Brain and nerve = Shinkei kenkyū no shinpo
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After large CT-based clinical trials have failed to prove the benefits of intravenous tissue plasminogen activator (tPA) administration for ischemic stroke patients beyond 3 hours of the onset of the concept of PWI/DWI mismatch which is the volume difference between a PWI lesion and DWI lesion on MRI scans, has been proposed to facilitate the selection of patients with a salvageable area. PWI/DWI mismatch is considered to represent the tissue that is not irreversibly injured and can respond to early reperfusion therapy. When an ischemic lesion is divided into 4 regions, namely, ischemic core, reversible DWI lesion, penumbra and benign oligemia, both the reversible DWI lesion and penumbra are considered to be an optimal targets for thrombolysis. ⋯ Most useful parameters of PWI should be determined to standardize volume evaluation using MRI scans. For the institutes where MRI scans are not available 24 hours a day, clinical DWI mismatch has been proposed as an alternative to of PWI/DWI mismatch. The application of MRI-based decision making strategy for stroke patients may facilitate the assessment and treatment of stroke patients beyond 3 hours of stroke onset, and is expected to allow the use of tPA for a substantially greater number of patients.
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Intracranial arteriovenous malformations (AVMs) are congenital lesions that can cause serious neurological deficits or even death. They can manifest as intracranial hemorrhage, epileptic seizure, or other symptoms such as headache or tinnitus. They are detected by computed tomography or magnetic resonance imaging. ⋯ Technological advances in endovascular surgery have provided new alternatives in the treatment of AVMs. Currently indications for embolization can be divided into (1) presurgical embolization in large AVMs to occlude deep arterial feeding vessels and (2) embolization before stereotactic radiosurgery to reduce the size of the nidus. Palliative embolization can be also applied for patients with large, inoperable AVMs who are suffering from progressive neurological deficits secondary to venous hypertension and/or arterial steal phenomenon.
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Alpha-dystroglycan (alpha-DG) is a glycoprotein that binds to laminin in the basal lamina and helps provide mechanical support. A group of muscular dystrophies are caused by glycosylation defects of alpha-DG and are hence collectively called alpha-dystroglycanopathy (alpha-DGP). Alpha-DGP is clinically characterized by a combination of muscular dystrophies, structural brain anomalies, and ocular involvement. ⋯ Clinically, these patients presented with minimal muscle weakness and dilated cardiomyopathy and had normal intelligence. These data clearly indicate that FKTN mutations can cause a broad spectrum of muscular dystrophies. Therefore, clinicians should always bear in mind the possibility of alpha-DGP when they have a patient suspected to have muscular dystrophy.