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Letter to the Editor
Acute disseminated encephalomyelitis after Mycoplasma pneumoniae infection: unfavourable clinical course, excellent recovery
Encefalomielitis aguda diseminada tras infección por Mycoplasma pneumoniae: evolución tórpida, recuperación excelente
J. Rodríguez-Montolio
Corresponding author
jrodriguezm@salud.aragon.es

Corresponding author.
, S. Ballesta-Martínez, Y. Martín-Alemán, E. Muñoz-Farjas
Servicio de Neurología, Hospital Clínico Universitario Lozano Blesa, Zaragoza, Spain
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Acute disseminated encephalomyelitis &#40;ADEM&#41; is an autoimmune demyelinating disease of the central nervous system typically occurring in childhood and characterised by multifocal white matter involvement&#46; It is usually monophasic&#44; although up to 20&#37; of patients may present recurrence&#46; Between 50&#37; and 75&#37; of cases are associated with history of infection&#44; whether viral &#40;measles&#44; mumps&#44; influenza&#44; hepatitis&#44; herpes&#41; or bacterial &#40;<span class="elsevierStyleItalic">Chlamydia</span>&#44; <span class="elsevierStyleItalic">Legionella</span>&#44; <span class="elsevierStyleItalic">Campylobacter</span>&#41;&#44; with <span class="elsevierStyleItalic">Mycoplasma pneumoniae</span> being the most common bacterial cause&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> Cases have also been described of ADEM in the context of SARS-CoV-2 infection&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> The aetiopathogenesis of ADEM is unknown&#59; the disease is thought to result from an autoimmune response against infectious agents with epitopes similar to myelin-associated peptides&#44; causing demyelinating lesions&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> The condition may present with a wide range of symptoms&#46; It usually manifests with initially systemic symptoms&#44; followed by acute&#44; rapidly-progressing multifocal neurological symptoms&#46;<a class="elsevierStyleCrossRefs" href="#bib0020"><span class="elsevierStyleSup">4&#8211;7</span></a> As no specific biological markers have been identified&#44; diagnosis is clinical and radiological&#59; furthermore&#44; no diagnostic criteria have been established for adults&#44; unlike in the paediatric population&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a> Adults usually present a more aggressive course&#44; with poorer functional outcomes and survival rates &#40;10&#37;-30&#37; mortality&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">We report the case of a 38-year-old woman who had presented pneumonia 3 weeks previously in the context of an epidemic outbreak in her workplace&#44; receiving treatment with amoxicillin&#47;clavulanic acid&#46; She consulted due to one week&#8217;s history of blurred vision in the left eye and right-sided faciobrachial paraesthesia&#46; The neurological examination revealed bilateral&#44; asymmetric loss of visual acuity with normal eye fundus&#44; right-sided ataxic hemiparesis&#44; right-sided facial hypoaesthesia&#44; generalised hyperreflexia&#44; and wide-based gait with inability to walk in tandem&#46; Given the current epidemiological situation&#44; we requested SARS-CoV-2 serology and PCR studies&#44; which yielded negative results&#46; Focal neurological signs progressed over the first few days&#44; with the patient presenting sensorimotor aphasia&#46; A brain MRI scan revealed multiple large&#44; oval-shaped lesions in the white matter and basal ganglia&#59; the lesions were hyperintense on T2-weighted and FLAIR sequences&#44; with no mass effect&#44; and displayed peripheral contrast uptake &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46; A cerebrospinal fluid &#40;CSF&#41; analysis revealed elevated protein levels &#40;0&#46;59&#8239;g&#47;L&#59; normal range&#44; 0&#46;35-0&#46;45&#41; with no cells&#59; other analyses &#40;autoimmune tests&#44; culture of mycobacteria&#44; and PCR for <span class="elsevierStyleItalic">Neisseria meningitidis</span>&#44; <span class="elsevierStyleItalic">Streptococcus pneumoniae</span>&#44; <span class="elsevierStyleItalic">Streptococcus agalactiae</span>&#44; <span class="elsevierStyleItalic">Haemophilus influenzae</span>&#44; <span class="elsevierStyleItalic">Listeria monocytogenes</span>&#44; and neurotropic viruses&#41; yielded negative results&#46; Blood serology tests yielded positive results for IgM and IgG antibodies against <span class="elsevierStyleItalic">M&#46; pneumoniae</span> 15 days after the onset of neurological symptoms&#59; the remaining serology studies &#40;HIV&#44; EBV&#44; CMV&#44; <span class="elsevierStyleItalic">Legionella</span>&#44; <span class="elsevierStyleItalic">Chlamydia</span>&#44; <span class="elsevierStyleItalic">Coxiella burnetii</span>&#41; and autoimmune studies yielded negative results&#46; A chest-abdomen-pelvis CT scan and transthoracic echocardiography study identified no abnormalities&#46; We started treatment with 1&#8239;g intravenous boluses of methylprednisolone&#44; which had to be discontinued on the third day due to clinical worsening&#46; The patient also did not respond to intravenous immunoglobulins&#46; Plasmapheresis was started&#44; with a good response&#46; We would like to highlight the discrepancy between clinical and radiological findings &#40;<a class="elsevierStyleCrossRef" href="#fig0010">Fig&#46; 2</a>&#41;&#44; with the patient presenting radiological worsening despite clinical improvement&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0015" class="elsevierStylePara elsevierViewall">Clinical presentation is particularly important in ADEM&#46; Fever&#44; headache&#44; and meningeal signs are rare in adult patients&#46; Encephalopathy as the initial symptom may be highly relevant in differential diagnosis with other demyelinating diseases&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> In our patient&#44; the absence of these symptoms and the MRI findings led us to broaden the differential diagnosis to include neuromyelitis optica spectrum disorders and autoimmune encephalitis&#46;<a class="elsevierStyleCrossRefs" href="#bib0015"><span class="elsevierStyleSup">3&#44;7</span></a> Tests for anti-aquaporin-4 &#40;AQP4&#41; antibodies and oligoclonal bands &#40;OCB&#41; in the CSF yielded negative results&#46; Testing for antimyelin oligodendrocyte glycoprotein &#40;MOG&#41; antibodies is recommended in these cases due to their implications for treatment&#44; prognosis&#44; and risk of recurrence&#59; testing for anti-AQP4 antibodies is also recommended for the differential diagnosis of neuromyelitis optica spectrum disorders&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> Patients with ADEM rarely present OCBs in the CSF&#59; however&#44; OCB determination may be useful in predicting future risk of multiple sclerosis&#44; a condition that is more frequent in patients with recurrent demyelination testing negative for anti-MOG antibodies&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> The imaging technique of choice is MRI&#44; which frequently reveals hyperintense lesions on T2-weighted and FLAIR sequences&#46; Unlike in multiple sclerosis&#44; MR images of ADEM typically display thalamic lesions&#44; with no &#8220;black holes&#46;&#8221;<a class="elsevierStyleCrossRefs" href="#bib0030"><span class="elsevierStyleSup">6&#44;9</span></a> The first-line treatment in the acute management of patients with ADEM is high-dose corticosteroid therapy&#44; frequently with methylprednisolone &#40;maximum dose of 1000&#8239;mg&#47;day&#41; for 3 to 5 days&#46; This treatment achieves complete recovery in 50&#37; to 80&#37; of cases&#46; In refractory cases&#44; such as that reported here&#44; plasmapheresis or intravenous immunoglobulins are recommended&#46;<a class="elsevierStyleCrossRefs" href="#bib0035"><span class="elsevierStyleSup">7&#44;10</span></a> Our patient presented signs of poor prognosis &#40;hyperacute onset&#44; aggressive course&#44; severe focal neurological signs&#44; and lack of response to corticosteroid therapy&#41;&#44; despite which she progressed favourably&#59; 6 months after diagnosis&#44; she is oligosymptomatic&#46;<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">10</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">In conclusion&#44; the highly variable clinical presentation of ADEM and the lack of specific biological markers and established diagnostic criteria for adults make this entity a diagnostic challenge&#46; Identifying adult-onset ADEM and providing early treatment is essential to improving functional and vital prognosis&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of interest</span><p id="par0025" class="elsevierStylePara elsevierViewall">The authors have no conflicts of interest to declare&#46;</p></span></span>"
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