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.
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.