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PubMed2001

[Tonic pupil and tendon areflexia: the Holmes-Adie's syndrome].

The Holmes-Adie syndrome (HAS) is characterised by initially monolateral, then bilateral enlargement of the pupil with delayed responses to near vision and subsequent redilation, and absent tendon reflexes. The diameter of the affected pupil is oval or irregular, sometimes with spontaneous movements of the pupillary sphincter muscle. Reaction to light may require several minutes' exposure to bright light, as it does redilation after a prolonged stay in a dark room. The reaction to near vision is tonic and delayed, as the subsequent redilation. In 10% of cases there is a permanent failure of the pupil to react either to light or to near vision. Absence of deep tendon reflexes is acquired and permanent, most frequently involving the Achilles' tendon reflex. Loss of different degrees of ciliary and spinal ganglia neurons, without evidence of inflammatory findings, are the neuropathological data accounting for the clinical signs of HAS. Polyneuropathies of different origin can be complicated by a symptomatic form of HAS.

Adie Syndrome↗
PubMed1977

Adie's syndrome: some new observations.

Adie's syndrome is a disease of unknown etiology. We known where the damage is, and which nerves are involved. We even know something of how the nerves react after the damage is done, but we don't known what causes the primary injury. The first step in working a jigsaw puzzle is to getall of the pieces right side up and take a good look at them. Some of the jigsaw pieces handled in this paper are listed below. Some of them are new observations; many of them are old concepts, partly modified and partly made secure by new facts. 1. Not all "tonic pupils" are due to "Adie's syndrome"; some are due to local injury and some to a generalized peripheral neuropathy (Table II). 2. All patients should have serologic tests for shyphilis. In this series one in six had positive serology. 3. The incidence of Adie's syndrome in Iowa in the early 1970's was approximately 4.7 per 100,000 population per year. 4. The prevalence of Adie's syndrome, therefore, was approximately 2 per 1000. 5. The mean age of onset of Adie's syndrome was about 32.2 years (Figure 1A). 6. The sex ratio was 2.6 females to each male. 7. Right eyes and left eyes were involved at approximately the same rate (Figure 2). 8. The incidence of second eye involvement in unilateral cases was about 4% per year during the first decade of the disease (Figure 18). 9. If this rate of second eye involvement (4% per year) persists during subsequent decades, then most Adie's pupils will eventually become bilateral. 10. The incidence of Adie's syndrome in a largely caucasian patient group is independent of iris color (Figure 4). 11. Only 10% of patients with Adie's syndrome had completely normal muscle stretch reflexes. 12. The muscle stretch reflexes in the arms were just as frequently imparied as those in th elegs, but the degree of impariment tended to be more severe in the ankles and triceps. 13. When there was any light reaction remaining in an Adie's pupil, a segmental paralysis of the sphincter muscle could be seen. 14. The near reaction of the pupil was often segmental and frequently involved segments which did not respond to light. 15. The segmental paralysis to light was randomly distributed around the sphincter (Figure 6B). 16. There was some tendency for the sphincter palsy to gradually become worse. This progression was also random (Figure 8). 17. Almost all patients with Adie's syndrome had an accommodative paresis at the time of onset. 18. Reading glasses given to a patient with a fresh Adie's pupil were soon discarded as accommodation recovered (Figure 9). 19. Accomodative effort induced an astigmatism in about half of the eyes with Adie's--presumably the result of a segmental palsy of the ciliary muscle. 20. Tonicity of accommodation was present in about 1/2 of the eyes with Adie's, making it difficut for the patient to maintain a steady level of ciliary muscle tone. 21. An occasional patient complained of brow ache from ciliary spasm with near work. 22. In most patients with Adie's syndrome the ciliary muscle was supersensitive to pilocarpine 0...

Accommodation, Ocular↗
PubMed2000

The Holmes-Adie plus syndrome.

A clinical syndrome of tonic pupil associated with tendon areflexia was first described by Holmes and Adie; autonomic neuropathy and peripheral neuropathy can be associated. The postulated mechanism of areflexia in Holmes-Adie syndrome is a synaptic disorder of the spinal reflex pathways. We report a case of a Holmes-Adie syndrome variant with hitherto unreported cranial neuropathy. A 41 year old woman developed insidious onset of sensory symptoms related to her left trigeminal and chorda tympani nerves over a few months. Physical examination showed generalised tendon areflexia and a left sided Adie's pupil. Imaging did not reveal any structural abnormality. Electrophysiological studies demonstrated an absent blink reflex on stimulating the left supraorbital and infraorbital nerves. These findings were suggestive of a dysfunction affecting the brain stem reflex arc. The pathophysiological process of Holmes-Adie syndrome may be more widespread than previously thought.

Adie Syndrome↗
PubMed1951

Adie's syndrome.

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Adie Syndrome↗
PubMed1980

Morphological basis of Adie's syndrome.

A female patient with Adie's syndrome died from unrelated disease at the age of 62. Both ciliary ganglia were seen to be severely depleted of nerve cells and still ongoing degeneration was seen in lumbar spinal ganglia, as well as in the posterior funiculi. This confirms earlier reports that primary pathological changes in Adie's syndrome are localized in the ciliary and spinal ganglia. Furthermore, it indicates that the underlying disease is still progressive after years.

Adie Syndrome↗
PubMed1987

Improved photographic assessment of the pupils in the syndromes of Horner and Holmes-Adie.

The use of photographic methods to assess pupillary abnormalities has usually been restricted to the measurement of anisocoria in light and darkness. An improved, accurate and relatively inexpensive photographic technique of recording pupillary movement was described, and tested in normal individuals and in the Horner and Holmes-Adie syndromes. A modern SLR camera, preprogrammable for exposure frequency and interval, was used for serial flash-lit photographs of the eyes during the course of darkness and near vision/accommodation reflexes. Measurement of pupillary diameter from these photographs permitted graphs of pupillary reflexes to be drawn that resemble traces obtained by other authors, who used less readily available and cumbersome cinematographic and electronic infra-red pupillometric methods. In Horner's syndrome, the affected pupil was invariably smaller, and the anisocoria was more marked in bright light or darkness, depending on the individual. The rate of dark mydriasis was abnormally slow, and most effectively quantified by measuring the pupillary 'half opening time', which was the interval required for the initial 50% of dark-induced pupillary dilatation. Constriction of tonic pupils during near vision/accommodation in subjects with the Holmes-Adie syndrome was consistently slow, and these pupils also failed to dilate fully in darkness. The amplitude of the darkness and near vision accommodation reflexes correlated significantly. The diverse pathophysiological mechanisms implicated by these changes were discussed.

Adie Syndrome↗
PubMed1978

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.

Accommodation, Ocular↗
PubMedDate not supplied

Adie's syndrome as a cause of amblyopia.

Adie's syndrome comprises a tonic pupil, which may be associated with impairment of accommodation, in the presence of diminished or absent deep tendon reflexes. We report a case of a 4-year-old boy with Adie's syndrome in which latent hypermetropia was made manifest by accommodative paresis and resulted in reversible amblyopia.

Accommodation, Ocular↗
PubMedDate not supplied

[On Adie's syndrome].

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Adie Syndrome↗
PubMed1959

Adie's syndrome.

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Adie Syndrome↗