ReviewNeurocritical care2004
Cerebral vasospasm: a consideration of the various cellular mechanisms involved in the pathophysiology.
Review in Neurocritical care, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed, 60 citations in OpenAlex.
- Trial
- Retinal Arterial Vasospasm in Retinal Vein Occlusion and Its Association with Aqueous Humor Endothelin-1.Ophthalmology and therapy · 2026Article
- A Case of Severe Delayed Vasospasm after Clipping Surgery for an Unruptured Intracranial Aneurysm.Neurointervention · 2024Article
- The blood-brain barrier and the neurovascular unit in subarachnoid hemorrhage: molecular events and potential treatments.Fluids and barriers of the CNS · 2022Review
- Peroxisome proliferator‑activated receptor β/δ regulates cerebral vasospasm after subarachnoid hemorrhage via modulating vascular smooth muscle cells phenotypic conversion.Molecular medicine reports · 2021Article
- When the Blood Hits Your Brain: The Neurotoxicity of Extravasated Blood.International journal of molecular sciences · 2021Review
- The Stabilization of Central Sympathetic Nerve Activation by Renal Denervation Prevents Cerebral Vasospasm after Subarachnoid Hemorrhage in Rats.Translational stroke research · 2020Article
- The Updated Role of the Blood Brain Barrier in Subarachnoid Hemorrhage: From Basic and Clinical Studies.Current neuropharmacology · 2020Article
- Asymmetric and Symmetric Dimethylarginines are Markers of Delayed Cerebral Ischemia and Neurological Outcome in Patients with Subarachnoid Hemorrhage.Neurocritical care · 2018Article
- The rise of soluble platelet-derived growth factor receptor β in CSF early after subarachnoid hemorrhage correlates with cerebral vasospasm.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2018Article
- High Compliance with Scheduled Nimodipine Is Associated with Better Outcome in Aneurysmal Subarachnoid Hemorrhage Patients Cotreated with Heparin Infusion.Frontiers in neurology · 2017Article
- Hyperacute Vasospasm After Aneurysmal Subarachnoid Hemorrhage.Neurocritical care · 2016Article
- Article
- Diagnosis of cerebral vasospasm and risk of delayed cerebral ischemia related to aneurysmal subarachnoid haemorrhage: an overview of available tools.Neurosurgical review · 2015Review
- Correlation between plasma total nitric oxide levels and cerebral vasospasm and clinical outcome in patients with aneurysmal subarachnoid hemorrhage in Indian population.Journal of neurosciences in rural practice · 2014Article
- Article
- Low-dose intravenous heparin infusion in patients with aneurysmal subarachnoid hemorrhage: a preliminary assessment.Journal of neurosurgery · 2013Article
- Significance of C-reactive protein and transcranial Doppler in cerebral vasospasm following aneurysmal subarachnoid hemorrhage.Journal of Korean Neurosurgical Society · 2013Article
- Angiographically documented cerebral vasospasm following transsphenoidal surgery for pituitary tumors.Pituitary · 2013Article
- Post-subarachnoid hemorrhage vasospasm in patients with primary headache disorders.Neurocritical care · 2013Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cellular mechanisms responsible for cerebral vasospasm (CVS) occurring after subarachnoid hemorrhage (SAH) have been of major interest over the past 50 years. The present review describes how each of the discrete anatomic components that comprise the cerebral artery may contribute to the pathology of CVS. The blood extravasated after SAH is hemolyzed and undergoes degradation with resultant production of free radicals, known to be powerful initiators of vascular damage. An inflammatory response is generated activating both leukocytes and platelets with subsequent release of inflammatory agents. The cerebral artery affected by CVS undergoes phenotypic change involving both the endothelial and smooth muscle cells. In the endothelium the production of nitric oxide and prostacyclin is affected. In the smooth muscle cells signal transduction pathways that enhance the function of the contractile proteins and induce the upregulation of contractile receptors are activated. In parallel, there is evidence that nervous reflex pathways involving the trigeminal ganglion and the hypothalamus are activated. However, the relative contributions of each of the systems are speculative. Therapy may be directed at disrupting the cascade leading from the SAH insult to CVS or at overcoming the dysfunction incurred by CVS; possible therapeutical interventions are considered.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.