Cases reported "Blindness"

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21/127. Position, size and luminosity of phosphenes generated by direct optic nerve stimulation.

    Pulses of low intensity current, delivered through a cuff electrode chronically implanted around the optic nerve of a blind retinitis pigmentosa patient generate visual sensations. These phosphenes are obtained at lower thresholds for a train of stimuli than for single pulses, which suggests the existence of a spatial and temporal integrating mechanism. The perceptions are much smaller than those predicted from model simulations. A set of equations are derived which show the effect of pulse current, duration, number and frequency on the position, size and, to some extent, luminosity of the resulting phosphenes.
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22/127. Self-inflicted blindness and brown-sequard syndrome.

    A 30-year-old paranoid schizophrenic man suffered a psychotic episode while flying on an airplane, locked himself in the bathroom, detached the temples of his sunglasses, and stabbed them deeply into both medial orbits. He then secured one temple into the door hinge and rammed the back of his neck repeatedly against it. The injuries caused no light perception from optic nerve trauma and a Brown-Sequard hemitransection of the spinal cord.
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23/127. Posterior ischemic optic neuropathy after hemodialysis.

    PURPOSE: To report a case of visual loss from posterior ischemic optic neuropathy (PION) after hemodialysis. DESIGN: Observational case report. methods: Neuro-ophthalmic examination, neuro-imaging including computed tomography (CT) scan, magnetic resonance imaging (MRI) of the head and orbits, and magnetic resonance angiography (MRA) of the neck and cerebral vasculature, as well as electrophysiologic testing including electroretinogram (ERG) and visually evoked response (VER) were performed. RESULTS: Acute onset of painless bilateral no light perception vision with absent pupillary response to light and normal funduscopic examination occurred shortly after completion of hemodialysis. Computed tomography scan and MRA results were normal. magnetic resonance imaging scan showed small vessel ischemic white matter changes. Electroretinogram results were normal and the VER was unrecordable. CONCLUSIONS: Visual loss after hemodialysis is a rare complication and is associated with anemia and hypotensive events. The visual loss is usually a result of anterior ischemic optic neuropathy. We were unable to find another instance in the literature of visual loss after hemodialysis resulting from PION.
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24/127. Acute visual loss in a child with autosomal recessive polycystic kidney disease: case report and review of the literature.

    Acute visual loss secondary to ischemic optic neuropathy in children is extremely rare. The causes are usually hypotension or anemia. We describe the clinical course of a 9-year-old boy with a functional renal transplant who presented to the emergency room hemodynamically stable after waking up with complete bilateral loss of vision (no light perception). Examination showed that he had suffered massive nocturnal blood loss from esophageal varices secondary to portal hypertension. The patient's end-stage renal disease was secondary to autosomal recessive polycystic kidney disease (ARPKD), an entity comprised of renal cysts and hepatic fibrosis. Ophthalmologic findings in ARPKD are rarely cited in the literature. A literature search revealed 3 other cases of sudden visual loss reported in nonophthalmologic journals in patients with ARPKD. Funduscopic examination showed bilateral optic nerve head pallor and swelling with associated flame hemorrhages. The fact that this patient already had mildly pale nerves on presentation, along with hemodynamically compensated blood pressure and pulse, suggested chronic as well as acute ischemia. Based on our findings and other reported cases in the literature, ophthalmologic examinations may be indicated in all patients with ARPKD.
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25/127. visual perception in a blind subject with a chronic microelectronic retinal prosthesis.

    A retinal prosthesis was permanently implanted in the eye of a completely blind test subject. This report details the results from the first 10 weeks of testing with the implant subject. The implanted device included an extraocular case to hold electronics, an intraocular electrode array (platinum disks, 4 x 4 arrangement) designed to interface with the retina, and a cable to connect the electronics case to the electrode array. The subject was able to see perceptions of light (spots) on all 16 electrodes of the array. In addition, the subject was able to use a camera to detect the presence or absence of ambient light, to detect motion, and to recognize simple shapes.
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26/127. Sudden blindness in a child: presenting symptom of a sphenoid sinus mucocele.

    A 10-year-old girl with no nasal or respiratory symptoms developed a headache lasting a few hours. The next day she became totally blind in the right eye and over 5 days vision in the left eye deteriorated to bare light perception. The diagnosis of a sphenoid sinus mucocele was made radiologically and drainage via an endonasal sphenoidectomy produced 12 ml of brownish fluid. Endoscopic biopsy of the wall confirmed the diagnosis of a mucocele. Steroid treatment was given postoperatively, but vision recovered to 6/12 in the left eye only. The importance of urgent clinical diagnosis and treatment is stressed.
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27/127. Perception of optical flow in cortical blindness: a case report.

    motion perception was studied in a subject with bilateral lesion of the visual cortex, involving severe damage to cortical areas V1 and V4, but with no apparent damage to visual associative areas situated in occipito-parietal and lateral occipito-temporal (presumably V5) zones. He was able to perceive optical flow motions simulating motion in depth in "blind" parts of his visual field, provided that the stimulus-onset was temporally dissociated from its motion. Moreover, he was able to discriminate between different velocities and directions of motion. The results suggest that perimetrically "blind" parts of the visual field in this patient have true capacities to process visual motion. They are discussed in reference to the subject's ability to move freely in his environment and in reference to the role of extrastriate visual pathways in visual motion processing.
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28/127. Irreversible blindness due to multiple tuberculomas in the suprasellar cistern.

    A 14-year-old girl developed fever, severe headache, vomiting, and no light perception in both eyes over a 3-day period without a previous complaint of visual or other neurologic difficulties. Neuro-ophthalmologic examination was normal apart from meningismus and blindness. brain imaging showed ventriculomegaly and multiple enhancing nodules around the optic chiasm. Lumbar puncture showed an elevated opening pressure with lymphocytic pleocytosis. polymerase chain reaction and enzyme-linked immunoabsorbent antibody tests on the cerebrospinal fluid were positive for mycobacterium tuberculosis. There was no evidence of tuberculosis elsewhere in the body. Standard antituberculous treatment, including corticosteroids, did not reverse the blindness.
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29/127. Sudden blindness caused by anterior ischemic optic neuropathy in 5 children on continuous peritoneal dialysis.

    The authors report the occurrence of sudden blindness in 5 children (mean age, 32 months; range, 11 to 60) during continuous peritoneal dialysis regimen. All children presented with loss of light perception, visual fixation and ocular pursuit, and bilateral mydriasis unreactive to bright light. Fundoscopic examination found signs of anterior ischemic optic neuropathy with disc swelling, edema, and hemorrhages. Whereas 1 patient was dehydrated, the 4 other patients appeared well and not dehydrated. Nevertheless, blood pressure was below the normal range in all of them. Therefore, hypovolemia is highly suspected to have been the cause of ischemic optic neuropathy in all cases. Treatment consisted of steroids (4 patients), anticoagulation or antiagregation drugs (3 patients), plasma or macromolecules infusions (2 patients), vasodilatators (2 patients), and transient dialysis interruption (1 patient). One child with hepatic cirrhosis died 4 days later of acute liver insufficiency owing to ischemic hepatic necrosis. The other children had only partial improvement of vision during the following months. Because the prognosis of ischemic optic neuropathy is very poor, diagnosis and treatment of chronic hypovolemia in children on continuous peritoneal dialysis is essential to prevent such a devastating complication.
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30/127. Consequence of perforation during peribulbar anesthesia in an only eye.

    A patient with a blind fellow eye had cataract surgery in the right eye; anesthesia comprised an intraocular injection of lidocaine and bupivacaine. Forty-eight hours after surgery, visual acuity in the right eye was light perception (LP). Three days later, fundus examination showed inferotemporal hemorrhage, retinal whitening consistent with needle tracking, and a diffusely pale optic disc in the operated eye. Computed tomography showed an intact optic nerve in both eyes and high-density vitreal lesions in the right eye. Laser photocoagulation was applied to the retinal break. We believe that a jet stream of anesthetic agent may have transiently increased intraocular volume enough to occlude the central retinal artery. Although the retina remained attached, visual acuity failed to improve beyond LP.
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