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Stroke
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Subarachnoid hemorrhage causes aseptic meningitis. This usually increases intracranial pressure for days to weeks. Focal brain ischemia may be due to secondary vasospasm. Approximately 25% of affected patients develop signs of an ischemic stroke or transient ischemic attack. There is significant brain edema. Risks for vasospasm and infarction, known as angry brain, are highest between 72 hours and 10 days. Another common development is secondary acute hydrocephalus. Another rupture may occur. When it does, it is usually within 1 week. The incidence of nonaneurysmal subarachnoid hemorrhage is high in patients with type 1 diabetes. Of cerebrovascular deaths in this group of patients, 23% are due to hemorrhagic strokes. The association of type 2 diabetes with subarachnoid hemorrhage from a ruptured saccular intracranial aneurysm is unclear.
Neurosurgery: Supratentorial tumors
Published in Hemanshu Prabhakar, Charu Mahajan, Indu Kapoor, Essentials of Geriatric Neuroanesthesia, 2019
Monica S. Tandon, Kashmiri Doley, Daljit Singh
Significant postoperative brain edema can occur due to several reasons: presence of extensive preoperative edema, direct brain tissue manipulation/excessive retraction during the surgery, subtotal resection of malignant gliomas (effect of edema exerted from the residual tumor and necrosis on adjacent normal brain tissue), surgery of deep intrinsic tumors in which only minimal resection was possible, and after resection of highly infiltrating tumors that involve a large amount of WM. Maximal postoperative swelling usually occurs within one to the first five days after the surgery, however it may also manifest earlier, in the immediate postoperative period, in patients with high-grade gliomas; though rare, this “wounded glioma syndrome” can evolve rapidly and result in acute brain herniation.
Postirradiation Emesis
Published in John Kucharczyk, David J. Stewart, Alan D. Miller, Nausea and Vomiting: Recent Research and Clinical Advances, 2017
Gregory L. King, Milan T. Makale
The neurons of the CNS may be indirectly affected by radiation via cerebral edema. It is possible that cerebral inflammation, edema, or increased cerebrospinal fluid (CSF) pressure, which all result from brain irradiation in humans and other species, leads to emesis.77–80,88–90 Neurologic conditions, such as cerebral infarct, meningitis, head trauma, and brain tumor, can produce a brain edema, which is often accompanied by vomiting.91
Clinical manifestation, management and prognosis of clear cell meningioma: an evidence-based review
Published in International Journal of Neuroscience, 2023
Masum Rahman, Priyata Dutta, Preeti Agarwala, Samar Ikram, Eram Ahsan, Md Manjurul Islam Shourav, Cecile Riviere-cazaux, Amro Abuleil, Aprajita Milind Bhorkar, Rezaur Rahman Reza, Abu Bakar Siddik
CCMs are mostly spherical in shape, accounting for up to 83% of cases [5]. 45% of CCMs have a cystic component, which is relatively higher than that of a WHO grade I meningioma. Cranial CCM with cystic parts has shown greater mean size [10]. However, no difference between cranial and spinal CCM has been identified regarding the size of the tumor. The mean maximal diameter of the cranial was 4.5 cm and of spinal CCM was 4.7 cm [5]. The majority of CCM are solitary, regardless of anatomical location, while multiple lesions are identified in only about 7–16% of cases [5, 14]. Moreover, peritumoral brain edema has also been observed in about 44% of cases [5]. According to Wang et al. [13], the pathophysiology of peritumoral brain edema is multifactorial, including the amount of tumor infiltrates, blood supply, site and pathological type. The most prominent MRI feature of CCM has been reported is microcystic degeneration [5].
Hydrogen sulfide attenuates hyperhomocysteinemia-induced blood-brain barrier permeability by inhibiting MMP-9
Published in International Journal of Neuroscience, 2022
Brain edema is the condition of water accumulation in the intracellular or extracellular spaces of the brain resulting in disturbed osmotic gradient and intracranial pressure [62]. In the present study, increased brain edema was observed in the hippocampus of Hcy treated animals, which might be due to increased permeability of BBB following HHcy. Aquaporin (AQP) family of water channels are a group of small membrane proteins that regulate the transport of water molecules across the plasma membrane [63]. AQP-4 is the major water transporting channel found in the mammalian brain mainly expressed in the astrocytic end feet at the blood-brain interface [64]. According to a recent study [16], Hcy treatment increases the mRNA expression of AQP-4 in astrocytes. However, increase in AQP-4 expression might be responsible for increased water levels in the hippocampus of the animals following HHcy. Interestingly, NaHS supplementation reduced the edema in hippocampus of the Hcy treated animals. H2S has been reported to attenuate SAH and stroke-induced edema by reducing the expression of AQP-4 via protein kinase c and inflammation mediated mechanisms [25,65]. There are only a few reports suggesting the role of H2S in response to AQPs. Therefore, more comprehensive research is needed to explore the mechanism of action of H2S in regulation of AQPs expression.
Isolated brainstem involvement in posterior reversible encephalopathy syndrome: a case report and review of the literature
Published in International Journal of Neuroscience, 2019
Chenchen Liu, Jie Cao, Zhuyi Su, Shabei Xu
Posterior reversible encephalopathy syndrome (PRES) is a disorder characterized by acute neurological symptoms, such as headache, vomiting, visual disturbances, seizures, confusion and focal neurological signs. Neuroimaging usually reveals reversible vasogenic edema predominantly involving the white matter of both cerebral hemispheres, especially parieto-occipital regions [1]. Brain edema affecting regions other than typical parieto-occipital regions is not uncommon, including frontal and temporal lobes, basal ganglia, cerebellum and brainstem [2]. However, those unusual lesions are always accompanied by involvement of parieto-occipital regions, isolated brainstem involvement in PRES (IBPRES) has been rarely reported. Little is known about its clinical manifestations, radiological features and outcomes. The aim of this study was to perform a systematic review of published cases on IBPRES.