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Scientific letter
Late leukoencephalopathy in patients with methanol intoxication
Leucoencefalopatía tardía posterior a intoxicación por metanol
Dannys Rivero Rodrigueza,b,
Corresponding author
dannyriverorodriguez@gmail.com

Corresponding author.
, Kimberly Sama, Michelle Bravoc,d
a San Francisco University of Quito USFQ, Ecuador
b Neurology Department, Eugenio Espejo Hospital, Quito, Ecuador
c Neurology Department, Donald, United States
d Barbara Zucker School of Medicine at Hofstra/Northwell, United States
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Methanol is a clear substance with pronounced similarities in flavor and aroma to ethanol&#46; It is highly toxic to the CNS and damage to the optic nerve and basal ganglia&#44; accompanied by severe metabolic acidosis&#44; have been observed within hours following ingestion&#46; Common clinical manifestations of methanol intoxication &#40;MI&#41; include blindness&#44; headache&#44; abdominal pain&#44; drowsiness&#44; seizures&#44; coma&#44; and death&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">The most recurrent neuroradiological finding demonstrated by CT and MR imaging &#40;MRI&#41; is putaminal necrosis&#44; with varying degrees of putaminal hemorrhage&#59; however&#44; optic nerve damage and white and grey matter lesions in various locations have also been reported&#44; though less frequently&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">In this study&#44; we report two patients &#40;P<span class="elsevierStyleInf">1&#44; 2</span>&#41; with accidental methanol ingestion who developed late toxic leukoencephalopathy&#46; The symptoms most frequently reported during the first medical evaluation &#40;6-h after ingestion&#41; were abdominal pain&#44; headache&#44; diaphoresis&#44; and declined visual acuity&#46; The progressive decrease in Glasgow coma score &#40;GCS&#41; during the initial 24<span class="elsevierStyleHsp" style=""></span>h &#40;P<span class="elsevierStyleInf">1</span>&#44; 13-9&#47;15-GCS&#46; P<span class="elsevierStyleInf">2</span>&#44; 15-12&#47;15-GCS&#41; of hospitalization&#44; coupled with metabolic acidosis &#40;P<span class="elsevierStyleInf">1</span>&#44; PH-6&#46;80&#44; PCO<span class="elsevierStyleInf">2</span>-25&#46;7&#44; HCO<span class="elsevierStyleInf">3</span>-3&#46;90&#44; Lactic acid-12&#46;1<span class="elsevierStyleHsp" style=""></span>mmol&#47;L&#46; P<span class="elsevierStyleInf">2</span>&#44; PH-7&#46;13&#44; PCO<span class="elsevierStyleInf">2</span>-12&#46;0&#44; HCO<span class="elsevierStyleInf">3</span>-4&#46;0&#44; Lactic acid-1&#46;9<span class="elsevierStyleHsp" style=""></span>mmol&#47;L&#41; and a notably high anion gap &#40;P<span class="elsevierStyleInf">1</span>-41&#46;8<span class="elsevierStyleHsp" style=""></span>mEq&#47;l&#46; P<span class="elsevierStyleInf">2</span>-39&#46;0<span class="elsevierStyleHsp" style=""></span>mEq&#47;l&#41;&#44; suggested the diagnosis of MI&#46; The diagnosis was confirmed after methanol levels in the blood were tested and exceeded 20<span class="elsevierStyleHsp" style=""></span>mg&#47;dL &#40;P<span class="elsevierStyleInf">1</span>-43<span class="elsevierStyleHsp" style=""></span>mg&#47;l&#46; P<span class="elsevierStyleInf">2</span>-28<span class="elsevierStyleHsp" style=""></span>mg&#47;l&#41;&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">In the both cases &#40;P<span class="elsevierStyleInf">1</span>&#44; P<span class="elsevierStyleInf">2</span>&#41; was it possible to perform an initial MRI scan&#44; allowed by their stable clinical status&#59; more than 30 days later&#44; follow-up MRI was performed&#44; demonstrating the progression of active toxic leukoencephalopathy &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46; In all patients&#44; putaminal hemorrhagic necrosis was observed&#44; with subcortical and deep white matter damage&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0025" class="elsevierStylePara elsevierViewall">MI causes severe damage to the CNS&#46; Putaminal hemorrhagic necrosis has been described as the most frequent radiological and clinical-pathological finding in these patients&#46; White matter &#40;WM&#41; lesions are another finding seen in MI&#59; they have been observed to be bilateral&#44; deep&#44; or subcortical&#44; although occasionally the subcortical fibers have been preserved&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> There are few case studies in the literature investigating DWI findings that use follow-up MRI evaluation after MI&#46;<a class="elsevierStyleCrossRefs" href="#bib0015"><span class="elsevierStyleSup">3&#44;4</span></a> It is probable that the prominent obstacles leading to difficulties in studying the severity of illness is the high level of morbidity and mortality associated with MI&#44; which can cause difficulties in performing follow-up MRI studies&#44; and the unstable initial state of the patient upon admission&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">One of the few descriptions of serial MRI studies in MI patients was described in a 2006 case study&#46; Takao et al&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> reported restricted diffusion in the putamen and subcortical fibers&#44; with a putaminal lesion in the initial MRI scan&#46; Following three days&#44; MRI revealed a new lesion in the subcortical fibers&#44; leading the authors to hypothesize that the new lesion was related to the cytotoxic edema observed in the first MRI scan&#46; On the 19th day&#44; MRI revealed progressed&#44; hemorrhagic damage to the subcortical fibers&#46;</p><p id="par0035" class="elsevierStylePara elsevierViewall">In our two patients&#44; we were able to demonstrate how relatively symmetric leukoencephalopathy in the frontal and&#47;or occipital lobes continued to worsen more than 30 days after MI&#46; We hypothesize that the initial restricted diffusion in the subcortical fibers in the DWI&#44; indicative of cytotoxic edema&#44; represents an early marker of potential WM damage seen in later imaging&#46; In the patient with more extensive leukoencephalopathy detected in the later stages of MI &#40;P<span class="elsevierStyleInf">1</span>&#41;&#44; we observed worsened morbidity at three months following hospital discharge&#44; leading us to suspect that WM lesions predict poor outcome following MI&#46; From our patients&#8217; imaging studies&#44; we suspect that progressive WM lesions may be a significant finding in these patients&#44; highlighting the severity over time following MI&#46;</p><p id="par0040" class="elsevierStylePara elsevierViewall">Further investigation of the relationship between the development of chronic leukoencephalopathy and the quantity of methanol ingested provides additional insight that can be used as a valuable predictive tool for prognostics&#46;</p><p id="par0045" class="elsevierStylePara elsevierViewall">Due to the few studies that have conducted follow-up MRI studies during the later stages of MI&#44; and with our sample size being small&#44; we cannot conclude that leukoencephalopathy is a long-term finding associated with MI&#46; Nevertheless&#44; it is worth exploring whether there is a relationship between worsened neuronal damage on serial MRI and patient outcomes&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Funding</span><p id="par0050" class="elsevierStylePara elsevierViewall">This research received no external funding&#46;</p></span></span>"
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ISSN: 23870206
Original language: English
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