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Intracranial haemorrhage
Published in Ibrahim Natalwala, Ammar Natalwala, E Glucksman, MCQs in Neurology and Neurosurgery for Medical Students, 2022
Ibrahim Natalwala, Ammar Natalwala, E Glucksman
v – Vasospasm. Cerebral vasospasm is delayed narrowing of cerebral vessels following a SAH. It normally begins 3 days after the haemorrhage with a peak at 5–14 days. It can cause reduced distal blood flow and can lead to DIND and cerebral infarction if left untreated. It is worth noting that vasospasm on angiography does not necessarily always correlate with clinical symptoms of vasospasm.3
Neurology
Published in Faye Hill, Sash Noor, Neel Sharma, Tiago Villanueva, Medical and Surgical Emergencies for Students and Junior Doctors, 2021
Faye Hill, Sash Noor, Neel Sharma
Monitoring and careful control of blood pressure is important in such cases. Surgical clipping or endovascular coiling should be performed to reduce the risk of re-bleeding. Cerebral vasospasm is a common occurrence after a subarachnoid haemorrhage. This can be appropriately managed through the use of oral nimodipine. Because of the risk of hydrocephalus associated with subarachnoid haemorrhage, temporary or permanent cerebrospinal fluid diversion is required. Seizures should be best controlled with anti-epileptic therapy (see below) and in cases of hyponatraemia, which can occur in up to 30% of cases, patients may benefit from fludrocortisone and hypertonic saline.
Intracranial Hemorrhage (ICH)
Published in Swati Goyal, Neuroradiology, 2020
It depends on the underlying cause. Monitoring of raised intracranial pressure, drainage for hydrocephalus. Cerebral vasospasm is a crucial complication, resulting in delayed cerebral ischemia and requires treatment with nimodipine (calcium channel blocker) and endovascular intervention (intra-arterial delivery of vasodilating agents and balloon angioplasty).
Comparison of radiological versus clinical cerebral vasospasm after aneurysmal subarachnoid hemorrhage: is vasospasm always present?
Published in Neurological Research, 2020
Djula Djilvesi, Igor Horvat, Bojan Jelaca, Jagos Golubovic, Filip Pajicic, Petar Vulekovic
Control CTA findings were analyzed independently by a radiologist and researcher. Data about the presence, region and intensity of vasospasm were determined by radiologist comparing control and admission CTA findings, without exact measuring the blood vessels. Researcher measured seven segments of the proximal blood vessels of the brain in their distal parts at admission and control CTA: 1. suprasellar part of the Internal carotid artery; 2. M1 segment of the Medial cerebral artery; 3. A1 segment of the Anterior cerebral artery; 4. A2 segment of the Anterior cerebral artery; 5. P1 segment of the Posterior cerebral artery; 6. vertebral artery, and 7. basilar artery. If there were signs of vasospasm in distal circulation (M2 and M3), these data were noted and taken into account in statistical analysis. In determining the presence of vasospasm, findings by both a radiologist and researcher were taken into account. The presence of cerebral vasospasm was classified as: 1. present (degree of narrowing of the blood vessel 5–100%, taking into account the possibility of error in the measurement) and 2. absent (0–5% narrowing). Narrowing of the arteries on angiographic images on the basis of the measured values was classified into: 1. mild (5–33%); 2. moderate (34–66%), and 3. severe (67–100%).
Brain ultrasound for diagnosis and prognosis in the neurological intensive care unit: a mini review for current development
Published in Neurological Research, 2019
Haomeng Zhu, Xiaokun Geng, Gary B. Rajah, Paul Fu, Huishan Du
Cerebral vasospasm after subarachnoid hemorrhage is a well-known phenomenon that leads to a decrease in the diameter of the blood vessels [21]. This is detected by TCD monitoring through a change in cerebral blood flow velocity of the cerebral blood and a reduction in cross-sectional areas of blood vessels. Symptomatic vasospasm (VSP) refers to direct mechanical damage or circulating vascular wall stimulating factors in the blood that cause cerebral vasoconstriction which leads to severe cerebral blood flow reduction and possibly cerebral ischemia [22]. VSP can cause localized contraction of the cerebral blood vessels, and if the amount of cerebral blood perfusion decreases enough, delayed cerebral ischemia will ensue. VSP is a common complication of aneurysmal SAH. At present, global cerebral angiography is the gold standard for diagnosing vasospasm, but it is invasive and cannot be continuously monitored. TCD is easy to use, non-invasive, and inexpensive thus making it an ideal tool for dynamic monitoring of VSPs [23] Statistics show that up to 70% of SAH patients have cerebral vasospasm, and 30% of patients have clinical ischemic symptoms [24]. Cerebral vasospasm usually begins on the third day, with peak between the 6th and 10th day, and can last up to three weeks [25]. One report noted that if vasospasms continue up until the 20th day, patient mortality rates can be as high as 20% [26].
Delayed ischaemia due to vasospasm after fenestration of a large arachnoid cyst
Published in British Journal of Neurosurgery, 2019
Jochem K. H. Spoor, Hugo P. Aben, Bachtiar Burhani, Geert-Jan Rutten
Cerebral vasospasm is a major cause of morbidity and mortality after subarachnoid haemorrhage. Incidentally, it also occurs after traumatic brain injury, brain surgery or meningitis.1 After brain tumour removal, several mechanisms have been postulated in the pathogenesis of vasospasm: accumulation of blood in the basal cisterns, manipulation or damage of blood vessel walls, and release of tumour material.2 A number of studies specifically reported on vasospasm after resection or rupture of an intracranial cyst (craniopharyngioma, colloid cyst, dermoid tumour).3 It is suggested that in these cases the content of the cyst caused a sterile inflammation, which subsequently led to the vasospasm. Inflammation, and in particular leukocyte-endothelial cell interactions, have been hypothesized to play a critical role in the pathogenesis of vasospasm.