Cases reported "Hypoxia, Brain"

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1/7. Delayed encephalopathy after strangling.

    An 11-year-old boy who had been the victim of a strangling attempt was asymptomatic for one week whereupon involuntary movements involving the trunk and limbs developed, along with repetitive episodes of opisthotonos and autonomic dysfunction. Meanwhile, he remained alert and appeared to be mentally intact. An electroencephalogram was normal. He died 13 weeks after the onset of the neurological disorder. The neuropathological examination showed cavitating lesions in the caudate nucleus, putamen, and globus pallidus bilaterally, with sparing of the white matter. The delayed onset of a progressively evolving neurological disorder has been noted in various forms of hypoxicischemic insult, including previously reported cases of strangling, but its occurrence cannot be predicted from the preceding clinical state or course. In the cases in which abnormal movements have been predominant, the pathological findings have been similar despite diversity in the preceding circumstances. We suggest the underlying metabolic disorder common to these cases may be lactic acidosis, and that they should be studied for evidence of a biochemical defect.
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2/7. Athetoid cerebral palsy with cysts in the putamen after hypoxic-ischaemic encephalopathy.

    Three cases of athetoid cerebral palsy after hypoxic-ischaemic encephalopathy (HIE) are reported. All three neonates had haemorrhagic lesions in the basal ganglia and thalami on magnetic resonance imaging (MRI). Prior cranial ultrasound had detected the lesions in only two cases. In all three children athetoid movements began within the first year of life. Follow up MRI scans showed bilateral symmetrical cystic lesions in the posterior putamen. Although haemorrhagic lesions within the basal ganglia are a common MRI finding in neonates with HIE, few of these babies develop athetoid cerebral palsy. We believe this to be the first report of discrete cystic lesions found in the basal ganglia of children with athetoid cerebral palsy.
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3/7. Delayed postanoxic encephalopathy after strangulation. Serial neuroradiological and neurochemical studies.

    A 13-year-old boy was the victim of attempted strangulation. His condition had returned to normal by the sixth day after the assault; however, from the seventh day, choreoathetosis, dystonia, and marked pseudobulbar paralysis developed in the boy. The computed tomographic scans and T2-weighted magnetic resonance images that were obtained at this time revealed low-density and high-signal intensities in the region of the bilateral putamen and caudate nucleus. These symptoms and the changes in his computed tomographic scans and magnetic resonance images subsided gradually during a 2-month period. Sequential analysis of the cerebrospinal fluid for gamma-aminobutyric acid and dopamine concentrations during his illness revealed reciprocal changes with normal recovery. Because of the delayed onset of neurological changes and the cerebrospinal fluid showing reversible symptoms, the delayed encephalopathy after strangulation had been related to the biochemical alterations that followed anoxia in the vulnerable basal ganglia.
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4/7. MRI demonstration of cortical laminar necrosis and delayed white matter injury in anoxic encephalopathy.

    We performed serial radiological examinations on a patient with anoxic encephalopathy. In the early term after the anoxic insult, T1-weighted MRI revealed high signal intensity areas distributed laminarly in the cerebral cortex and diffusely in the putamen, which were thought to reflect the cortical necrosis and necrosis in the putamen. Single photon emission computed tomography using I-123 isopropylamphetamine showed persistent hypoperfusion in the arterial watershed zones. T2-weighted MRI performed several months after the anoxic episode revealed diffuse high-intensity lesions in the arterial water-shed zones. These delayed-onset white matter lesions continued to extend over several months.
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keywords = putamen
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5/7. Hypoxic-ischemic damage of the basal ganglia. case reports and a review of the literature.

    Three cases of movement disorders secondary to hypoxic-ischemic encephalopathy are reported. Despite similarities among the clinical events, the neurological syndromes produced were dissimilar. Cerebral hypoxia-ischemia typically produces lesions of the globus pallidus that may result in an akinetic rigid syndrome. Due to its unique blood supply, vascular insufficiency is found to be a major factor. Lesions in the putamen also occur, and these tend to be associated with dystonia. Recent evidence supports a specific neuronal sensitivity in the striatum, possibly due to afferent excitatory amino acid connections. These two components and changes in the levels of neurotransmitters during hypoxia-ischemia may interact to produce varied clinical outcomes. These factors must also be considered when planning therapeutic interventions.
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6/7. brain magnetic resonance imaging in suspected extrapyramidal cerebral palsy: observations in distinguishing genetic-metabolic from acquired causes.

    Experienced clinicians recognize that some children who appear to have static cerebral palsy (CP) actually have underlying genetic-metabolic disorders. We report a series of patients with motor disorders seen in children with extrapyramidal CP in whom brain magnetic resonance imaging abnormalities provided important diagnostic clues in distinguishing genetic-metabolic disorders from other causes. One cause of static extrapyramidal CP, hypoxic-ischemic encephalopathy at the end of a term gestation, produces a characteristic pattern of hyperintense signal and atrophy in the putamen and thalamus. Other signal abnormalities and atrophy in the putamen, globus pallidus, or caudate can point to genetic-metabolic diseases, including disorders of mitochondrial and organic acid metabolism. Progress in understanding and treating genetic diseases of the developing brain makes it essential to diagnose disorders that masquerade as static CP. brain magnetic resonance imaging is a useful diagnostic tool in the initial evaluation of children who appear to have CP.
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keywords = putamen
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7/7. MR findings of hypoxic damage of the bilateral striate cortices: a case report.

    MR imaging of a patient with cortical blindness revealed areas of abnormal signal bilaterally in the lateral putamen and the striate cortices. The coronal T2-weighted image clearly demonstrated the selective involvement of the bilateral striate cortices. The differential diagnosis and the vulnerability of the striate cortex are discussed.
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