A man in his late forties had lived as a recluse for more than ten years. He was found dead in his room. At autopsy, subarachnoid hemorrhage (SAH) was detected at the base of the brain, which weighed 1333 g. The cerebellar tonsil was swollen. The cerebral ventricle was enlarged and filled with blood. A hematoma was observed in the upper part of the left side of the cerebellar hemisphere. The location and size of SAH in this case indicated that the rupture of a cerebral aneurysm (CA) had occurred; however, CA was not detected. A mass of blood vessels buried in the hematoma was observed at the left cerebellopontine angle (CPA). The vascular lesion showed round-shaped blood vessels as well as flat-shaped vessels with the appearance of veins, but with elastic fibers indicative of arteries. The lesion was considered to be the nidus and was 5-8 mm in size. Feeding arteries appeared to be from the anterior inferior cerebellar artery (AICA). However, the draining vein and anastomotic parts of the artery and vein were not confirmed. Based on these histopathological features, this vascular lesion was diagnosed as arteriovenous malformation (AVM). A differential diagnosis between AVM at CPA and CA is needed in order to identify the source of non-traumatic SAH.
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http://dx.doi.org/10.1111/neup.12383 | DOI Listing |
J Cereb Blood Flow Metab
January 2025
Neurovascular Research Unit, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, USA.
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AP-HP, Hôpital Lariboisière, Department of Anaesthesia and Critical Care, Paris, France.
In patients with acute brain injury (ABI), optimizing cerebral perfusion parameters relies on multimodal monitoring. This include data from systemic monitoring-mean arterial pressure (MAP), arterial carbon dioxide tension (PaCO), arterial oxygen saturation (SaO), hemoglobin levels (Hb), and temperature-as well as neurological monitoring-intracranial pressure (ICP), cerebral perfusion pressure (CPP), and transcranial Doppler (TCD) velocities. We hypothesized that these parameters alone were not sufficient to assess the risk of cerebral ischemia.
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December 2024
Molecular pharmacology, Department of Biofunctional Evaluation, Gifu Pharmaceutical University, Gifu, Japan.
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January 2025
Faculty of Health and Medical Sciences, The University of Adelaide, Australia.
The Glasgow Coma Scale (GCS) was first published in The Lancet by Sir Graham Teasdale and Bryan Jennett 50 years ago based on their pioneering work on developing a numerical scale to describe coma in clear and reproducible terms and to avoid the confusion associated with the wide variety of descriptive terms for consciousness that were in use at the time. It's difficult to know if Teasdale and Jennett could have predicted how influential, widespread and long-lasting the GCS would become, but in retrospect it seems clear that the GCS was introduced at a perfect stage in the development of modern clinical neurosurgery and neuroscience research. The simplicity of the scale, its recognition by senior academics and the emerging radiology technologies in the 1970s heralded a new era of neuroscience and an approach to the management of not only traumatic brain injury (TBI) but other types of central nervous system disease in which consciousness was affected, such as aneurysmal subarachnoid haemorrhage and stroke.
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Department of Neurosurgery, Jingjiang People's Hospital, Jingjiang, China.
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