Cases reported "Hypoxia, Brain"

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1/8. 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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2/8. 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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3/8. The auditory pathology of brain death as revealed by auditory evoked potentials.

    A case of brain death is reported in which the auditory brainstem response, middle latency component, and slow vertex response were recorded before and after the cessation of cortical activity, and in which histological examination of the temporal bone and central auditory pathways was performed post mortem. brain death of at least 48 hours' duration was demonstrated by neurological examination, flat electroencephalographic recording, and persistent absence of auditory evoked responses. The postmortem examination was performed 3 hours after death. The pathological studies of the whole length of the auditory pathway revealed total autolysis of the organ of corti, marked cell loss in the dorsal cochlear nucleus, and moderate cell loss in other nuclei of the central auditory pathway. It should be considered that total autolysis of the organ of corti and severe cell loss of the cochlear nucleus may occur if the auditory brainstem response becomes absent in comatose patients.
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4/8. homicide of an aggressive adolescent boy with right temporal lesion: a case report.

    The case is reported of a 14-year-old male who killed an 8-year-old child following an alleged insult. The subject had been known to be aggressive throughout his school career. He had suffered one nocturnal seizure at the age of 13, but he never was amnesic for any of his fights. There was a history of possible hypoxic birth trauma. Neuropsychiatric investigation revealed developmental lags in speech and other psychosocial skills and, on computer tomography, a circumscribed lesion (cystic defect) lateral to the right nucleus amygdalae.
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5/8. Localized brainstem ischemic damage and Ondine's curse after near-drowning.

    A 19-year-old man was a victim of near-drowning in fresh water. After he was resuscitated, examination showed nystagmus, absent gag reflex, diminished facial sensation, dysmetria of all limbs, and failure of automatic respiration. His intellect was perfectly preserved. Eight months later, he died suddenly, and the essential neuropathologic findings were limited to the lower brainstem. There was marked neuronal depletion bilaterally in the nucleus gracilis, nucleus cuneatus, nucleus of the tractus solitarius, nucleus ambiguus, and nucleus retroambiguus; several other lower-brainstem nuclei showed evidence of damage, but to lesser extent. The neuropathologic findings seem to have been an unusual consequence of anoxia-ischemia and support previous concepts of the anatomical localization of the human respiratory centers.
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6/8. Prenatal symmetrical thalamic degeneration with flexion spasticity at birth.

    The unusual occurrence of spasticity at birth with symmetrical thalamic damage was found in a male infant delivered at 36 weeks' gestation following an episode of traumatically induced premature labor at 32 weeks. The infant was found to be spastic in flexion with increased stretch reflexes, depressed primitive reflexes, and moderate flexion contractures. Computerized tomographic scans showed bilateral nonenhancing thalamic densities. Neuropathologically, the lateral thalamic nuclei and the red nucleus showed neuron loss, astrocytosis, and, as confirmed by electron microprobe analysis, calcified neurons. The striatum was uninvolved. These findings closely resemble those reported as "symmetrical thalamic degeneration in infancy" and are strongly reminiscent of the pattern of thalamic involvement frequently seen in status marmoratus. It would appear that there is a period during perinatal life in which the lateral thalamus can be rendered vulnerable to hypoxic-ischemic injury, and that the thirty-second week of gestation must be included within this period.
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7/8. reflex blepharospasm associated with bilateral basal ganglia lesion.

    A patient with a bilateral striatal lesion secondary to anoxia presented reflex blepharospasm associated with parkinsonism and dystonia in the limbs. The blink reflex excitability curve was enhanced and the R-2 response prolonged as in patients with essential blepharospasm. The findings in this patient support the notion that blepharospasm may be secondary to basal ganglia dysfunction through abnormal facilitation of reticular formation neurons controlling facial nucleus motoneuron excitability.
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8/8. Rolandic type cerebral palsy in children as a pattern of hypoxic-ischemic injury in the full-term neonate.

    Magnetic resonance images (MRIs) of the brains of 11 patients aged from 1 week to 12 years with a distinctive type of cerebral palsy were selected based on distribution of cerebral lesions, which were restricted to bilateral perirolandic cortical and subcortical regions, including frequent symmetric involvement of basal ganglia and ventrolateral nucleus of thalami. Retrospectively, the perinatal history and clinical features were reviewed to correlate clinical data with this distinctive pattern of brain injury. Clinically affected neonates had an encephalopathy associated with a severe perinatal asphyxial event. Older children with cerebral palsy survived a similar perinatal course and demonstrated spastic quadriparesis with bulbar or pseudobulbar involvement, lack of verbal speech and variable delays in cognitive development. The distribution of hypoxic-ischemic lesions involving bilateral perirolandic regions, basal ganglia, and thalami, appears to correlate with increased metabolic areas of primary myelination in full-term neonates, but not with arterial border zones nor a single cerebral artery distribution. Myelination is a critical process in maturing brain associated with marked increase in tissue respiration and thus greater susceptibility to oxygen deprivation. It is believed that the extent of hypoxic-ischemic brain injury is determined principally by brain maturity and regional metabolic rates at time of insult and this correlates with active myelination in full-term neonates. This study confirms previous data from neuropathologic literature and recent reports of neuroimaging studies of asphyxiated neonates. In addition, retrospective analysis of the clinical data enables recognition of a type of cerebral palsy that might be the hallmark of hypoxic-ischemic injury in term neonates.
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