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Biomedical subjects

J F Rizzo

Publications and source records attributed to J F Rizzo.

At least 37 records · Page 2Linked to original sources
PubMed1996

Neural network differentiation of optic neuritis and anterior ischaemic optic neuropathy.

AIMS: The efficacy of an artificial intelligence technique, neural network analysis, was examined in differentiating two optic neuropathies with overlapping clinical profiles-idiopathic optic neuritis (ON) and non-arteritic anterior ischaemic optic neuropathy (AION). METHODS: A neural network was trained with data from 116 patients with 'gold standard' diagnoses of ON or AION. It was then tested with data from 128 patients with presumed ON or AION, and the correlation of the network's diagnosis with that of expert clinicians tabulated. RESULTS: The network agreed with the clinicians on 97.8% (88 of 90) of the patients with presumed ON and 94.7% (36 of 38) of the patients with presumed AION. Youth, female sex, better initial acuity, a central scotoma, subsequent improvement in acuity, or progressive disease biased the network towards a diagnosis of ON, while advanced age, male sex, presence of hypertension, poor initial acuity, an altitudinal field defect, disc oedema, or less improvement in acuity biased the network towards a diagnosis of AION. CONCLUSION: Neural network analysis is a useful technique for classification of optic neuropathies, particularly where there is overlap of clinical findings.

Adult↗
PubMed1996

Recurrent chiasmal apoplexy due to cavernous malformation.

We report a case of chiasmal apoplexy due to a cavernous malformation (CM). Surgery was delayed because of the patient's advanced pregnancy, and nearly complete recovery of vision occurred spontaneously. Recurrent hemorrhage prompted surgical extirpation. The patient was left with a residual deficit. The literature pertaining to chiasmal apoplexy and CMs is reviewed. Nearly half of the reported cases of chiasmal CM had recurrent hemorrhages. The co-occurrence of hemorrhage from CM and pregnancy is too rare to merit any conclusions about cause and effect.

Adult↗
PubMed1995

Suppression of melatonin secretion in some blind patients by exposure to bright light.

BACKGROUND: Complete blindness generally results in the loss of synchronization of circadian rhythms to the 24-hour day and in recurrent insomnia. However, some blind patients maintain circadian entrainment. We undertook this study to determine whether some blind patients' eyes convey sufficient photic information to entrain the hypothalamic circadian pacemaker and suppress melatonin secretion, despite an apparently complete loss of visual function. METHODS: We evaluated the input of light to the circadian pacemaker by testing the ability of bright light to decrease plasma melatonin concentrations in 11 blind patients with no conscious perception of light and in 6 normal subjects. We also evaluated circadian entrainment over time in the blind patients. RESULTS: Plasma melatonin concentrations decreased during exposure to bright light in three sightless patients by an average (+/- SD) of 69 +/- 21 percent and in the normal subjects by an average of 66 +/- 15 percent. When two of these blind patients were tested with their eyes covered during exposure to light, plasma melatonin did not decrease. The three blind patients reported no difficulty sleeping and maintained apparent circadian entrainment to the 24-hour day. Plasma melatonin concentrations did not decrease during exposure to bright light in seven of the remaining blind patients; in the eighth, plasma melatonin was undetectable. These eight patients reported a history of insomnia, and in four the circadian temperature rhythm was not entrained to the 24-hour day. CONCLUSIONS: The visual subsystem that mediates light-induced suppression of melatonin secretion remains functionally intact in some sightless patients. The absence of photic input to the circadian system thus constitutes a distinct form of blindness, associated with periodic insomnia, that afflicts most but not all patients with no conscious perception of light.

Adolescent↗
PubMed1995

Visual loss after neurosurgical repair of paraclinoid aneurysms.

OBJECTIVE: To describe three cases of unexplained visual loss after technically successful clipping of paraclinoid aneurysms. DESIGN: Three case reports are presented. RESULTS: Profound blindness occurred in all three patients. Only one patient had marked visual recovery. Two clinical patterns were observed. A fulminant orbital syndrome presumably from compromise of large draining veins of the orbit was observed in one patient. A retrobulbar optic neuropathy that might have resulted from either direct injury or damage to small dural vessels of the posterior optic nerve was observed in the other two patients. CONCLUSIONS: There is a risk of postoperative blindness after clipping of paraclinoid aneurysms. The frequency of this complication may increase because attempts to repair these aneurysms are becoming more common. Patients with paraclinoid aneurysms should receive preoperative and postoperative neuro-ophthalmologic examinations.

Adult↗
PubMed1995

Quantitative analysis of optic disc cupping in compressive optic neuropathy.

PURPOSE: Cupping of the optic disc, a characteristic sign of glaucoma, has been anecdotally described in association with compressive optic neuropathy. The aim of this study is to perform a masked, controlled, and quantitative measurement of the optic disc cup to determine if compressive lesions of the afferent visual pathway were associated with increased cupping. METHODS: The ratio of cup area:disc area of 29 patients with intracranial lesions impinging on the optic nerves and the chiasm (14 with pituitary adenomas, 7 with meningiomas, 6 with craniopharyngiomas, and 2 with aneurysms) was compared with those of 20 age-matched control subjects. The areal ratios were derived planimetrically from hand-drawn images of magnified stereophotographs. Patients were divided into three groups based on the degree of laterality of visual compromise. Uninvolved eyes served as an internal control for patients with unilateral disease. RESULTS: The median ratio of cup area:disc area was 0.37 for all eyes with visual compromise (n = 51) and 0.10 for control eyes, which was statistically significant (P = 0.0001). The median intereye difference in the ratio of cup area:disc area was 0.13 for patients with unilateral lesions and 0.04 for control subjects. This difference also was statistically significant (P = 0.0001). CONCLUSIONS: The finding of intereye asymmetry in patients with unilateral optic nerve compression is convincing evidence that the enlarged cup is an acquired feature. Several types of compressive lesions of the anterior visual pathway can be associated with increased cupping of the optic disc in the absence of increased intraocular pressure.

Adolescent↗
PubMed1995

Adenosine triphosphate deficiency: a genre of optic neuropathy.

PURPOSE: To offer clinical evidence that deficiency of vitamin B12 may adversely affect the neuronal function of patients who also have the 14,484 mitochondrial DNA mutation associated with Leber's hereditary optic neuropathy (LHON). METHODS: A case of a 27-year-old man with vitamin B12 deficiency and the 14,484 mitochondrial DNA mutation is presented and the literature on causes of some metabolic optic neuropathies reviewed. RESULTS: Visual loss and neurologic symptoms of vitamin B12 deficiency occurred together, at a time when the level of vitamin B12 was subnormal. Vision and other sensory functions began to improve within 2 months of vitamin therapy, and normal vision eventually was restored. CONCLUSIONS: The relatively prompt improvement and the eventual complete recovery of vision following vitamin replacement therapy suggest that the subnormal level of vitamin B12 precipitated visual loss. Given the clinical similarities of subnormal vitamin B12, LHON, and nutritional/tobacco amblyopia, deficiency of adenosine triphosphate might be a unifying etiology for several types of optic neuropathy. This energy hypothesis provides a theoretical basis for the enigmatic phenomena of centrocecal scotomata and recovery of visual function after prolonged blindness.

Adenosine Triphosphate↗
PubMed1994

Choroidal infarction after optic nerve sheath fenestration.

PURPOSE: To describe a visual complication of optic nerve sheath fenestration. METHODS: Case review of two patients who underwent seemingly uncomplicated optic nerve sheath fenestration. FINDINGS: Both patients had a surgical complication that resulted in significant depression of their temporal visual field and development of a wedge-shaped region of subretinal pigmentation in the nasal fundus. CONCLUSIONS: Both patients had choroidal infarctions as a complication of optic nerve sheath fenestration. Choroidal infarction should be considered in cases of unexpected loss of visual field after this type of surgery, although the funduscopic signs that assist in making the diagnosis may not be evident for several weeks after surgery.

Adult↗
PubMed1994

Optic canal decompression in indirect optic nerve trauma.

BACKGROUND: The proper management of neurogenic visual loss after blunt head trauma is controversial. Non-treatment, corticosteroids, and surgical decompression of the optic canal are all currently considered to be reasonable alternatives. The goal of this study was to identify factors affecting improvement in patients treated with canal decompression. METHODS: A retrospective analysis of 31 cases in which transethmoidal decompression of the optic canal had been performed for neurogenic visual loss after closed head trauma was conducted. Each patient was alert and free of injury to the globe when evaluated before surgery. Surgery was performed within 6 days of injury, and all were given perioperative steroids. RESULTS: Visual acuity improved in 22 (71%) patients, with 6 (19%) regaining visual acuity of 20/40 or better. The mean improvement from preoperative visual deficit was 42.0% +/- 6.6%, with a median improvement of 45.2%. Both univariate and multivariate analysis suggested that vision improved more in patients who were younger than 40 years of age than in patients who were 40 years of age or older. Interval between injury and surgery, preoperative visual acuity, and the presence of optic canal fracture did not affect outcome. CONCLUSION: Any future randomized trials of therapy should stratify patients based on age. Enrollment of patients with no light perception or who experienced delay between injury and treatment may be reasonably considered.

Adolescent↗
PubMed1993

Tobacco amblyopia.

Tobacco amblyopia, once an important cause of bilateral optic neuropathy, has become so rare in the United States that some investigators doubt its existence. However, we treated two men who appeared to have this disorder. These two patients demonstrate that tobacco amblyopia can develop without malnutrition, alcoholism, or disordered vitamin B12 metabolism. Both patients recovered, one with cessation of smoking and the other with intramuscular administration of hydroxocobalamin despite continued smoking.

Adult↗
PubMed1993

Occult retinal and choroidal vascular disease. The value of timed and directed fluorescein angiography.

BACKGROUND: Acute vascular disease of the choroid or large vessels of the retina is usually accompanied by funduscopic signs. In instances of monocular visual loss, such objective signs are important diagnostic clues that the pathology is in the eye and not in the optic nerve. METHODS: Fluorescein angiography was timed in a consistent manner, and photographs were taken at two frames per second. Orientation of the camera was customized for each patient based on the location of the visual field defect. RESULTS: Eight patients with monocular visual loss were referred because the cause of the visual loss was not evident. In each patient, fluorescein angiography showed vascular disease of either the choroid or retina, despite normal-appearing fundi. CONCLUSIONS: Fluorescein angiography can detect otherwise occult vascular disease of the retina or choroid. In eyes with monocular scotomas, the angiogram should be performed with the camera oriented with respect to the location of the visual field defect. Accurately timed, rapid sequence photography provides additional information about rate and symmetry of flow. Focal areas of hypoperfusion often are incidental but deserve added consideration when they correspond to the location of a scotoma.

Adult↗
PubMed1993

Developmental variation in the structure of the retina.

Events traditionally called "developmental errors" are known to occur in both vertebrate and invertebrate nervous systems. This study was concerned with the frequency and mode of generation of such events in the mammalian retina. We studied three anomalous structures observed in the rabbit's retina after staining of the cell populations that accumulate indoleamines: type 3 cells, stray processes in the optic fiber layer, and displaced cells. They were counted in rabbit retinas prepared as whole-mounts, and in most cases topological maps were made. For comparison, the conventional indoleamine-accumulating amacrine cells and the tyrosine hydroxylase (TH)-positive cells, which are members of the mammalian retina's recognized complement of amacrine cells, were also counted. A further comparison was made with the number and distribution of TH-positive amacrine cells in highly inbred mice. The ordinary amacrine cells did not vary much in number from animal to animal. Especially in inbred mice, the reproducibility was striking: the extreme variation in number of TH amacrine cells between any two of the 14 retinas studied was 22%, and the mean difference between two eyes of individual mice was 2.5 +/- 1.7%. The three anomalous structures were rare and variable. Their numbers varied more than fourfold from animal to animal. However, their numbers in two eyes from the same animal varied by an overall average of only 14 +/- 10%. The anomalous structures were present in all rabbits, and their morphology was the same in all cases: they are under precise control by the developmental program. The anomalous cells share many phenotypic features with the regular amacrine cells of the indoleamine-accumulating class.(ABSTRACT TRUNCATED AT 250 WORDS)

Amines↗
PubMed1992

Retinocalcarine function in Alzheimer's disease. A clinical and electrophysiological study.

Impaired visual function in Alzheimer's disease (AD) could result from either precortical or cortical lesions, or both. In a parallel psychophysical study of visual function in AD, we found that contrast sensitivity function, color vision, stereoacuity, and backward masking were impaired relative to the performance of age-matched control subjects, whereas performance on a critical flicker fusion test was normal. The intent of the present study was to determine whether abnormalities of the retinocalcarine pathway contribute to visual dysfunction. We performed neuro-ophthalmological examinations on 38 patients with AD; from this group, 25 received additional psychophysical testing and 13 underwent electrophysiological testing. Clinical neuro-ophthalmological examinations, full-field electroretinograms, focal electroretinograms, and pattern visual evoked potentials were normal in all patients tested. There was no evidence of retinocalcarine abnormality specific to AD. We conclude that the visual impairment experienced by some patients with AD primarily results from involvement of the visual association cortices rather than from precortical damage, at least before the end stage of the disease.

Aged↗
PubMed1992

Selective immunohistochemical staining in the paraneoplastic retinopathy syndrome.

BACKGROUND: The mechanism leading to visual loss in paraneoplastic retinopathy is not known. An autoimmune process has been imputed based on immunologic investigations of several patients and by analogy to certain other paraneoplastic syndromes. METHODS: Two patients with documented small cell carcinoma of the lung who had clinical evidence of paraneoplastic retinopathy are described. Histopathologic examination of the retina from one patient and immunohistochemical staining of human retina with serum from control subjects and both patients were performed. RESULTS: Electroretinograms demonstrated dysfunction of photoreceptors in both patients, with predominant loss of rod function in one patient. Post mortem examination showed patchy loss of photoreceptors of the extramacular retina and relative sparing of cones, findings consistent with the clinical and electrophysiologic test results. Serum from both patients stained the retina in an identical manner, with restriction of the stain to the outer retina. Stain was present over the outer plexiform layer, the outer nuclear layer, and the inner and outer segments of most photoreceptors. A sharp demarcation was present between those areas that did and did not stain. All rod inner and outer segments appeared to stain, and many cone inner segments were not stained. Immunologic tests obtained elsewhere did not show serum antibody to the 23 kD protein. CONCLUSION: These findings support the concept of an autoimmune pathogenesis by showing selectivity of the immune response and correlation between the apparent target of the immune response and the clinical and pathologic findings. The mechanism by which cell loss occurs in the retina is not answered by this study. The absence of antibody to the 23 kD protein does not exclude the diagnosis of paraneoplastic retinopathy.

Aged↗
PubMed1991

Optic neuritis and ischemic optic neuropathy. Overlapping clinical profiles.

A retrospective analysis of the clinical features of 81 patients with acute idiopathic optic neuritis and 58 patients with nonarteritic anterior ischemic optic neuropathy revealed a surprising overlap of manifestations. The rate of visual decline and the range of visual acuities were the same for both. Central scotomas and improvement in acuity were more common in optic neuritis, but occurred often enough in nonarteritic anterior ischemic optic neuropathy to limit their value as single diagnostic criteria. The similarities observed in this study suggest that it may be difficult to differentiate between optic neuritis and nonarteritic anterior ischemic optic neuropathy solely on nosologic grounds in some instances of acute, unilateral optic neuropathy.

Adult↗
PubMed1991

Visual dysfunction in Alzheimer's disease: relation to normal aging.

In patients with Alzheimer's disease (AD), compared with age-matched and young healthy control subjects, visual deficits in the following functions were observed: color, stereoacuity, contrast sensitivity, and backward masking (homogeneous and pattern). Critical flicker fusion thresholds were normal, relative to age-matched healthy subjects. For color, the majority of the errors were tritanomalous (blue axis). Color and stereoacuity deficits were unrelated to severity of dementia, in accordance with models of vision that describe these functions as modular rather than diffuse for cortical localization. Although contrast sensitivity was depressed throughout the frequency range in AD, more patients were impaired at low than at high spatial frequencies, contrasting with the observed normal aging pattern of high-frequency loss. Healthy elderly subjects showed depressed critical flicker fusion thresholds and reduced contrast sensitivity at high frequencies, relative to the young group; differences between these groups were not found for the other vision tests. A subset of the AD group received detailed neuro-ophthalmological examination, and no abnormalities were found. This finding, taken together with normal thresholds for critical flicker fusion, suggests that the widespread visual dysfunction reported here is more likely to be related to known pathological changes in primary visual and association cortex in AD than to changes in the retina or optic nerve.

Adolescent↗