<clinical_study>
  <!-- This xml conforms to an XML Schema at:
    https://clinicaltrials.gov/ct2/html/images/info/public.xsd -->
  <required_header>
    <download_date>ClinicalTrials.gov processed this data on September 20, 2023</download_date>
    <link_text>Link to the current ClinicalTrials.gov record.</link_text>
    <url>https://clinicaltrials.gov/ct2/show/NCT03284801</url>
  </required_header>
  <id_info>
    <org_study_id>ADEM</org_study_id>
    <nct_id>NCT03284801</nct_id>
  </id_info>
  <brief_title>Management Of Acute Disseminating Encephalomyelitis</brief_title>
  <official_title>Management of Acute Disseminated Encephalomyelitis in Neurology Unit of Assiut University Children Hospital</official_title>
  <sponsors>
    <lead_sponsor>
      <agency>Assiut University</agency>
      <agency_class>Other</agency_class>
    </lead_sponsor>
  </sponsors>
  <source>Assiut University</source>
  <oversight_info>
    <is_fda_regulated_drug>No</is_fda_regulated_drug>
    <is_fda_regulated_device>No</is_fda_regulated_device>
  </oversight_info>
  <brief_summary>
    <textblock>
      Acute disseminated encephalomyelitis is an immune-mediated inflammatory demyelinating disease&#xD;
      of the central nervous system, which is typically transitory and self-limiting. It is&#xD;
      characterized by an acute or subacute encephalopathy with neurological deficits, and magnetic&#xD;
      resonance imaging evidence of widespread demyelination that predominantly involves the white&#xD;
      matter of the brain and spinal cord. In the absence of specific biological markers, the&#xD;
      diagnosis of Acute disseminated encephalomyelitis is still based upon a combination of&#xD;
      clinical and neuro imaging features and exclusion of diseases that mimic Acute disseminated&#xD;
      encephalomyelitis&#xD;
    </textblock>
  </brief_summary>
  <detailed_description>
    <textblock>
      Acute disseminated encephalomyelitis can occur at any age, but usually affects children and&#xD;
      young adults. The mean age of clinical presentation in pediatric cohorts ranges from 5 to 8&#xD;
      years. The annual incidence of Acute disseminated encephalomyelitis is reported to be 0.4-0.8&#xD;
      per 100,000 and the disease more commonly affects children and young adults, probably related&#xD;
      to the high frequency of exanthematous and other infections and vaccination in this age&#xD;
      group.Initial symptoms and signs of Acute disseminated encephalomyelitis usually begin within&#xD;
      2 days to 4 weeks after a viral infection or vaccination, and include a rapid onset&#xD;
      encephalopathy (behavioral change or altered consciousness) associated with a combination of&#xD;
      multifocal neurological deficits, leading to hospitalization within a week. Typically Acute&#xD;
      disseminated encephalomyelitis presents with systemic symptoms such as fever, malaise,&#xD;
      headache, nausea, and vomiting, which may occur shortly before the appearance of neurological&#xD;
      signs and symptoms. The clinical course is rapidly progressive, developing maximum deficits&#xD;
      within a few days (mean 4.5 days) . A wide variety of neurological deficits have been&#xD;
      described in pediatric patients with Acute disseminated encephalomyelitis, including:&#xD;
      obtundation and depressed consciousness (invariable); unilateral or bilateral long tract&#xD;
      signs (60-95%); acute hemiplegia (76%); ataxia (18-59%); meningismus (26-31%); seizures&#xD;
      (13-35%); spinal cord involvement (24%); visual involvement (7-23%); and speech impairment or&#xD;
      aphasia (5-21%). Cerebellar mutism and prolonged focal motor seizures in the context of Acute&#xD;
      disseminated encephalomyelitis have been mainly reported in children younger than 5 years of&#xD;
      age.Acute combined peripheral nervous system demyelination is not rare in children with Acute&#xD;
      disseminated encephalomyelitis whereas it is more frequently described in adult patients,&#xD;
      with a reported frequency of 44% in one study. A particular Acute disseminated&#xD;
      encephalomyelitis phenotype affecting young children has been reported in association with&#xD;
      group A beta hemolytic streptococcal infection. Prominent behavioral disturbances, dystonic&#xD;
      movements, and basal ganglia abnormalities on MRI (in addition to typical white matter&#xD;
      lesions) characterize this syndrome.&#xD;
&#xD;
      Supportive care in the acute stage is critical and early antiviral treatment with acyclovir&#xD;
      (30 mg/kg/ day) is highly recommended on admission, considering that viral encephalitis and&#xD;
      particularly herpes simplex encephalitis is the usual primary diagnosis in a child with&#xD;
      fever, encephalopathy, seizures, and focal neurological signs. The treatment for Acute&#xD;
      disseminated encephalomyelitis includes primarily the management of acute attacks.&#xD;
      Corticosteroid treatment at high doses is the most widely reported therapy. Most authors&#xD;
      recommend a brief (3-5 days) high-dose intravenous steroid course, usually methylprednisolone&#xD;
      given at 20-30 mg/kg/day to a maximum dose of 1 g/day, or dexamethasone given at 1 mg/kg/day,&#xD;
      followed by oral prednisone taper for 4-6 weeks . Reported treatment approaches show a wide&#xD;
      variety in the specific steroid formulation employed, as well as in the dosing, routes of&#xD;
      administration, and tapering regimens. Treatment with corticosteroids requires careful&#xD;
      monitoring of blood pressure, urine glucose, and serum potassium, and administration of&#xD;
      gastric protection. The use of immunoglobulin has been reported in several case studies&#xD;
      either alone or in combination with corticosteroids. The recommended total dose of&#xD;
      immunoglobulin is 2 g/kg, administered over 2-5 days. The usefulness of immunoglobulin has&#xD;
      been reported both as a second-line treatment in steroid-unresponsive Acute disseminated&#xD;
      encephalomyelitis cases and in patients showing recurrent or steroid-dependent demyelination.&#xD;
&#xD;
      The use of plasma exchange has been recently established as possibly effective and it may be&#xD;
      considered as escalation therapy for steroid-unresponsive acute fulminant demyelinating&#xD;
      diseases including Acute disseminated encephalomyelitis, multiple sclerosis, and transverse&#xD;
      myelitis, . Plasmapheresis should be started as soon as the treatment failure is recognized.&#xD;
      The use of this procedure in Acute disseminated encephalomyelitis has been reported in only a&#xD;
      small number of severe cases. A median number of seven exchanges (range 2 to 20) were&#xD;
      reported in one study. Moderate to severe anemia, symptomatic hypotension, hypocalcemia,&#xD;
      potential transfusion reactions or transmission of transfusion-related diseases, and&#xD;
      heparin-associated thrombocytopenia have been described in relation to therapeutic plasma&#xD;
      exchange. There is also a risk of catheter-related complications, including thrombosis,&#xD;
      septic infections or pneumothorax.&#xD;
&#xD;
      Acute hemorrhagic leukoencephalitis is often considered the most acute and severe form of&#xD;
      Acute disseminated encephalomyelitis, with a universally fatal course within hours to days&#xD;
      after the onset of neurological symptoms without treatment. Survival in pediatric patients&#xD;
      has been reported with combined therapy including high-dose intravenous corticosteroid,&#xD;
      immunoglobulin, Therapeutic plasma exchange, and decompressive craniotomies. Aggressive&#xD;
      treatment strategies such as surgical decompression have to be considered and performed in&#xD;
      patients with fulminant variants of Acute disseminated encephalomyelitis, with evidence of&#xD;
      continued clinical deterioration due to increased intracranial pressure, unresponsive to&#xD;
      conventional medical treatment and critical care measures.&#xD;
    </textblock>
  </detailed_description>
  <overall_status>Unknown status</overall_status>
  <last_known_status>Not yet recruiting</last_known_status>
  <start_date type="Anticipated">January 2018</start_date>
  <completion_date type="Anticipated">March 2019</completion_date>
  <primary_completion_date type="Anticipated">January 2019</primary_completion_date>
  <study_type>Observational</study_type>
  <has_expanded_access>No</has_expanded_access>
  <study_design_info>
    <observational_model>Case-Only</observational_model>
    <time_perspective>Prospective</time_perspective>
  </study_design_info>
  <primary_outcome>
    <measure>clinical audit on management of acute disseminating encephalomyelitis</measure>
    <time_frame>within one year</time_frame>
    <description>To improve diagnosis and management of acute disseminated encephalomyelitis in Neurology Unit of Assiut University Children Hospital and to decrease the mortality and residual deficits from this disease.&#xD;
The aim of this audit is to measure the current practice within the Neurology Unit of Assiut University Children Hospital team in the diagnosis and management of acute disseminated encephalomyelitis against the recommendations in American Academy of Neurology guidance by using checklist and designed questionnaire.</description>
  </primary_outcome>
  <enrollment type="Anticipated">40</enrollment>
  <condition>Acute Disseminated Encephalomyelitis</condition>
  <intervention>
    <intervention_type>Other</intervention_type>
    <intervention_name>management of acute disseminating encephalomyelitis</intervention_name>
    <description>clinical audit on management of acute disseminating encephalomyelitis</description>
  </intervention>
  <eligibility>
    <study_pop>
      <textblock>
        - All patient presented with manifestation of acute disseminating encephalomyelitis&#xD;
        admitted in Assiut University Children Hospital&#xD;
      </textblock>
    </study_pop>
    <sampling_method>Non-Probability Sample</sampling_method>
    <criteria>
      <textblock>
        Inclusion Criteria:&#xD;
&#xD;
          -  All patient presented with manifestation of acute disseminating encephalomyelitis&#xD;
             admitted in Assiut University Children Hospital&#xD;
&#xD;
        Exclusion Criteria:&#xD;
&#xD;
          -  Patients presented with viral encephalitis,bacterial meningitis&#xD;
&#xD;
          -  Cases not fulfilling MRI criteria for diagnosis of acute disseminated&#xD;
             encephalomyelitis&#xD;
      </textblock>
    </criteria>
    <gender>All</gender>
    <minimum_age>12 Months</minimum_age>
    <maximum_age>18 Years</maximum_age>
    <healthy_volunteers>No</healthy_volunteers>
  </eligibility>
  <overall_official>
    <last_name>Marwa Alsaid Ahmed, resident doctor</last_name>
    <role>Principal Investigator</role>
    <affiliation>Assiut University</affiliation>
  </overall_official>
  <overall_contact>
    <last_name>Farouk Alsayed hassanen, prof</last_name>
    <phone>01006178123</phone>
    <email>Farouk.hassan@med.eu.edu.eg</email>
  </overall_contact>
  <overall_contact_backup>
    <last_name>Eman Fath Allah, Lecturer</last_name>
    <phone>01115191158</phone>
    <email>Fathalaeman@yahoo.com</email>
  </overall_contact_backup>
  <reference>
    <citation>Wingerchuk DM. Postinfectious encephalomyelitis. Curr Neurol Neurosci Rep. 2003 May;3(3):256-64. doi: 10.1007/s11910-003-0086-x.</citation>
    <PMID>12691631</PMID>
  </reference>
  <reference>
    <citation>Tenembaum S, Chitnis T, Ness J, Hahn JS; International Pediatric MS Study Group. Acute disseminated encephalomyelitis. Neurology. 2007 Apr 17;68(16 Suppl 2):S23-36. doi: 10.1212/01.wnl.0000259404.51352.7f.</citation>
    <PMID>17438235</PMID>
  </reference>
  <reference>
    <citation>Menge T, Kieseier BC, Nessler S, Hemmer B, Hartung HP, Stuve O. Acute disseminated encephalomyelitis: an acute hit against the brain. Curr Opin Neurol. 2007 Jun;20(3):247-54. doi: 10.1097/WCO.0b013e3280f31b45.</citation>
    <PMID>17495616</PMID>
  </reference>
  <reference>
    <citation>Dale RC, de Sousa C, Chong WK, Cox TC, Harding B, Neville BG. Acute disseminated encephalomyelitis, multiphasic disseminated encephalomyelitis and multiple sclerosis in children. Brain. 2000 Dec;123 Pt 12:2407-22. doi: 10.1093/brain/123.12.2407.</citation>
    <PMID>11099444</PMID>
  </reference>
  <reference>
    <citation>Hynson JL, Kornberg AJ, Coleman LT, Shield L, Harvey AS, Kean MJ. Clinical and neuroradiologic features of acute disseminated encephalomyelitis in children. Neurology. 2001 May 22;56(10):1308-12. doi: 10.1212/wnl.56.10.1308.</citation>
    <PMID>11376179</PMID>
  </reference>
  <reference>
    <citation>Anlar B, Basaran C, Kose G, Guven A, Haspolat S, Yakut A, Serdaroglu A, Senbil N, Tan H, Karaagaoglu E, Karli Oguz K. Acute disseminated encephalomyelitis in children: outcome and prognosis. Neuropediatrics. 2003 Aug;34(4):194-9. doi: 10.1055/s-2003-42208.</citation>
    <PMID>12973660</PMID>
  </reference>
  <reference>
    <citation>Pohl D, Tenembaum S. Treatment of acute disseminated encephalomyelitis. Curr Treat Options Neurol. 2012 Jun;14(3):264-75. doi: 10.1007/s11940-012-0170-0.</citation>
    <PMID>22476745</PMID>
  </reference>
  <reference>
    <citation>Cortese I, Chaudhry V, So YT, Cantor F, Cornblath DR, Rae-Grant A. Evidence-based guideline update: Plasmapheresis in neurologic disorders: report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology. 2011 Jan 18;76(3):294-300. doi: 10.1212/WNL.0b013e318207b1f6.</citation>
    <PMID>21242498</PMID>
  </reference>
  <reference>
    <citation>Keegan M, Pineda AA, McClelland RL, Darby CH, Rodriguez M, Weinshenker BG. Plasma exchange for severe attacks of CNS demyelination: predictors of response. Neurology. 2002 Jan 8;58(1):143-6. doi: 10.1212/wnl.58.1.143.</citation>
    <PMID>11781423</PMID>
  </reference>
  <verification_date>September 2017</verification_date>
  <study_first_submitted>September 8, 2017</study_first_submitted>
  <study_first_submitted_qc>September 13, 2017</study_first_submitted_qc>
  <study_first_posted type="Actual">September 15, 2017</study_first_posted>
  <last_update_submitted>September 13, 2017</last_update_submitted>
  <last_update_submitted_qc>September 13, 2017</last_update_submitted_qc>
  <last_update_posted type="Actual">September 15, 2017</last_update_posted>
  <responsible_party>
    <responsible_party_type>Principal Investigator</responsible_party_type>
    <investigator_affiliation>Assiut University</investigator_affiliation>
    <investigator_full_name>Marwa Alsaid Ahmed</investigator_full_name>
    <investigator_title>Principle Investigator</investigator_title>
  </responsible_party>
  <condition_browse>
    <!-- CAUTION:  The following MeSH terms are assigned with an imperfect algorithm            -->
    <mesh_term>Encephalomyelitis</mesh_term>
    <mesh_term>Encephalomyelitis, Acute Disseminated</mesh_term>
  </condition_browse>
  <patient_data>
    <sharing_ipd>No</sharing_ipd>
  </patient_data>
  <!-- Results have not yet been posted for this study                                          -->
</clinical_study>


download date: ClinicalTrials.gov processed this data on September 20, 2023
link text: Link to the current ClinicalTrials.gov record.
url: https://clinicaltrials.gov/ct2/show/NCT03284801
org study id: ADEM
nct id: NCT03284801
lead sponsor: 
is fda regulated drug: No
is fda regulated device: No
Acute disseminated encephalomyelitis is an immune-mediated inflammatory demyelinating disease
      of the central nervous system, which is typically transitory and self-limiting. It is
      characterized by an acute or subacute encephalopathy with neurological deficits, and magnetic
      resonance imaging evidence of widespread demyelination that predominantly involves the white
      matter of the brain and spinal cord. In the absence of specific biological markers, the
      diagnosis of Acute disseminated encephalomyelitis is still based upon a combination of
      clinical and neuro imaging features and exclusion of diseases that mimic Acute disseminated
      encephalomyelitis
Acute disseminated encephalomyelitis can occur at any age, but usually affects children and
      young adults. The mean age of clinical presentation in pediatric cohorts ranges from 5 to 8
      years. The annual incidence of Acute disseminated encephalomyelitis is reported to be 0.4-0.8
      per 100,000 and the disease more commonly affects children and young adults, probably related
      to the high frequency of exanthematous and other infections and vaccination in this age
      group.Initial symptoms and signs of Acute disseminated encephalomyelitis usually begin within
      2 days to 4 weeks after a viral infection or vaccination, and include a rapid onset
      encephalopathy (behavioral change or altered consciousness) associated with a combination of
      multifocal neurological deficits, leading to hospitalization within a week. Typically Acute
      disseminated encephalomyelitis presents with systemic symptoms such as fever, malaise,
      headache, nausea, and vomiting, which may occur shortly before the appearance of neurological
      signs and symptoms. The clinical course is rapidly progressive, developing maximum deficits
      within a few days (mean 4.5 days) . A wide variety of neurological deficits have been
      described in pediatric patients with Acute disseminated encephalomyelitis, including:
      obtundation and depressed consciousness (invariable); unilateral or bilateral long tract
      signs (60-95%); acute hemiplegia (76%); ataxia (18-59%); meningismus (26-31%); seizures
      (13-35%); spinal cord involvement (24%); visual involvement (7-23%); and speech impairment or
      aphasia (5-21%). Cerebellar mutism and prolonged focal motor seizures in the context of Acute
      disseminated encephalomyelitis have been mainly reported in children younger than 5 years of
      age.Acute combined peripheral nervous system demyelination is not rare in children with Acute
      disseminated encephalomyelitis whereas it is more frequently described in adult patients,
      with a reported frequency of 44% in one study. A particular Acute disseminated
      encephalomyelitis phenotype affecting young children has been reported in association with
      group A beta hemolytic streptococcal infection. Prominent behavioral disturbances, dystonic
      movements, and basal ganglia abnormalities on MRI (in addition to typical white matter
      lesions) characterize this syndrome.

      Supportive care in the acute stage is critical and early antiviral treatment with acyclovir
      (30 mg/kg/ day) is highly recommended on admission, considering that viral encephalitis and
      particularly herpes simplex encephalitis is the usual primary diagnosis in a child with
      fever, encephalopathy, seizures, and focal neurological signs. The treatment for Acute
      disseminated encephalomyelitis includes primarily the management of acute attacks.
      Corticosteroid treatment at high doses is the most widely reported therapy. Most authors
      recommend a brief (3-5 days) high-dose intravenous steroid course, usually methylprednisolone
      given at 20-30 mg/kg/day to a maximum dose of 1 g/day, or dexamethasone given at 1 mg/kg/day,
      followed by oral prednisone taper for 4-6 weeks . Reported treatment approaches show a wide
      variety in the specific steroid formulation employed, as well as in the dosing, routes of
      administration, and tapering regimens. Treatment with corticosteroids requires careful
      monitoring of blood pressure, urine glucose, and serum potassium, and administration of
      gastric protection. The use of immunoglobulin has been reported in several case studies
      either alone or in combination with corticosteroids. The recommended total dose of
      immunoglobulin is 2 g/kg, administered over 2-5 days. The usefulness of immunoglobulin has
      been reported both as a second-line treatment in steroid-unresponsive Acute disseminated
      encephalomyelitis cases and in patients showing recurrent or steroid-dependent demyelination.

      The use of plasma exchange has been recently established as possibly effective and it may be
      considered as escalation therapy for steroid-unresponsive acute fulminant demyelinating
      diseases including Acute disseminated encephalomyelitis, multiple sclerosis, and transverse
      myelitis, . Plasmapheresis should be started as soon as the treatment failure is recognized.
      The use of this procedure in Acute disseminated encephalomyelitis has been reported in only a
      small number of severe cases. A median number of seven exchanges (range 2 to 20) were
      reported in one study. Moderate to severe anemia, symptomatic hypotension, hypocalcemia,
      potential transfusion reactions or transmission of transfusion-related diseases, and
      heparin-associated thrombocytopenia have been described in relation to therapeutic plasma
      exchange. There is also a risk of catheter-related complications, including thrombosis,
      septic infections or pneumothorax.

      Acute hemorrhagic leukoencephalitis is often considered the most acute and severe form of
      Acute disseminated encephalomyelitis, with a universally fatal course within hours to days
      after the onset of neurological symptoms without treatment. Survival in pediatric patients
      has been reported with combined therapy including high-dose intravenous corticosteroid,
      immunoglobulin, Therapeutic plasma exchange, and decompressive craniotomies. Aggressive
      treatment strategies such as surgical decompression have to be considered and performed in
      patients with fulminant variants of Acute disseminated encephalomyelitis, with evidence of
      continued clinical deterioration due to increased intracranial pressure, unresponsive to
      conventional medical treatment and critical care measures.
observational model: Case-Only
time perspective: Prospective
measure: clinical audit on management of acute disseminating encephalomyelitis
time frame: within one year
description: To improve diagnosis and management of acute disseminated encephalomyelitis in Neurology Unit of Assiut University Children Hospital and to decrease the mortality and residual deficits from this disease.
The aim of this audit is to measure the current practice within the Neurology Unit of Assiut University Children Hospital team in the diagnosis and management of acute disseminated encephalomyelitis against the recommendations in American Academy of Neurology guidance by using checklist and designed questionnaire.
intervention type: Other
intervention name: management of acute disseminating encephalomyelitis
description: clinical audit on management of acute disseminating encephalomyelitis
study pop: 
sampling method: Non-Probability Sample
criteria: 
gender: All
minimum age: 12 Months
maximum age: 18 Years
healthy volunteers: No
last name: Marwa Alsaid Ahmed, resident doctor
role: Principal Investigator
affiliation: Assiut University
last name: Farouk Alsayed hassanen, prof
phone: 01006178123
email: Farouk.hassan@med.eu.edu.eg
last name: Eman Fath Allah, Lecturer
phone: 01115191158
email: Fathalaeman@yahoo.com
citation: Wingerchuk DM. Postinfectious encephalomyelitis. Curr Neurol Neurosci Rep. 2003 May;3(3):256-64. doi: 10.1007/s11910-003-0086-x.
PMID: 12691631
citation: Tenembaum S, Chitnis T, Ness J, Hahn JS; International Pediatric MS Study Group. Acute disseminated encephalomyelitis. Neurology. 2007 Apr 17;68(16 Suppl 2):S23-36. doi: 10.1212/01.wnl.0000259404.51352.7f.
PMID: 17438235
citation: Menge T, Kieseier BC, Nessler S, Hemmer B, Hartung HP, Stuve O. Acute disseminated encephalomyelitis: an acute hit against the brain. Curr Opin Neurol. 2007 Jun;20(3):247-54. doi: 10.1097/WCO.0b013e3280f31b45.
PMID: 17495616
citation: Dale RC, de Sousa C, Chong WK, Cox TC, Harding B, Neville BG. Acute disseminated encephalomyelitis, multiphasic disseminated encephalomyelitis and multiple sclerosis in children. Brain. 2000 Dec;123 Pt 12:2407-22. doi: 10.1093/brain/123.12.2407.
PMID: 11099444
citation: Hynson JL, Kornberg AJ, Coleman LT, Shield L, Harvey AS, Kean MJ. Clinical and neuroradiologic features of acute disseminated encephalomyelitis in children. Neurology. 2001 May 22;56(10):1308-12. doi: 10.1212/wnl.56.10.1308.
PMID: 11376179
citation: Anlar B, Basaran C, Kose G, Guven A, Haspolat S, Yakut A, Serdaroglu A, Senbil N, Tan H, Karaagaoglu E, Karli Oguz K. Acute disseminated encephalomyelitis in children: outcome and prognosis. Neuropediatrics. 2003 Aug;34(4):194-9. doi: 10.1055/s-2003-42208.
PMID: 12973660
citation: Pohl D, Tenembaum S. Treatment of acute disseminated encephalomyelitis. Curr Treat Options Neurol. 2012 Jun;14(3):264-75. doi: 10.1007/s11940-012-0170-0.
PMID: 22476745
citation: Cortese I, Chaudhry V, So YT, Cantor F, Cornblath DR, Rae-Grant A. Evidence-based guideline update: Plasmapheresis in neurologic disorders: report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology. 2011 Jan 18;76(3):294-300. doi: 10.1212/WNL.0b013e318207b1f6.
PMID: 21242498
citation: Keegan M, Pineda AA, McClelland RL, Darby CH, Rodriguez M, Weinshenker BG. Plasma exchange for severe attacks of CNS demyelination: predictors of response. Neurology. 2002 Jan 8;58(1):143-6. doi: 10.1212/wnl.58.1.143.
PMID: 11781423
responsible party type: Principal Investigator
investigator affiliation: Assiut University
investigator full name: Marwa Alsaid Ahmed
investigator title: Principle Investigator
mesh term: Encephalomyelitis
mesh term: Encephalomyelitis, Acute Disseminated
sharing ipd: No