Related Experiment Video
Updated: Jul 5, 2026
Neurobehavioral Assessments in a Mouse Model of Neonatal Hypoxic-ischemic Brain Injury
Published on: November 24, 2017
[Clinical evaluation of neonatal hypoglycemic brain injury demonstrated by serial MRIs]
Jian Mao1, Li-Ying Chen, Jian-Hua Fu
1Department of Pediatrics, Shengjing Hospital of China Medical University, Shenyang 110004, China. maoj@cmu2h.com
Insights
Neonatal hypoglycemic brain injury, particularly affecting occipital and parietal cortexes, correlates with hypoglycemia severity. Diffusion-weighted imaging (DWI) effectively detects early brain injury in newborns.
Area of Science:
- Neonatal neurology
- Pediatric radiology
- Neuroimaging
Context:
- Hypoglycemia is a common metabolic disturbance in neonates.
- Brain injury resulting from hypoglycemia can lead to long-term neurological deficits.
- Understanding the relationship between clinical presentation and imaging findings is crucial for timely intervention.
Purpose:
- To investigate the correlation between clinical and imaging features in neonates diagnosed with hypoglycemic brain injury.
- To identify the most vulnerable brain regions affected by neonatal hypoglycemia.
- To evaluate the utility of serial Magnetic Resonance Imaging (MRI) sequences, including Diffusion-Weighted Imaging (DWI), in assessing the severity and progression of hypoglycemic brain injury.
Summary:
- Clinical manifestations of hypoglycemic brain injury in neonates include seizures, lethargy, and hypotonia, with severe cases presenting with coma or cardiorespiratory arrest.
- Occipital and parietal cortexes (OPC) were consistently affected in all neonates studied, with severe hypoglycemia leading to widespread cortical involvement and potential damage to white matter, basal ganglia, and thalamus.
- Diffusion-weighted imaging (DWI) demonstrated high-intensity signals as an early indicator of hypoglycemic brain injury, with serial MRIs revealing cerebral atrophy and encephalomalacia in severe cases, and delayed myelination or spastic diplegia in follow-up.
Impact:
- Establishes a direct relationship between the severity of hypoglycemia and the extent of brain injury visualized on serial MRIs.
- Highlights the occipital and parietal areas as primary targets of neonatal hypoglycemic brain injury.
- Demonstrates the diagnostic value of DWI in detecting early-stage hypoglycemic brain injury and informs prognosis based on imaging patterns.
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.
