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

Notable historical aspects relating to the etiology and treatment of pes cavus have been critically examined. The characteristic features of the deformity are described and an explanation offered for the mechanism of their production. Although its etiology remains uncertain, a study of the literature and a great deal of clinical material has established certain well supported conclusions regarding the etiology and pathology of the condition. Certain aspects of cerebral palsy serve to strengthen impressions of earlier authors that the primary center of origin of pes cavus lies somewhere in the central nervous system. Localized foci of partial damage lying adjacent to tracts of nerve cells more seriously affected by a neurological disease could emit irritating stimuli capable of producing degrees of over-action of the invertor muscles varying from obvious spasm to clinically undetectable increase in muscle tone. Biral or other factors which stop short at creating nothing more than such a focus of irration could explain the insidious onset of the deformity in the idiopathic group. Over-action of invertor muscles for one reason or another, including ischemia, is almost certainly responsible for initiating the deformity, though primary contracture of the plantar fascia could possibly do so. With the appearance of supination of the heel, the calcanean tendon becomes an active invertor adding its force to that of the plantar fascia to produce structural varus of the calcaneum. Contracture of the plantar fascia and supination of the heel are regarded as features of major importance. Correction of the latter can be achieved more effectively by suitable osteotomy than by subtaloid fusion, which is regarded with great disfavor. Conservative treatment consists of exercises and shoe appliances. Surgical correction is based on calcanean osteotomy and plantar fasciotomy supplemented where necessary by suitable tendon transplantations, correction of clawing of the toes, and tarsal or metatarsal wedge resections. Preservation of the midtarsal subtaloid joint complex is essential. With the heel correctly aligned the degree of improvement to be expected in the forefoot deformity is such that any structural operation on it should be deferred until a fair period of walking has been tried.
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PMID:The present status of the problem of pes cavus. 109 4

Fetal ischemia or hypoxia can lead to cerebral palsy, mental retardation and epilepsy. We propose that the production of nitric oxide and oxygen radicals by neurons when ischemic or hypoxic brain is reperfused may contribute to cerebral injury. Ischemia will depolarize neuronal membranes causing the synaptic discharge of the excitatory neurotransmitter glutamate, which in turn opens the voltage-dependent, N-methyl-D-aspartic acid-specific glutamate receptor/ionophore, allowing calcium to accumulate in the neuron. Calcium in turn activates an oxygen-dependent neuronal nitric oxide synthetase, which oxidizes arginine to produce nitric oxide (.NO) when oxygen is readmitted to brain by reperfusion. Nitric oxide reacts with the oxygen radical superoxide (O2-), also produced by reperfusion, to form peroxynitrite (ONOO-). Peroxynitrite can diffuse for several micrometers before decomposing to form the powerful and cytotoxic oxidants hydroxyl radical and nitrogen dioxide. The hypothesis is consistent with available evidence on the protective action of glutamate antagonists and of oxygen radical scavengers for limiting cerebral infarction following focal ischemia.
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PMID:The double-edged role of nitric oxide in brain function and superoxide-mediated injury. 167 55

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

Cerebral hypoxia-ischemia remains a major cause of acute perinatal brain injury, leading ultimately to neurologic dysfunction manifest as cerebral palsy, mental retardation, and epilepsy. Research in experimental animals over the past 10 or more years has expanded greatly our understanding of the cellular and molecular events that occur during a hypoxic-ischemic insult to brain, and recent discoveries have suggested that metabolic perturbations arising in the recovery period after resuscitation contribute substantially to the nature and extent of neuronal destruction. The review focuses on those neurochemical processes responsible for the maintenance of cellular homeostasis and how these mechanisms fail in hypoxia-ischemia to culminate in brain damage. Knowledge of these critical events has opened new avenues of potential therapy for the fetus and newborn infant subjected to cerebral hypoxia-ischemia to prevent the serious delayed effects of perinatal brain injury.
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PMID:Experimental biology of cerebral hypoxia-ischemia: relation to perinatal brain damage. 197 36

Although the static encephalopathies of childhood are common, little is known of the underlying alterations in the neurochemical anatomy of the brain. Using quantitative morphological techniques, we examined the effect of perinatal hypoxia-ischemia on the number and distribution of cholinergic (ACh) neurons in a unilateral experimental striatal lesion in rats. The striatal pathology simulates status marmoratus, a recognized correlate of human dystonic cerebral palsy. We found that striatal injury results in a mean 22% decrease in the number of ACh neurons at the age of 3 to 4 weeks. The loss of neurons was relatively less than the volume loss, resulting in a mean 16% increase in neuron density. This effect was not uniform throughout the striatum; it was more pronounced caudally, resulting in a mean 52% increase in density in the most caudal striatal plane. These changes in immature rats were also seen in adult rats, indicating that there were lasting alterations in striatal cholinergic morphology. Hypoxic-ischemic injury to the striatum also resulted in a persistent decrease in the mean area of ACh neurons. The increased density of these neurons may imply that they are relatively resistant to hypoxic-ischemic injury. These findings may be relevant to the observation that anticholinergic drugs are among the most effective for treating dystonias, including those observed in static encephalopathies.
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PMID:Quantitative morphological analysis of striatal cholinergic neurons in perinatal asphyxia. 230 30

Baclofen, the most effective drug for treating spasticity, is a specific agonist of gamma-aminobutyric acid-B receptors, and is very abundant in the superficial layers of the spinal cord. Given orally, baclofen does not easily penetrate the blood-brain barrier, and is distributed equally to the brain and spinal cord. Direct intrathecal administration was given in order to change the distribution of the drug by preferentially perfusing the spinal cord. Eighteen patients presenting a severe spastic syndrome were treated with chronic intrathecal infusion of baclofen in the lumbar cerebrospinal fluid. After clinical preselection, 38 patients were implanted with a lumbar access port allowing long-term trials in order to determine the efficacy of baclofen therapy and the effective 12-hour dose. The 18 patients selected for chronic administration were implanted with a programmable pump. The pathology in these cases was: multiple sclerosis (6 cases), posttrauma spastic syndrome (eight cases), and (one case each) cerebral palsy, ischemic cerebral lesion, spinal ischemia, and transverse myelitis. The mean follow-up period was 18 months (range 4 to 43 months). The clinical results were evaluated according to muscular hypertony on Ashworth's scale (changed for occurrence of painful spasms) and functional improvement. Results were better for spastic syndrome secondary to traumatic medullary lesion than for demyelinating disease. Hypertonia was improved in all cases as confirmed by the registration of the Hoffman (H) reflex. Painful muscular spasms disappeared in 14 of the 16 affected patients. Significant functional improvement was noted in nine patients and was considerable in three. The risk of side effects secondary to overdose (such as excessive hypotonia or central depression) and the absence of a specific baclofen antagonist stresses the necessity for accurate determination of the efficient dose. After an initial titration period and adjustment of the therapeutic dose, the individual doses were from 21 to 500 micrograms/24 hrs (mean 160 micrograms/24 hrs). This new conservative method is very effective, perfectly reversible, and safe when administered in conditions favorable to its use.
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PMID:Chronic intrathecal baclofen administration for control of severe spasticity. 230 74

There is no known glutamatergic innervation of globus pallidus (GP) in adult mammals, but we report that during postnatal development of the GP there are large, transient increases in both presynaptic high-affinity glutamate uptake and postsynaptic Na+-independent glutamate receptor binding. These glutamatergic markers increase rapidly in rat GP after birth and then decrease to adult levels over a period of weeks. A similar developmental pattern of pallidal glutamate binding was found in human brains. In contrast, binding in rat caudate-putamen (CPu) increases after birth, reaches a peak, and remains constant into adulthood. The results suggest that a glutamatergic pathway transiently innervates the globus pallidus during the perinatal period. Because glutamate is an excitotoxin, this pathway may account, in part, for the basal ganglia damage seen in some forms of cerebral palsy after perinatal hypoxia/ischemia.
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PMID:Evidence for transient perinatal glutamatergic innervation of globus pallidus. 288 65

Perinatal asphyxia is associated with an increased risk of cerebral palsy and significant mortality. We investigated the use of flunarizine, a calcium antagonist and MK-801, an excitatory amino acid antagonist, in preventing the sequelae of severe hypoxic/ischemic insults. Flunarizine was neuroprotective in the infant rat subjected to unilateral carotid ligation and 2 h of hypoxia. Preliminary analysis of experiments in a novel model of cerebral ischemia in the fetal sheep suggests that prophylactic treatment with flunarizine greatly modified the outcome after 30 min of total ischemia. Treatment with MK-801 prevented post-ischemic seizures. The background to these developments is outlined and future prospects considered.
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PMID:Perinatal cerebral asphyxia: pharmacological intervention. 307 20

We report the neuropathologic findings in a 63-year-old white male with a history of birth asphyxia, cerebral palsy, seizures and mild mental retardation in conjunction with similar brain pathologic findings in animal models of perinatal asphyxia. The human case showed a left cerebral hemispheric hemiatrophy associated with an extensive ulegyria involving all cerebral lobes on that side and a single microscopic focus of cortical atrophy in the right hemisphere. Among a large number of experimental perinatal asphyctic exposures only an occasional animal, like the human case described, showed unilateral hemispheric injury with softening and necrosis if examined early and ulegyria with hemispheric hemiatrophy if examined late. The present paper suggests that perinatal asphyxia under specific pathophysiologic conditions may cause unilateral brain injury. Our experimental studies suggest the specific condition of perinatal asphyxia potentially causing unilateral or asymmetrical brain damage is marked hypoxemia combined with substantial reductions in blood pressure but without circulatory collapse. Given these conditions, the asymmetry of the brain damage likely reflects fetal head position within the gravitational field relative to the heart. With disturbed cerebral blood flow autoregulation from asphyxia, the gravitational field likely accentuates the ischemia of those brain areas most elevated above the level of the heart. Thus, we postulate head position may play a pivotal role in defining brain regions that are damaged in hypotensive perinatal asphyxia. This interpretation may affect the intensive care of hypoxemic, hypotensive newborns aimed at minimizing the risk of brain damage.
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PMID:Cerebral hemiatrophy--correlation of human with animal experimental data. 325 12

The dramatic reduction in perinatal morbidity and mortality over the last decade has not been accompanied by any diminution in the incidence of cerebral palsy. We investigated retrospectively the relationship of certain perinatal events to the subsequent development of cerebral palsy in 75 infants. Cerebral palsy occurred in association with acute intrapartum asphyxia in 8% and traumatic delivery in 11%. Thirty-five percent of cases were associated with chronic fetal distress, defined by a unique fetal heart rate (FHR) pattern consisting of a normal baseline rate with persistently absent variability and mild variable decelerations with overshoot. This pattern was found frequently in association with postmaturity, meconium staining, intrauterine growth retardation, and neonatal seizures. Acid-base studies, when available, did not reveal acidosis. Twenty-seven percent of the cases involved a combination of chronic fetal distress, acute intrapartum fetal asphyxia, and/or traumatic delivery. We postulate that antenatal intermittent umbilical cord compression secondary to oligohydramnios results in repetitive transient central nervous system ischemia, insufficient to cause death, but resulting in a characteristic FHR pattern and impaired neurologic development. If these data are confirmed, this FHR pattern may be an important marker for the development of subsequent neurologic handicap or other adverse outcome.
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PMID:Perinatal antecedents of cerebral palsy. 270 35


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