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Case ReportCase Report
Open Access

Brainstem encephalitis

A diagnostic dilemma

Sarah A. Bin Abdulqader, Hisham M. Alkhalidi and Abdulrazag M. Ajlan
Neurosciences Journal April 2018, 23 (2) 152-157; DOI: https://doi.org/10.17712/nsj.2018.2.20170401
Sarah A. Bin Abdulqader
From the Department of Neurosurgery (Bin Abdulqader, Ajlan), Department of Pathology (Alkhalidi), College of Medicine, King Saud University, Riyadh, Kingdom of Saudi Arabia, and from the Department of Neurosurgery (Ajlan), Stanford School of Medicine, Palo Alto, CA, United States of America
MBBS
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  • For correspondence: [email protected]
Hisham M. Alkhalidi
From the Department of Neurosurgery (Bin Abdulqader, Ajlan), Department of Pathology (Alkhalidi), College of Medicine, King Saud University, Riyadh, Kingdom of Saudi Arabia, and from the Department of Neurosurgery (Ajlan), Stanford School of Medicine, Palo Alto, CA, United States of America
MBBS, FRCPC
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Abdulrazag M. Ajlan
From the Department of Neurosurgery (Bin Abdulqader, Ajlan), Department of Pathology (Alkhalidi), College of Medicine, King Saud University, Riyadh, Kingdom of Saudi Arabia, and from the Department of Neurosurgery (Ajlan), Stanford School of Medicine, Palo Alto, CA, United States of America
MBBS, FRCSC
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    Figure 1

    Timeline figure of the clinical event.

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    Figure 2

    Initial brain MRI showing A, G & H) focal lesion in the right side of medulla oblongata posteriorly with extension into middle cerebellar peduncle and posterior pons. Post contrast images show multiple ring-like enhancing areas are around the central hemorrhagic focus. D) Susceptibility weighted image (SWI) shows multiple foci of dark signal indicating hemorrhagic foci. E) Diffusion weighted image (DWI) shows no restricted diffusion in central non enhancing area to suggest any purulent material. F) Central hemmohagic areas give relatively increased rCBV values. The surrounding FLAIR hyperintensity show slightly lower rCBV values compared to normal appearing cerebral white matter. I) Single voxel MR spectroscopy at TE of 135 with region of interest in normal appearing tissue around the lesion shows nearly normal NAA, choline and J) creatine peaks and at TE of 135 with region of interest in the lesion shows decreased NAA and increased choline peaks. There is also increased lipid-lactate peak around 0.9 to 1.5 ppm.

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    Figure 3

    Histopathological findings. A) Axial T2 weighted brain MRI showing post biopsy changes at the right cerebellar hemisphere. B) The biopsies exhibit fragments with cellular areas, formed by mixture of chronic inflammatory cells, with dominance of histiocytes, in addition to lymphocytes, plasma cells and glial cells. C) A major component of the cellular infiltrate reacts to CD 68, confirming histiocytic nature. D) In areas, the CNS tissue sampled exhibit gliosis and foci of chronic inflammation, in keeping with encephalitis.

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    Figure 4

    The progression of the disease demonstrated on axial T1 weighted post contrast imaging.

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    Figure 5

    Follow-up brain MRI at 57th week of presentation. (A) axial, (C) coronal, (D) sagittal T1 weighted post contrast imaging and (B) axial flair imaging show regression in the size of the lesion at the right aspect of the pons and right middle cerebellar peduncle with a mild volume loss of the right side of pons.

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    Table 1

    Laboratory findings of the patient presented.

    VariablesResults
    CSF chemistry
     Glucose4.4
     Protein0.5 g/L
     WBC0 cells
     RBC30
    Blood culturesNegative
    Cryptococcus antigenNegative
    Asperigillous galactomannan antigenNegative
    Mycoplasm IgMNegative
    Herpes simplex virus PCRNegative
    HIVNegative
    Autoimmune markers
     ESR3
     Complement 3 level137
     ANANegative
     Anti ds DNANegative
     Jo 1 antibodyNegative
    Tuberculosis investigations
     Acid fast bacilli cultureNegative
     Acid fast bacilli PCRNegative
     QuantiferonNegative
    CSF cultures & gram stainNegative
    Pneumocystitis pneumoniaNegative
    Toxoplasma IgGNegative
    Brucella serologyNegative
    Hepatitis B & CNon reactive
    CRP2.6
    Complement 4 level45
    ANCANegative
    SS-A and SS-B antibodiesNegative
    CryoglobulinNegative
    • CSF - cerebrospinal fluid, WBC - white blood cells, RBC - red blood cells, PCR - polymerase chain reaction, ESR - erythrocyte sedimentation rate, ANA - antinuclear antibody, CRP - C reactive protein, ANCA - antineutrophil cytoplasmic antibodies

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Neurosciences Journal: 23 (2)
Neurosciences Journal
Vol. 23, Issue 2
1 Apr 2018
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Brainstem encephalitis
Sarah A. Bin Abdulqader, Hisham M. Alkhalidi, Abdulrazag M. Ajlan
Neurosciences Journal Apr 2018, 23 (2) 152-157; DOI: 10.17712/nsj.2018.2.20170401

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Brainstem encephalitis
Sarah A. Bin Abdulqader, Hisham M. Alkhalidi, Abdulrazag M. Ajlan
Neurosciences Journal Apr 2018, 23 (2) 152-157; DOI: 10.17712/nsj.2018.2.20170401
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