Ischemic model of optic nerve injury

Cioffi, George A.

doi:10.1016/j.ajo.2006.02.013

Cited by 51 publications

(59 citation statements)

References 117 publications

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“…Alternatively, the GCC loss might be related to interference in axoplasmic flow induced by local ischaemia at the level of optic chiasm. 22 This hemodynamic perturbation might be related to the action of vasoactive peptide endothelin-1 that is released by pituitary tumours. 23 GCC and RNFL dysfunction, measured by SD-OCT, has also been demonstrated in early glaucoma.…”

Section: Eyementioning

confidence: 99%

“…1,2 They comprise 20% of all primary brain and central nervous system tumours and represent the second most common type identified by histology in young adults (20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34) years) according to the Central Brain Tumor Registry of the USA. 3 A population-based study conducted in the province of Liège, Belgium, reported a 3-5 times higher prevalence of clinically relevant pituitary tumours (1:1064) than previously estimated.…”

Section: Introductionmentioning

confidence: 99%

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Evaluation of the retinal nerve fibre layer and ganglion cell complex thickness in pituitary macroadenomas without optic chiasmal compression

Cennamo

Auriemma²,

Cardone

et al. 2015

Eye

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Purpose The aim of this prospective study was to measure the thickness of the circumpapillary retinal nerve fibre layer (cpRNFL) and the ganglion cell complex (GCC) using spectral domain optical coherence tomography (SD-OCT) in a cohort of consecutive de novo patients with pituitary macroadenomas without chiasmal compression. Patients and methods Twenty-two consecutive patients with pituitary macroadenoma without chiasmal compression (16 men, 6 women, aged 45.2 ± 14.6 years, 43 eyes) entered the study between September 2011 and June 2013. Among them, 31.8% harboured a growth hormone-secreting pituitary adenoma, 27.3% a prolactin-secreting pituitary adenoma, 27.3% a corticotrophin-secreting pituitary adenoma, and 13.6% a non-secreting pituitary tumour. Eighteen subjects (nine females, nine males, mean age 36.47 ± 6.37 years; 33 eyes) without pituitary adenoma, with normal ophthalmic examination, served as controls. In both patients and controls, cpRNFL and GCC thicknesses were measured by SD-OCT. Results Patients were significantly older (P = 0.02) than controls. Best corrected visual acuity, intraocular pressure, colour fundus photography, and automatic perimetry test were within the normal range in patients and controls. Conversely, cpRNFL (P = 0.009) and GCC (Po0.0001) were significantly thinner in patients than in controls. The average GCC (r = 0.306, P = 0.046) significantly correlated with the presence of arterial hypertension. OCT parameters did not differ significantly between patients with a tumour volume above the median and those with a tumour volume below the median. Conclusion Pituitary macroadenomas, even in the absence of chiasmal compression, may induce GCC and retinal nerve fibre layer thinning. SD-OCT may have a role in the early diagnosis and management of patients with pituitary tumours.

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Section: Eyementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Evaluation of the retinal nerve fibre layer and ganglion cell complex thickness in pituitary macroadenomas without optic chiasmal compression

Cennamo

Auriemma²,

Cardone

et al. 2015

Eye

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“…A number of GluR antagonists have been used experimentally to show that some do protect against ischemia-induced damage 568 . Ischemia-induced axonal loss in large retinal ganglion cell axons is similar to that seen in glaucoma 569 . (2) Glaucoma: Although raised intraocular pressure [IOP] is a significant risk factor for developing glaucoma, there is no set threshold for IOP that causes glaucoma.…”

Section: Other Neurological Conditionsmentioning

confidence: 51%

A Review of Glutamate Receptors II: Pathophysiology and Pathology

Rousseaux

2008

J Toxicol Pathol

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Seventy years ago it was discovered that glutamate plays a central role in brain metabolism and is abundant in the brain. Glutamate was then found to be the principal excitatory neurotransmitter in the brain. As stated in the first article of this series, there are three families of ionotropic receptors with intrinsic cation permeable channels: Nmethyl-D-aspartate [NMDA], α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid [AMPA] and kainate [Ka].Among these there are three groups of metabotropic, G protein-coupled glutamate receptors [mGluR] that modify neuronal and glial excitability through G protein subunits acting on membrane ion channels and second messengers such as diacylglycerol and cAMP. There are also two glial glutamate transporters and three neuronal transporters in the brain. Although glutamate is the most abundant amino acid in the diet, there is no evidence for brain damage in humans resulting from dietary glutamate. However, a Ka analog, domoate, is sometimes ingested accidentally in blue mussels; this potent toxin causes limbic seizures, which can lead to hippocampal and related pathology and amnesia. Endogenous glutamate may contribute to the brain damage occurring acutely after status epilepticus, cerebral ischemia or traumatic brain injury by activating NMDA, AMPA or mGluR 1 receptors. Glutamate may also contribute to chronic neurodegeneration in such disorders as amyotrophic lateral sclerosis and Huntington's disease. In animal models of cerebral ischemia and traumatic brain injury, NMDA and AMPA receptor antagonists protect against acute brain damage and delayed behavioral deficits. Other clinical conditions that may respond to drugs acting on glutamatergic transmission include epilepsy, amnesia, anxiety, hyperalgesia and psychosis. In this second part of this review, we will explore those diseases in which the pathophysiology and pathology are associated, in part, with the glutamate system. (J Toxicol Pathol 2008; 21: 133-173)

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“…This decrease in RI can be interpreted as a beneficial effect on ocular blood flow. In primates, chronic optic nerve ischemia has been shown to induce retinal ganglion cell loss independently of high IOP (3) . Consequently, this reduction of the RI of the OA could also be helpful in glaucoma treatment, by potentially preventing retinal ganglion cell Values are the mean ± standard deviation.…”

Section: Discussionmentioning

confidence: 99%

“…There is compelling accumulated evidence supporting the theory that decreased ocular blood flow contributes to glaucomatous optic neuropathy (1,2) . In a model of optic nerve injury, it was demonstrated that alterations of perfusion and oxygen delivery to the retinal ganglion cells may significantly contribute to vision loss (3) . Therefore, detailed hemodynamic evaluation of the orbital circulation is needed to better understand this complex disorder.…”

Section: Introductionmentioning

confidence: 99%

Effects of prostaglandin analogs on blood flow velocity and resistance in the ophthalmic artery of rabbits

Giannico¹,

Lima²,

Shaw³

et al. 2016

Arquivos Brasileiros De Oftalmologia

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Approved by the following research ethics committee: Universidade Federal do Paraná, protocol #011/2011. ABSTRACTPurpose: The aim of this study was to investigate the effects of prostaglandin analogs on blood flow in the ophthalmic artery of clinically healthy rabbits. Methods: Fifty-five clinically healthy New Zealand white rabbits were divided into six groups, and the left eyes were treated for four weeks with the preservative benzalkonium chloride (BAK) only or a topical formulation of different prostaglandin analogs (bimatoprost BAK, tafluprost BAK-free, travoprost BAK, travoprost POLYQUAD, and latanoprost BAK). Color Doppler imaging was performed before and after the treatments. The mean values of the peak systolic velocity (PSV) and end diastolic velocity and the resistive index (RI) were calculated. Statistical analysis was performed to compare the differences pre-and post-treatment for each drug and post-treatment among the drugs. Results: The prostaglandin analogs did not affect PSV. Bimatoprost BAK, travoprost POLYQUAD, and latanoprost BAK did not change RI. Tafluprost BAK-free and travoprost BAK therapy resulted in similar reductions in RI. No significant differences pre-and post-treatment were found when BAK was administered alone. Conclusion:The prostaglandin analogs tafluprost BAK-free and travoprost BAK improved blood flow in the ophthalmic artery in healthy New Zealand white rabbits, which suggests that these drugs enhance the prevention of the progression the progression of glaucoma. Keywords

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Ischemic model of optic nerve injury

Cited by 51 publications

References 117 publications

Evaluation of the retinal nerve fibre layer and ganglion cell complex thickness in pituitary macroadenomas without optic chiasmal compression

Evaluation of the retinal nerve fibre layer and ganglion cell complex thickness in pituitary macroadenomas without optic chiasmal compression

A Review of Glutamate Receptors II: Pathophysiology and Pathology

Effects of prostaglandin analogs on blood flow velocity and resistance in the ophthalmic artery of rabbits

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