Publications by authors named "Masaki Namekawa"

4 Publications

  • Page 1 of 1

[Herpes simplex encephalitis presenting as a stroke-like episode following a migraine attack: a case report].

Rinsho Shinkeigaku 2022 Jul 24;62(7):567-570. Epub 2022 Jun 24.

Department of Neurology, Nagaoka Red Cross Hospital.

A 23-year-old woman, who had been suffering from migraine since primary school age, presented with left arm paralysis three days after one such migraine attack. On admission, brain MRI diffusion-weighted imaging (DWI) demonstrated high-signal-intensity lesions in the white matter of the right fronto-parietal lobe, and no abnormal lesions were evident in the limbic system. Although the patient had a fever of 38.7°C, the CSF cell count was not elevated. On the 4‍ day, the left arm paralysis worsened, with an increase in body temperature to 39.8°C. Brain MRI revealed that the white matter lesions had spread to the right postcentral gyrus and the bilateral insular cortex. Also, MR angiography demonstrated no spasms or dissection of the major vessels. On the 6‍ day, the CSF cell count was elevated to 54/μl and herpes simplex virus DNA was detected. Acyclovir and steroid pulse therapy ameliorated the symptoms. Cervical artery dissection and reversible cerebral vasoconstriction are well known complications of migraine attack. However, herpes simplex encephalitis should also be considered as a differential diagnosis in patients with a high fever of unknown origin.
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http://dx.doi.org/10.5692/clinicalneurol.cn-001745DOI Listing
July 2022

[Recurrent autoimmune glial fibrillary acidic protein (GFAP) astrocytopathy with long cervical cord lesions: a case report].

Rinsho Shinkeigaku 2022 May 26;62(5):386-390. Epub 2022 Apr 26.

Department of Neurology, Nagaoka Red Cross Hospital.

A 61-year-old man who had suffered two episodes of generalized convulsion in a two-year period was admitted to our hospital because of progressive gait disturbance during the previous five months. Neurological examination revealed cognitive impairment, spasticity of the lower limbs, truncal ataxia, and dysautonomia including orthostatic hypotension, dysuria and hypohydrosis. Brain fluid-attenuated inversion recovery (FLAIR) MRI detected high-signal-intensity lesions in the periventricular white matter and centrum semiovale, with punctate gadolinium (Gd) enhancement. Spinal MRI detected swollen cervical long cord lesions extending from C2 to C6. Although methylprednisolone pulse treatment initially ameliorated the symptoms and MRI abnormal findings, clinical symptoms and MRI abnormalities including new cervical lateral column lesions reminiscent of those in autoimmune glial fibrillary acidic protein (GFAP) astrocytopathy (GFAP-A) relapsed two months later. At this point, anti-GFAPα antibody was detected in the cerebrospinal fluid. Although the clinical course of GFAP-A has been well reported, the present case showed a chronic refractory course.
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http://dx.doi.org/10.5692/clinicalneurol.cn-001713DOI Listing
May 2022

Progressive micrographia without parkinsonism caused by autoimmune brainstem encephalitis: A case report.

Clin Neurol Neurosurg 2021 Mar 15;202:106496. Epub 2021 Jan 15.

Department of Neurology, Brain Research Institute, Niigata University, Japan.

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http://dx.doi.org/10.1016/j.clineuro.2021.106496DOI Listing
March 2021

Strategies to prevent hemorrhagic transformation after reperfusion therapies for acute ischemic stroke: A literature review.

J Neurol Sci 2020 Dec 4;419:117217. Epub 2020 Nov 4.

Department of Neurology, Brain Research Institute, Niigata University, Niigata, Japan. Electronic address:

Background: Reperfusion therapies by tissue plasminogen activator (tPA) and mechanical thrombectomy (MT) have ushered in a new era in the treatment of acute ischemic stroke (AIS). However, reperfusion therapy-related HT remains an enigma.

Aim: To provide a comprehensive review focused on emerging concepts of stroke and therapeutic strategies, including the use of protective agents to prevent HT after reperfusion therapies for AIS.

Methods: A literature review was performed using PubMed and the ClinicalTrials.gov database.

Results: Risk of HT increases with delayed initiation of tPA treatment, higher baseline glucose level, age, stroke severity, episode of transient ischemic attack within 7 days of stroke onset, and hypertension. At a molecular level, HT that develops after thrombolysis is thought to be caused by reactive oxygen species, inflammation, remodeling factor-mediated effects, and tPA toxicity. Modulation of these pathophysiological mechanisms could be a therapeutic strategy to prevent HT after tPA treatment. Clinical mechanisms underlying HT after MT are thought to involve smoking, a low Alberta Stroke Program Early CT Score, use of general anesthesia, unfavorable collaterals, and thromboembolic migration. However, the molecular mechanisms are yet to be fully investigated. Clinical trials with MT and protective agents have also been planned and good outcomes are expected.

Conclusion: To fully utilize the easily accessible drug-tPA-and the high recanalization rate of MT, it is important to reduce bleeding complications after recanalization. A future study direction could be to investigate the recovery of neurological function by combining reperfusion therapies with cell therapies and/or use of pleiotropic protective agents.
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http://dx.doi.org/10.1016/j.jns.2020.117217DOI Listing
December 2020
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