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PubMed2000

Choroidal thickness changes during altered eye growth and refractive state in a primate.

PURPOSE: In the chick, compensation for experimentally induced defocus involves changes in the thickness of the choroid. The choroid thickens in response to imposed myopic defocus and thins in response to imposed hyperopic defocus. This study was undertaken to determine whether similar choroidal changes occur in the primate eye with induced refractive errors. METHODS: Thirty-three common marmosets were used. Eyes in 26 monkeys served as untreated control eyes, and eyes in 7 received 3 weeks of monocular lid suture to induce changes in eye growth and refractive state. Refractive errors were measured using refractometry and retinoscopy, and axial ocular dimensions, including choroidal thickness, were measured using high-frequency A-scan ultrasonography. Eyes were measured before the lids were sutured and at frequent intervals after lid opening. RESULTS: In the marmoset, choroidal thickness ranges from 88 to 150 microm and increases significantly during the first year of life. Monocular lid suture initially results in short, hyperopic eyes that then become elongated and myopic. In these animals the choroids of both the experimental and the fellow control eyes also increase in thickness with age but additionally show interocular differences that vary significantly with the relative changes in vitreous chamber depth and refraction. In eyes that are shorter and more hyperopic than control eyes the choroids are thicker, and in eyes that are longer and more myopic than control eyes the choroids are thinner. CONCLUSIONS: In marmosets, the thickness of the choroid increases during postnatal eye growth. Superimposed on this developmental increase in choroidal thickness there are changes in thickness that are correlated with the induced changes in eye size. These changes are small (<50 microm) in comparison with those observed in the chick, contributing to less than a diopter change in refractive error.

Aging↗
PubMed2005

Differentiation of choroid plexus tumors by advanced magnetic resonance spectroscopy.

OBJECT: The management of pediatric intraventricular tumors is highly dependent on identification of the tumor type. Choroid plexus papillomas, a common intraventricular tumor in children, can be difficult to distinguish radiographically from choroid plexus carcinomas and other common pediatric central nervous system (CNS) tumors. In this study to overcome the limitations of current noninvasive imaging modalities, the authors use novel magnetic resonance (MR) spectroscopy techniques in vivo to elucidate the identifying biochemical features of choroid plexus tumors that may facilitate diagnosis and treatment. METHODS: Based on an Internal Review Board-approved protocol, six children with newly diagnosed, untreated intraventricular brain tumors were identified. On retrospective review, this series included three choroid plexus papillomas and three choroid plexus carcinomas. Single-voxel proton MR spectroscopy with a short echo time was performed, and absolute metabolite concentrations (in mmol/kg) were determined using fully automated quantitation. These results were compared with MR spectroscopy profiles obtained in 54 other untreated CNS neoplasms in children. The myo-inositol (mI) level was significantly higher in choroid plexus papillomas (> 10 mmol/kg), uniquely distinguishing these tumors from choroid plexus carcinomas and all other tumors. Choroid plexus carcinomas, on the other hand, had significantly elevated levels of choline when compared with choroid plexus papillomas. CONCLUSIONS: In this study the authors find that mI is a biochemical constituent that uniquely identifies choroid plexus papillomas and can be used as a noninvasive means of diagnosis and for follow-up evaluations in patients with this disease.

Adolescent↗
PubMed1998

Ocular axial length and choroidal thickness in newly hatched chicks and one-year-old chickens fluctuate in a diurnal pattern that is influenced by visual experience and intraocular pressure changes.

Low coherence laser Doppler interferometry (LDI) allows high precision measurements of the axial length of the eye and of the thickness of the individual layers of the ocular fundus. Here, we used LDI to monitor diurnal changes in these dimensions in eyes of newly hatched chicks and one-year-old chickens with normal or altered visual input. In chicks and chickens with normal visual experience, axial eye length displays diurnal fluctuations increasing during the light phase. Choroidal thickness also exhibits a diurnal pattern, shrinking during the day and expanding during the night. Retinal thickness does not vary. Based on the pressure compliance of the enucleated chick eye, the diurnal intraocular pressure (IOP) fluctuation could contribute both to the increase in axial length and to daytime choroidal shrinkage. Following deprivation of form vision by unilateral goggle wear, occluded chick eyes demonstrate enhanced axial elongation. Diurnal fluctuations in axial length but not in choroidal thickness are temporarily disrupted. The retina of form deprived eyes thins approximately 10% in five days. In contralateral eyes, the diurnal patterns of both axial length and choroidal thickness fluctuations are also disrupted. Following occluder removal in chicks, choroidal thickness increases for several days during both the light and dark phase, leading to its overall expansion. Retinal thickness returns to baseline. When deprived of form vision for five days, the eyes of year-old chickens do not exhibit measurable axial elongation. Diurnal patterns of fluctuation in axial length and choroidal thickness are however disrupted. After goggle removal, axial length fluctuation is restored to normal, but the diurnal choroidal thickness pattern is inverted. In contralateral eyes, choroidal thickness exhibits normal diurnal fluctuations both during and after form vision deprivation. In conclusion, axial length and choroidal thickness fluctuations are influenced by visual experience in both newborn chicks and one-year-old chickens. In selected instances a binocular interaction regarding axial length and choroidal thickness changes is suggested, the effect weakening with age.

Animals↗
PubMed1999

Influence of ophthalmic nerve fibers on choroidal blood flow and myopic eye growth in chicks.

Ophthalmic sensory nerve fibers containing substance P and calcitonin gene-related peptide' innervate the choroid in mammals and are known to vasodilate choroidal blood vessels. The avian choroid is also innervated by ophthalmic nerve fibers containing substance P and calcitonin gene-related peptide. The present studies were carried out to determine the influence of these sensory fibers on choroidal blood flow in birds and characterize their interaction with manipulations affecting eye growth. In these studies, ChBF was measured using laser Doppler flowmetry in both eyes in the following groups of birds: (1) normal chicks; (2) chicks with right optic nerve transected for 2 weeks; (3) chicks with right optic nerve transected and a goggle over the right eye for 2 weeks; and (4) chicks with right optic and ophthalmic nerves transected and a goggle over the right eye for 2 weeks. The eyes were refracted and various ocular dimensions measured after the blood-flow measurements. It was found that optic nerve transection reduced ChBF to 30% of normal. Placing a goggle (which increases ocular temperature by 4 degrees C) over an optic nerve transected eye nearly doubled choroidal blood flow over that in an optic nerve transected eye without a goggle. Additional transection of the ophthalmic nerve in a goggled optic nerve-transected eye, yielded choroidal blood flow that was indistinguishable from that in a nongoggled optic nerve-transected eye. Optic nerve transection had a slight stunting effect on axial growth of the eye. While myopic axial elongation was observed in goggled eyes with the optic nerve cut, the extent of myopia was less than in normal goggled eyes. Ophthalmic nerve transection further reduced the myopia induced by goggling in an optic nerve cut eye. These results suggest that ophthalmic nerve input to the choroid exerts a vasodilatory influence, which is activated in a goggled eye. This increased choroidal blood flow may be in response to elevated ocular temperatures caused by the goggling and this increase appears to be masked in goggled eyes with an intact optic nerve by the reduction in choroidal blood flow normally accompanying myopic eye growth. Our results thus show that the induction of myopic eye growth (as in our optic nerve cut eyes with a goggle) need not be accompanied by a decrease in choroidal blood flow from the baseline no-goggle condition (in this case, with the optic nerve cut).

Animals↗
PubMed2002

Improved leukocyte tracking in mouse retinal and choroidal circulation.

The purpose of this study is to develop a new method with which to visualize leukocyte dynamics in murine choroidal and retinal circulation. Both pigmented (B10.RIII) and non-pigmented (BALB/c) mice were used in this study. One hundred microl of 0.05% sodium fluorescein was injected via the mice tail vein to outline the vessel, followed by 150 microl (10(7) cells) C-AM labelled leukocytes. Fundus images were obtained with a confocal scanning laser ophthalmoscope. The dynamic image sequences were recorded simultaneously on videotape (S-VHS) and digitally at 25 frames per sec. The digital images were later analysed with a custom-made personal computer-based image analysis system. Both the choroidal and retinal circulation can be visualized in non-pigmented mice in the first few seconds of fluorescein angiography. However, the view of the choroidal and the retinal capillary circulation is soon blurred due to the rapid fluorescein leakage in the choroid. In contrast, in pigmented mice, retinal circulation is clear against the dark background of the choroid, while choroidal circulation is masked behind the pigment epithelial layer and cannot be seen at all. C-AM labelled leukocytes were clearly seen in the retinal circulation of all experimental mice and in the choroidal circulation of non-pigmented mice for as long as 30 min. The number of labelled circulating cells decreased as time clasped. Cells moved rapidly in the retinal arteries, slowing down or even stopping for a few seconds in the capillary system, and then moved slightly faster again through the postcapillary venules and veins. In non-pigmented mice, significant number of cells were seen to have arrested in the choroidal circulation. There was no difference between B10.RIII mice and BALB/c mice in vessel diameters, leukocyte velocities and shear stresses. This method allows the visualization of leukocytes and provides data on their behavior as they move through the choroidal and retinal circulation of non-pigmented mice, and in the retinal circulation of pigmented mice. It provides a valuable new tool for the investigation of real time leukocyte dynamics in murine retinal and choroidal microcirculations both under physiological conditions and during the development of ocular disease.

Animals↗
PubMed2000

[Morphometric changes in the choriocapillaris and choroid in eyes with advanced glaucoma damage].

BACKGROUND: In addition to elevated intraocular pressure, a compromised ocular blood supply has been implicated in the pathogenesis of primary open-angle glaucoma (PCOG). METHODS AND MATERIALS: We analyzed 20 eyebank eyes with end-stage PCOG and compared these with 20 age-matched controls. The following variables were measured: density and diameter of large choroidal vessels in the macular and equatorial choroid; thickness of the choroid in the macular and equatorial region; and density and thickness of choriocapillaris in the macular, peripapillary, and equatorial choroid. RESULTS: Eyes with glaucoma displayed a lower density of the capillaries of the choriocapillaris than control eyes in the macular, temporal peripapillary, and equatorial choroid, with 0.50 vs. 0.55 (P = 0.018), 0.46 vs. 0.51 (P = 0.016), and 0.50 vs. 0.55 (P = 0.038), respectively. Assessment of large choroidal vessels in the macular choroid showed that eyes with glaucoma had less density of veins (11.7 vs. 38.9/mm2; P < 0.001) and arteries (7.7 vs. 12.4/mm2; P = 0.005) and arteries with a higher diameter (45.6 vs. 28.2 microns; P < 0.001) than control eyes. The large vessels in the equatorial choroid displayed no significant difference in diameter but a lower density (21.2 vs. 44.1/mm2; P = 0.017) in eyes with glaucomatous damage than controls. CONCLUSION: Eyes with advanced glaucomatous damage after long-standing PCOG exhibit many changes in the choroidal vasculature. We cannot conclude from our study whether the observed vascular changes in the choroid are primary pathogenic factors or secondary phenomena.

Capillaries↗
PubMed2006

Acquired choroidal folds: a sign of idiopathic intracranial hypertension.

BACKGROUND: Choroidal folds may be caused by several underlying ocular and orbital diseases; they are classified as idiopathic when no obvious cause is found. The objective of this study was to determine whether acquired choroidal folds are associated with idiopathic intracranial hypertension. METHODS: In this observational case series, three patients with normal fundus examination later developed choroidal folds. They underwent complete ocular examination, B-scan ultrasonography, fluorescein angiography, optic coherent tomography (OCT) and magnetic resonance imaging. A neurological consultation, lumbar puncture and measurement of opening pressure of cerebrospinal fluid (CSF) were also obtained for all patients. RESULTS: Three patients with previously normal ocular fundus developed choroidal folds, and optic nerve subarachnoid space enlargement was seen on B-scan. Clinical and radiological evaluations identified elevation of intracranial pressure, and biochemical analysis of CSF was normal, suggesting a diagnosis of pseudotumour cerebri, which was later confirmed. The first patient developed choroidal folds in one eye first, and 4 years later in the fellow eye. The second patient presented with bilateral optic disk swelling secondary to intracranial hypertension. After treatment, which lowered CSF pressure, bilateral choroidal folds were identified by OCT, fluorescein angiography and ocular fundus photograph. The third patient also developed choroidal folds in one eye, but his fellow eye was difficult to evaluate due to a chorioretinitis scar on the macula. OCT identified choroidal folds in all three patients and in the second patient, it also revealed retinal nerve fiber layer damage. CONCLUSIONS: Acquired choroidal folds and optic nerve subarachnoid space enlargement may be signs of idiopathic intracranial pressure elevation. Nevertheless, this diagnosis should be confirmed by lumbar puncture. Comprehensive imaging studies should be performed to rule out expanding tumors. The lower CSF pressure in our first two patients suggests that choroidal folds or optic disk swelling may depend on the level of intracranial pressure and may be points in a continuum of clinical presentations.

Adult↗
PubMed2005

Anatomical and functional evidence for progressive age-related decline in parasympathetic control of choroidal blood flow in pigeons.

The choroid receives extensive parasympathetic innervation, which in birds arises largely from the ciliary ganglion (CG). Since age-related changes in parasympathetic regulation of choroidal blood flow (ChBF) could contribute to age-related retinal decline, we used anatomical and functional methods to determine if ChBF control by the CG shows age-related decline in pigeons. The efficacy of the choroidal vasodilatory response to activation of the CG preganglionic input from the medial subdivision of the nucleus of Edinger-Westphal (EWM) was assessed using laser Doppler flowmetry (LDF). The EWM receives bisynaptic retinal input, and electrical stimulation of EWM or light stimulation of the retina in young animals produces dramatic choroidal vasodilation. Transcleral LDF was therefore used to measure both basal ChBF and the increases in ChBF elicited by electrical stimulation of EWM or by retinal illumination in 0.5-18 year old pigeons. Fixed cryostat sections of the eye from 0.5 to 22 year old pigeons were immunolabeled for the 3A10 neurofilament-associated antigen to determine if intrachoroidal nerve fibers arising from CG exhibited age-related loss. We focused on superior choroid, since it is the primary target for CG nerve fibers. There was a marked age-related loss in the ChBF vasodilatory response elicited by either EWM stimulation or retinal illumination, as was also true for basal ChBF. A progressive decrease in choroidal nerve fibers of CG origin, to 17% of youthful abundance by 22 years of age, was also observed. The evoked ChBF increase, and basal ChBF, achieved 50% of their age-related decline between the ages of 3 and 4 years, while half the loss in CG innervation of choroid was later, occurring by 10 years. Age-related loss of choroidal nerve fibers occurs in parallel with but more slowly than the reduction in basal ChBF and the choroidal vasodilation that can be elicited via natural (light) or electrical activation of the central neural input to CG choroidal neurons. The prominent age-related decline in parasympathetic control of ChBF early in the pigeon life span could contribute to the age-related retinal decline observed in pigeons.

Aging↗
PubMed1997

Choroid plexus cysts--association with trisomy: prospective review of 16,059 patients.

OBJECTIVE: The purpose of the study was to determine the incidence of isolated choroid plexus cysts in association with trisomy 18 and other abnormalities. STUDY DESIGN: All patients from June 1992 through December 1995 were followed up after a screening ultrasonography. Any patient with a choroid plexus cyst was offered genetic counseling and an amniocentesis. Screening ultrasonographic examinations were performed on 16,059 patients, and 301 patients had a fetus with a choroid plexus cyst. One hundred thirty patients elected to have an amniocentesis. Patients were followed up to delivery. RESULTS: Two hundred sixty-three patients had an isolated choroid plexus cyst. Thirty-eight patients had a choroid plexus cyst associated with additional risk factors. Risk factors included advanced maternal age, additional ultrasonographic abnormalities, past obstetric history, or family history. No abnormalities were noted in the group with an isolated choroid plexus cyst. Four patients had an abnormality when the choroid plexus cyst was associated with an additional risk factor, including two patients with trisomy 18 and one with trisomy 21. CONCLUSION: An isolated choroid plexus cyst was not associated with a trisomy or other abnormalities in this study. When a choroid plexus cyst was associated with an additional risk factor, 10.5% of the patients had an abnormality. Amniocentesis is recommended when a choroid plexus cyst is found in association with additional risk factors.

Adult↗
PubMed2000

Optical coherence tomographic features of idiopathic submacular choroidal neovascularization.

PURPOSE: To clarify the morphologic features of idiopathic submacular choroidal neovascularization using optical coherence tomography. METHODS: Using optical coherence tomography, we prospectively examined 17 consecutive eyes (17 patients; eight men, nine women; mean age +/- SD, 36.0 +/- 9.3 years) with idiopathic submacular choroidal neovascularization. During the follow-up period (mean +/- SD, 7.5 +/- 3.8 months), we repeated optical coherence tomography in 15 eyes; optical coherence tomography was performed only at the initial examination in two eyes that underwent submacular surgery. RESULTS: Choroidal neovascularization was observed in the subsensory retinal space anterior to the retinal pigment epithelium as a highly or moderately reflective mass, which protruded from the retinal pigment epithelium in 13 of 17 eyes (protruding type). In four eyes, choroidal neovascularization was a highly reflective fusiform mass at the level of the retinal pigment epithelium and choriocapillaris (fusiform type). During the follow-up period, choroidal neovascularization regressed and the protruding mass became a highly reflective fusiform mass in 10 of 11 eyes with the protruding type that underwent repeated examination. In three of the 10 eyes, during 5 to 10 months from initial examination, the choroidal neovascularization was exacerbated and it again protruded into the subsensory retinal space anterior to the retinal pigment epithelium. Four eyes with the fusiform type remained the same throughout the follow-up period. The overlying retina was thickened and had low reflectivity in all 17 eyes at the initial examination. Optical coherence tomography identified subretinal fluid in only 11 of the 13 eyes with protruding type choroidal neovascularization. CONCLUSIONS: Optical coherence tomography confirmed subsensory retinal location of idiopathic submacular choroidal neovascularization anterior to the retinal pigment epithelium. Protruding choroidal neovascularization transforms to fusiform tissue at the level of the retinal pigment epithelium during the process of regression. Sensory retinal edema was always associated with choroidal neovascularization.

Adult↗
PubMed1999

Angiotensin II regulates choroid plexus blood flow by interacting with the sympathetic nervous system and nitric oxide.

Blood flow to the rat choroid plexus has minimal variability when plasma angiotensin II (AII) concentration is changed within a broad range of levels. We tested the hypothesis that a complex interplay of the vasoconstrictor and vasodilator AII actions in choroidal tissue results in small net changes in choroidal blood flow. Blood flow was measured with 123I- or 125I-N-isopropyl-p-iodoamphetamine. AII was infused intravenously (i.v.) at 30 (moderate dose) and 300 ng kg-1 min-1 (high dose), which respectively decreased (15%) and did not change choroidal blood flow. To determine whether AII regulates choroidal blood flow by interacting with the sympathetic nervous system, rats were given phentolamine (1 mg kg-1, i.v.). This alpha-adrenoceptor antagonist by itself did not alter blood flow; however, it attenuated the blood flow-lowering effect of moderate AII dose. Phentolamine also unmasked the vasodilator AII actions at high peptide concentration. beta-Adrenoceptor blockade, with propranolol (1 mg kg-1, i.v.), reduced blood flow (18-20%) and increased vascular resistance (23-26%). During beta-adrenoceptor blockade, a further decrease in blood flow (15-21%) and increase in vascular resistance (23%) was noted when high AII dose was administered. The direct vasoconstrictor effect of AII at moderate dose on choroidal vasculature was examined in rats subjected to chronic bilateral superior cervical ganglionectomy. In these animals, AII decreased blood flow (24%) and increased vascular resistance (24%). To find out whether the hemodynamic AII actions in choroidal tissue are mediated by nitric oxide (NO), Nomega-nitro-l-arginine methyl ester (l-NAME) was used. l-NAME (0.1 mg kg-1, i.v.) by itself did not alter blood flow; however, in l-NAME-treated rats high AII dose lowered blood flow (25-32%) and increased vascular resistance (30-43%). We conclude that the vasoconstrictor AII actions involve a direct peptide effect on the choroidal vascular bed, and the AII-mediated potentiation of sympathetic activity, which results in the activation of alpha-adrenoceptors. The AII-mediated stimulation of sympathetic nerves also results in the beta-adrenoceptor-dependent relaxation of choroidal blood vessels. In addition, choroidal vasodilatory actions of AII are NO-mediated.

Adrenergic alpha-Antagonists↗
PubMed2003

Isolation of a set of genes expressed in the choroid plexus of the mouse using suppression subtractive hybridization.

The choroid plexus produces cerebrospinal fluid, providing a specialized environment for the CNS. We previously demonstrated that choroid plexus ependymal cells can enhance nerve regeneration in vivo and promote neurite outgrowth in vitro. To understand the molecular mechanisms of choroid plexus functions, we isolated genes predominantly expressed in the mouse choroid plexus using suppression subtractive hybridization. Out of the 49 complementary DNA (cDNA) fragments isolated in two types of screening, 43 matched known sequences in the database and six were novel. In one type of screening where choroid plexus cDNAs were subtracted with cerebral cortex cDNAs, transthyretin and phosphodiesterase I alpha were predominant. This is consistent with previous reports and supports the authenticity of our approach. In the other type of screening, cDNAs derived from the choroid plexus of neonatal (postnatal day 5) mice were subtracted with cDNAs from the choroid plexus of adult mice. RNA blot and/or in situ hybridization confirmed abundant expression, in the mouse choroid plexus, of the mRNA encoding gelsolin, phospholipid transfer protein, ATP-binding cassette transporter A8 (ABCA8), androgen-inducible aldehyde reductase, and Na(+)/sulfate cotransporter SUT-1. Also, one novel gene (FS88) was found to be expressed in the choroid plexus from neonatal mice. Our data suggest that the choroid plexus cells produce molecules involved in processes such as prevention of fibrillization of amyloid beta-protein (transthyretin and gelsolin), lipid metabolism (phospholipid transfer protein and ABCA8), and detoxification (androgen-inducible aldehyde reductase).

Animals↗
PubMed2000

Choroid plexus recovery after transient forebrain ischemia: role of growth factors and other repair mechanisms.

1. Transient forebrain ischemia in adult rats, induced by 10 min of bilateral carotid occlusion and an arterial hypotension of 40 mmHg, caused substantial damage not only to CA-1 neurons in hippocampus but also to epithelial cells in lateral ventricle choroid plexus. 2. When transient forebrain ischemia was followed by reperfusion (recovery) intervals of 0 to 12 hr, there was moderate to severe damage to many frond regions of the choroidal epithelium. In some areas, epithelial debris was sloughed into cerebrospinal fluid (CSF). Although some epithelial cells were disrupted and necrotic, their neighbors exhibited normal morphology. This patchy response to ischemia was probably due to regional differences in reperfusion or cellular metabolism. 3. Between 12 and 24 hr postischemia, there was marked restoration of the Na+, K+, water content, and ultrastructure of the choroid plexus epithelium. Since there was no microscopical evidence for mitosis, we postulate that healthy epithelial cells either were compressed together on the villus or migrated from the choroid plexus stalk to more distal regions, in order to "fill in gaps" along the basal lamina caused by necrotic epithelial cell disintegration. 4. Epithelial cells of mammalian choroid plexus synthesize and secrete many growth factors and other peptides that are of trophic benefit following injury to regions of the cerebroventricular system. For example, several growth factors are upregulated in choroid plexus after ischemic and traumatic insults to the central nervous system. 5. The presence of numerous types of growth factor receptors in choroid plexus allows growth factor mediation of recovery processes by autocrine and paracrine mechanisms. 6. The capability of choroid plexus after acute ischemia to recover its barrier and CSF formation functions is an important factor in stabilizing brain fluid balance. 7. Moreover, growth factors secreted by choroid plexus into CSF are distributed by diffusion and convection into brain tissue near the ventricular system, e.g., hippocampus. By this endocrine-like mechanism, growth factors are conveyed throughout the choroid plexus-CSF-brain nexus and can consequently promote repair of ischemia-damaged tissue in the ventricular wall and underlying brain.

Animals↗
PubMed2006

Accuracy of choroidal melanoma diagnosis by general ophthalmologists: a prospective study.

PURPOSE: To estimate the proportion of 'false positives' in patients referred with a diagnosis of suspected choroidal melanoma by general ophthalmologists to an ocular oncology centre. METHODS: A prospective study of patients referred by general ophthalmologists to an ocular oncology centre was undertaken over a 14-week period. The diagnosis was made clinically in patients receiving radiotherapy or phototherapy and was confirmed by histopathology in patients requiring fine needle aspiration biopsy (FNAB) or enucleation. RESULTS: A total of 132 new patients were seen in 10 consecutive ocular oncology clinics between 29 March 2004 and 5 July 2004. The mean age was 62 years (range 28-88 years) and 60 (55%) were female. Among the 83 suspected malignant posterior segment lesions, the suspected diagnosis included choroidal melanoma (73), choroidal metastasis (6), 'choroidal tumour' (3), and 'Solid retinal detachment' (1). Only 50 of the 73 suspected melanomas were confirmed (68.5%; 95% CI, 57-78%), the oncologist's diagnosis in the remaining 23 being choroidal naevus (10), choroidal metastasis (1), circumscribed choroidal haemangioma (2) and others (10). Only one of six patients with suspected metastases had this condition, the remainder having melanoma (1), lymphoma (1), circumscribed choroidal haemangioma (1), and others (2). The 'choroidal tumours' and 'solid detachments' were found to be chorio-retinal disciform scar (1), varix of vortex vein (1), eccentric CNV (1), and subretinal haemorrhage (1) CONCLUSION: Approximately 30% of patients referred to an ocular oncology service with the diagnosis of choroidal melanoma have an incorrect diagnosis.

Adult↗
PubMed1996

Choroid plexus cysts: not associated with Down syndrome.

We sought to determine whether there is an association between choroid plexus cysts identified in the second-trimester fetus and trisomy 21. Over a 7-year period, fetuses scanned between 14 and 22 weeks were prospectively evaluated for the presence of choroid plexus cysts. Follow-up on fetuses with choroid plexus cysts was obtained by review of the medical records. Over the same time period, the scans and reports of all fetuses with trisomy 21 detected in our laboratory by mid-trimester amniocentesis were reviewed. The prevalence of choroid plexus cysts in fetuses with and without trisomy 21 were compared by means of X2 analysis. A total of 473 fetuses with choroid plexus cysts were identified among 32,053 second-trimester fetuses. Sixteen fetuses were lost to follow-up, three had structural defects and normal karyotypes and 21 had abnormal karyotypes, two of which were trisomy 21. Other abnormal karyotypes included trisomy 18, unbalanced translocation and triploidy, previously reported elsewhere. The remaining 433 fetuses either had normal karyotypes or were normal newborns. The prevalence of choroid plexus cysts (excluding fetuses with trisomy 18) was 1.38% in our general population. During the study period, 143 fetuses with trisomy 21 were karyotyped in our laboratory, and two of these (1.40%) had choroid plexus cysts. Both had other sonographic abnormalities suggesting trisomy 21. The difference in prevalence of fetuses with choroid plexus cysts and trisomy 21 vs. those without trisomy 21 was not statistically significant (X2 = 0.98; relative risk (RR) = 1.02; 95% CI = 0.26, 4.03). We conclude that choroid plexus cysts occur with similar frequency in fetuses with trisomy 21 to that in fetuses from the general population. The finding of choroid plexus cysts should not be used to increase the patient's calculated risk of having a fetus with trisomy 21.

Adult↗
PubMed2003

Transport of L-[125I]thyroxine by in situ perfused ovine choroid plexus: inhibition by lead exposure.

Lead (Pb) exposure hinders brain development in children by mechanisms that remain unknown. Previous evidence shows that sequestration of Pb in the choroid plexus lowers the production and secretion of transthyretin (TTR), a thyroxine (T4) transport protein, from the choroid plexus into the cerebrospinal fluid (CSF). This study was undertaken to characterize the uptake kinetics of T4 by the choroid plexus and to determine if in vivo Pb exposure altered the T4 uptake in an in situ perfused ovine choroid plexus model. Sheep received i.p. injections of Pb acetate (20 mg Pb/kg) or Na acetate (as the controls) every 48 h for a period of 16 d. The [125I]T4 uptake was determined by a paired-tracer perfusion method using 0.5 microCi [125I]T4 and 2 microCi [14C]mannitol at various concentrations of unlabeled T4 (trace to 20 microM). The flux of [125I]T4 into the choroid plexus followed Michaelis-Menten kinetics with the maximum flux (Vmax) of 56.6 nmol/min/g and half-saturation constant (Km) of 10.7 mumol/L, suggesting an evident saturable influx of T4 into the choroid epithelium. In vivo Pb exposure in these sheep resulted in a significant accumulation of Pb in the choroid plexus and hippocampus. Pb treatment diminished the Vmax by 63.7% of control, but did not alter Km. The maximal cellular uptake (Umax) and net uptake (Unet) in Pb-treated animals were 2.1-fold and 1.9-fold, respectively, lower than those of control. Exposure to Pb, however, did not significantly change the flow rate through the choroid plexus. Data suggest that the choroid plexus may serve as a significant site for T4 transport into the CSF, and Pb exposure may hinder the influx of T4 from the blood into the choroid plexus.

Animals↗
PubMed2004

The effect of the nonspecific nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester on the choroidal compensatory response to myopic defocus in chickens.

PURPOSE: Chick eyes show rapid compensation to retinal defocus. One component of this mechanism involves changes in the thickness of the choroid: when the retina is exposed to myopic defocus, the choroid thickens, pushing the retina forward; conversely, when the eye is exposed to hyperopic defocus, the choroid thins. The underlying mechanism(s) for these changes are unknown. We tested the hypothesis that nitric oxide might play a role. METHODS: We examined the effect of the nonspecific nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) on the compensatory choroidal thickening in response to myopic defocus using two visual paradigms: first, in previously form-deprived "recovering" eyes and, second, in eyes wearing +15 D spectacle lenses. L-NAME was injected intravitreally after removal of the diffuser or immediately before putting on the lenses. In addition, we looked at the effect of L-NAME on experimentally thickened choroids (induced by 1 week of recovery from deprivation myopia or 1 week of +15 D lens wear) and on choroids of normal eyes. Eyes were measured using A-scan ultrasonography before the injections and at subsequent intervals for several days. As a control for the injection procedure, eyes with the same visual conditions were injected with saline. Fellow eyes were untreated and uninjected. RESULTS: L-NAME inhibited choroidal thickening in both previously form-deprived eyes (2 vs. 117 microm; p < 0.001) and eyes wearing +15 D lenses (3 vs. 137 microm; p < 0.02). The effect was rapid, transient, and dose dependent (ED50, 0.26 micromoles). L-NAME produced thinning in experimentally thickened choroids (recovering: -116 microm; lenses: -219 microm) and in normal choroids (-47 microm) within 7 hours. CONCLUSIONS: Nitric oxide may play a role in modulating choroidal thickness. The mechanism is as yet unknown.

Adaptation, Physiological↗
PubMed1993

Choroidal invasion of retinoblastoma: metastatic potential and clinical risk factors.

There is considerable debate about the significance of choroidal invasion of retinoblastoma with regard to metastatic disease. The charts of patients with retinoblastoma were reviewed over a 17 year period to determine the frequency of histopathological choroidal invasion of retinoblastoma and its risk for eventual metastatic disease. Sixty seven of 289 eyes (23%) enucleated for retinoblastoma had histopathological evidence of choroidal invasion. Those patients with choroidal invasion (with or without optic nerve invasion) were more likely to develop metastases than those without choroidal invasion (p = 0.0001). When considering those patients with isolated choroidal invasion of retinoblastoma, excluding those with associated optic nerve invasion, there was no significant risk but there was a trend towards the development of metastases (p = 0.10). The clinical factors found to be predictive for choroidal invasion from retinoblastoma from a univariate analysis included increased intraocular pressure (p = 0.04) and iris neovascularisation (p = 0.007) and, from a multivariate analysis, iris neovascularisation (p = 0.02). The histopathological factors statistically associated with choroidal invasion included the presence of optic nerve invasion (p = 0.002) and poorly differentiated retinoblastoma (p = 0.003). Factors not predictive for choroidal invasion included the age, race, and sex of the patient and the tumour laterality, inheritance, size, and growth pattern. Choroidal invasion of retinoblastoma is a risk for metastases, especially if it is associated with any degree of optic nerve invasion.

Adolescent↗