Safety Profile of Nimodipine in Patients with Subarachnoid Hemorrhage

Tettenborn, D; Dycka, J.; Kurtz, Natalie; Porto, L. Hermida

doi:10.1007/978-3-642-48695-1_11

Cited by 3 publications

(1 citation statement)

References 14 publications

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“…Drugs & Aging 2 (4) 1992 adverse effect in patients treated with oral or intravenous nimodipine and was observed in up to 5% of patients with subarachnoid haemorrhage (Langley & Sorkin 1989;Tettenborn et al 1991). It should be noted that reductions in blood pressure were more likely if the patient was previously hypertensive (Tettenborn et a!.…”

Section: Tolerabilitymentioning

confidence: 99%

Nimodipine

Wadworth¹,

McTavish²

1992

Drugs & Aging

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Nimodipine is a dihydropyridine calcium antagonist which dilates cerebral blood vessels and increases cerebral blood flow in animals and humans. Preliminary findings reveal its potential benefit for the treatment of a wide range of cerebrovascular disorders, particularly for prophylaxis and treatment of delayed ischaemic neurological deficits resulting from cerebral vasospasm in patients with subarachnoid haemorrhage. Studies involving patients aged up to 79 years have confirmed these preliminary findings by showing that nimodipine reduces the incidence of severe ischaemic deficit after subarachnoid haemorrhage. Initial results from studies of patients with acute ischaemic stroke indicate that nimodipine, started within 72 hours of onset, improved recovery, particularly in patients over 65 years. However, other investigators have found no marked difference in 6-month mortality or morbidity rates of stroke patients aged up to 97 years. Findings from other studies suggest that nimodipine may improve symptoms of cognitive dysfunction in elderly patients. Nimodipine is well tolerated by both younger and older patients. The most frequently reported adverse event has been hypotension. Thus, nimodipine therapy offers important benefits as part of the approach to management of patients with subarachnoid haemorrhage and has potential in other cerebral disorders, including stroke and impaired cognitive function, although confirmation of initial results in patients with cerebral impairment are required.

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Section: Tolerabilitymentioning

confidence: 99%

Nimodipine

Wadworth¹,

McTavish²

1992

Drugs & Aging

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Endothelial Cell Dysfunction and Injury in Subarachnoid Hemorrhage

Kumar¹,

McBride²,

Dash³

et al. 2018

Mol Neurobiol

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In the brain, vascular endothelial cells conserve blood viscosity, control blood flow, and form the interface between central nervous system and circulating blood. Clinical outcome after aneurysmal subarachnoid hemorrhage is linked to early brain injury, cerebral vasospasm, and other causes of delayed cerebral ischemia. The cerebral vasculature remains a unique target for therapies since it becomes rapidly disrupted after subarachnoid hemorrhage, and damage to the blood vessels continues into the delayed injury phase. The current failure of therapies to improve clinical outcome warrants a re-evaluation of current therapeutic approaches. The mechanisms of endothelial cell injury and blood-brain barrier breakdown are critical to the pathway of cerebral injury, and an improved understanding of these mechanisms may lead to novel therapeutic targets. This review provides an update on the current understanding of endothelial cell injury following aneurysmal subarachnoid hemorrhage, including blood-brain barrier dysfunction.

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