XD
Mao
Jian
J
Chen
Li-ying
LY
Wang
Xiao-ming
XM
D001921:Brain / Q000473:pathology*; D002540:Cerebral Cortex / Q000378:metabolism*; D002544:Cerebral Infarction / Q000378:metabolism*; D004058:Diffusion; D006801:Humans; D020925:Hypoxia-Ischemia, Brain / Q000378:metabolism*; D007223:Infant; D007231:Infant, Newborn; D008279:Magnetic Resonance Imaging / Q000379:methods*; D020521:Stroke / Q000378:metabolism