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  1. Wong CK, Ng CF, Tan HJ, Mukari SAM
    BMJ Case Rep, 2021 May 24;14(5).
    PMID: 34031085 DOI: 10.1136/bcr-2021-242090
    Bickerstaff brainstem encephalitis (BBE) is a rare autoimmune encephalitis characterised by ataxia, ophthalmoplegia and altered consciousness. An overlap between BBE with Guillain-Barré syndrome (GBS) shows similar clinical and immunological features. We report a case of BBE with GBS overlap secondary to Chlamydia pneumoniae infection. The triad of altered consciousness, ataxia and ophthalmoplegia were present in the patient. The investigations included cerebrospinal fluid cytoalbuminological dissociation, nerve conduction test that showed prolonged or absent F wave latencies, hyperintensity in the left occipital region on brain MRI and diffuse slow activity on the electroencephalogram. The chlamydia serology was positive indicating a postinfectious cause of BBE syndrome. He required artificial ventilation as his consciousness level deteriorated with tetraparesis, oropharyngeal and respiratory muscle weakness. Immunotherapy with intravenous immunoglobulin and methylprednisolone was commenced. He made good recovery with the treatment. Prompt recognition of this rare condition following chlamydia infection is important to guide the management.
    Matched MeSH terms: Autoimmune Diseases of the Nervous System*
  2. Miyaji K, Paul F, Shahrizaila N, Umapathi T, Yuki N
    J Neuroimmunol, 2014 Nov 15;276(1-2):172-4.
    PMID: 25156074 DOI: 10.1016/j.jneuroim.2014.08.004
    Given their localization and important role in regulating complement, complement regulatory proteins may act as target antigens and their antibodies as biomarkers in demyelinating neuropathies. We investigated the binding of autoantibodies to complement regulatory proteins (CD46, 55 and 59) in demyelinating diseases. In 42 acute inflammatory demyelinating polyneuropathy, 23 chronic inflammatory demyelinating polyneuropathy, 13 acute motor axonal neuropathy, 71 multiple sclerosis, and 19 neuromyelitis optica patients as well as 55 healthy controls, we were unable to detect significant titers of antibodies to CD46, CD55 and CD59. These autoantibodies are unlikely to be biomarkers in acute and chronic inflammatory demyelinating polyneuropathies.
    Matched MeSH terms: Autoimmune Diseases of the Nervous System/pathology*
  3. Viswanathan S, Hiew FL
    J Clin Apher, 2019 Aug;34(4):434-444.
    PMID: 30829434 DOI: 10.1002/jca.21696
    There has been an increase in the use of therapeutic plasma exchange (TPE) in immune-mediated neurological disorders in recent years. However, accessibility and availability of TPE remains low and costly, especially for a country with limited healthcare funding like Malaysia. With expanding clinical indications in neurological disorders, and increasingly expensive conventional immunomodulatory treatment such as intravenous immunoglobulin and monoclonal antibodies, TPE remains an effective part of first or second-line treatment. In this article, we detailed the historical aspects of the use of TPE in neurological disorders in Malaysia over the last four decades and discussed the challenges behind the establishment of the first in-house neurology-driven TPE service in the country. Local TPE database from a national neurology centre in Kuala Lumpur over the past 20 years was analyzed. We observed a remarkable three folds increase in the use of TPE at our center over the past 10 years (total 131 TPE treatments) compared to a decade prior, with expanding clinical indications predominantly for central nervous system demyelinating disorders. Besides using membrane filtration method, centrifugal technique was adopted, providing new opportunities for other clinical beneficiaries such as a neurologist driven "in-house TPE unit". However, there were real world challenges, especially having to provide services with limited funding, human resources, and space. In addition, much has to be done to improve accessibility, availability, and sustainability of TPE services at our center and nationwide. Nevertheless, even with limited resources and support, it is possible with concerted efforts to work within the confines of these limitations to establish a safe, successful, and sustainable TPE service.
    Matched MeSH terms: Autoimmune Diseases of the Nervous System/therapy
  4. Lim JA, Lee ST, Moon J, Jun JS, Kim TJ, Shin YW, et al.
    Ann Neurol, 2019 03;85(3):352-358.
    PMID: 30675918 DOI: 10.1002/ana.25421
    OBJECTIVE: There is no scale for rating the severity of autoimmune encephalitis (AE). In this study, we aimed to develop a novel scale for rating severity in patients with diverse AE syndromes and to verify the reliability and validity of the developed scale.

    METHODS: The key items were generated by a panel of experts and selected according to content validity ratios. The developed scale was initially applied to 50 patients with AE (development cohort) to evaluate its acceptability, reproducibility, internal consistency, and construct validity. Then, the scale was applied to another independent cohort (validation cohort, n = 38).

    RESULTS: A new scale consisting of 9 items (seizure, memory dysfunction, psychiatric symptoms, consciousness, language problems, dyskinesia/dystonia, gait instability and ataxia, brainstem dysfunction, and weakness) was developed. Each item was assigned a value of up to 3 points. The total score could therefore range from 0 to 27. We named the scale the Clinical Assessment Scale in Autoimmune Encephalitis (CASE). The new scale showed excellent interobserver (intraclass correlation coefficient [ICC] = 0.97) and intraobserver (ICC = 0.96) reliability for total scores, was highly correlated with modified Rankin scale (r = 0.86, p

    Matched MeSH terms: Autoimmune Diseases of the Nervous System/complications; Autoimmune Diseases of the Nervous System/physiopathology*; Autoimmune Diseases of the Nervous System/psychology*
  5. Jha NK, Ojha S, Jha SK, Dureja H, Singh SK, Shukla SD, et al.
    J Mol Neurosci, 2021 Nov;71(11):2192-2209.
    PMID: 33464535 DOI: 10.1007/s12031-020-01767-6
    The coronavirus disease 2019 (COVID-19) pandemic is an issue of global significance that has taken the lives of many across the world. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the virus responsible for its pathogenesis. The pulmonary manifestations of COVID-19 have been well described in the literature. Initially, it was thought to be limited to the respiratory system; however, we now recognize that COVID-19 also affects several other organs, including the nervous system. Two similar human coronaviruses (CoV) that cause severe acute respiratory syndrome (SARS-CoV-1) and Middle East respiratory syndrome (MERS-CoV) are also known to cause disease in the nervous system. The neurological manifestations of SARS-CoV-2 infection are growing rapidly, as evidenced by several reports. There are several mechanisms responsible for such manifestations in the nervous system. For instance, post-infectious immune-mediated processes, direct virus infection of the central nervous system (CNS), and virus-induced hyperinflammatory and hypercoagulable states are commonly involved. Guillain-Barré syndrome (GBS) and its variants, dysfunction of taste and smell, and muscle injury are numerous examples of COVID-19 PNS (peripheral nervous system) disease. Likewise, hemorrhagic and ischemic stroke, encephalitis, meningitis, encephalopathy acute disseminated encephalomyelitis, endothelialitis, and venous sinus thrombosis are some instances of COVID-19 CNS disease. Due to multifactorial and complicated pathogenic mechanisms, COVID-19 poses a large-scale threat to the whole nervous system. A complete understanding of SARS-CoV-2 neurological impairments is still lacking, but our knowledge base is rapidly expanding. Therefore, we anticipate that this comprehensive review will provide valuable insights and facilitate the work of neuroscientists in unfolding different neurological dimensions of COVID-19 and other CoV associated abnormalities.
    Matched MeSH terms: Autoimmune Diseases of the Nervous System/etiology
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