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Biomedical subjects

H S Thompson

Publications and source records attributed to H S Thompson.

At least 55 records · Page 3Linked to original sources
PubMed1990

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.

Adult↗
PubMed1990

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.

Glaucoma, Open-Angle↗
PubMed1990

Could specific oral tolerance be a therapy for autoimmune disease?

Several experimental autoimmune diseases have been successfully suppressed by the induction of specific oral tolerance. Here, Stephen Thompson and Norman Staines review the nature and mechanisms of this form of tolerance and discuss its possible applications in the control of human autoimmune diseases.

Administration, Oral↗
PubMed1990

A unilateral cataract produces a relative afferent pupillary defect in the contralateral eye.

The relative afferent pupillary defect (RAPD) was measured with neutral density filters in ten patients, each of whom had a dense cataract in one eye only. In each instance, the cataract reduced visual acuity to counting fingers or worse, whereas visual acuity in the other eye was 20/25 or better. All patients with mature or nuclear cataracts had a measureable RAPD in the other eye (mean, 0.44 log unit). In each instance, after extraction of the cataract, the RAPD disappeared. Thus, a dense cataract causes an RAPD in the contralateral eye by increasing the pupillomotor effectiveness of the stimulus light and that this is the reason why even a brunescent cataract does not cause an RAPD in the same eye. In addition, two clinical cases are reported. One case records the development of a cataract in an eye with a preexisting RAPD resulting from optic neuritis; as the cataract became more opaque, the afferent defect became smaller and finally was reversed. The other case shows that a traumatic cataract can produce an RAPD in the contralateral eye. Thus, when an afferent pupillary defect is seen in an eye with a cataract, a visual pathway defect in that eye should definitely be suspected.

Adult↗
PubMed1990

Low affinity antibodies against collagen type II are associated with pathology in collagen-induced arthritis in mice.

The relationship between the functional affinity of antibodies against type II collagen (CII) and the development of arthritis was studied in mice with collagen-induced arthritis. The responses of DBA/1 strain mice were compared with those of mice selectively bred to produce antibodies of high functional affinity (HA mice) and low functional affinity (LA mice). HA and LA mice did not develop arthritis in response to immunization with CII whereas 86% of DBA/1 mice did, with 33% showing severe and 53% mild disease. Anti-CII antibodies of the highest titre, the lowest functional affinity, and the greatest affinity heterogeneity were associated with the development of the severest arthritis in DBA/1 mice: even in DBA/1 mice with moderate or no disease the amount of antibody and heterogeneity were higher and functional affinity lower than in either HA or LA mice. Antibodies of the G1, 2a, 2b and 3 subclasses were produced in all mice, and none of these alone accounted for the overall difference in IgG antibody titres or affinity in the groups of mice. Antibodies of the IgG2a subclass showed the closest association with the development of arthritis in the different groups. It is concluded that anti-CII antibodies of low functional affinity, and presumably also of the IgG2a subclass, influence the disease process in collagen arthritis.

Animals↗
PubMed1990

Seizure-induced miosis and ptosis: association with temporal lobe magnetic resonance imaging abnormalities.

Two patients with seizure-associated miosis and ptosis are described. In both there are magnetic resonance imaging abnormalities of the temporal lobe. In one patient, increased magnetic resonance imaging signal intensity is present in the temporal lobe contralateral to ptosis and miosis. In the other, there is temporal lobe asymmetry with the smaller temporal lobe ipsilateral to the miotic pupil and ptotic lid. The relevant human and experimental literature related to cortical control of pupil size and lid movement is reviewed. Based on the available literature and the findings in these two patients, it is proposed that the increased signal intensity in the temporal lobe of one patient represents an irritative stimulus causing contralateral miosis and ptosis, whereas the temporal lobe hypoplasia in the second patient permitted impulses from the contralateral normal temporal lobe to predominate, resulting in miosis and ptosis homolateral to the hypoplastic temporal lobe.

Adolescent↗
PubMed1989

Kestenbaum's number as an indicator of pupillomotor input asymmetry.

We compared the direct light response of both eyes in 90 patients who had anterior visual pathway disease using two different testing methods. We measured Kestenbaum's number in millimeters of pupillary diameter. Kestenbaum's number (K) is the difference in the pupil size attained in each eye under direct illumination while the other eye is occluded. We then measured the relative afferent pupillary defect (RAPD) in log units using neutral density filters. The two tests gave similar results (K = 0.88 x RAPD). Kestenbaum's number is the less precise measure, but it can be quickly and cheaply estimated even in dark brown eyes. The filter test requires a set of filters and at least one well-innervated iris sphincter. Kestenbaum's number can be measured without filters, but the iris sphincter and dilator muscles in both eyes must be normally innervated.

Filtration↗
PubMed1989

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.

Female↗
PubMed1989

Amaurosis fugax and ocular infarction in adolescents and young adults.

Because the cause and natural history of amaurosis fugax and ocular infarction are unknown in most younger patients, we reviewed the records of 83 patients who had become symptomatic before the age of 45. Cerebral transient ischemic attacks had occurred in 9 of these patients but no case of stroke was found. A striking feature of these patients was that 41% had headache or orbital pain accompanying their amaurotic spells and an additional 25.3% had severe headaches independent of the visual loss. Results of laboratory studies were rarely abnormal and echocardiography disclosed that only 1 patient had previously unknown heart disease. Mitral valve prolapse was detected in 6.5%, a figure similar to that expected for the general population. Of the original 83 patients, 42 were reexamined after a mean period of 5.8 years. None of the patients in this group had had a stroke, and the clinical status at follow-up was not found to correlate with the duration of the visual loss (amaurosis fugax versus ocular infarction), frequency (single versus recurrent episodes), sex, presence of headache or heart disease, cigarette smoking, use of oral contraceptives, or abnormal findings on echocardiograms or laboratory studies. We conclude that amaurosis fugax and ocular infarction occurring in the younger patient are probably associated with a more benign clinical course than that seen in older persons and that migraine is a likely cause for the episodes of visual loss in a majority of this group. Because of this, we believe that a conservative approach to the evaluation of such patients seems warranted.

Adolescent↗
PubMed1989

X-linked progressive cone dystrophy. Clinical characteristics of affected males and female carriers.

The authors evaluated nine affected males and six female carriers from a four-generation family with X-linked cone dystrophy. As the affected males grew older, visual acuity deteriorated, central scotomas deepened, and macular changes became more prominent. There was granularity of the macula in younger individuals and bull's eye lesions and central geographic atrophy of the retinal pigment epithelium (RPE) in the older subjects. The retinas of some affected males had a bronze-green tapetal-like sheen. Color vision was impaired in all affected males and resembled an acquired type II defect (Verriest classification). One younger subject had paradoxical pupillary constriction to darkness. Visual-evoked potential (VEP) latencies were prolonged in some affected males, suggesting that photoreceptor degeneration caused transsynaptic degeneration of ganglion cells. All female carriers had visual acuities of 20/30 or better, but some showed mild ophthalmoscopic changes and abnormalities of color vision, electroretinograms (ERGs), and VEPs.

Adolescent↗
PubMed1989

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.

Cranial Nerve Diseases↗
PubMed1988

Enlargement of the blind spot caused by papilledema.

Blind spot enlargement in papilledema has been attributed to either mechanical disruption of the integrity of the peripapillary percipient elements by the swollen optic disk or to the Stiles-Crawford effect. We investigated the possibility that blind spot enlargement in papilledema is caused, at least in part, by a refractive scotoma due to peripapillary hyperopia. We reduced the enlarged blind spot in a patient with focal peripapillary hyperopia, without papilledema, to near normal size by using progressively stronger plus lenses. Similarly, with the addition of plus sphere, we reduced the size of the blind spot in five of six patients with papilledema, but in none of our normal subjects.

Adult↗
PubMed1988

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.

Aged↗
PubMed1988

Tolerogenic activity of polymerized type II collagen in preventing collagen-induced arthritis in rats.

Rats were exposed parenterally or pergastrically to polymerized type II collagen (POLCII) and became resistant to the subsequent induction of disease with arthritogenic type II collagen (CII) administered intradermally in Freund's incomplete adjuvant (FIA). POLCII was prepared by cross-linking native soluble arthritogenic CII, from bovine nasal septal cartilage, with glutaraldehyde. POLCII injected intradermally in FIA did not induce arthritis. Animals treated in this manner were resistant for a period of at least 100 days to induced disease. The change in the properties of the CII from an arthritogen to a tolerogen was related to the amount of glutaraldehyde (used to polymerize the CII) which was assumed to control the extent of cross-linking of the CII. Highly cross-linked POLCII administered pergastrically, like soluble CII, was not arthritogenic but was tolerogenic, inducing a state of unresponsiveness to a challenge with arthritogenic CII. In general serum anti-CII antibody levels were higher in arthritic than in tolerized non-arthritic rats. It is concluded that the breaking of self-tolerance to CII depends upon its physical state. When polymerized and insoluble, a form analogous to that in which it exists naturally, it is tolerogenic.

Animals↗