神経感染症の治療の進歩（2021）

抄録

COVID–19, which has been raging in Japan since 2020, has been reported to cause various syndromes and neurological disorders, including stroke, Guillain–Barré syndrome (GBS), encephalitis/encephalopathy, and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) as sequelae. These mechanisms are mainly immune–mediated mechanisms rather than direct viral effects, and GBS and encephalitis/encephalopathy have slightly different characteristics from the conventional COVID–19 non–associated course. In addition, in stroke, not only neurological damage but also multi–organ damage may occur, and rehabilitation may be time–consuming. Furthermore, 14.3% of patients with sequelae of COVID–19 infection develop ME/CFS. Since no treatment for ME/CFS has been established, patients are forced to seek treatment by hand, such as rTMS therapy and carnitine replacement, and future treatment methods are awaited.

In infectious meningoencephalitis, Multiplex PCR, although not approved by insurance in Japan, has the potential to rapidly identify the pathogen and is expected to be utilized in clinical practice as soon as possible. Although no new drugs have been introduced, meta–analysis has shown the usefulness of naloxone combination therapy for viral meningitis, dexamethasone combination therapy for tuberculous meningitis, and a single high–dose amphotericin B liposome regimen for HIV–positive cryptococcal meningitis, respectively.

The recent widespread use of biologics for neuroimmune diseases has focused attention on progressive multifocal leukoencephalopathy (PML), a serious complication of some agents. However, since this therapy may result in brain damage, it is no longer recommended, and the focus is on discontinuation of the causative agent and symptomatic treatment.

In HTLV–1–associated myelopathy (HAM), the pathogenesis has become clearer over the years, and CXCL–10 and neopterin are already established biomarkers of disease activity. Oral steroids and interferon–alpha have been shown to improve motor function and are already being utilized in clinical practice, but the development of HAM–specific therapeutic agents that affect CXCL–10 and neopterin levels is also underway daily, and we look forward to future drug discovery efforts.