Articles: brain-pathology.
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Three to 12 h of mild hypothermia (HT) starting after hypoxia-ischemia is neuroprotective in piglets that are anesthetized during HT. Newborn infants suffering from neonatal encephalopathy often ventilate spontaneously and are not necessarily sedated. We aimed to test whether mild posthypoxic HT lasting 24 h was neuroprotective if the animals were not sedated. ⋯ Cortisol reached 3 times the NT value at the end of HT. We speculate that the stress of shivering and feeling cold interfered with the previously shown neuroprotective effect of HT. Research on the appropriateness of sedation during clinical HT is urgent.
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Arch Neurol Chicago · Aug 2001
Brain single-photon emission computed tomography and magnetic resonance imaging in Machado-Joseph disease.
Machado-Joseph disease (MJD) is one of the most frequently encountered spinocerebellar ataxias. However, few reports on brain single-photon emission computed tomographic (SPECT) imaging (BSI) with hexylmethylpropylene amineoxine labled with technetium Tc 99m and magnetic resonance imaging (MRI) have been performed for the evaluation of patients with MJD. ⋯ Brain SPECT imaging and MRI were capable of identifying subclinical abnormalities in individuals with MJD. These findings may be helpful for a better understanding of the pathophysiology of this disease.
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Journal of neurotrauma · Jul 2001
Case ReportsDelayed hemispheric neuronal loss in severely head-injured patients.
Recent experimental studies have revealed that traumatic brain injury as well as ischemic brain injury can cause chronic progressive neuronal damage. In the present study, we demonstrate previously unreported delayed cerebral atrophy on computerized tomography (CT) scans in severely head-injured patients. Seventeen severely head-injured patients who required mild hypothermia to control intracranial hypertension after the failure of conventional therapies were retrospectively analyzed. ⋯ Six of these eight patients with DNL achieved functional recovery despite progressive atrophic changes demonstrated on CT scans. On CT scans, DNL was characterized by (1) the sudden appearance at several months postinjury of a low-density area in the hemisphere ipsilateral to the injury; (2) the preservation of essential cortical structure although related white matter structures showed severe atrophic changes; and (3) no spread of the low-density area to the contiguous territory of the other main cerebral artery. It is concluded that focal primary injury to underlying brain, if severe enough, can result in delayed hemispheric atrophy.
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Journal of neurosurgery · Jun 2001
Clinical and economic consequences of early discharge of patients following supratentorial stereotactic brain biopsy.
The goal of this study was to determine the clinical and economic consequences of early discharge (< 8 hours) of patients following stereotactic brain biopsy (SBB). ⋯ Early discharge of patients following SBB of supratentorial lesions is safe in the absence of excessive intraoperative bleeding, new postoperative deficit, and clot on a postoperative CT scan. Extended outpatient observation (8-23 hours) is not clinically necessary and may be economically prohibitive in the setting of a teaching hospital.
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J. Neurol. Neurosurg. Psychiatr. · Jun 2001
A longitudinal study of brain atrophy and cognitive disturbances in the early phase of relapsing-remitting multiple sclerosis.
(a) To establish whether the cognitive decline of the early phase of relapsing-remitting multiple sclerosis depends on the progression of the burden of disease, or on the loss of brain parenchyma, or is influenced by both; (b) to monitor the loss of brain parenchyma in the early phase of the disease; and (c) to examine its possible relation with the progression of physical disability. ⋯ In the early phase of relapsing-remitting multiple sclerosis the cognitive deterioration relies more on the development of brain parenchymal volume atrophy than on the extent of burden of disease in the brain. The loss of brain parenchymal volume underlies the progressive accumulation of physical disability from the initial phase of the disease, which becomes more demonstrable only if studied with longer observation periods. Probably, the main pathological substrate of brain atrophy in the early stage of the disease is early axonal loss, which causes the progression of neurological deficits and the development of cognitive impairment. These data support the debated opinion that disease modifying therapy should be initiated as early as possible.