Cases reported "Hypoxia-Ischemia, Brain"

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1/27. Parasagittal cerebral injury: magnetic resonance findings.

    Parasagittal cerebral injury is a specific pathologic lesion that can be found in full-term newborn babies suffering from hypoxic-ischemic encephalopathy. It is defined by the presence of cortical and subcortical white-matter necrosis involving the parasagittal and superomedial areas of the cerebral convexities. We report on two patients who showed parasagittal cerebral injury on magnetic resonance imaging. In both cases antecedents of hypoxic-ischemic encephalopathy were noted. In one of the patients basal ganglia involvement was also detected by cranial magnetic resonance imaging. In the follow-up studies the presence of upper-limb pyramidal signs and dyspraxia were two of the more pronounced symptoms. We will discuss the usefulness of neuroimaging, especially magnetic resonance imaging with coronal views, in the diagnosis of the parasagittal cerebral injury.
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ranking = 1
keywords = encephalopathy
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2/27. Hypoxic-ischemic encephalopathy with cystic brain stem necroses and thalamic calcifications in a preterm twin.

    A severe and rare ischemic brain lesion in a preterm twin boy is reported. The boy was born after two weeks of anhydramnios and amnionic infection at 24 weeks of gestation. Following a difficult Caesarean section and prolonged umbilical cord compression he developed prenatal acidosis with an umbilical cord pH of 6.96. At the age of 7 h, heart rate variability narrowed due to severely disturbed brain stem function and the patient developed clinical signs of hypoxic-ischemic encephalopathy. Sonography demonstrated extensive symmetrical brain stem and basal ganglia lesions. After a prolonged comatose and apneic state, death occurred at the age of 25 days. autopsy confirmed columnar bilateral cavitation of basal ganglia, diencephalon, brain stem and spinal gray matter, as well as focal calcifications in the palladium, thalamus, and brain stem. The findings highly resemble those observed after experimental or clinical cardiac arrest.
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ranking = 2.5
keywords = encephalopathy
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3/27. Cytochrome oxidase deficiency presenting as birth asphyxia.

    Hypoxic-ischaemic encephalopathy (HIE) was diagnosed in an infant with acidosis. At 7 weeks of age further investigations revealed abnormal neuroimaging (CT and MRI scans) and a raised plasma and CSF lactate. A skeletal-muscle biopsy at 2 months of age confirmed the diagnosis of cytochrome oxidase deficiency. The course of the patient's disorder has taken that of a static encephalopathy (cerebral palsy). Inborn disorders of the respiratory chain should be considered in the differential diagnosis of HIE.
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ranking = 1
keywords = encephalopathy
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4/27. Possible mechanisms in infants for selective basal ganglia damage from asphyxia, kernicterus, or mitochondrial encephalopathies.

    magnetic resonance imaging and neuropathologic studies have demonstrated remarkably selective patterns of injury to subregions of the basal ganglia in children. Examples are kernicterus and certain mitochondrial encephalopathies, which cause selective injury to the globus pallidus, and near-total perinatal asphyxia, which causes lesions in the putamen and thalamus. To explain the differential vulnerability of nuclei within millimeters of each other, we hypothesize that their locations within the neurotransmitter-specific circuitry of the basal ganglia motor loop are important. In severe hypoxic-ischemic encephalopathy, excitatory glutamatergic pathways into the putamen and thalamus are overactive, but the globus pallidus might be protected because its activity is silenced by inhibitory neuronal activity. In contrast, the relatively high resting neuronal activity in the globus pallidus might make it more vulnerable to less intense, subacute oxidative stresses from mitochondrial toxins such as bilirubin or from genetic mitochondrial disorders. This hypothesis has implications for designing neuroprotective therapies and for treating associated chronic movement disorders.
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ranking = 0.5
keywords = encephalopathy
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5/27. molybdenum cofactor deficiency: report of three cases presenting as hypoxic-ischemic encephalopathy.

    We report three infants with the diagnosis of molybdenum cofactor deficiency. The key findings leading to diagnosis were neonatal seizures unresponsive to treatment, craniofacial dysmorphic features, hyperexcitability, low blood uric acid levels, and neuroimaging findings. The parents were consanguineous in two of these patients. The diagnosis was established by the presence of low blood uric acid levels, positive urine sulfite reaction, quantitative aminoacid analysis, and high-voltage electrophoresis of the urine sample showing a typical increase of S-sulfo-L-cysteine. skin fibroblast cultures confirmed the diagnosis. magnetic resonance imaging findings were suggestive of encephalomalacia with cystic changes due to hypoxic-ischemic encephalopathy. We conclude that molybdenum cofactor deficiency must be included in the differential diagnosis of patients presenting with intractable seizures in the newborn period who have computed tomography and magnetic resonance imaging findings reminiscent of those of hypoxic-ischemic encephalopathy, and the urine sulfite dipstick test can be a part of the evaluation of these infants in neonatal intensive care units.
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ranking = 3
keywords = encephalopathy
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6/27. Acute hepatic encephalopathy with diffuse cortical lesions.

    Acute hepatic encephalopathy is a poorly defined syndrome of heterogeneous aetiology. We report a 49-year-old woman with alcoholic cirrhosis and hereditary haemorrhagic telangiectasia who developed acute hepatic coma induced by severe gastrointestinal bleeding. Laboratory analysis revealed excessively elevated blood ammonia. MRI showed lesions compatible with chronic hepatic encephalopathy and widespread cortical signal change sparing the perirolandic and occipital cortex. The cortical lesions resembled those of hypoxic brain damage and were interpreted as acute toxic cortical laminar necrosis.
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ranking = 3.4251650388667
keywords = encephalopathy, hepatic encephalopathy, hepatic
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7/27. time course of changes in diffusion-weighted magnetic resonance imaging in a case of neonatal encephalopathy with defined onset and duration of hypoxic-ischemic insult.

    The onset and duration of hypoxic-ischemic (HI) insults rarely can be determined precisely in perinatal asphyxia. The need to establish the timing of HI insults will be critical for the successful application of evolving neuroprotective therapies that may be administered to the asphyxiated newborn. diffusion-weighted magnetic resonance imaging has emerged as an imaging technique that can be used to identify HI brain injury before the detection of abnormalities by conventional magnetic resonance imaging. This case illustrates the early changes in diffusion-weighted and conventional magnetic resonance imaging studies and in quantitative values of the apparent diffusion coefficient in a unique case of neonatal asphyxia in which the onset and duration of the HI insult were known.hypoxia-ischemia, newborn brain, perinatal asphyxia, diffusion-weighted imaging, proton magnetic resonance spectroscopy.
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ranking = 2
keywords = encephalopathy
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8/27. Pseudo-subarachnoid hemorrhage of the head diagnosed by computerized axial tomography: a postmortem study of ten medical examiner cases.

    In this report, we describe ten cases of pseudo-subarachnoid hemorrhage on computer axial tomography (CT) scan of the head. A pseudo-subarachnoid hemorrhage is a false positive finding by CT of the head in which the scan is interpreted as being positive for a subarachnoid hemorrhage not substantiated by subsequent neuropathologic findings. This study is a retrospective review of postmortem cases brought into the Office of the Chief Medical Examiner for the State of maryland over a three-year period (from 1997 to 2000). We compared the clinician's impression of the CT scan with the postmortem neuropathology. The clinical diagnosis of subarachnoid hemorrhage was based on misinterpretation of non-contrast CT scans of the head. In six of the ten cases, the reading was performed by a radiologist and in four cases by nonradiologist physicians (emergency room physician, neurologist, or neurosurgeon). All the patients survived between a few hours to a few days after being admitted to the hospital. For most of the cases (80%), the neuropathology showed hypoxic/ischemic encephalopathy. The most common cause of death (four out of ten cases) was narcotic intoxication. This report is submitted so that clinicians and pathologist become more familiar with this entity.
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ranking = 0.5
keywords = encephalopathy
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9/27. diffusion MRI in three types of anoxic encephalopathy.

    We report the clinical and diffusion-weighted MRI (DWI) features of three patients with different types of anoxic brain injury: attempted hanging (hypoxic hypoxia), carbon monoxide poisoning (histotoxic hypoxia), and hanging with cardiac arrest (hypoxic-ischemic encephalopathy, HIE). The first two patients, but not the third, recovered substantial neurological function. The distribution of DWI abnormalities was different and correlated well with the distinct neuropathological features of these entities. The prognosis after anoxic encephalopathy depends on the underlying mechanism and its severity, which may be reflected by DWI abnormalities.
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ranking = 3
keywords = encephalopathy
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10/27. mandibular nerve block treatment for trismus associated with hypoxic-ischemic encephalopathy.

    BACKGROUND AND OBJECTIVES: We describe the use of mandibular nerve block for the management of bilateral trismus associated with hypoxic-ischemic encephalopathy. CASE REPORT: The patient was a 65-year-old man with bilateral trismus due to hypoxic-ischemic encephalopathy. Despite his impaired consciousness, we performed fluoroscopically guided bilateral mandibular nerve block. The bilateral symptoms were sufficiently improved, without obvious side effects, by injecting a local anesthetic near the right mandibular nerve and a neurolytic near the left mandibular nerve. CONCLUSIONS: mandibular nerve block may be an effective treatment for patients with bilateral trismus due to ischemic-encephalopathy, even when consciousness is impaired.
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ranking = 3.5
keywords = encephalopathy
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