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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We previously reported a predominance of left focal motor seizures in infants receiving extracorporeal membrane oxygenation (ECMO), raising concerns about possible ischemia resulting from the right common carotid artery ligation. We therefore evaluated the neurologic and psychologic outcome at 2 years of age of all infants with ECMO-related seizures. Although 8 of 12 infants had left focal seizures in infancy, there was no lateralization of motor findings at 2 years of age; left hemiparesis was present in three of the infants and right hemiparesis in three. The developmental quotient was normal in 6 of 12 infants, low-average in three, borderline in two, and in the mentally handicapped range in one. We conclude that any ischemia resulting from carotid ligation is not great enough to produce long-term lateralizing findings but that seizures during ECMO are a risk factor for later cerebral palsy or developmental delay.
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PMID:Significance of seizures associated with extracorporeal membrane oxygenation. 194 88

Although numerous etiological or triggering factors have been suggested in sudden infant death syndrome (SIDS), the underlying mechanism of death is ultimately cardiac and/or respiratory in nature. As there is no evidence of lung or heart abnormalities, attention has focussed on the neural control of respiration and cardiac function. It is important to appreciate the methodological limitations involved in utilizing autopsy material and the criteria for selection of appropriate controls. This report reviews the pathological evidence for developmental delay in SIDS emphasizing delay of neural maturation of both myelination and synapses. Other abnormalities of the nervous system apparently associated with hypoxia-ischemia such as brainstem astrogliosis are also discussed. The occurrence of SIDS at a precise age together with our preliminary studies indicate that neural development delay is an important link in the chain of events leading to SIDS.
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PMID:Neural maturational delay as a link in the chain of events leading to SIDS. 227 93

Our objective was to determine the clinical spectrum of pediatric hemiparesis by identifying the relative frequency of various diagnoses and comorbid conditions seen in these children. Case records of all patients with hemiparesis in a single practice over an 11-year period were reviewed with reference to clinical features, etiologic determination, and comorbid conditions. Ninety-two children were identified: 73 (79.3%) had a congenital hemiparesis and 19 (20.7%) had an acquired hemiparesis. An abnormal perinatal history (P = .003), prematurity (P = .016), and younger age at onset of symptoms (P < .001) were associated with a congenital hemiparesis. The overall etiologic yield was 83.7% (82.2% in the congenital and 89.5% in the acquired). The top four etiologic entities were cerebrovascular ischemia (40.2%), periventricular leukomalacia (18.5%), intracranial hemorrhage (16.3%), and cerebral dysgenesis (13%). Factors predictive of establishing an underlying etiology included birth prior to 34 weeks' gestation (P = .034), global developmental delay (P = .048), epilepsy (P = .024), and having appropriate imaging modalities (P = .001). Half of these children had a concurrent global developmental delay, associated epilepsy (odds ratio 3.67; 95% confidence interval 1.40-9.72), and prematurity (odds ratio 5.41; 95% confidence interval 1.56-18.80). A third of these children developed epilepsy. Multivariate predictive factors for epilepsy included global developmental delay (odds ratio 4.20; 95% confidence interval 1.44-12.27), cerebrovascular ischemia (odds ratio 5.10; 95% confidence interval 1.76-14.77), and term birth (odds ratio 3.87; 95% confidence interval 1.20-12.56). The majority of children with hemiparesis have a congenital etiology. The diagnostic yield is higher than previously reported; however, specific underlying etiologies need to be better determined. Comorbid conditions of global developmental delay and epilepsy have a high prevalence in this population, contributing to overall morbidity.
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PMID:Profile of pediatric hemiparesis. 1599 94

Hypoxia (H) and hypoxia-ischemia (HI) are major causes of foetal brain damage with long-lasting behavioral implications. The effect of hypoxia has been widely studied in human and a variety of animal models. In the present review, we summarize the latest studies testing the behavioral outcomes following prenatal hypoxia/hypoxia-ischemia in rodent models. Delayed development of sensory and motor reflexes during the first postnatal month of rodent life was observed by various groups. Impairment of motor function, learning and memory was evident in the adult animals. Activation of the signaling leading to cell death was detected as early as three hours following H/HI. An increase in the counts of apoptotic cells appeared approximately three days after the insult and peaked about seven days later. Around 14-20 days following the H/HI, the amount of cell death observed in the tissue returned to its basal levels and cell loss was apparent in the brain tissue. The study of the molecular mechanism leading to brain damage in animal models following prenatal hypoxia adds valuable insight to our knowledge of the central events that account for the morphological and functional outcomes. This understanding provides the starting point for the development and improvement of efficient treatment and intervention strategies.
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PMID:The effect of prenatal hypoxia on brain development: short- and long-term consequences demonstrated in rodent models. 1676 7

A 22-year-old female with a history of developmental delay and seizures successfully treated with carbamazepine and levetiracetam developed fulminant hepatic failure and subsequently died. She had been admitted to the hospital following secondary generalized seizures of 35 min duration. A circulatory shock as well as intoxication was taken into consideration during the clinical course. Autopsy failed to reveal a macroscopically discernible cause of death. Significant findings on microscopic examination included acute tubular necrosis in the kidneys, pre-existing marked accumulation of neutral lipid within the hepatocytes as well as hyperacute liver damage with evidence of almost complete hepatocyte necrosis. Carbamazepine and levetiracetam were simultaneously determined from blood and tissues such as liver, lungs, muscle and kidneys by LC-MS/MS following addition of lamotrigine as an internal standard and liquid-liquid extraction. Validation data are given for levetiracetam. Both carbamazepine and levetiracetam were present in blood at concentrations within or below the therapeutic range, respectively. Moreover, tissue concentrations suggested long-term administration of anticonvulsant drugs, which is in accordance with the medical history. After excessive drug concentrations could be ruled out, the metabolic consequences of a prolonged carbamazepine therapy to cause severe hepatic injury in the present case are discussed. A mechanism of injury to the hepatocytes may be membrane damage by either an increased production of free radicals and/or a decreased free radical scavenging capacity. Following ischemia with reperfusion and during hyperthermia, large amounts of free radicals are formed. Induction of the mixed oxidase activity during longterm administration of carbamazepine may also increase production of free radicals, leaving the hepatic cell more vulnerable to oxidative injury.
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PMID:[Fulminant liver failure in a patient on carbamazepine and levetiracetam treatment associated with status epilepticus]. 1691 Mar

Gastrointestinal causes of sudden and/or unexpected death in the young are uncommon and only rarely involve congenital anomalies of the mesentery. Two cases are reported of unexpected deaths following herniation of intestine through congenital mesenteric defects to illustrate the forensic issues that may arise. Case 1 involves a 2.5-year-old girl who collapsed on arrival to hospital following 18 hours of fever and apparently mildly nonspecific symptoms. Resuscitation was unsuccessful, and at autopsy a segment of gangrenous small intestine was found that had herniated through a congenital mesenteric defect. Case 2 involves a 23-year-old woman with a past history of severe mental and physical disabilities who was found dead in her bed. She had a recent history of mild diarrhea and vomiting, but had not appeared particularly ill. At autopsy the peritoneal cavity was filled with a very dilated and obstructed colon as a result of herniation of a segment of sigmoid colon through a distal small intestinal mesenteric defect. These cases demonstrate that symptoms and signs of intestinal ischemia may not be clearly manifested in early childhood and that developmental delay may also result in older individuals presenting in a nonspecific manner. Although rare, congenital mesenteric abnormalities with compromise of the intestinal vasculature remain a possibility to be considered at autopsy in all cases of unexpected death, despite the lack of a clear history of significant gastrointestinal disturbance. Death may relate to ischemic compromise of either the herniated portion of intestine (as in case 1) or to the stretched intestine bordering the hernial orifice (as in case 2).
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PMID:Congenital mesenteric defects and unexpected death-a rare finding at autopsy. 1820 27

It is rare for both limb ischemia and arterial ischemic stroke to occur in the same child during the perinatal period. Two children who appear to have had perinatal emboli to both an arm and a middle cerebral artery territory are presented here. One child required amputation of the ischemic limb below the shoulder, and the other required skin grafts to the distal ischemic fingers. Each of these children later received cerebral magnetic resonance imaging for evaluation of developmental delay and was found to have what appeared to be old perinatal arterial ischemic stroke. Both children were homozygous for the methylenetetrahydrofolate reductase C677T gene variant. Eight other children with perinatal limb ischemia and stroke were found on literature review; several also had delayed diagnosis of perinatal stroke. This report examines the approach to diagnosis and treatment in each of these and makes suggestions for the similar cases in the future.
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PMID:Two children with both arm ischemia and arterial ischemic stroke during the perinatal period. 2186 33

Schizencephaly is a rare malformation of the central nervous system. Both genetic and non-genetic etiologies like prenatal infections or ischemia have been postulated. Clinical manifestations most often include varying degrees of developmental delay, motor impairment and seizures. It can be associated with septo-optic dysplasia (SOD), optic nerve hypoplasia and absence of septum pellucidum, pachygyria, polymicrogyria, heterotopia and arachnoid cysts. We report a case of unilateral closed lip schizencephaly with SOD.
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PMID:Unilateral closed lip schizencephaly with septo-optic dysplasia. 2476 Dec 55

Cerebral artery infarction as a complication of acute otitis media is a rare complication. The mechanism appears to be the spread of meningeal inflammation to involve the walls of intracranial vessels, resulting in arterial thrombosis with ischemia or rupture with hemorrhage. We report the case of a 3 year old female with a history of global developmental delay who sustained a large left hemispheric stroke after middle cerebral artery infarction as a complication of an acute otitis media.
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PMID:Massive ischemic stroke as a complication of otitis media. 2630 69

Antenatal brain hypoxia-ischemia, which occurs in cerebral palsy, is considered a significant cause of motor impairments in children. The mechanisms by which antenatal hypoxia-ischemia causes brain injury and motor deficits still need to be elucidated. Tetrahydrobiopterin is an important enzyme cofactor that is necessary to produce neurotransmitters and to maintain the redox status of the brain. A genetic deficiency of this cofactor from mutations of biosynthetic or recycling enzymes is a well-recognized factor in the development of childhood neurological disorders characterized by motor impairments, developmental delay, and encephalopathy. Experimental hypoxia-ischemia causes a decline in the availability of tetrahydrobiopterin in the immature brain. This decline coincides with the loss of brain function, suggesting this occurrence contributes to neuronal dysfunction and motor impairments. One possible mechanism linking tetrahydrobiopterin deficiency, hypoxia-ischemia, and neuronal injury is oxidative injury. Evidence of the central role of the developmental biology of tetrahydrobiopterin in response to hypoxic ischemic brain injury, especially the development of motor deficits, is discussed.
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PMID:Tetrahydrobiopterin in antenatal brain hypoxia-ischemia-induced motor impairments and cerebral palsy. 2880 28


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