ABSTRACT. Non-perinatal hypoxic-ischaemic encephalopathy (HIE) has varying anatomical patterns dependent on the type of insult, the degree and duration of cerebral hypoxia, or presence and degree of hypoperfusion. Profound insults can affect the entire cerebral cortex or just the perirolandic cortex, the cerebellum and the deep grey matter structures. Less severe insults may affect only the watershed regions. The objective of this article is to review the anatomical patterns of non-perinatal HIEs by MRI. Non-perinatal hypoxic-ischaemic encephalopathy (HIE) can be a devastating neurological injury and prompt recognition of it can result in significant changes in patient management. HIE insults develop in varying regions of the brain depending on the severity and duration of hypoperfusion or hypo-oxygenation [1]. Brain parenchyma changes have corresponding MR signal characteristics that are often obvious but can be subtle [2]. It is important for radiologists to be aware of the variations in the appearance of HIE in order to be alert to the diagnosis in subtle cases, recognise unusual patterns and be aware of the clinical ramifications.This review shows cases of HIE beyond the perinatal period. Aetiological factors and timing of imaging findings are delineated. The cases involve the usual HIE-specific neuroanatomical locations: the cerebral cortex, cerebellum, hippocampus, basal ganglia and thalamus. In addition, cases of HIE showing damage to the cerebral white matter and limbic system are demonstrated. Also, cases that mimic the appearance of HIE are presented. It is critical for a radiologist to be aware of potentially confounding cases.
Multinodular and vacuolating neuronal tumor is a recently described seizure-associated entity with overlapping features of a malformative and neoplastic process. We report a case of multinodular and vacuolating neuronal tumor in a 29-year-old man with a history of recent headaches and complex partial seizures. Neuroimaging revealed a nonenhancing, T2 and T2 fluid-attenuated inversion recovery hyperintense multinodular lesion in the right temporal lobe. Lesional tissue demonstrated well-demarcated nodules of ganglioid cells with vacuolation of both the perikarya and the fibrillary neuropil-like background. The ganglioid cells showed weak cytoplasmic reactivity for synaptophysin and were nonreactive for neurofilament and chromogranin. CD34-positive stellate cells were present within the nodules. A 50-gene next-generation sequencing panel did not identify any somatic mutations in genomic DNA extracted from the tumor.
Unknown ethiology Background:Over-the-counter medications that contain aspirin are widely used, and patients generally regard them as safe. However, the side effects of salicylate toxicity can be severe, and delay in the diagnosis may increase the risk of mortality. Neurologic symptoms are a common presenting feature of salicylate toxicity in the elderly, and their recognition may allow earlier diagnosis. This report is of a case of a 61-year-old woman who presented with acute focal neurologic deficit associated with salicylate toxicity and who had a previous history of stroke. Case Report:A 61-year-old woman presented to the Emergency Department after awakening with left-sided weakness. She had a history of ischemic stroke with an associated seizure disorder. The patient denied recent seizure, and brain magnetic resonance imaging (MRI) showed no evidence of an acute stroke. Following her arrival, she became acutely confused and complained of tinnitus, shortness of breath, and blurred vision. On direct questioning, she gave a history of excessive use of salicylate for the previous two to three weeks. Her initial serum salicylate level was significantly increased at 78.1 mg/dl (upper therapeutic limit, 19.9 mg/dl). She recovered completely following treatment with oral activated charcoal, intravenous sodium bicarbonate, and potassium replacement.
Conclusions:This case demonstrates that physicians should consider salicylate toxicity as a possible cause of exacerbation of neurological deficit in elderly patients.
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