Case StudyTransient splenial lesion in a case with carbon monoxide poisoning: A clue supporting the excitotoxicity hypothesis?
Introduction
Transient splenial lesion (TSL) is an isolated, non-enhancing, ovoid, T2-hyperintense lesion manifested by prominent restricted diffusion in the center of the corpus callosum splenium. This rare phenomenon initially first identified in status epilepticus and the use and withdrawal of antiepileptic drugs.1 In recent years, a stereotypic appearance TSL have been repeatedly reported, and thought not to be uncommon. It has been reported in many various clinical conditions including viral encephalitis/encephalopathy, metabolic derarangements such as hypoglicemia and hypernatremia, malnutrition, vitamin B12 deficiency, alcohol poisoning, and eclampsia.2,3 We believe that the reported case herein will also widen the spectrum of the TSL, since this is the first case of carbon monoxide (CO) poisoning associated with TSL, to the best of our knowledge.
Section snippets
Case study
A 17-year-old, previously healthy boy was referred to our emergency department for hyperbaric oxygen therapy with a comatose and intubated state that was caused by sleeping in a poorly ventilated room with a coal heater. His initial venous blood gas analysis showed pH 7.10, PaO2 54 mmHg, PaCO2 64.8 mmHg, HCO3 19 mmol/L. COHb (carboxyhemoglobin) was 18% (normal range 0.5–1.5%), and blood glucose level was 119 mg/dl at the referring hospital. Neither the patient nor any family member had a
Discussion
We reported a distinct patient with coexisting CO intoxication associated TSL. CO poisoning result in the formation of COHb which reduces the amount of Hb available for O2 transport. COHb can cause profound hypoxic/anoxic injury in the brain.4 Different areas of the brain can be affected by CO poisoning. Globus pallidus, putamen, caudat nucleus, thalamus, periventricular or subcortical white matter, cerebral cortex, cerebellum, and hippocampus of the temporal lobe may be involved. Globus
Conflict of interest
Authors declare that they have no conflict of interest.
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Cited by (4)
Cytotoxic lesions of the corpus callosum in children: Etiology, clinical and radiological features, and prognosis
2021, Brain and DevelopmentCitation Excerpt :Infection- and trauma-associated causes are the most common etiologies of CLOCCs [9]. Although many case reports and a small series of patients have been presented since the first description of CLOCCs, these sources mainly focus on infection-associated patient series with a reversible outcome or isolated case reports of rare presentations [10-14]. While most patients with CLOCCs have only splenial CC involvement, such etiologies as metachromatic leukodystrophy, urea cycle defects (by causing hyperammonemia), and diffuse axonal injury (DAI) may all cause lesions in different parts of the brain with splenium involvement, potentially resulting in irreversible damage [15,16].
Transient Splenial Lesion of the Corpus Callosum After Cabergoline Treatment
2018, World NeurosurgeryCitation Excerpt :On diffusion-weighted images (DWI), they are restricted diffusion in the center of the splenium of the corpus callosum. It has been reported in various clinical conditions including viral encephalopathy, hypoglicemia, hypernatremia, malnutrition, vitamin B12 deficiency, alcohol poisoning, and eclampsia.1,2 In this case report, we describe a 24-year-old man with a microprolactinoma in the pituitary region.
Mild encephalitis/encephalopathy with a reversible splenial lesion in children
2018, Diagnostic and Interventional RadiologyLesions in the Splenium of the Corpus Callosum on MRI in Children: A Review
2017, Journal of Neuroimaging