Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)  

BACKGROUND: Some reports are suggesting the efficacy of continuous irrigation therapy for brain abscesses, but the way how to irrigate and perfusion abscesses and cerebral spinal fluid has not yet been established. Here, we present the case of successfully treated by continuous irrigation therapy for the severe bacterial brain abscess, meningitis, and encephalitis. CASE DESCRIPTION: A 62-year-old man presented to our hospital with a chief complaint of headache and vomiting. Magnetic resonance imaging revealed an encapsulated lesion with peripheral contrast in the left cerebellar hemisphere, and the lesion showed high signal intensity on diffusion-weighted imaging. We diagnosed him with a brain abscess. In addition to drainage of the cerebellar lesion by small craniotomy and systemic administration of antibiotics, continuous irrigation therapy was performed for 7 days until the cell count of the cerebrospinal fluid became negative. Saline with antibiotics was infused through from ventricular drain, which was inserted through the anterior horn of the lateral ventricle to spiral drainage. His state of consciousness improved, and he was able to live at home. CONCLUSION: Our proposed novel continuous irrigation therapy may lead to a positive outcome in brain abscesses.

DOI： 10.25259/SNI_940_2024

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Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)  

Demyelination and axonal degeneration are fundamental pathological characteristics of multiple sclerosis (MS), an inflammatory disease of the central nervous system (CNS). Although the molecular mechanisms driving these processes are not fully understood, hepatocyte growth factor (HGF) has emerged as a potential regulator of neuroinflammation and tissue protection in MS. Elevated HGF levels have been reported in MS patients receiving immunomodulatory therapy, indicating its relevance in disease modulation. This study investigated HGF's neuroprotective effects using transgenic mice that overexpressed HGF. The experimental autoimmune encephalomyelitis (EAE) model, which mimics MS pathology, was employed to assess demyelination and axonal damage in the CNS. HGF transgenic mice showed delayed EAE progression, with reduced CNS inflammation, decreased demyelination, and limited axonal degeneration. Scanning electron microscopy confirmed the preservation of myelin and axonal integrity in these mice. In addition, we explored HGF's effects using a cuprizone-induced demyelination model, which operates independently of the immune system. HGF transgenic mice exhibited significant protection against demyelination in this model as well. We also investigated the expression of key HGF receptors, particularly c-Met and KAI-1. While c-Met, which is associated with increased inflammation, was upregulated in EAE, its expression was significantly reduced in HGF transgenic mice, correlating with decreased neuroinflammation. Conversely, KAI-1, which has been linked to axonal protection and stability, showed enhanced expression in HGF transgenic mice, suggesting a protective mechanism against axonal degeneration. These findings underscore HGF's potential in preserving CNS structure and function, suggesting it may be a promising therapeutic target for MS, offering new hope for mitigating disease progression and enhancing neuroprotection.

DOI： 10.3390/ijms252011261

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Authorship：Lead author  

J-GLOBAL

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Language：English   Publishing type：Research paper (scientific journal)  

Multiple sclerosis (MS) is the chronic inflammatory demyelinating disease of the CNS. Relapsing-remitting MS (RRMS) is the most common type of MS. However, the mechanisms of relapse and remission in MS have not been fully understood. While SJL mice immunized with proteolipid protein (PLP) develop relapsing-remitting experimental autoimmune encephalomyelitis (RR-EAE), we have recently observed that some of these mice were resistant to the active induction of relapsing EAE after initial clinical and histological symptoms of EAE with a severity similar to the relapsing EAE mice. To clarify the mechanism of relapsing, we examined myelin morphology during PLP139-151-induced RR-EAE in the SJL mice. While RR-EAE mice showed an increased EAE severity (relapse) with CNS inflammation, demyelination with abnormal myelin morphology in the spinal cord, the resistant mice exhibited a milder EAE phenotype with diminished relapse. Compared with the RR-EAE mice, the resistant mice showed less CNS inflammation, demyelination, and abnormalities of the myelin structure. In addition, scanning electron microscopic (SEM) analysis with the osmium-maceration method displayed ultrastructural abnormalities of the myelin structure in the white matter of the RR-EAE spinal cord, but not in that of the resistant mice. While the intensity of myelin staining was reduced in the relapsing EAE spinal cord, immunohistochemistry and immunoblot analysis revealed that the 21.5 kDa isoform of degenerating myelin basic protein (MBP) was specifically induced in the relapsing EAE spinal cord. Taken together, the neuroinflammation-induced degenerating 21 kDa isoform of MBP sheds light on the development of abnormal myelin on the relapse of MS pathogenesis.

DOI： 10.3390/ijms24098160

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Language：English   Publishing type：Research paper (scientific journal)  

BACKGROUND: Several treatments for traumatic facial paralysis have been reported, but the role of surgery is still controversial. CASE DESCRIPTION: A 57-year-old man was admitted to our hospital with head trauma due to a fall injury. A total body computed tomography (CT) scan showed a left frontal acute epidural hematoma associated with a left optic canal and petrous bone fractures with the disappearance of the light reflex. Hematoma removal and optic nerve decompression were performed immediately. The initial treatment was successful with complete recovery of consciousness and vision. The facial nerve paralysis (House and Brackmann scale grade 6) did not improve after medical therapy, and thus, surgical reconstruction was performed 3 months after the injury. The left hearing was lost entirely, and the facial nerve was surgically exposed from the internal auditory canal to the stylomastoid foramen through the translabyrinthine approach. The facial nerve's fracture line and damaged portion were recognized intraoperatively near the geniculate ganglion. The facial nerve was reconstructed using a greater auricular nerve graft. Functional recovery was observed at the 6-months follow-up (House and Brackmann grade 4), with significant recovery in the orbicularis oris muscle. CONCLUSION: Interventions tend to be delayed, but it is possible to select a treatment method of the translabyrinthine approach.

DOI： 10.25259/SNI_995_2022

PubMed

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Presentation type：Oral presentation (general)  

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