目的：探讨新生儿低血糖性脑损伤的影像特征与临床及预后关系，为低血糖性脑损伤的诊断及预防提供依据。方法：16例低血糖性脑损伤新生儿于入院24~48小时（n=16），生后2周左右（n=11），1~5月(n=3)进行了常规的MRI 与MRI-DWI动态观察与临床随访。结果：惊厥、嗜睡、肌张力减低为常见的症状和体征，昏迷和呼吸衰竭5例。低血糖脑损伤时最低血糖值为0.98±0.43 mmol/L,5例重者血糖为0.72±0.42 mmol/L。脑电图提示轻者为间断低电压，重者电压平坦，甚至电静息。16例均有顶枕部皮层受累，合并脑室周围白质损伤2例，弥漫性皮层受累5例，其中1例合并广泛的脑白质损伤，2例合并丘脑基底节受累。弥漫性皮层受累5例和顶枕部合并脑白质损伤2例血糖明显低于仅有顶枕部受累者（0.71±0.35 mmol/L vs 1.19±0.42 mmol/L，t=2.4124,P<0.05）。早期信号改变在DWI表现最明显为高信号。4例弥漫性脑水肿者再次检查已发生广泛性脑萎缩和多发脑软化；顶枕部受累者7例接受了再次检查，5例T1WI与T2WI信号异常，而DWI信号异常3例。临床表现轻者以顶枕部皮层受累为主，重者弥漫性皮层受累为主。顶枕部受累1例随访发现髓鞘发育落后；合并白质受累1例发生双下肢痉挛性瘫痪；弥漫性皮层受累1例发生广泛脑软化。结论：新生儿低血糖性脑损伤与低血糖的严重程度密切相关，顶枕部皮层是易损区，但重度的损伤可表现为弥漫性皮层受累甚至合并广泛的白质或基底节丘脑受损，DWI可以早期反映脑损伤情况。

OBJECTIVE: To study the relationship between clinical and imaging features in neonates with hypoglycemic brain injury. METHODS: Sixteen neonates with hypoglycemic brain injury received a MRI scan with the sequences of T1WI, T2WI and DWI within 48 hrs after admission. Of the 16 patients, 11 received second MRI scan at two weeks of their lives, and 3 received a third scan at ages of 1-5 months. RESULTS: Repeated seizures, lethargy and hypotonia were common clinical manifestations. Five severe hypoglycemia cases presented coma, respiratory failure and even cardiorespiratory arrest. The minimum mean value of whole blood glucose (WBG) in the 16 patients was 0.98±0.43 mmol/L, and that of the 5 severe cases was 0.72±0.42 mmol/L. EEG showed intermittent low voltage in the mild hypoglycemia cases. Flatten pattern and even electrocerebral silence was noted in the severe cases. Occipital and parietal cortexes (OPC) injuries were found in all of the 16 patients and 2 patients had concurrent periventricular white matter injury. A widespread involvement of cortex was found in the 5 severe hypoglycemia cases in which 1 showed widespread involvement of white matter, and 2 showed involvement of basal ganglia and thalamus. The 5 patients with widespread cortex injury and the 2 patients with OPC and periventricular white matter injury showed lower minimum WBG levels compared with those with OPC alone (0.71±0.35 mmol/L vs 1.19±0.42 mmol/L; t= 2.4124,P<0.05). The appearance of high-intensity signals on DWI was shown as early changes of signals in all of the 16 patients. The second MRI scan for 7 patients with OPC showed abnormal signals on T1WI and T2WI in 5 patients and abnormal signals on DWI in 3 cases. Cerebral atrophy and multicystic encephalomalacia were found in four patients with widespread involvement of cortex on DWI. In the follow-up one patient with OPC presented delayed myelination and one with concurrent white matter injury showed spastic diplegia. One patient with widespread involvement of cortex showed diffused encephalomalacia. CONCLUSIONS: The severity of hypoglycemic brain injury demonstrated by serial MRIs relates to the severity of hypoglycemia. The occipital and parietal areas are the most vulnerable following hypoglycemia in neonates. Severe hypoglycemic brain injury manifests as a widespread involvement of cortex, or combined with white matter, or basal ganglia and thalamus. DWI can show early hypoglycemic brain injury.