Biomedical subjects
Publications and source records attributed to H S Thompson.
A 52-year-old woman complained of progressive loss of vision in the right eye. Although the visual acuity was normal, there was a relative afferent pupillary defect, and a mild decrease in color vision, mild optic disk pallor, and a nasal field defect along the central vertical meridian. The left eye was normal. Craniotomy disclosed a giant right-sided carotid-ophthalmic artery aneurysm.
We measured relative afferent pupillary defects in 105 patients with various stages of optic neuritis. We detected pupillary defects in 96% of acute unilateral cases, 92% of recovered unilateral cases 91.7% of acute cases with evidence of optic neuropathy in the other eye, and 65.8% of recovered bilateral cases. With careful testing, one can find relative afferent pupillary defects in nearly all patients with unilateral optic neuritis and in most patients with bilateral disease. A patient without a pupillary defect after apparent unilateral optic neuritis frequently has evidence of disease in the other eye when visual-evoked potentials are tested.
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.
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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.
A patient is described who suffered from intermittent spasms of the pupillary sphincter and ciliary muscle. Both intraocular muscles contracted several times a minute, producing sporadic darkening of vision in the affected eye. The spasms continued for eleven days, so it was possible to document them pupillographically. This curious phenomenon seems to have been the result of a transient "irritability" of the ciliary ganglion.
We measured pupil cycle time before and after treatment in 11 patients with compressive optic nerve disease. Nine patients had chiasmal tumors and two had optic neuropathy of Grave's disease. Pupil cycle time before treatment was abnormal in at least one eye of all patients and in each case, pupil cycle time improved or worsened in accordance with the response to treatment of the patient's visual acuity and visual fields. This suggests that the pupil cycle time may be used as a simple objective office test for following up patients with impaired optic nerve conduction as the result of optic nerve compression. This information is similar to that gained from visual evoked response and may be used together with other objective clinical data such as disk pallor, nerve fiber loss, and relative afferent pupillary defect.
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Two studies were carried out in volunteers without any abnormal ocular conditions to assess the effects and safety of an ophthalmic preparation of oxymetazoline (0.025%). In the first study in which oxymetazoline was compared with placebo and phenylephrine, the results of infra-red electronic pupillography showed that oxymetazoline in therapeutic doses had no effect on pupil size or near point recession. The second study, which was a double-blind forced choice comparison of two different formulations against placebo and 1% naphazoline, showed from assessments of the degree of ocular discomfort and hyperaemia that oxymetazoline was well tolerated and the subjects preferred oxymetazoline in a boric acid rather than in a phosphate solution.
Unequal pupils are common and can be difficult to sort out. A flow chart is presented to help in localizing the cause for anisocoria. Also, an inexpensive and simple camera is suggested for use in accurately measuring pupils.
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.
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.
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We saw four patients with optic tract lesions and complete homonymous hemianopia. In each patient, the visual acuity was good in both eyes. All four patients had a relative afferent pupillary defect in the eye with the temporal field loss. This pupillary sign is to be expected in all such cases and may serve to differentiate acute optic tract lesions from acute geniculostriate lesions when the characteristic midnasal pallor of the nerve head has not had time to develop.
A thin slit-lamp beam illuminating the pupil margin produced clearly visible pupil oscillations. These oscillations were timed with a stopwatch, thus producing a measurement of the "pupil cycle time". The pupil cycle time was remarkably stable in various testing situations and repeatable within +/- 3% over extended periods of time. When the iris muscles were normally innervated and responsive, the pupil cycle time was dependent on the speed of conduction and the number and strength of optic nerve impulses. Pupil cycle time can be measured in most persons with active or inactive optic neuritis. In the few patients whose light reflex is so poor that the pupil cycle time cannot be measured, the inability to induce cycling can itself be taken as a definite abnormality of the light reflex arc. Only 5% of normal persons 12 to 50 years of age are expected to have a pupil cycle time in either eye longer than 954 msec, or a difference in pupil cycle time between the two eyes longer than 70 msec. Pupil cycle time was significantly longer in patients with optic neuritis, with a P-value less than .001. The pupil cycle time is similar to visual evoked response latency time in that it can detect and quantitate subclinical defects in optic nerve conduction time. Pupil cycle time is objective and quantitative for each eye individually. It is a fast, simple, and reliable clinic test of optic nerve function.
In patients with unilateral Adie's syndrome, we compared the relative supersensitivity of the tonic pupil to methacholine hydrochloride (Mecholyl 2.5%) and pilocarpine 0.125%. We tested a large series of patients and photographed the pupils before and 30 minutes after the eyedrops. In a group of 36 patients, Mecholyl was positive in 64% of the tests; and in a group of 20 patients, pilocarpine 0.125% was positive in 80% of the tests. Eight patients who failed to show supersensitivity with Mecholyl were tested with pilocarpine and five of the eight were shown to be supersensitive. We concluded that pilocarpine, in this concentration is not only an adequate substitute for Mecholyl 2.5%, but is a more sensitive testing substance in unilateral cases, simply because it has a slightly stronger miotic action.
A thin slit-lamp beam illuminating the pupil margin produces clearly visible pupil oscillations. These oscillations can be timed with a stopwatch, thus producing a measurement of the "edge-light" pupil cycle time'. The pupil cycle time is remarkably stable in various testing situations and is repeatable within about +/- 3% over extended periods of time. Expected normal distribution and 95% confidence intervals are given in Table 3. When the iris muscles are normally innervated and responsive, the pupil cycle time is dependent on the speed of nerve conduction and the number and strength of optic nerve impulses. Only 5% of normal persons aged 12 to 50 years are expected to have a pupil cycle time in either eye longer than 954 ms or a difference in pupil cycle time between the two eyes longer than 70 ms.
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