Síndrome de hipermetropía adquirida con pliegues coroideos / Acquired hypermetropia syndrome with choroidal folds

Desde el primer reporte de pliegues coroideos, en el año 1884, el conocimiento sobre su etiología, el mecanismo de producción y su manejo se ha incrementado notablemente. Las causas de los pliegues coroideos abarcan un extenso número de condiciones muy variadas; entre ellas se encuentran los idiopáticos, la hipertensión intracraneana, algunas drogas como el topiramato, las infiltraciones difusas de la coroides por linfomas e hiperplasia linfoide, la hipotonía por contracción de tejido fibrovascular, los tumores coroideos y orbitarios (intraconales y extraconales), entre otras. Se presenta una paciente femenina de 57 años de edad quien acudió por vez primera a la Consulta de Oftalmología en el año 2008 por disminución lenta y progresiva de la agudeza visual de ambos ojos. El examen de fondo de ojo mostró discos ópticos con bordes definidos, buena coloración y presencia de pliegues coroideos radiales al disco en polo posterior de ambos ojos. La refracción arrojó una hipermetropía que fue en aumento en las consultas de seguimiento hasta el presente sin variar el aspecto del fondo de ojo. Se concluye que el caso presenta síndrome de hipermetropía adquirida con pliegues coroideos(AU)

Since the first reported case of choroidal folds in 1884, the understanding of their mechanisms, aetiologies, and management has expanded signally. With ophthalmoscopy, choroidal folds can be appreciated by the light and dark bands observed deep to the retina. While choroidal folds are visible on ophthalmoscopic examination, they are more easily identified using fluorescein angiography. A-scan ultrasound may reveal a shortened axial length. Common B-scan ultrasonographic findings include thickening of the choroid or flattening of the posterior aspect of the globe. Causes of choroidal folds are many, among them are idiophatic, increased intracranial pressure, diffusely infiltrative conditions (lymphomas and benign lymphoid hiperplasia), hypotony, drug induced (an unusual complication of certain medications such as Topiramate), contraction of fibrovascular tissue, choroidal neoplasms and orbital mass lesions (intraconal and extraconal tumours). We report a 57 years old woman who came to ophthalmogy consultation first in 2008 complaning of slowly progressive loss of vision. Fundoscopy showed well defined optic disc with radial choroidal folds of the posterior pole in both eyes. Manifest refraction showed hyperopia that increased in the following visits until the present. Fundoscopy showed not changes. Definitive diagnosis was syndrome of acquired hyperopia with choroidal folds(AU)

Ischemic penumbra as a trigger for intracranial pressure rise - A potential cause for collateral failure and infarct progression?

We have recently shown that intracranial pressure (ICP) increases dramatically 24 h after minor intraluminal thread occlusion with reperfusion, independent of edema. Some of the largest ICP rises were observed in rats with the smallest final infarcts. A possible alternate mechanism for this ICP rise is an increase of cerebrospinal fluid (CSF) volume secondary to choroid plexus damage (a known complication of the intraluminal stroke model used). Alternatively, submaximal injury may be needed to induce ICP elevation. Therefore, we aimed to determine (a) if choroid plexus damage contributes to the ICP elevation, (b) if varying the patency of an important internal collateral supply to the middle cerebral artery (MCA), the anterior choroidal artery (AChA), produces different volumes of ischemic penumbra and (c) if presence of ischemic penumbra (submaximal injury) is associated with ICP elevation. We found (a) no association between choroid plexus damage and ICP elevation, (b) animals with a good internal collateral supply through the AChA during MCAo had significantly larger penumbra volumes and (c) ICP elevation at ≈24 h post-stroke only occurred in rats with submaximal injury, shown in two different stroke models. We conclude that active cellular processes within the ischemic penumbra may be required for edema-independent ICP elevation.

Infarction of the lateral posterior choroidal artery territory after manipulation of the choroid plexus at the atrium: causal association with subependymal artery injury.

OBJECT: The atrium of the lateral ventricle is often affected by tumors, and some patients with these tumors suffer neurological deficits, including hemiparesis after surgery. The authors of this study investigated the possible mechanisms causing the relatively high incidences of ischemic complications associated with surgery approaching the atrium of the lateral ventricle. METHODS: Clinical records and radiological images of 28 patients were retrospectively studied. These patients had their lateral ventricles opened at the atrium during the resection of gliomas as well as other nonbenign brain tumors, and were treated for gliomas at our tertiary referral center in the Tohoku district, Japan, between January 2008 and December 2010. RESULTS: Routine postoperative diffusion-weighted MR images obtained within 72 hours after surgery detected infarction in the periatrial/periventricular regions in 7 patients, presumably corresponding to the lateral posterior choroidal artery (LPChA) territory. Five of these 7 patients suffered neurological sequelae with varying severities. The choroid plexus at the atrium was coagulated to achieve hemostasis during the surgery in all of these patients. Detailed analysis of microangiograms revealed ventriculofugal arteries arising from the lateral ventricle. Damage of the subependymal artery that supplies the ventriculofugal arteries caused by coagulation of the choroid plexus at the atrium probably resulted in the infarction in these patients. CONCLUSIONS: Neurosurgeons must be aware of the possibility of LPChA territory infarction during surgery in the atrial or periatrial regions caused by subependymal artery obstruction after manipulating or coagulating the choroid plexus near the atrium.

The effects of impulse noise on the epithelial cells of the choroid plexus.

AIM: The aim of this study was to investigate the effects of impulse noise on the epithelial cells of the choroid plexus. MATERIAL AND METHODS: Forty Sprague Dawley rats were used and divided into the 2 groups as control and study groups. In the control group, the rats did not suffer noise injury. The rats were exposed to impulse noise at 20 minute durations at 10 times each day for one month in study group. Then, the rats were sacrificed and the choroid plexuses were examined histologically. The number of cells was counted and the cells were analyzed. RESULTS: There were clear signs of nuclear condensation and cell body shrinkage, suggesting the presence of apoptosis. Severe desquamation of villus and the cell loss were observed in the study group. The numbers of the normal cells decreased, and the number of apoptotic cells increased significantly (p < 0.05). CONCLUSION: Impulse noise causes apoptotic death of epithelial cells in the choroid plexus, decrease the normal cells and increase the apoptotic cells.

Quiste del plexo toroide: reporte de tres casos / Torus plexus cyst: report of three cases

Una gran variedad de lesiones con efecto de masa pueden crecer en el sistema ventricular, dentro de ellas los quistes del plexo coroide. Estas son lesiones congénitas que asientan frecuentemente en el trígono ventricular. Histológicamente se caracterizan por una capa externa fibrosa y otra interna con un epitelio cuboidal. Los pequeños quistes son asintomáticos mientras que los grandes causan síntomas secundarios a la dilatación u obstrucción ventricular, se diagnostican con el apoyo de la TAC, la RMN y el ultrasonido, en los niños con fontaneras abiertas. Las lesiones sintomáticas son tratadas quirúrgicamente por diferentes procederes. En nuestro trabajo se presentan tres casos clínicos, dos pediátricos con crecimiento progresivo del quiste, durante la observación clínico-radiológica y el tercero un adulto que debuta con un síndrome de hipertensión endocraneana, todos fueron tratados con abordaje quirúrgico directo y exéresis total de la lesión, con una evolución favorable.

Fatal cerebral injury from blows to the site of a nonadherent bone fragment from a previous craniotomy.

A young man with a prior left temporal craniotomy was brought to the emergency room after being beaten, including a blunt trauma to the head. After receiving a cranial X-ray, the patient was discharged home. He was found in a deep coma eight hours later. Autopsy revealed an approximately 4 x 5 cm bone fragment fixed to the left temporal bone, except at the inferior margin, where it had no osseous connection. There were a 44 g subdural hematoma in the left frontotemporal region, small hematomata within the left temporal lobe, and bilateral subarachnoid hemorrhage. Microscopically, we detected ruptured choroid plexus at the surface of the left temporal lobe. We speculated that the combination of the unfixed bone fragment and hyperplastic choroid plexus after craniotomy increased the decedent's vulnerability to external trauma at that site.

Manual occipital ventricular puncture for cerebrospinal fluid shunt surgery: can aiming be standardized?

The manual occipital ventricular puncture is a standard surgical procedure, but specific targeting has not received sufficient attention despite the experience of anatomical disorientation. This study tried to identify an exact site for the ideal trajectory with this method, especially in the sagittal plane, which avoids contact with the choroid plexus that may be the major source of complications. A total of 44 consecutive adult cases undergoing cerebrospinal fluid shunting through the occipital route for hydrocephalus were retrospectively reviewed for the following: correlations between burr hole site, direction of puncture, and location of the ventricular catheter based on postsurgical radiological studies; calculation of the ideal trajectory to place the catheter tip in the anterior horn of the lateral ventricle without contact with the choroid plexus through the standard occipital burr hole. In addition, the relationships between the location of the ventricular structure, the cranial base line connecting the nasion and inion, and the size of the ventricle were evaluated. Incorrect catheter emplacement was found in five cases, which suggested that this procedure using the standard burr hole site and aim point might result in incorrect catheter placement. The ideal external aim points were widely distributed because of the variable heights of ventricular structures from the cranial baseline. No correlation between the locations of the anatomical points and ventricular size was found. The present study could not define a standard external aim point. Tailored preoperative planning of the trajectory is recommended.

Lesões expansivas do plexo coróide: [revisão] / Choroid plexus mass lesions: [review]

As lesões expansivas do plexo coróide constituem um grupo bastante amplo e heterogêneo de doenças e seus simuladores. Tumores, infecções, anomalias congênitas, hemorragias, cistos e fenômenos degenerativos são alguns dos exemplos de causas de lesões expansivas do plexo coróide. No presente trabalho fizemos revisão da literatura pertinente, descrevendo os achados de imagem e ilustrando-os com alguns casos do nosso serviço. Apesar de não existir na literatura descrição de sinais patognomônicos, a avaliação criteriosa e sistemática das características das lesões pode sugerir determinada etiologia.

Choroid plexus mass lesions encompass a broad and heterogeneous group of diseases and their simulators. Tumors, infections, congenital anomalies, hemorrhage, cysts and degenerative diseases are some examples of mass lesions affecting the choroid plexus. In this article we review the current literature, describing the imaging findings and illustrating choroid plexus mass lesions with some cases diagnosed at our facility. Despite the inexistence of pathognomonic signs, a careful and systematic evaluation of the imaging characteristics may suggest many etiologies.

Intraventricular contrast medium leakage during ethanol embolization of an arteriovenous malformation.

We report the unusual phenomenon of abrupt intraventricular contrast medium leakage from the choroid plexus occurring during ethanol embolization of a periventricular arteriovenous malformation. There was no evidence of any associated intraventricular hemorrhage to suggest that leakage arose from a vessel perforation, as was first suspected. Intraventricular contrast medium leakage has been reported previously in the setting of ependymitis, and it is likely that similar pathogenetic mechanisms apply in this case. To our knowledge, this is the first reported case of intraventricular contrast medium leakage occurring during an embolization procedure.

Could antioxidant therapy reduce the incidence of deafness following bacterial meningitis?

Sensorineural hearing loss following acute bacterial meningitis could be caused by hydroxyl radicals generated by the inflammatory response. Obstruction of cerebrospinal fluid circulation through the tela choroidae of the choroid plexuses, with subsequent rupture of the tela choroidae, would expose the auditory nerve to selective radical damage. Acute administration of lipophilic antioxidants might provide the auditory nerve with increased protection.

Studies of the choroid plexus and its associated epiplexus cells in the lateral ventricles of rats following an exposure to a single non-penetrative blast.

The choroid plexus in rats exhibited ultrastructural changes following a non-penetrative blast. The immunophenotypic features of epiplexus cells associated with the choroid plexus epithelium were also altered. In rats killed at 1 and 7 days after the blast, the intercellular spaces between the epithelial cells were greatly widened, coupled with the massive eruption and possible extrusion of the apical cytoplasm into the ventricular lumen. Associated with these changes was the passage of some monocytes/lymphocytes across the epithelium. The incidence of such a migratory phenomenon was more frequent in rats killed 7 days after the blast. In rats killed 14 days after the blast, the ultrastructural changes of the epithelial cells became less pronounced. At 21 and 28 days after the blast, the ultrastructure of the choroid plexus was comparable to that of normal specimens. The immunoreactivity of epiplexus cells in terms of their cell number and staining intensity with the monoclonal antibodies OX-42, OX-18, OX-6 and ED1 was noticeably augmented at 7 and 14 days after the blast; this, however subsided at 21 and 28 days. It is concluded that the choroid plexus is extremely sensitive to a blast wave as manifested by its structural alterations and the vigorous expression of CR3 receptors and MHC antigens by the epiplexus cells. It is suggested that a possible immune response might have been triggered in the cerebrospinal fluid ventricular system following the blast.

Cytologic manifestations of ballistic injury.

The adherent residue from 60 projectiles in 38 consecutive gunshot wound deaths was analyzed by cytologic technique to determine whether a bullet, while passing through the body or intermediate target, retains tissue and other trace evidence. The projectiles, which were recovered from both the body and shooting area, contained microscopically recognizable cellular and inert material in all cases. Direct ballistic trauma could be documented in several tissue types, most notably in muscular tissue. Progressive damage to skeletal and cardiac muscle was seen in multiple preparations. This ranged from partial separation of the fascicles to cytoplasmic homogenization and nuclear rupture. Except in cases of severe ballistic trauma, skeletal and cardiac muscle could be distinguished on the preparations. In addition to neural tissue, projectiles traversing the central nervous system (CNS) contained elongated fragments of intact microvascular structures, sheets of cerebral covering cells, and connective tissue from the scalp. The vascular structures present in CNS preparations may clarify some of the clinical findings in victims of gunshot wounds and elucidate possible pathophysiologic mechanisms in craniocerebral projectile injuries.

Avulsion of choroid plexus during revision of ventricular shunting: its high incidence and predictive value on computed tomography scan.

Over a 2-year period, 5 of 10 patients with revision of ventricular shunting were complicated by intraventricular and/or intracerebral hemorrhage due to avulsion of the choroid plexus. Retrospective analysis of computed tomography scans prior to the revision disclosed the presence of an intraventricular or periventricular mass adjoining the ventricular catheter in four of the five patients. Histologic findings of the soft tissue at the tip of the removed catheter were compatible with the choroid plexus accompanied by granulation tissue. The risk factors useful for detecting the possible occurrence of this complication are discussed.

Traumatic tears of the tela chorioidea: a hitherto unrecognized cause of post-traumatic hydrocephalus.

A new and hitherto unrecognized phenomenon of rupture of the tela chorioidea in closed head injury of acceleration-deceleration type is described. It occurs very frequently, especially in association with blows in the centro-axial plane even if the acceleration forces are relatively mild. These tears are regularly followed by intraventricular bleeding which follows the flow of the CSF into the subarachnoid space producing a leptomeningeal reaction with impairment of absorption of CSF and consequent communicating hydrocephalus.