ABSTRACT
Multicystic encephalomalacia is varying sized cystic lesions in the brain encountered in developing fetuses or infants. These cysts start at the periventricular area and may extend onto the cortex. The cause of the formation of these cystic lesions is secondary to an ischemic or hypoxic insult, which leads to liquefactive necrosis and subsequent formation of gliotic cyst walls having an admixture of microglia. We discuss four autopsy cases that had multicystic encephalomalacia to highlight the scenarios in which these lesions are encountered.
Subject(s)
Humans , Male , Infant, Newborn , Encephalomalacia/complications , Autopsy , Microglia , Gliosis , HypoxiaABSTRACT
The magnetic resonance imaging findings of multicystic encephalomalacia are featured by bilateral frontal large cystic lesion with corpus callosum involvement,evident heterogeneous enhancement of the lesion margin,ring hyperintensity on diffusion weighted imaging,and high choline peak and low N-acetylaspartate peak of the enhanced lesion margin on magnetic resonance spectroscopy.This article reports a case of multicystic encephalomalacia.
Subject(s)
Humans , Corpus Callosum , Encephalomalacia , Magnetic Resonance Imaging , Magnetic Resonance SpectroscopyABSTRACT
Background: Neonatal respiratory distress due to coexisting subglosso-palatalmembrane and tongue dermoid has not been reported yet. Case characteristics: Anewborn with respiratory distress having a membrane in the oral cavity. Excision ofmembrane revealed a tongue mass with cleft palate, obstructing the nasopharynxcompletely. Elective ventilation was followed by excision of mass. Outcome: The childwas cured with uneventful course at follow-up of six months. Message: Co-existingcongenital anomalies causing airway obstruction may be missed in presence ofsubglosso-palatal membrane.
ABSTRACT
PURPOSE: Encephalomalacia is one of the major causes of symptomatic epilepsy. However, no previous study has examined the correlation between encephalomalacia and epilepsy in children. In this study, we aimed to quantify the prevalence, clinical features, and risk factors of epilepsy associated with encephalomalacia. METHODS: We performed a retrospective review of the medical records of 95 patients who were diagnosed with encephalomalacia by neuroimaging techniques at Pusan National University Children's Hospital between November 2008 and July 2013. Patients were classified into two groups: epilepsy (Group A) and non-epilepsy (Group B). We compared the demographics, underlying causes, and distribution of encephalomalacic lesions of these two groups. RESULTS: Groups A and B comprised 35 (36.8%) and 60 (63.1%) patients, respectively. Compared to Group B, Group A showed shorter mean gestational period (35.99+/-4.63 vs. 38.09+/-3.70, P=0.02), lower birth weight (2.60+/-0.94 vs. 3.02+/-0.64, P=0.02), and earlier onset of encephalomalacia (2.74+/-3.52 vs. 5.60+/-5.96, P=0.01). In comparing the underlying cause of encephalomalacia, the occurrence of epilepsy was lower after cerebrovascular disease (P<0.01), but trended towards a higher incidence after a central nervous system infection (P=0.09). Multifocal encephalomalacic lesions were significantly higher in Group A (P=0.04). CONCLUSION: The risk factors for epilepsy associated with encephalomalacia are early gestational age, low birth weight, early onset of encephalomalacia, and multifocal encephalomalacic lesions. It may be necessary for clinicians to search for these risk factors, and make a particularly close observation on these patients.
Subject(s)
Child , Humans , Infant, Newborn , Birth Weight , Central Nervous System Infections , Demography , Encephalomalacia , Epilepsy , Gestational Age , Incidence , Infant, Low Birth Weight , Medical Records , Neuroimaging , Prevalence , Retrospective Studies , Risk FactorsABSTRACT
The antepartum death of a fetus in a twin pregnancy may cause significant risk of mortality and morbidity in the surviving infant. Especially, one fetal demise of a twin pregnancy in the second or third trimester is an uncommon and difficult problem in the management of pregnancy. In this report, we present a case of single intrauterine death in a twin gestation diagnosed in the 27th week of pregnancy and the surviving fetus exhibits multicystic encephalomalacia three weeks later, antenatally.
Subject(s)
Female , Humans , Infant , Pregnancy , Encephalomalacia , Fetus , Mortality , Pregnancy Trimester, Third , Pregnancy, TwinABSTRACT
Encephalomalacia is a spongiform white matter change, which consists of rarefaction, vacuoles, larger cavities, and sometimes coalesces into cysts. We experienced a 14-year-old male with cystic encephalomalacia developed after cerebral infarction associated with hypertensive encephalopathy. Hypertensive encephalopathy is related to edema within the cerebral white matter. He visited another hospital because of generalized seizure, and his blood pressure was 180/100 mmHg. Nifedipine was given immediately, but seizure couldn't be controlled, so he was transferred to our hospital for further evaluation. When he arrived, his BP was 130/80mmHg. Initial laboratory findings were hematuria, proteinuria, decreased C3, and increased ASO. We diagnosed the encephalopathy as a complication of acute poststreptococcal glomerulonephritis. On the first day, hypodense lesion in white matter of left parietal lobe showed on the brain CT, suggesting cerebral edema. On the 20th day, there was strong enhancement in the same site, suggesting cerebral infarction on Gd-DTPA enhanced T1WI. After 7 months, on follow-up MRI scan, we found the encephalomalatic change. The cause of encephalomalacia was presumed to be a rapid lowering of BP in the initial treatment. We report this very rare case with a brief review of some related literatures.
Subject(s)
Adolescent , Humans , Male , Blood Pressure , Brain , Brain Edema , Cerebral Infarction , Edema , Encephalomalacia , Follow-Up Studies , Gadolinium DTPA , Glomerulonephritis , Hematuria , Hypertensive Encephalopathy , Magnetic Resonance Imaging , Nifedipine , Parietal Lobe , Proteinuria , Seizures , VacuolesABSTRACT
Encephalomalacia is a spongiform white matter change, which consists of rarefaction, vacuoles, larger cavities, and sometimes coalesces into cysts. We experienced a 14-year-old male with cystic encephalomalacia developed after cerebral infarction associated with hypertensive encephalopathy. Hypertensive encephalopathy is related to edema within the cerebral white matter. He visited another hospital because of generalized seizure, and his blood pressure was 180/100 mmHg. Nifedipine was given immediately, but seizure couldn't be controlled, so he was transferred to our hospital for further evaluation. When he arrived, his BP was 130/80mmHg. Initial laboratory findings were hematuria, proteinuria, decreased C3, and increased ASO. We diagnosed the encephalopathy as a complication of acute poststreptococcal glomerulonephritis. On the first day, hypodense lesion in white matter of left parietal lobe showed on the brain CT, suggesting cerebral edema. On the 20th day, there was strong enhancement in the same site, suggesting cerebral infarction on Gd-DTPA enhanced T1WI. After 7 months, on follow-up MRI scan, we found the encephalomalatic change. The cause of encephalomalacia was presumed to be a rapid lowering of BP in the initial treatment. We report this very rare case with a brief review of some related literatures.
Subject(s)
Adolescent , Humans , Male , Blood Pressure , Brain , Brain Edema , Cerebral Infarction , Edema , Encephalomalacia , Follow-Up Studies , Gadolinium DTPA , Glomerulonephritis , Hematuria , Hypertensive Encephalopathy , Magnetic Resonance Imaging , Nifedipine , Parietal Lobe , Proteinuria , Seizures , VacuolesABSTRACT
Various anatomical defects have been described in the surviving co-twin who had stillborn, macerated monozygotic co-twin with disseminated intravascular coagulation. The suggested mechanism was the transfer of emboli or thromboplastic materials of dead fetus to co-twin through placental vascular anastomoses. Multicystic encephalomalacia is the condition defined anatomically by the presence of multiple cavities in the great part of both cerebral hemispheres. The most common pathogenesis is circulatory disturbance caused by neonatal asphyxia during the perinatal period. We experienced two cases of monozygotic twin with deceased co-twin at 26 weeks, 33 weeks of gestation and confirmed the diffuse multicystic encephalomalacia by cranial ultrasonography and MRI in a surviving co-twin. Only one patient has been followed who showed spastic cerebral palsy and severe mental retardation. We report two cases of multicystic encephalomalacia in a surviring co-twin with a intrauterine fetal death and its related literatures.
Subject(s)
Humans , Pregnancy , Asphyxia , Cerebral Palsy , Cerebrum , Disseminated Intravascular Coagulation , Encephalomalacia , Fetal Death , Fetus , Intellectual Disability , Magnetic Resonance Imaging , Pregnancy, Twin , Twins, Monozygotic , UltrasonographyABSTRACT
Multicystic encephalomalacia is the condition defined anatomically by the presence of multiple cavities in the great part of both cerebral hemispheres. The most common cause of the condition was regarded as the circulatory disturbance during the perinatal period. Also, neonatal asphyxia was the most important cause of the circulatory disturbance. But we experienced a case of multicystic encephalomalacia in a liveborn twin with a stillborn co-twin without perinatal asphyxia. It seems likely that intrauterine disseminated intravascular coagualation owing to fetofetal transfer of thromboplastic material from the dead fetus through vascular shunts in a monochorionic placenta without neonatal asphyxia constitute the main cause of the neurologic complication in our patient. So we report with a brief review and its related literatures.
Subject(s)
Humans , Asphyxia , Cerebrum , Encephalomalacia , Fetus , Placenta , TwinsABSTRACT
Objective To evaluate the epileptic focus localization value of MSI in patients with refractory epilepsy and encephalomalacia. Method MSI examination was proceeded in 11 patients with refractory epilepsy and encephalomalacia. Five of them were treated with gamma-knife; the others were treated with surgery. Results In the five patients treated with gamma-knife, the result was satisfied in 3 patients, one patient improved significantly, the other one useless. The distance between the encephalomalacia and the epileptic focus was 4cm in one patient; one patient′s encephalomalacia was located in right frontal-parietal lobe but the epileptic focus mainly located in right temporal lobe, only a little located around the encephalomalacia. Overall agreement among VEEG,ECoG and MEG (presence of concordant spikes with the same localization shown by three techniques) was obtained in three patients, the areas localized by ECoG were larger than VEEG and MSI in two patients. The localization was different in VEEG, MSI and ECoG in one patient, then he was given a resection of bilateral occipital epileptic focus. The results of patients treated with surgery were satisfied. Conclusion The MSI localization of epileptic focus in patients with refractory epilepsy and encephalomalacia is precise, and it can direct the advanced clinical treatment.