China ; Humans ; Hypoxia-Ischemia, Brain ; diagnosis ; therapy ; Infant, Newborn

Humans ; Hypoxia-Ischemia, Brain ; diagnosis ; therapy ; Infant, Newborn ; Infant, Premature

Humans ; Hypoxia-Ischemia, Brain ; diagnosis ; therapy ; Infant, Newborn ; Time Factors

BACKGROUNDMild hypoxic-ischemic encephalopathy (HIE) injury is becoming the major type in neonatal brain diseases. The aim of this study was to assess brain maturation in mild HIE neonatal brains using total maturation score (TMS) based on conventional magnetic resonance imaging (MRI).

METHODSTotally, 45 neonates with clinically mild HIE and 45 matched control neonates were enrolled. Gestated age, birth weight, age after birth and postmenstrual age at magnetic resonance (MR) scan were homogenous in the two groups. According to MR findings, mild HIE neonates were divided into three subgroups: Pattern I, neonates with normal MR appearance; Pattern II, preterm neonates with abnormal MR appearance; Pattern III, full-term neonates with abnormal MR appearance. TMS and its parameters, progressive myelination (M), cortical infolding (C), involution of germinal matrix tissue (G), and glial cell migration bands (B), were employed to assess brain maturation and compare difference between HIE and control groups.

RESULTSThe mean of TMS was significantly lower in mild HIE group than it in the control group (mean ± standard deviation [SD] 11.62 ± 1.53 vs. 12.36 ± 1.26, P < 0.001). In four parameters of TMS scores, the M and C scores were significantly lower in mild HIE group. Of the three patterns of mild HIE, Pattern I (10 cases) showed no significant difference of TMS compared with control neonates, while Pattern II (22 cases), III (13 cases) all had significantly decreased TMS than control neonates (mean ± SD 10.56 ± 0.93 vs. 11.48 ± 0.55, P < 0.05; 12.59 ± 1.28 vs. 13.25 ± 1.29, P < 0.05). It was M, C, and GM scores that significantly decreased in Pattern II, while for Pattern III, only C score significantly decreased.

CONCLUSIONSThe TMS system, based on conventional MRI, is an effective method to detect delayed brain maturation in clinically mild HIE. The conventional MRI can reveal the different retardations in subtle structures and development processes among the different patterns of mild HIE.

Brain ; pathology ; Female ; Humans ; Hypoxia-Ischemia, Brain ; diagnosis ; Infant, Newborn ; Magnetic Resonance Imaging ; methods ; Male

OBJECTIVETo elucidate that diffusion weighted imaging (DWI) can be used to predict the injured regions of neonatal brain with hypoxic-ischemic encephalopathy (HIE) in the early phase of injury, and to measure the apparent diffusion coefficient (ADC) values in the multiple regions of the brain.

METHODThe participants in this study were twenty-six infants with HIE from neonatology ward hospitalized between July 2006 and July 2009. Nineteen patients had severe HIE, and seven had moderate HIE. DWI and conventional magnetic resonance imaging (MRI) were performed for each case within the first 72 hrs. The ADC values of eight regions of interest (ROIs) were measured in ten cases with severe HIE (ADC values group). ROIs included posterior limb of internal capsule (PLIC), ventrolateral thalami, basal ganglia, perirolandic cortex, occipital cortex, centrum semiovale, brainstem, and frontal white matter. Twelve neonates were enrolled as the control subjects.

RESULTSDuring the first 72 hrs, the conventional MRI of 26 patients showed subarachnoid hemorrhage in 5, subdural hemorrhage in 2, and mild high signal intensity in the cortex of only one patient. In the 19 cases with severe HIE, abnormal signal intensities were seen in ventrolateral thalami and perirolandic cortex of 17 patients (89%), and the remaining 2 infants showed abnormal cortex and subcortical white matter. In 7 cases with moderate HIE, 4 had abnormal signal intensity in the cortex and subcortical white matter, 2 had abnormal periventricular white matter, and only one showed abnormal signal intensity in the ventrolateral thalami and perirolandic cortex. In the ADC values group, the average ADC values of posterior limb of internal capsule (PLIC), ventrolateral thalami, basal ganglia, perirolandic cortex, occipital cortex, centrum semiovale, brainstem, and frontal white matter respectively were 0.68 (0.56 - 0.88), 0.73 ± 0.13, 0.67 ± 0.11, 0.78 ± 0.22, 0.90 ± 0.16, 0.87 ± 0.21, 0.73 ± 0.19, 1.32 ± 0.22 × 10(-3) mm(2)/S. In the control group, the average ADC values of posterior limb of internal capsule (PLIC), ventrolateral thalami, basal ganglia, perirolandic cortex, occipital cortex, centrum semiovale, brainstem, and frontal white matter respectively were 0.96 (0.95 - 1.02), 1.02 ± 0.90, 1.15 ± 0.99, 1.08 ± 0.07, 1.09 ± 0.08, 1.39 ± 0.20, 0.96 ± 0.05, 1.58 ± 0.18× 10(-3) mm(2)/S. There was statistically significant difference in the average ADC values between each of 8 ROIs of infants with HIE and healthy neonates (P < 0.01).

CONCLUSIONIn the first days after birth, the major injured regions of severe HIE were ventrolateral thalami and perirolandic cortex, the minor injured regions were cortex and subcortical white matter. Multiple regions of moderate HIE were injured, including cortex with subcortical white matter, periventricular white matter, and ventrolateral thalami with perirolandic cortex. The ADC values of the regions with abnormal signal intensity decreased, also some regions with the normal signal intensity.

Brain ; pathology ; Diffusion Magnetic Resonance Imaging ; methods ; Female ; Humans ; Hypoxia-Ischemia, Brain ; diagnosis ; Infant, Newborn ; Male

OBJECTIVETo explore the value of electroencephalogram (EEG) in early diagnosis of brain injury in neonates with asphyxia.

METHODSEEG examination was performed in 49 neonates with asphyxia (mild: n=9; severe: n=40) within 6 hrs of their births. Of the 49 asphyxiated neonates, 33 had concurrent HIE, including 20 cases of mild, 9 cases of moderate and 4 cases of severe HIE.

RESULTSTwenty-one (63.6%) out of the 33 patients with HIE showed abnormal EEG, but only one (6.3%) in the asphyxia group without HIE. All of 13 patients with moderate-severe HIE showed abnormal EEG. The degree of EEG abnormality in neonates with HIE was consistent with the clinical grading of HIE. The neonates whose EEG showed electrical silence and burst suppression and the abnormalities were kept unrecoverable for more than 2 weeks had very poor prognosis.

CONCLUSIONSEEG can reflect brain injury caused by neonatal asphyxia and the severity of brain injury. It may be useful for early diagnosis of brain injury following asphyxia in neonates.

Asphyxia Neonatorum ; complications ; physiopathology ; Early Diagnosis ; Electroencephalography ; Female ; Humans ; Hypoxia-Ischemia, Brain ; diagnosis ; Infant, Newborn ; Male

Female ; Humans ; Hydrogen ; Hypoxia-Ischemia, Brain ; diagnosis ; Infant, Newborn ; Magnetic Resonance Spectroscopy ; methods ; Male

The neonatal burst suppression is a severe EEG pattern and always demonstrates serious damage of nerve system. But the outcome of these patients depends on the different etiology. A total of 256 cases of video EEG recordings were analyzed in order to summarize the etiology and outcome of burst suppression. The results showed that some patients in all 17 cases of burst suppression showed EEG improvement. The etiology was the dominant factor in long term outcome. It was suggested that effective video EEG monitoring is helpful for etiologic study and prognosis evaluation.
Electroencephalography/*methods ; Hypoxia-Ischemia, Brain/diagnosis ; Monitoring, Physiologic/methods ; Neonatology/methods ; Video Recording

OBJECTIVETo establish a neonatal Tibet minipig model of hypoxic-ischemic encephalopathy and evaluate the magnetic resonance imaging (MRI) manifestations and pathological findings.

METHODSSix neonatal (1-3 days old) Tibet minipigs were randomized into model group (n=4) and control group (n=2). In model group, hypoxic-ischemic encephalopathy was induced by surgical ligation of the bilateral carotid artery followedimmediately by hypoxic exposure in a hypoxia chamber for 1 h. ESWAN was performed at 2 h, 24 h, 3 days and 5 days after induction of HIE or at 2 h after sham surgery in the control animals to evaluate the brain damage. Conventional MRI scans (T2FLAIR, T2WI, and DWI) were also performed at 24 h after the modeling.

RESULTSIn the neostriatum, values of T(2)*-weighted MRI increased and reached the peak level at 3 days post-injury (P<0.05). Subcortical white matter T(2)* values reached the peak level at 24 h (P<0.05). Neostriatum R(2)* values were at the lowest level at 3 days (P<0.05). Magnitude values were significantly increased after the model establishment (P<0.05). DWI showed multiple mild focal high signals in the bifrontal subcortical white matter and bilateral neostriatum; T2FLAIR showed slightly increased signal; T2WI showed no obvious abnormalities. SWI showed dilated medulla veins adjacent to the bilateral lateral ventricles and basal ganglia. In the early stage of HIE, brain pathologies were characterized mainly by edema and venous congestion with occasional focal necrosis and hemosiderin deposition.

CONCLUSIONESWAN sequence is capable of detecting bleeding and brain edema, and T(2)*, R(2)*, and magnitude values can be used to estimate the changes of brain damage following HIE.

Animals ; Disease Models, Animal ; Hypoxia-Ischemia, Brain ; diagnosis ; pathology ; Magnetic Resonance Imaging ; Swine ; Swine, Miniature ; Tibet

BACKGROUND: Ocular dipping (OD), or inverse ocular bobbing, consists of slow, spontaneous downward eye movements with rapid return to the primary position. It has been mainly reported following hypoxic-ischemic encephalopathy, but has also been described in association with other types of diffuse or multifocal encephalopathies and structural brainstem damage. CASE REPORT: We report the case of a previously asymptomatic 66-year-old woman who presented with confusion, recent memory disturbances, and abnormal involuntary movements, followed by a coma. Abnormal spontaneous vertical eye movements consistent with OD developed from the fourth day after admission, and the patient died 20 days later. The pathological examination of the brain confirmed the diagnosis of Creutzfeldt-Jakob disease. CONCLUSIONS: The precise location of damage causing OD is unknown. In contrast to ocular bobbing, OD has no localizing value itself, but structural brainstem damage is likely when it appears combined with other spontaneous vertical eye movements.
Aged ; Brain ; Brain Stem ; Coma ; Creutzfeldt-Jakob Syndrome* ; Diagnosis ; Dyskinesias ; Eye Movements ; Female ; Humans ; Hypoxia-Ischemia, Brain ; Memory