Intracarotid slow bolus injection of nimodipine during angiography for treatment of cerebral vasospasm after SAH. A preliminary report.

@article{Grotenhuis1984IntracarotidSB,
  title={Intracarotid slow bolus injection of nimodipine during angiography for treatment of cerebral vasospasm after SAH. A preliminary report.},
  author={Joachim Andreas Grotenhuis and W. Bettag and B. J. O. Fiebach and K. Dabir},
  journal={Journal of neurosurgery},
  year={1984},
  volume={61 2},
  pages={
          231-40
        }
}
Nimodipine was given as an intracarotid slow bolus injection in six patients with subarachnoid hemorrhage (SAH) due to rupture of a cerebral aneurysm, with angiographically demonstrated vasospasm. The patients were followed by serial angiograms for demonstration of the effect of nimodipine on vasospasm. After angiography, all patients were treated with a constant venous infusion of this new calcium antagonist. Although the therapeutic regimen was started only a few hours after onset of… 
View on PubMed
thejns.org
69 Citations
Highly Influential Citations
1
Background Citations
10
Results Citations
4

69 Citations

Citation Type

Citation Type

Intra-Arterial Nimodipine for Severe Cerebral Vasospasm after Aneurysmal Subarachnoid Hemorrhage: Influence on Clinical Course and Cerebral Perfusion
TLDR
IAN in a selective patient group resulted in a positive response with reduction of angiographic vasospasm and increase in cerebral perfusion as detected by PCT after 24 hours, therefore, IAN appears more effective than intra-arterial papaverine.
Intra-arterial nimodipine for the treatment of symptomatic cerebral vasospasm after aneurysmal subarachnoid hemorrhage: preliminary results.
TLDR
Intra-arterial nimodipine is effective and safe for the treatment of symptomatic vasospasm after subarachnoid hemorrhage and further prospective randomized studies of cerebral blood flow are needed to confirm these results.
Intra-arterial nimodipine to treat symptomatic cerebral vasospasm following traumatic subarachnoid haemorrhage. Technical case report
TLDR
A patient with symptomatic and angiographically documented vasospasm following traumatic SAH which was refractory to maximal medical therapy and successfully treated with intra-arterial infusion of Nimodipine is described.
Treatment of Symptomatic Cerebral Vasospasm After Subarachnoid Hemorrhage by Intraarterial Perfusion with Nimodipine
TLDR
Clinical and experimental experiences with the calcium antagonist nimodipine after intravenous and/or oral administration indicate that the incidence of neurological deficits attributed to vasospasm may be reduced and the use of calcium antagonists could be beneficial in the prevention or treatment of cerebral vasospasms.
Continuous intra-arterial nimodipine infusion in patients with severe refractory cerebral vasospasm after aneurysmal subarachnoid hemorrhage: a feasibility study and outcome results
TLDR
Key to the effective administration of continuous intra-arterial nimodipine infusion is multimodal neuromonitoring and the individual adaptation of dosage and time of infusion for each patient.
Prevention of symptomatic vasospasm after SAH by constant venous infusion of nimodipine.
TLDR
Early administration of a specific 'cerebral' calcium antagonist like Nimodipine after SAH will prevent the intracellular Ca2+ overloading, thus protecting the neural cells and preventing Ca2-induced smooth-muscle contraction of cerebral vessels, which encourages ischaemic deficits after SAh.
Angiographic Features and Clinical Outcomes of Intra-Arterial Nimodipine Injection in Patients with Subarachnoid Hemorrhage-Induced Vasospasm
TLDR
IA nimodipine injection for SAH-induced vasospasm led to significant vasodilation in angiography and improvement in clinical symptoms without significant complications, and the findings suggest that IA nimmodipine injections should be utilized when intractable vasospasms develops despite rigorous conservative management.
Continuous Local Intra-arterial Nimodipine Administration in Severe Symptomatic Vasospasm After Subarachnoid Hemorrhage
TLDR
Preliminary data show that CLINA is a straightforward, effective, and safe option for patients with severe CV refractory to medical therapy.
Intra-arterial nimodipine for cerebral vasospasm after subarachnoid haemorrhage: Influence on clinical course and predictors of clinical outcome
TLDR
Intra-arterial nimodipine treatment appears to be effective in reversing angiographic CV, however, it is not alwayseffective in reversing clinical deterioration, as several other factors including treatment delay affect the clinical course.
Continuous Intra-Arterial Nimodipine for the Treatment of Cerebral Vasospasm
Two patients with refractory symptomatic cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH) were treated by continuous intra-arterial nimodipine infusion via a catheter placed in the…
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 55 REFERENCES
Cerebral arterial spasm--a controlled trial of nimodipine in patients with subarachnoid hemorrhage.
TLDR
It is concluded that nimodipine should be given to patients who are neurologically normal after subarachnoid hemorrhage in order to reduce the occurrence of severe neurologic deficits due to cerebral arterial spasm.
Role of prostaglandin F2a in the genesis of experimental cerebral vasospasm
TLDR
Findings suggest that a role of prostaglandin F2a in the genesis of cerebral vasospasm seen clinically is suggested, together with reports in the literature that the brains is rich in prostaglandsin F 2a which it releases into the CSF, suggest a role in this disease.
Cerebral vasospasm with ruptured saccular aneurysm--the clinical manifestations.
TLDR
It was concluded that in this study vasospasm accounted for all DID's and that in the absence of vasospasms DID did not occur.
Cerebral arterial spasm: part 10. Reversal of acute and chronic spasm in dogs with orally administered nifedipine.
TLDR
Sublingual administration of nifedipine 20 minutes before the subarachnoid injection of blood prevented the acute spasm and reversed both the acute and the delayed cerebral arterial spasm.
The pathophysiology of cerebral vasospasm, and pharmacological approaches to its management
  • R. Towart
  • Medicine, Biology
    Acta neurochirurgica
  • 1982
TLDR
A new group of drugs, the calcium antagonists, has selective and potent relaxant actions against the contractions of cerebral vessels produced by a wide range of agonists, and may be of therapeutic use in both the prophylaxis and treatment of cerebral vasospasm.
Cerebral arterial spasm. 2. Experimental evaluation of mechanical and humoral factors in pathogenesis.
TLDR
The arteries at the base of the brain are especially suited for study of arterial spasm, for it is only here that arteries are found bathed by clear fluid and covered by an avascular membrane which can be incised without exposing the outside of the artery to blood.
Attempted prevention or treatment of intracranial arterial spasm: a survey.
TLDR
It may be possible in the future to identify those patients at risk of developing cerebral vasospasm by assessing the location and amount of subarachnoid blood by computerized tomography, which would aid the development of measures to prevent intracranial arterial spasm.
Report on the cooperative study of intracranial aneurysms and subarachnoid hemorrhage. IV. Cerebral angiography. An analysis of the diagnostic value and complications of carotid and vertebral angiography in 5,484 patients.
TLDR
C cerebral angiography was used extensively in European countries for diagnosis of tumors, arteriovenous malformations, aneurysms, hematomas, and other lesions and a brief history and survey of the literature can be found in Wickbom's 1948 monograph.
Pial arterial vasodilation by intravenous nimodipine in cats.
TLDR
In a series of animal experiments, isopropyl (2-methoxyethyl)-1,4-dihydro-2,6-dimethyl-4(3-nitrophenyl)-3,5-pyridinedicarboxylate (nimodipine) was administered by infusion to 10 anesthetized cats, causing marked dilation and drop in blood pressure.
Intracranial arterial spasm: a clinical analysis.
TLDR
It has been postulated that preoperative intracranial arterial spasm originates locally as a result of arterial distortion and irritation by aneurysmal rupture and perivascular clot formation, and is propagated to other areas by the nerves and smooth muscle fibers of the involved cerebral arteries.
...
1
2
3
4
5
...