Biomedical subjects

J F Rizzo

Publications and source records attributed to J F Rizzo.

46 records · Page 3Linked to original sources

PubMed1991

Visual function in Alzheimer's disease and normal aging.

We examined a wide range of visual behaviors in 59 patients with Alzheimer's disease (AD), 35 elderly control subjects, and 12 young control subjects. A subset of the patients with AD received neuro-ophthalmologic and electrophysiologic examinations in order to evaluate the integrity of the retino-calcarine pathway. Patients with AD showed significant, selective losses in visual function, including color discrimination, stereoacuity, contrast sensitivity, and backward masking, but not in critical flicker fusion. The deficits were not attributable to clinically apparent lesions of the retina or optic nerve. We therefore suggest that AD lesions in primary visual and posterior association cortices underlie the observed behavioral abnormalities.

Adolescent↗

PubMed1991

Optic nerve head blood speed as a function of age in normal human subjects.

We used the laser Doppler technique to determine the relation between age and the speed of blood cells moving through the capillaries of the optic nerve head. We studied 22 normal human volunteers ranging in age from 16-76 years. The results were best described by a statistically significant quadratic relationship between capillary blood speed and age. Blood speeds were lowest in the youngest and oldest subjects and highest in subjects between 27 and 35 years old. A two-phase linear model showed a statistically significant 20% decrease in blood speed in volunteers between the ages of 31 and 76. The results were not affected by gender, degree of refractive error, systemic blood pressure, intraocular pressure, cup/disc ratio of the optic nerve head, or by site-to-site differences in the light scattering properties of the optic nerve head tissue. Capillary blood speed was, on average, 15% greater from temporal sites than from nasal sites, corresponding to the equally greater distribution of ganglion cell axons within the same area. The results provide a baseline of normal age-controlled data that can be compared to measurements obtained from patients with disorders of the optic nerve head thought to have a vascular etiology.

Adolescent↗

PubMed1990

The dural shunt syndrome. I. Management of glaucoma.

The authors present four cases of the dural shunt syndrome in which shallowing of the anterior chamber or rubeosis developed. All patients were female, ranging in age from 66 to 79 years, exhibiting elevated intraocular pressure (IOP), decreased extraocular movements, injected tortuous episcleral vessels, and proptosis. The authors managed these four cases with laser iridotomy, gonioplasty, panretinal photocoagulation, or medical treatment. It is important to recognize associated findings in patients with shallow anterior chambers and elevated IOPs so that a diagnosis of a dural shunt is considered and appropriately treated. Theories on the mechanisms of increased IOP in the dural shunt syndrome and the management of various types of glaucoma in four different cases are reviewed.

Aged↗

PubMed1988

Risk of developing multiple sclerosis after uncomplicated optic neuritis: a long-term prospective study.

We prospectively studied 60 white patients living in New England who presented with uncomplicated optic neuritis (ON) to determine the risk of developing multiple sclerosis (MS). The diagnoses of ON and MS were made solely on the basis of clinical criteria. Patients were followed for a mean of 14.9 years. Life table analysis indicated that 74% of the women and 34% of the men will have developed MS 15 years after their attack of ON. The risk of developing MS was 3.4 times greater for women than for men. Onset of ON between the ages of 21 and 40 years may have had a modest effect in increasing the risk of developing MS. Recurrence of ON did not appear to affect the risk.

Adult↗

PubMed1987

Transient visual loss in ornithine transcarbamoylase deficiency.

We examined a 32-year-old, previously healthy man who developed episodic bilateral visual impairment and confusion. Coincident hyperammonemia led to the diagnosis of ornithine transcarbamoylase deficiency, which was established by enzymatic analysis of a liver biopsy specimen. The available data were insufficient to determine if the metabolic derangement impaired vision at the level of the optic nerves or at the cerebral level.

Adult↗

PubMed1987

Posterior ischemic optic neuropathy during general surgery.

We examined two patients who awoke with profound bilateral visual loss after operations under general anesthesia. Their fundi, initially normal, later showed bilateral optic atrophy. Neither patient showed other neurologic deficits, although one demonstrated radiologic evidence of a small cerebral infarction in the deep white matter. These patients probably suffered intraoperative infarction of the retrobulbar segments of both optic nerves, producing posterior ischemic optic neuropathy. Profound systemic hypotension may have been a contributing factor in one patient, the use of the pump-oxygenator in the other, and anemia in both.

Coronary Artery Bypass↗

PubMed1986

Ocular neuromyotonia after radiation therapy.

Ocular neuromyotonia is a paroxysmal monocular deviation that results from spasm of eye muscles secondary to spontaneous discharges from third, fourth, or sixth nerve axons. We observed this rare disorder in four patients who had been treated with radiation for tumors in the region of the sella turcica and cavernous sinus. Based on these cases and four others identified in the literature it would appear that radiation predisposes to a cranial neuropathy in which ocular neuromyotonia may be the major manifestation. Radiation appears to be the most common cause of ocular neuromyotonia.

Adolescent↗

PubMed1986

Optic atrophy in familial dysautonomia.

We examined three patients with classic findings of familial dysautonomia (Riley-Day syndrome) whose visual impairment was associated with optic atrophy. The presence of an optic atrophy in familial dysautonomia is indicative of central nervous system involvement, at least in these cases. Each of these patients was first noted to have visual impairment after the first decade. The late onset of optic atrophy may partly explain its apparent rarity. Since the life span of patients with familial dysautonomia is increasing, optic atrophy may be more commonly recognized in the future.

Adult↗

PubMed1986

Retinal and neurologic findings in the Laurence-Moon-Bardet-Biedl phenotype.

The nosology of the Laurence-Moon and Bardet-Biedl syndromes has been controversial. Presented is a patient with polydactyly, retinopathy, ataxia, low-average intellectual function, and obesity. These features constitute a composite of both syndromes and reflect the clinical heterogeneity that may be seen. Accordingly, the authors suggest the use of the term "Laurence-Moon-Bardet-Biedl phenotype" until these syndromes can be defined in some other manner. The neuroradiologic studies document atrophy of the cerebellum that accounts for the ataxia. Electroretinograms (ERG) demonstrate the decline in retinal function over a 16-year interval and the delayed cone ERG b-wave implicit time with normal cone amplitudes to 30 Hz white flicker that can exist in the early stage of this disorder.

Adult↗

PubMedDate not supplied

Broad-band visual capacities are not selectively impaired in Alzheimer's disease.

Histological examination of the optic nerves of Alzheimer's disease (AD) patients has revealed a selective degeneration of large axon ganglion cells. This morphological abnormality raises the possibility of a selective impairment of broad-band channel visual function. To test this hypothesis, we administered visual psychophysical tests associated with either the color-opponent or the broad-band retinocortical channel to 14 AD patients and 29 elderly control subjects (ECS). In previous studies in monkeys, these tests had been sensitive to the effects of either parvocellular or magnocellular LGN lesions. In the present study, the color-opponent channel was assessed by tests of texture and color discrimination; the broad-band channel was assessed by tests of flicker and motion detection. Logistic regression analysis indicated that all tests collectively discriminated diagnostic groups at a borderline level of significance (p = 0.09). ANOVA also indicated a trend towards overall depressed function for AD patients on some capacities tested. Analyses comparing the prevalence of deficits in the AD and ECS groups showed that a significantly greater number of AD patients than ECS had deficits on texture discrimination, blue-violet discrimination, and 4.72 degrees/s motion detection. No individual subject demonstrated a selective impairment of broad-band channel function. The visual deficits in AD did not resemble those caused by lesions of magnocellular LGN in monkeys, indicating that the visual impairment in AD is not a functional reflection of damage limited to the broad-band channel.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗