1/176. Post-traumatic pituitary apoplexy--two case reports.A 60-year-old female and a 66-year-old male presented with post-traumatic pituitary apoplexy associated with clinically asymptomatic pituitary macroadenoma manifesting as severe visual disturbance that had not developed immediately after the head injury. skull radiography showed a unilateral linear occipital fracture. magnetic resonance imaging revealed pituitary tumor with dumbbell-shaped suprasellar extension and fresh intratumoral hemorrhage. Transsphenoidal surgery was performed in the first patient, and the visual disturbance subsided. decompressive craniectomy was performed in the second patient to treat brain contusion and part of the tumor was removed to decompress the optic nerves. The mechanism of post-traumatic pituitary apoplexy may occur as follows. The intrasellar part of the tumor is fixed by the bony structure forming the sella, and the suprasellar part is free to move, so a rotational force acting on the occipital region on one side will create a shearing strain between the intra- and suprasellar part of the tumor, resulting in pituitary apoplexy. Recovery of visual function, no matter how severely impaired, can be expected if an emergency operation is performed to decompress the optic nerves. Transsphenoidal surgery is the most advantageous procedure, as even partial removal of the tumor may be adequate to decompress the optic nerves in the acute stage. Staged transsphenoidal surgery is indicated to achieve total removal later.- - - - - - - - - - ranking = 1keywords = brain (Clic here for more details about this article) |
2/176. Visual loss with Langerhans cell histiocytosis: multifocal central nervous system involvement.A 42-year-old woman with a 6-year history of diabetes insipidus and progressive hypersomnolence presented with visual loss. neuroimaging showed infiltration in the hypothalamus, the optic nerve, and the chiasm, as well as multiple lesions in other areas of the brain parenchyma. biopsy showed Langerhans cell histiocytosis. This is an unusual presentation of Langerhans cell histiocytosis, involving the visual pathways without manifestations outside of the central nervous system. The differential diagnosis and the magnetic resonance imaging findings will be discussed.- - - - - - - - - - ranking = 4.9839525198143keywords = brain, central nervous system, nervous system (Clic here for more details about this article) |
3/176. Creutzfeldt-Jakob disease presenting with visual blurring, diplopia and visual loss: Heidenhain's variant.Focal electroencephalographic abnormalities as described in Heidenhain's variant of Creutzfeldt-Jakob disease are uncommon. We report a 73-year-old male presenting with visual symptoms, right hemianopia and rapidly progressive dementia. myoclonus was synchronous with generalised periodic epileptiform discharges on electroencephalography (EEG). In addition, there were periodic focal sharp waves at the left occipital region. diffusion-weighted magnetic resonance brain images showed slightly increased signal intensity in the occipital parasagittal area, left more than right. 14-3-3 protein was detected in the cerebrospinal fluid. The patient died within 5 months of presentation.- - - - - - - - - - ranking = 1keywords = brain (Clic here for more details about this article) |
4/176. Spontaneous intracranial hypotension.PURPOSE: To describe a patient with classic presentation of spontaneous intracranial hypotension and subsequent improvement with targeted epidural blood patch. methods: Report of one case and review of the literature. RESULTS: Examination of cerebrospinal fluid after lumbar puncture disclosed a reduced opening pressure, an increased level of protein, and lymphocytic pleocytosis. magnetic resonance imaging of the brain with gadolinium showed diffuse enhancement of the pachymeninges, no evidence of leptomeningeal enhancement, and chronic subdural fluid collection. Radionuclide cisternography demonstrated reduced activity over the cerebral convexities, early accumulation of radiotracer in the urinary bladder, and direct evidence of leakage at the cervicothoracic junction (C7-T1). Clinical, laboratory, and radiologic features were consistent with the diagnosis of spontaneous intracranial hypotension. Therapy with a targeted epidural blood patch resulted in the rapid resolution of symptoms. CONCLUSIONS: In this report, we describe a classic case of spontaneous intracranial hypotension in a 63-year-old man with an initial presentation of postural headaches, blurred vision, pain in the left eye, diplopia on left gaze, and neck soreness.- - - - - - - - - - ranking = 1keywords = brain (Clic here for more details about this article) |
5/176. Acquired dural fistulae in benign intracranial hypertension: a short case report.Venous sinus thrombosis has been regarded as a known cause of intracranial hypertension. We report a case of long-standing raised intracranial hypertension (ICT) that presented with deteriorating vision in both eyes. Magnetic resonance (MR) imaging of the brain and cerebral angiography showed blockage of superior saggital sinus and sigmoid sinuses with bilateral dural arteriovenous fistulae (DAVF) formation.- - - - - - - - - - ranking = 1keywords = brain (Clic here for more details about this article) |
6/176. The "thin man" phenomenon: a sign of cortical plasticity following inferior homonymous paracentral scotomas.AIM: To investigate an image distortion, experienced by patients with homonymous paracentral scotomas. methods: Two consecutive patients with right inferior homonymous paracentral scotomas resulting from ischaemic brain insults were examined. Neuro-ophthalmological examination included tangent screen and Amsler grid evaluation. In addition, the patients were asked to describe a figure showing two vertical lines, identical in length and symmetrically located on either side of a fixation point. This figure was presented in such a way that when the subject looked at the fixation point the right line crossed the scotoma. Finally, the patients were asked whether, when looking at the face of an interlocutor, both sides of the body looked the same. RESULTS: In both patients field defects were markedly smaller when delineated with Amsler grids than using a tangent screen. With the parallel line test, the right line appeared uninterrupted in patient 1, whereas in patient 2 it looked slightly blurred in a two degree long segment corresponding to the middle of the scotoma. To both subjects the right line appeared shorter than the left line. Finally both subjects indicated that, after steadily fixating their interlocutor's face or neck for 5-10 seconds, the left shoulder appeared narrower than the right one, which made him look surprisingly thin. This perceptual alteration was called the "thin man" phenomenon. CONCLUSIONS: Paracentral homonymous scotomas can be associated with perceptual completion and shape distortion, owing to apparent displacement of images adjacent to the scotoma towards the field defect. Occurrence of such a perceptual change should alert one to the possibility of paracentral homonymous scotomas, which often go undetected when using routine visual field testing procedures.- - - - - - - - - - ranking = 1keywords = brain (Clic here for more details about this article) |
7/176. The clinical spectrum of schwannomas presenting with visual dysfunction: a clinicopathologic study of three cases.Schwannomas (neurilemomas) are benign tumors that arise from schwann cells in the peripheral nervous system. The most commonly involved nerves that cause neuro-ophthalmic manifestations are cranial nerves V and VIII. In this series of three women, schwannomas presented as intraconal masses that mimicked a cavernous hemangioma, a superior orbital mass transgressing the superior orbital fissure, and an expansive frontal lobe mass with clinical symptoms and signs of increased intracranial pressure. Although all three complained of visual blurring, none of our patients presented with Vth or VIIIth cranial nerve dysfunction. Histopathologic studies demonstrated well-circumscribed, encapsulated spindle-cell lesions with classic Antoni A and B patterns. Histopathologic examination is essential to confirm the diagnosis of a schwannoma that may be otherwise clinically confusing. Direct optic nerve compression, globe indentation with induced hyperopia, or increased intracranial pressure with optic nerve compromise may be responsible for visual symptoms. A multidisciplinary approach is often required because of the size and location of schwannomas.- - - - - - - - - - ranking = 0.23482619999724keywords = nervous system (Clic here for more details about this article) |
8/176. brain imaging in a patient with hemimicropsia.Hemimicropsia is an isolated misperception of the size of objects in one hemifield (objects appear smaller) which is, as a phenomenon of central origin, very infrequently reported in literature. We present a case of hemimicropsia as a selective deficit of size and distance perception in the left hemifield without hemianopsia caused by a cavernous angioma with hemorrhage in the right occipitotemporal area. The symptom occurred only intermittently and was considered the consequence of a local irritation by the hemorrhage. Imaging data including a volume-rendering MR data set of the patient's brain were transformed to the 3-D stereotactic grid system by Talairach and warped to a novel digital 3-D brain atlas. Imaging analysis included functional MRI (fMRI) to analyse the patient's visual cortex areas (mainly V5) in relation to the localization of the hemangioma to establish physiological landmarks with respect to visual stimulation. The lesion was localized in the peripheral visual association cortex, Brodmann area (BA) 19, adjacent to BA 37, both of which are part of the occipitotemporal visual pathway. Additional psychophysical measurements revealed an elevated threshold for perceiving coherent motion, which we relate to a partial loss of function in V5, a region adjacent to the cavernoma. In our study, we localized for the first time a cerebral lesion causing micropsia by digital mapping in Talairach space using a 3-D brain atlas and topologically related it to fMRI data for visual motion. The localization of the brain lesion affecting BA 19 and the occipitotemporal visual pathway is discussed with respect to experimental and case report findings about the neural basis of object size perception.- - - - - - - - - - ranking = 4keywords = brain (Clic here for more details about this article) |
9/176. Peduncular hallucinosis: an unusual sequel to surgical intervention in the suprasellar region.Peduncular hallucinations are formed visual images often associated with sleep disturbance, and are caused by lesions in the midbrain, pons and diencephalon. In the present study, we report two patients who developed peduncular hallucinations following surgery in the suprasellar region. In one of these, the peduncular hallucinations were a sequel to endoscopic third ventriculostomy, while in the other, they were due to diencephalon and mid-brain compression by a postoperative clot following excision of a hypothalamic astrocytoma.- - - - - - - - - - ranking = 2keywords = brain (Clic here for more details about this article) |
10/176. Childhood blindness and visual loss: an assessment at two institutions including a "new" cause.PURPOSE: This study was initiated to investigate the causes of childhood blindness and visual impairment in the united states. We also sought a particular etiology--congenital lymphocytic choriomeningitis virus (LCMV)--which has been considered exceedingly rare, in a fixed target population of children, the severely mentally retarded. methods: We undertook a library-based study of the world literature to shed light on the causes of childhood blindness internationally and to put our data in context. We prospectively examined all consented children (159) at 2 institutions in the united states to determine their ocular status and the etiology of any visual loss present. One of the institutions is a school for the visually impaired (hereafter referred to as Location V), in which most of the students have normal mentation. The other is a home for severely mentally retarded, nonambulatory children (hereafter referred to as Location M). This institution was selected specifically to provide a sample of visual loss associated with severe retardation because the handful of cases of LCMV in the literature have been associated with severe central nervous system insults. Histories were obtained from records on site, and all children received a complete cyclopleged ophthalmic examination at their institution performed by the author. patients at Location M with chorioretinal scars consistent with intrauterine infection (a possible sign of LCMV) had separate consents for blood drawing. Sera was obtained and sent for standard TORCHS titers, toxoplasmosis titers (Jack S. Remington, MD, Palo Alto, Calif), and ELISA testing for LCMV (Centers for Disease Control and Prevention, Atlanta, Ga). RESULTS: The diagnoses at Location V were varied and included retinopathy of prematurity (19.4%), optic atrophy (19.4%), retinitis pigmentosa (14.5%), optic nerve hypoplasia (12.9%), cataracts (8.1%), foveal hypoplasia (8.1%), persistent hyperplastic primary vitreous (4.8%), and microphthalmos (3.2%). The most common diagnosis at Location M was bilateral optic atrophy, which was found in 65% of the patients examined who had visual loss. Of these, the insults were most often congenital (42.6%), with birth trauma, prematurity, and genetics each responsible for about 15% of the optic atrophy. The second most common diagnosis was cortical visual impairment (24%), followed by chorioretinal scars (5%), which are strongly suggestive of intrauterine infection. Of 95 patients examined at Location M, 4 had chorioretinal scars. Two of these had dramatically elevated titers for LCMV, as did one of their mothers. One of the other 2 children died before serum could be drawn, and the fourth had negative titers for both TORCHS and LCMV. CONCLUSIONS: At both locations studied, visual loss was most often due to congenital insults, whether genetic or simply prenatal. The visual loss at Location V was twice as likely as that at Location M to be caused by a genetic disorder. The genetic disorders at Location V were more often isolated eye diseases, while those among the severely retarded at Location M were more generalized genetic disorders. Our study identified optic atrophy as a common diagnosis among the severely mentally retarded with vision loss, a finding that is supported by previous studies in other countries. In our population of severely retarded children, the target etiology of lymphocytic choriomeningitis virus was responsible for half the visual loss secondary to chorioretinitis from intrauterine infection. This is more common than would be predicted by the few cases previously described in the literature, and strongly suggests that LCMV may be a more common cause of visual loss than previously appreciated. We believe that serology for LCMV should be part of the workup for congenital chorioretinitis, especially if the TORCHS titers are negative, and that perhaps the mnemonic should be revised to "TORCHS L." Childhood blindness and visual impairment are tragic and co- - - - - - - - - - ranking = 0.79679050396286keywords = central nervous system, nervous system (Clic here for more details about this article) |
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