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Eight-and-a-half syndrome as manifestation of acute disseminated adenovirus encephalomyelitis
Síndrome del ocho y medio como manifestación de enfermedad desmielinizante aguda por adenovirus
S. Fathi Nieto
Corresponding author
gsolerenrique@gmail.com

Corresponding author.
, E. García-Soler, R. Butrón Ruiz, J. Orts Llácer, M. Aguilar González, H. Barranco González
Departamento de Oftalmología, Hospital Universitario La Fe, Valencia, Spain
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    "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Introduction</span><p id="par0005" class="elsevierStylePara elsevierViewall">Acute disseminated encephalomyelitis &#40;ADE&#41; is a demyelinating disease of the central nervous system &#40;CNS&#41; that affects children between the ages of 5 and 8 years&#44;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> with an average age of 7&#46;1 years&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">It should be suspected in pediatric patients mainly when&#44; after a history of infectious disease or previous vaccination in the last 2&#8211;4 weeks&#44; they manifest clinical symptoms of encephalitis with headache&#44; fever&#44; nausea&#44; vomiting and varied neurological focality reflecting multifocal CNS involvement&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">It is more frequent in winter and spring&#44; with a slight male predisposition&#46;<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1&#8211;3</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">Diagnosis is based on clinical history&#44; neurological symptoms and the findings visible on brain and spinal cord magnetic resonance imaging &#40;MRI&#41;&#44;<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1&#8211;4</span></a> the imaging test of choice when this entity is suspected&#46; MRI shows multiple hyper-reflective lesions with poorly defined margins on T2 and FLAIR sequences&#44; affecting the central and subcortical white matter&#59; the grey matter-white matter junction of both hemispheres&#44; cerebellum&#44; brainstem and spinal cord&#44; and the grey matter of the thalamus and basal ganglia&#46;<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1&#44;2</span></a> It is recommended to complete the study with a complete blood test with serology and antibodies and a lumbar puncture&#44; which is normal in 20&#37;&#8211;30&#37; of cases&#44; the rest being non-specific but reflecting inflammation data&#46;<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1&#44;3</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">The first line of treatment is based on the use of corticosteroids in megabolic boluses for 5 days&#44; followed by a tapering regime for 4&#8211;6 weeks&#46; Refractory or severe cases are combined with immunoglobulins 2&#8239;g&#47;kg for 2&#8211;5 days&#46; In cases refractory to previous treatment or sudden onset cases&#44; it has been combined with plasmapheresis<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1&#44;3</span></a> and even with hypothermia and decompressive craniotomy&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">The prognosis of the disease is favourable&#44; resolving in most cases without sequelae&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Clinical case</span><p id="par0035" class="elsevierStylePara elsevierViewall">Male&#44; aged 8&#44; who consulted the emergency department of the pediatric ophthalmology department of our centre for diplopia in dextroversion and abnormal eye movements with onset that same day&#46; He had no relevant personal history or recent vaccinations&#44; and reported an episode of gastroenteritis the previous week that resolved spontaneously without treatment&#46;</p><p id="par0040" class="elsevierStylePara elsevierViewall">On examination he had an uncorrected visual acuity of 0&#46;8 in both eyes&#46; Intraocular pressure with ICare tonometer was 14&#8239;mmHg in the right eye &#40;RE&#41; and 15&#8239;mmHg in the left eye &#40;LE&#41;&#46; Pupils were isochoric and normoreactive&#44; with no relative afferent pupillary defect&#46;</p><p id="par0045" class="elsevierStylePara elsevierViewall">Oculomotor examination revealed an inability of the LE to adduct accompanied by nystagmus of the RE in abduction &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#44; with preserved convergence&#46; In the remaining gaze positions&#44; a spring nystagmus of moderate frequency and fine amplitude was observed&#44; which was vertical in superior and inferior gaze and horizontal in levoversion&#44; with a much higher frequency and amplitude in dextroversion&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0050" class="elsevierStylePara elsevierViewall">There was no fever or other systemic symptoms&#46; It was decided to admit the patient for a left internuclear ophthalmoplegia &#40;LIO&#41;&#46;</p><p id="par0055" class="elsevierStylePara elsevierViewall">During the first 48&#8239;h of admission&#44; there was also evidence of limited abduction of the LE and adduction of the RE &#40;<a class="elsevierStyleCrossRef" href="#fig0010">Fig&#46; 2</a>&#41;&#44; left peripheral facial paralysis&#44; loss of sensation of the left hemiface and tongue deviation to the right&#46; In view of the freezing of the horizontal gaze of the LE together with the LIO of the new appearance of the RE and left facial paralysis&#44; a finding known as eight-and-a-half syndrome&#44; an emergency brain CT scan was requested&#44; pending the performance of a spinal and brain MRI scan&#44; the result of the CT scan being normal&#46;</p><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0060" class="elsevierStylePara elsevierViewall">The MRI showed a T2 hyperintense lesion in the floor of the fourth ventricle with cranial direction towards the left medial longitudinal fascicle &#40;MFL&#41; &#40;<a class="elsevierStyleCrossRef" href="#fig0015">Fig&#46; 3</a>&#41;&#44; as well as multiple hyperintense FLAIR lesions without uptake in bilateral parietal deep white matter and around the occipital horns&#44; suggestive of parainfectious and&#47;or autoimmune demyelinating lesion&#46;</p><elsevierMultimedia ident="fig0015"></elsevierMultimedia><p id="par0065" class="elsevierStylePara elsevierViewall">Serology&#44; nasopharyngeal swab&#44; antibody study and lumbar puncture were performed to complete the study&#44; and in view of the suspicion of demyelinating disease&#44; intravenous treatment was started with corticotherapy at megadoses &#40;30&#8239;mg&#47;kg&#47;day&#41; and immunoglobulins 0&#46;4&#8239;g&#47;kg&#47;day for 5 days&#46;</p><p id="par0070" class="elsevierStylePara elsevierViewall">The antibody study and microbiological results for the nasopharyngeal swab were negative&#46; Lumbar puncture showed non-specific inflammatory data and absence of oligoclonal bands&#44; with negative microbiology&#46; Serology was positive for adenovirus IgM and IgG&#44; establishing the diagnosis of adenovirus AED&#46;</p><p id="par0075" class="elsevierStylePara elsevierViewall">Twenty-four hours after starting treatment with glucocorticoids and immunoglobulins&#44; a favourable evolution was observed with complete recovery of the left peripheral facial paralysis&#46; After 72&#8239;h of treatment&#44; the adduction limitation of both the LE and the RE disappeared&#44; with only a slight limitation of abduction of the LE persisting during hospitalisation&#44; which disappeared in the check-up performed one month after hospital discharge&#46; MRI scans performed at 4 and 12 months after the episode revealed no new lesions&#44; although the above described lesions persisted&#46;</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Discussion</span><p id="par0080" class="elsevierStylePara elsevierViewall">Internuclear ophthalmoplegia &#40;INO&#41; is a disorder of the horizontal conjugate gaze caused by a lesion at the level of the MFL&#44; limiting adduction of the eye on the side of the lesion with a nystagmus on abduction of the contralateral side&#46; Etiology is varied&#44; the main causes in adults being ischemia or multiple sclerosis &#40;MS&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> In children&#44; LIO is less common&#44; and a thorough history and examination should be performed to discover the various causes&#58; trauma&#44; infectious or demyelinating meningoencephalitis&#44; brain tumours&#44; iatrogenesis&#44; vasculitis or cerebral haemorrhage&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a></p><p id="par0085" class="elsevierStylePara elsevierViewall">When a patient presents with an ipsilateral horizontal conjugate palsy &#40;one&#41; together with an ipsilateral LIO &#40;half&#41;&#44; it is called Fisher&#8217;s one-and-a-half syndrome&#46; This syndrome&#44; described by Fisher in 1967&#44; is the result of a lesion in the paramedian pontine reticular formation &#40;PPRF&#41;&#44; the ipsilateral MFL and the nucleus of the ipsilateral cranial VI par&#46;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a></p><p id="par0090" class="elsevierStylePara elsevierViewall">A variety of disorders fall within the spectrum of one-and-a-half syndrome depending on the structures affected at the level of the pons&#46; The most common variant is the eight-and-a-half syndrome&#44; first described in 1998 by Eggenberger<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a> after reporting 3 cases secondary to ischemic stroke&#46; This syndrome adds to horizontal conjugate palsy and ipsilateral LIO an ipsilateral paralysis of the cranial VII par&#46; With regard to its etiology&#44; the eight-and-a-half syndrome etiology matches that described for LIO&#44; the two pathologies being differentiated by the more extensive involvement of the pontine tegmentum in the case of the eight-and-a-half syndrome&#46; This anatomical area should be studied by means of imaging tests to determine the etiology and to be able to carry out specific treatment depending on the cause&#46; In adults&#44; ischemic origin is more frequent due to involvement of a perforating branch of the basilar artery&#44; while in children MS is more frequent&#46;<a class="elsevierStyleCrossRefs" href="#bib0030"><span class="elsevierStyleSup">6&#44;8</span></a> In pediatrics&#44; a single case of infectious eight-and-a-half syndrome secondary to tuberculoma has been reported in a 4 year-old girl&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a></p><p id="par0095" class="elsevierStylePara elsevierViewall">The imaging test of choice is brain and spinal cord MRI&#44; which will help to guide the diagnosis&#46; If demyelinating lesions are present&#44; the study should be expanded to differentiate between monophasic demyelination as the first manifestation of ADE or MS&#44; as 18&#37; of diagnoses of ADE have been reported to be a first attack of MS&#46;<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a> Radiological differences that may help differentiate between MS and ADE include location&#44; presence of bilateral involvement or black holes&#46; The periventricular location of hyperreflective lesions on T2 and FLAIR sequences&#44; the presence of black holes and the absence of bilateral diffuse involvement point to MS&#44; as opposed to ADE&#44; which is characterised by bilateral diffuse involvement in 45&#37; of patients&#44; with the presence of black holes and periventricular involvement in a very low percentage of patients&#46;<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a></p><p id="par0100" class="elsevierStylePara elsevierViewall">In addition to radiological features&#44; the diagnosis of ADE is based on a thorough clinical history&#44; with a history of recent vaccination or infectious symptoms in the last 2 days&#8211;4 weeks being characteristic&#46; It is more frequent in winter and spring&#44; with a slight male predisposition and an age between 5 and 8 years old&#46;<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1&#8211;3</span></a> At the time of diagnosis&#44; the patient presents with clinical signs of encephalitis&#44; with headache&#44; fever&#44; nausea&#44; vomiting and varied neurological focality&#44; reflecting multifocal CNS involvement&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a></p><p id="par0105" class="elsevierStylePara elsevierViewall">Lumbar puncture results may help to differentiate between the two entities&#44; the main discriminating feature being the presence of oligoclonal IgG bands in cerebrospinal fluid &#40;CSF&#41; but not in serum&#44; which occurs in 40&#37;&#8211;95&#37; of MS cases and only in 0&#37;&#8211;29&#37; of ADE cases&#46; ADE would yield a non-specific inflammatory result in CSF&#44; absent in MS&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> The presence of micro-organisms in the CSF also supports the diagnosis of ADE&#46; In the case of adenovirus&#44; encephalitis incidence data of 1&#46;9&#37; have been published&#46;<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">10</span></a> Since CSF was positive in only 15&#37; of cases&#44; it is postulated that the disease is caused by immune damage secondary to circulating antigen-antibody complexes rather than primary CNS infection&#46;<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">10</span></a></p><p id="par0110" class="elsevierStylePara elsevierViewall">First-line treatment in ADE is based on the use of corticosteroids at a dose of 30&#8239;mg&#47;kg&#47;day for 3&#8211;5 days&#44; followed by a tapering regimen for 4&#8211;6 weeks&#46; In cases with poor response&#44; use has been combined with immunoglobulins at a dose of 2&#8239;g&#47;kg for 2&#8211;5 days&#46; The combined use of corticosteroids&#44; immunoglobulins and plasmapheresis has been reported in refractory patients or those with immediate onset symptoms&#44;<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1&#44;3</span></a> and a single case was also treated with hypothermia and decompressive craniotomy&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a></p><p id="par0115" class="elsevierStylePara elsevierViewall">The prognosis is favourable in most patients&#44; with complete recovery reported in 50&#37;&#8211;75&#37; of cases within 1&#8211;6 months of onset and a mortality rate of less than 10&#37;&#46; The main sequelae described are ataxia and mild hemiparesis&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a></p><p id="par0120" class="elsevierStylePara elsevierViewall">Follow-up should be performed with brain MRI&#44; which shows complete resolution of lesions in 27&#37;&#8211;55&#37; and partial resolution in 45&#37;&#8211;64&#37;&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> Other authors have suggested figures of 37&#37;&#8211;75&#37; complete recovery in EDA and 25&#37;&#8211;53&#37; partial recovery&#46;<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> It is advisable to perform at least 2 Brain MRI during follow-up before discharge&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> Brain MRI may also be useful for long-term differentiation between the diagnosis of ADE and MS&#46; The presence of new lesions points towards a diagnosis of MS&#44; as their presence has been reported in only 0&#37;&#8211;9&#37; of patients with ADE&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a></p><p id="par0125" class="elsevierStylePara elsevierViewall">In conclusion&#44; we present a case of 8&#46;5 syndrome as a manifestation of adenovirus ADE&#46; It should be suspected in children of pediatric age who report viral symptoms in recent weeks or recent vaccination&#44; as well as in patients with neurological symptoms who present with lesions suspicious of demyelination on brain and spinal cord MRI together with a lumbar puncture with a non-specific result&#46; The prognosis of the disease is favourable&#44; with no or minimal sequelae after treatment with corticosteroids and immunoglobulins&#46;</p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Funding</span><p id="par0130" class="elsevierStylePara elsevierViewall">This research has not received specific support from public sector agencies&#44; the commercial sector or non-profit organisations&#46;</p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Conflict of interest</span><p id="par0135" class="elsevierStylePara elsevierViewall">No conflicts of interest were declared by the authors&#46;</p></span></span>"
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            0 => "S&#237;ndrome del ocho y medio"
            1 => "Oftalmoplej&#237;a internuclear"
            2 => "Encefalomielitis diseminada aguda"
            3 => "Adenovirus"
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        "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">Acute disseminated encephalomyelitis is an immune mediated inflammatory-demyelinizing disease that usually manifests after infection or vaccination in school-age children&#46; It typically presents a prodromal phase with flu-like symptoms&#44; followed by a phase with varied clinical symptoms&#44; neuro-ophthalmological alterations such as ophthalmoplegia or optic neuritis may occur&#46;</p><p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">The differential diagnosis includes tumor&#44; vascular&#44; infectious&#44; inflammatory and demyelinating diseases&#46; Diagnosis is based on the clinical history and the characteristics of brain magnetic resonance imaging&#44; the gold standard test&#46; The study of the cerebrospinal fluid can help to guide the clinical picture&#46;</p><p id="spar0030" class="elsevierStyleSimplePara elsevierViewall">The prognosis is favorable&#44; with an excellent response to corticosteroids and immunoglobulins&#44; with minimal long-term sequelae in most cases&#46;</p><p id="spar0035" class="elsevierStyleSimplePara elsevierViewall">We report the case of an 8-year-old male with acute demyelinating disease due to adenovirus whose manifestation was an eight-and-a-half syndrome&#46;</p></span>"
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        "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0040" class="elsevierStyleSimplePara elsevierViewall">La encefalomielitis diseminada aguda es una enfermedad inflamatoria-desmielinizante inmunomediada que suele manifestarse tras una infecci&#243;n o vacunaci&#243;n en ni&#241;os en edad escolar&#46; T&#237;picamente presenta una fase prodr&#243;mica con un cuadro pseudogripal seguida de una fase con cl&#237;nica muy variada&#44; pudiendo aparecer alteraciones neurooftalmol&#243;gicas como oftalmoplej&#237;a o neuritis &#243;ptica&#46;</p><p id="spar0045" class="elsevierStyleSimplePara elsevierViewall">La etiolog&#237;a es variada&#44; incluyendo enfermedades tumorales&#44; vasculares&#44; infecciosas&#44; inflamatorias y desmielinizantes&#46; El diagn&#243;stico se basa en la historia cl&#237;nica y en las caracter&#237;sticas de la resonancia magn&#233;tica cerebral&#44; prueba de imagen de elecci&#243;n&#46; El estudio del l&#237;quido cefalorraqu&#237;deo puede servir de ayuda en la orientaci&#243;n del cuadro cl&#237;nico&#46;</p><p id="spar0050" class="elsevierStyleSimplePara elsevierViewall">El pron&#243;stico es favorable&#44; con excelente respuesta a los corticoides e inmunoglobulinas y con m&#237;nimas secuelas a largo plazo en la mayor&#237;a de los casos&#46;</p><p id="spar0055" class="elsevierStyleSimplePara elsevierViewall">Presentamos el caso de un var&#243;n de 8 a&#241;os con enfermedad desmielinizante aguda por adenovirus cuya manifestaci&#243;n fue un s&#237;ndrome del ocho y medio&#46;</p></span>"
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                      "titulo" => "Encefalomielitis diseminada aguda postinfecciosa y posvacunal&#58; casos cl&#237;nicos y revisi&#243;n de la literatura"
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                            2 => "J&#46;L&#46; Guti&#233;rrez-Morales"
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                      "titulo" => "Eight-and-a-half syndrome&#58; video evidence and updated literature review"
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                          "etal" => false
                          "autores" => array:4 [
                            0 => "M&#46;A&#46; C&#225;rdenas-Rodr&#237;guez"
                            1 => "S&#46;A&#46; Castillo-Torres"
                            2 => "B&#46; Ch&#225;vez-Lu&#233;vanos"
                            3 => "L&#46; de Le&#243;n-Flores"
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Original language: English
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