Antioxidants: what role do they play in physical activity and health?

Exercise appears to increase reactive oxygen species, which can result in damage to cells. Exercise results in increased amounts of malondialdehyde in blood and pentane in breath; both serve as indirect indicators of lipid peroxidation. However, not all studies report increases; these equivocal results may be due to the large intersubject variability in response or the nonspecificity of the assays. Some studies have reported that supplementation with vitamins C and E, other antioxidants, or antioxidant mixtures can reduce symptoms or indicators of oxidative stress as a result of exercise. However, these supplements appear to have no beneficial effect on performance. Exercise training seems to reduce the oxidative stress of exercise, such that trained athletes show less evidence of lipid peroxidation for a given bout of exercise and an enhanced defense system in relation to untrained subjects. Whether the body's natural antioxidant defense system is sufficient to counteract the increase in reactive oxygen species with exercise or whether additional exogenous supplements are needed is not known, although trained athletes who received antioxidant supplements show evidence of reduced oxidative stress. Until research fully substantiates that the long-term use of antioxidants is safe and effective, the prudent recommendation for physically active individuals is to ingest a diet rich in antioxidants.

The rational management of idiopathic intracranial hypertension.

Idiopathic intracranial hypertension is a diagnosis most frequently made in young, overweight women. The chief hazard to the patient is permanent visual loss due to chronic papilledema. After the diagnosis has been clearly established using lumbar puncture and imaging techniques, the neurologist is involved in helping to lower the intracranial pressure, control the headaches, and encourage weight loss. Careful vision monitoring is essential and should be done in collaboration with an ophthalmologist. Visual fields, fundus photographs, intraocular pressure measurement, and visual acuity should be performed at each follow-up visit. The use of visual evoked response and repeated measurement of intracranial pressure by lumbar puncture do not provide data that help to guide therapeutic decisions. Indications for surgery are loss of visual field or decline in visual acuity in the fact of medical therapy, persistent headache, or the inability to perform visual-function studies. Optic nerve sheath fenestration and lumbar peritoneal shunt both appear to be effective surgical means to reduce the pressure on the optic disc. A neurologist and an ophthalmologist working together provide the evidence on which to base rational decisions in the care of the patient with idiopathic intracranial hypertension.

Visual loss in pseudotumor cerebri. Follow-up of 57 patients from five to 41 years and a profile of 14 patients with permanent severe visual loss.

The prognosis for vision in most patients with pseudotumor cerebri is excellent; however, visual loss, which is the only serious complication, may occur either early or late in the course of the disease. A group of 57 patients was followed up five to 41 years with visual fields, visual acuity, and fundus photographs. Blinding visual loss or severe visual impairment in one or both eyes occurred in 14 patients, and in seven patients, this occurred months to years after the initial symptoms. Systemic hypertension was a significant risk factor for visual loss in patients with pseudotumor cerebri, and blindness occurred in eight of 13 patients who were hypertensive. Despite suggestions that blind spot measurement is useful for following up patients with this condition, we believe that sequential quantitative perimetry gives more complete information and is essential to rational decision making in the treatment of pseudotumor cerebri.

Spatial contrast sensitivity in facial recognition.

Recognition and learning of complex images may depend on spatial processing characteristics of the visual system. Prosopagnosia, an impairment of visual learning and recognition of faces, might result from impaired perception in spatial channels carrying crucial information. We studied spatial contrast sensitivity (SCS) in two subjects with stable facial recognition defects. One had relative SCS reduction for high-frequency gratings but could process high frequencies in room light. The other had normal SCS. Both had intact spatial processing relative to image size. The results suggest that impairments in visual spatial channels are not necessary for the development of prosopagnosia.

Upbeat nystagmus changing to downbeat nystagmus with convergence.

A 35-year-old woman developed upbeating nystagmus while recovering from presumed Wernicke-Korsakoff syndrome. The upbeating nystagmus changed to downbeating nystagmus with convergence. The slow-phase velocity of the downbeating nystagmus varied with the convergence effort. We believe that this unusual nystagmus pattern implies convergence input to the supranuclear centers for vertical gaze.

Optic neuritis in the elderly: prognosis for visual recovery and long-term follow-up.

We evaluated 14 patients with idiopathic optic neuritis, 50 years of age or older, within 1 month of symptomatic onset from 1980 through 1985. We obtained follow-up information from case records an average of 13 months after initial examination and from telephone interviews an average of 57 months after initial evaluation. Four patients were men and ten were women. Visual loss was monocular in ten cases and binocular in four. Only one of 18 affected eyes initially had an acuity of 20/30 or better. Eleven eyes recovered acuities of 20/30 or better. There was no apparent benefit to those patients treated with corticosteroid agents. Six patients (43%) developed other neurologic sequelae an average of 16 months later; four (28%) had a second bout of optic neuritis and three (21%) developed clinically definite MS. Optic neuritis in the elderly behaves similarly to that disorder in younger age groups.

Downbeating nystagmus and other ocular motor defects caused by lithium toxicity.

We report the clinical and neuropathologic findings of a 63-year-old woman who died following an accidental lithium overdose that produced coma, respiratory depression, horizontal gaze palsy, and downbeating nystagmus. She also had mild hypomagnesemia. The pathology was cytotoxicity, predominantly in the regions of the nuclei prepositus hypoglossi and medial vestibular nucleus. Damage to this area with kainate and ibotenate in rhesus monkeys has produced horizontal gaze palsy and downbeating nystagmus. In addition, we report our clinical experience during the past 6 years with other examples of downbeating nystagmus in patients receiving lithium.

Suppression of collagen induced arthritis by oral administration of type II collagen: changes in immune and arthritic responses mediated by active peripheral suppression.

The oral administration of CII by gavage to WA/KIR rats before a conventional arthritogenic challenge with bovine CII in FIA reduced the incidence (by 23%) and delayed the onset of collagen-induced arthritis in about 50% of the animals. Selective changes in B cell and T cell responses to CII in animals treated this way are interpreted to indicate a state of tolerance or hyporesponsiveness to CII. Tolerant animals made less serum antibody, to bovine and rat CII, of the IgG2b isotype and more of the IgG1 isotype. Phenotypic and functional analysis of peripheral lymph node cells showed that those from tolerized animals expressed less MHC Class II, proliferated less and secreted less IgG2b anti-CII antibody in response to stimulation in vitro with CII when compared with cells from non-tolerant animals. However, this depression of the immune responses to CII seen in vitro was overcome when the cells were incubated with increasing amounts of CII. Tolerance could be transferred to normal animals. Spleen cells, and nylon wool-filtered splenic T cells (but not mesenteric lymph node cells) adoptively transferred hyporesponsiveness to normal recipients which were then less susceptible to collagen-induced arthritis. Transfer of serum from gavaged animals did not modify the susceptibility of normal recipients to arthritis. Spleen cells from gavaged animals suppressed proliferative and antibody responses in co-cultures in vitro with lymph node cells from animals immunized with CII in FIA. The suppressive spleen cell population contained more cells expressing MHC Class II, in both the CD8+ and CD4+ populations. These studies show that the oral administration of CII alters the subsequent immune response to the arthritogenic challenge and indicate that this oral tolerance of CII is due, not to clonal deletion or anergy, but rather to an antigen-driven active suppression mechanism that affects both T cells and B cells, most likely through the action of regulatory cytokines IL-4, IL-10 and TGF beta.

The iris sphincter in aberrant regeneration of the third nerve.

Fourteen patients with aberrant regeneration of the third cranial nerve were examined using self-developing photographs, motion pictures, and pupillography. These pupillary phenomena were noted: (1) sector contractions of the iris sphincter in response to light, (2) sector contractions of the iris sphincter associated with eye movements, and (3) an abnormal pupillary unrest. The observations strongly support the concept that after injury, fibers regenerate and sprout collateral branches that finally reach muscles of the oculomotor group other than those originally innervated.

Ciliary muscle dysfunction in Adie's syndrome.

Ciliary muscle function in patients with Adie's syndrome was studied retrospectively in 122 patients and prospectively in 17 patients. When a careful history was taken, two thirds of the patients had ciliary muscle-related symptoms. Most of the patients with Adie's syndrome had a moderate accomodative paresis, but there was a strong tendency for the ciliary muscle to recover with time. Many patients showed a tonicity of accommodation, especially those who had had the condition for several years. Astigmatism could be induced with accommodation in one third of patients. This may be related to segmental paralysis of the ciliary muscle. Seventy-three percent of the patients showed supersensitivity of the ciliary muscle in the involved eye, when both eyes were treated with a mixture of 0.25% pilocarpine hydrochloride and hydroxypropyl methylcellulose (Isopto Carpine). This may be a clinical aid in diagnosing Adie's syndrome. Two patients were found to have bilateral ciliary muscle dysfunction but only unilateral pupillary abnormalities. These two patients may have had a "pupil-sparing" Adie's syndrome.

Congenital Horner's syndrome.

Patients with congenital Horner's syndrome (who seemed, on the basis of their clinical history and the distribution fo anhidrosis, to have a preganglionic lesion) had partial mydriatic failure with hydroxyamphetamine hydrobromide and a supersensitivity to phenylephrine hydrochloride. This apparent paradox can be readily explained by postulating an aorthograde transsynaptic dysgenesis of the postganglionic neuron, such as has been demonstrated in the sympathetic nervous system of newborn animals. The failure of hydroxyamphetamine to cause mydriasis indicates damage to the postganglionic sympathetic neuron, but in the neonate this damage may be secondary to a preganglionic lesion.

Differentiation between recently resolved optic neuritis and central serous retinopathy. Use of tests of visual function.

A test battery was performed on 13 patients with resolved central serous retinopathy and on 13 patients with resolved optic neuritis to see whether the tests would help to distinguish between the two conditions. We found that the most useful discriminators were the relative afferent pupillary defect, followed by the visual evoked potential latency and the critical flicker frequency. The total error score on the Farnsworth-Munsell 100-Hue Test and the nature of the color vision defect were not helpful in separating the two diseases.

Visual evoked potential and pupillary signs. A comparison in optic nerve disease.

We measured the pupil cycle time, the relative afferent pupillary defect, and the pattern-reversal visual evoked potential (VEP) in 41 patients with unilateral anterior ischemic optic neuropathy (AION) and 24 patients with unilateral optic neuritis. We speculated that the relative afferent pupillary defect would match the VEP amplitude and that the pupil cycle time would correspond to the VEP latency. We found a correlation between the relative afferent pupillary defect and VEP amplitude in patients with AION, but not in patients with optic neuritis. We also found that the pupil cycle time and VEP latency were weakly correlated, but only in patients with optic neuritis. In these two groups of patients with unilateral optic neuropathy, the most sensitive objective indicator of disease was the relative afferent pupillary defect. The least sensitive indicator was the pupil cycle time.

Functional visual loss. Follow-up of 42 cases.

Forty-two patients with diagnosed functional visual loss were reexamined an average of four years after their initial visit. Twenty-three patients continued to have constricted or spiral visual fields at follow-up. Despite persistent evidence of functional visual defects, few patients were either socially or economically impaired by them. Patients who had other types of visual field loss or loss of visual acuity were more likely to have these signs resolve than were patients with constricted or spiral fields. Concurrent unrelated organic ocular disease was present in 11 patients. In 20 patients, it was not possible to identify psychiatric symptoms either related to the onset of functional eye signs or at follow-up. Treatment did not substantially alter the course.

Decreased visual acuity from optic disc drusen.

Although visual field defects occur commonly from optic disc drusen, reduction in visual acuity is rare. We describe four patients with reduced visual acuity and one with visual field constriction to the point of legal blindness that resulted from optic disc drusen. The acute episodic and stepwise nature of visual loss in some of the cases in our series suggests a vascular mechanism. Reduced visual acuity from drusen remains a diagnosis of exclusion. It should be considered, however, when visual loss has been acute and nonprogressive or stepwise in a nerve fiber bundle distribution and when visual acuity is not reduced until visual field constriction is severe.

Use of infrared videography to detect and record iris transillumination defects.

We have developed a technique of detecting and recording iris transillumination defects using an infrared sensitive video camera. This method is useful for assessing the loss of posterior iris pigment in patients with the pigmentary dispersion syndrome and pigmentary glaucoma. Some patients with no transillumination defects on slit-lamp examination were noted to have discrete defects on infrared videography. This technique is a rapid, convenient, and reproducible method of permanently recording posterior iris pigment changes. These high-quality video images can then be followed to determine the natural course and the results of therapy in these patients.

Critical evaluation of the cocaine test in the diagnosis of Horner's syndrome.

We evaluated the effectiveness of the cocaine test for diagnosing Horner's syndrome. The test was administered to 119 patients with a diagnosis of Horner's syndrome and to 50 normal subjects. We compared the cocaine-induced anisocoria in the two groups by measuring photographs of the pupils. We found the cocaine test to be highly effective in separating normal subjects from patients with Horner's syndrome. The chances of having Horner's syndrome increased with the amount of cocaine-induced anisocoria. Through the use of logistic regression analysis, we determined the odds ratio of having Horner's syndrome compared with not having it for each 0.1-mm increment of anisocoria measured after cocaine administration. A postcocaine anisocoria value of 0.8 mm gave a mean odds ratio of approximately 1050:1 that Horner's syndrome was present (lower 95% confidence limit = 37:1). We found that simply measuring the postcocaine anisocoria provided a better prediction of Horner's syndrome than taking the trouble to calculate the net change in anisocoria. Odds ratios should help the clinician decide if the result of a cocaine test is indicative of Horner's syndrome.

Visual function abnormalities in central serous retinopathy.

Eighteen patients with central serous retinopathy (CSR) underwent a battery of visual function tests when first seen and after resolution of the subretinal fluid. Eyes with CSR had minimal relative afferent pupillary defects, reduced critical flicker-fusion thresholds, prolonged visual evoked potential (VEP) latencies, increased errors on the Farnsworth-Munsell 100-hue (FM 100) test, and depressed central visual fields (Octopus). The afferent pupillary defect and critical flicker-fusion thresholds were the first to improve after resolution of the subretinal fluid. Next in rate of improvement were the visual acuity, the VEP latency, and the FM 100 test results. The threshold of the central Octopus at fixation improved the slowest and was still abnormal during long-term follow-up, indicating a prolonged depression in the threshold of central field sensitivity after resolution of the CSR. Many of these abnormalities are also seen in patients with optic nerve disease.

Raeder's syndrome. A clinical review.

The term "Raeder's syndrome," which now seems to mean any painful postganglionic Horner's syndrome, has been used in the past to describe patients with a wide variety of underlying pathology, including such serious lesions as middle cranial fossa neoplasms and such benign conditions as unilateral vascular headache syndromes. The purpose of this review which is based on the literature and some recent experience with 41 cases of Raeder's syndrome, is to help clarify this syndrome and to aid the clinician in its evaluation and treatment. Patients with Raeder's syndrome have been divided into three major groups. In the first group, the painful postganglionic Horner's syndrome is associated with multiple parasellar cranial nerve involvement and these patients require full neuroradiological investigation to uncover such lesions as local or metastatic tumors within the middle cranial fossa. The second and third groups do not have the multiple cranial nerve damage and their prognoses are benign. The characteristics, clinical investigation and medical therapy of each of these two benign groups are outlined and discussed. Extensive neuroradiological investigation is not recommended for patients in the second or third groups. Common to all three groups of Raeder's syndrome is the association of unilateral headache with the interruption of the postganglionic oculosympathetic fibers along the course of the internal carotid artery.

Oculomotor paresis with cyclic spasms. A critical review of the literature and a new case.

Oculomotor paresis with cyclic spasms is a rare syndrome, usually noticeable at birth or developing during the first year of life. On a background of oculomotor paresis, spastic movements occur at regular intervals: about every second minute the lid is raised, the globe wanders toward midline, the pupil contracts, and accomodation increases. These spasms last from 10 to 30 seconds, and then give way again to paresis. Since this phenomenon was first described, opinions were divided about its mechanism and about the site of the responsible defect. Based on a quantitative analysis of a new case, and of all previously published reports, a new theory is proposed which can account for all features of the syndrome.