Cyclosporine A for the prevention of neurological deficit following subarachnoid hemorrhage.

M, Ryba; Grieb, P; Bidziński, J; Pastuszko, M; Dziewiecki, C.; Iwańska, K

doi:10.1161/str.22.4.531a

Cited by 14 publications

(5 citation statements)

References 10 publications

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“…Clinical studies with cyclosporine are also varied, showing no beneficial effect of cyclosporine in the outcome patients with severe SAH [167], but showing improved outcome in patients who underwent early clipping after SAH when combined with nimodipine [168–170]. Tacrolimus (FK-506), a newer immunosuppressant, did not prevent vasoconstriction and lymphocytic infiltrations in experimental SAH models [171–173].…”

Section: The Role Of Inflammation In Vasospasm After Sahmentioning

confidence: 99%

“…Immunosuppressants such as cyclosporine cause T-cell dysfunction by inhibiting interleukin-2 (IL-2) transcription [ 164 ] and have been tested in experimental SAH with varied success [ 165 , 166 ]. Clinical studies with cyclosporine are also varied, showing no beneficial effect of cyclosporine in the outcome patients with severe SAH [ 167 ], but showing improved outcome in patients who underwent early clipping after SAH when combined with nimodipine [ 168 – 170 ]. Tacrolimus (FK-506), a newer immunosuppressant, did not prevent vasoconstriction and lymphocytic infiltrations in experimental SAH models [ 171 – 173 ].…”

Section: The Role Of Inflammation In Vasospasm After Sahmentioning

confidence: 99%

See 1 more Smart Citation

Inflammation, Vasospasm, and Brain Injury after Subarachnoid Hemorrhage

Miller

Turan

Chau

et al. 2014

BioMed Research International

170

120

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Subarachnoid hemorrhage (SAH) can lead to devastating neurological outcomes, and there are few pharmacologic treatments available for treating this condition. Both animal and human studies provide evidence of inflammation being a driving force behind the pathology of SAH, leading to both direct brain injury and vasospasm, which in turn leads to ischemic brain injury. Several inflammatory mediators that are elevated after SAH have been studied in detail. While there is promising data indicating that blocking these factors might benefit patients after SAH, there has been little success in clinical trials. One of the key factors that complicates clinical trials of SAH is the variability of the initial injury and subsequent inflammatory response. It is likely that both genetic and environmental factors contribute to the variability of patients' post-SAH inflammatory response and that this confounds trials of anti-inflammatory therapies. Additionally, systemic inflammation from other conditions that affect patients with SAH could contribute to brain injury and vasospasm after SAH. Continuing work on biomarkers of inflammation after SAH may lead to development of patient-specific anti-inflammatory therapies to improve outcome after SAH.

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Section: The Role Of Inflammation In Vasospasm After Sahmentioning

confidence: 99%

Section: The Role Of Inflammation In Vasospasm After Sahmentioning

confidence: 99%

Inflammation, Vasospasm, and Brain Injury after Subarachnoid Hemorrhage

Miller

Turan

Chau

et al. 2014

BioMed Research International

170

120

View full text Add to dashboard Cite

show abstract

“…Also treatment with immunosuppressants in experimental SAH in dogs and rabbits prevented the angiopathic changes in intracranial arteries, and in patients with SAH it markedly improved the neurological status 7,17,19,22,23,24,25 In conclusion, the experimental and clinical observations strongly suggest that the described IgM and/ or C3 immune deposits may play a role in the pathogenesis of post aneurysm rupture neurological complications.…”

Section: Discussionmentioning

confidence: 74%

Is vascular angiopathy following intracranial aneurysm rupture immunologically mediated?

Jarzabek-Chorzelska²,

Chorzelski³

et al. 1992

Acta neurochir

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Immunofluorescence studies showed the presence of IgM and/or C3 in the endothelium of intracranial aneurysms in 5 out of 6 patients with subarachnoid haemorrhage (SAH). In none of them were the immune deposits found in the gyrus rectus. Cortical tissue of 4 epileptic patients which served as a control give negative results. Serum studies on femoral artery wall used as an antigenic substrate did not reveal circulating antibodies of the IgM or IgG class. Our studies strongly suggest that the IgM and/or C3 immune deposits located in the endothelium of intracranial arteries may play a role in post SAH neurological complications.

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“…Cyclosporine is a potent immunosuppressant which inhibits T-lymphocyte activation [30], however it can also prevent neurological deterioration of patients with subarachnoid hemorrhage caused by the rupture of an aneurysm [31] because it relaxes cerebral vasospasm [32]. Ogawa et al also reported that it could prevent the late onset reduction of muscarinic acetylcholine receptors which occurred in the hippocampus 7 days after 5 min of cerebral ischemia.…”

Section: Discussionmentioning

confidence: 99%

Protective effects of cyclosporine and allopurinol on transient global cerebral ischemia in gerbils

Ogata

Luo

1995

J Anesth

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The effects of cyclosporine and allopurinol on neuronal death following global cerebral ischemia were evaluated in Mongolian gerbils. The animals were randomly divided into four groups of 12 each: (1) sham operation as control, (2) occlusion of the bilateral common carotid arteries for 12 min and treatment with physiological saline, (3) occlusion plus treatment with 5 mg/kg of cyclosporine, and (4) occlusion plus treatment with 100 mg/kg of allopurinol 30 min before cerebral ischemia and daily thereafter for 6 days. On the 7th day after ischemia or sham operation, the gerbils' brains were removed. The number of necrotic pyramidal cells in the cortex and hippocampal CA1 was evaluated and tissue chemiluminescence (reflecting the presence of superoxide radicals) and lipid peroxides were examined. The number of necrotic pyramidal cells in each field of view (×100) of the cortex was 115±79 after ischemia, which was significantly larger than 14±8 in the control group, and was 45±33 and 60±49 after treatment with cyclosporine and allopurinol, respectively. The number of surviving pyramidal cells per mm length after ischemia in CA1 was 37±14, which was significantly smaller than 174±30 in the control group, but 78±31 following treatment with was cyclosporine, and 108±53 with allopurinol. A reduced number of necrotic pyramidal cells was associated with lower tissue chemiluminescence and lipid peroxides. The results suggest that both cyclosporine and allopurinol can inhibit neuronal death after global cerebral ischemia, and that autoimmunization and superoxide radicals are partially responsible for neuronal death.

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Cyclosporine A for the prevention of neurological deficit following subarachnoid hemorrhage.

Cited by 14 publications

References 10 publications

Inflammation, Vasospasm, and Brain Injury after Subarachnoid Hemorrhage

Inflammation, Vasospasm, and Brain Injury after Subarachnoid Hemorrhage

Is vascular angiopathy following intracranial aneurysm rupture immunologically mediated?

Protective effects of cyclosporine and allopurinol on transient global cerebral ischemia in gerbils

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