Why patients with Alzheimer’s disease may show increased sensitivity to tropicamide eye drops: role of locus coeruleus

Hou, Ruihua; Samuels, E. R.; Raisi, Marwan Al; Langley, R. W.; Szabadi, E.; Bradshaw, C. M.

doi:10.1007/s00213-005-0227-9

Cited by 16 publications

(15 citation statements)

References 63 publications

(85 reference statements)

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“…However, diazepam is likely to interact with GABA A receptors at multiple sites in the sleep/arousal network, causing sedation, and this effect may be conveyed to the autonomic nervous system. Modified from Szabadi and Bradshaw (1996) and Hou et al (2006a) There were four treatment combinations. Subjects were allocated to treatment combinations and sessions according to a balanced doubleblind design (see text).…”

Section: Designmentioning

confidence: 99%

Arousal and the pupil: why diazepam-induced sedation is not accompanied by miosis

et al. 2007

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Section: Designmentioning

confidence: 99%

Arousal and the pupil: why diazepam-induced sedation is not accompanied by miosis

et al. 2007

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“…The neurotransmitter acetylcholine is deficient in the AD brain [67,79], hence cholinergic dysfunction in iris nerve cells is a possible explanation for the hypersensitive response, although in this case one would expect to find agonist hypersensitivity with antagonist subsensitivity, or vice versa. Alternative explanations more consistent with the dual hypersensitivity include AD related damage to the locus coeruleus brain region which is involved in pupillary control [80] or increased corneal penetration of the cholinergic eyedrops. One study using a fluorescent marker to evaluate corneal penetration of tropicamide found no difference between AD and controls [81], but further studies are required to confirm this result.…”

Section: (Figure 2)mentioning

confidence: 99%

Ocular Biomarkers for Early Detection of Alzheimer's Disease

Frost

Martins

Kanagasingam

2010

JAD

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Alzheimer's disease (AD) is the most common form of dementia and is characterized clinically by a progressive decline in memory, learning and executive function and neuropathologically by the presence of cerebral amyloid deposits. Despite a century of research, there is still no cure or conclusive pre-mortem diagnosis for the disease. A number of symptom-modifying drugs for AD have been developed, but their efficacy is minimal and short-lived. AD cognitive symptoms arise only after significant, irreversible neural deterioration has occurred, hence there is an urgent need to detect AD early, before the onset of cognitive symptoms. An accurate, early diagnostic test for AD would enable current and future treatments to be more effective, as well as contribute to the development of new treatments.While most AD related pathology occurs in the brain, the disease has also been reported to affect the eye, which is more accessible for imaging than the brain. AD-related proteins exist in the normal human eye and may produce ocular pathology in AD. There is some homology between the retinal and cerebral vasculatures and the retina also contains nerve cells and fibers that form a sensory extension of the brain. The eye is the only place in the body where vasculature or neural tissue is available for non-invasive optical imaging. This article presents a review of current literature on ocular morphology in AD and discusses the potential for an ocular based screening test for AD.

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“…92,93 Increased pupillary sensitivity to tropicamide could be due to loss of noradrenergic neurons in the locus caeruleus observed in AD and a number of dementias. 94 Hypersensitivity pupillary responses have also been reported using dilute solutions of the sympathetic agonist phenylephrine and the cholinergic agonist pilocarpine. 95 Phenylephrine 0.5% induced a larger mydriasis in LBD subjects compared to AD and control participants, a result attributed to the dysfunction in sympathetic innervation to the iris.…”

Section: Pupillary Functionmentioning

confidence: 99%

“…Significant response to mydriatics in AD [89][90][91][92][93][94][95][96] Eye movements Most significant in PDD and DLB. Defects in fixation, decline in saccadic latency, undershooting of target in AD.…”

Section: Visual Dysfunction In Dementiamentioning

confidence: 99%

Oculo‐visual changes and clinical considerations affecting older patients with dementia

Armstrong

Kergoat

2015

Ophthalmic Physiologic Optic

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Purpose Dementia is associated with various alterations of the eye and visual function. Over 60% of cases are attributable to Alzheimer's disease, a significant proportion of the remainder to vascular dementia or dementia with Lewy bodies, while frontotemporal dementia, and Parkinson's disease dementia are less common. This review describes the oculo‐visual problems of these five dementias and the pathological changes which may explain these symptoms. It further discusses clinical considerations to help the clinician care for older patients affected by dementia. Recent findings Visual problems in dementia include loss of visual acuity, defects in colour vision and visual masking tests, changes in pupillary response to mydriatics, defects in fixation and smooth and saccadic eye movements, changes in contrast sensitivity function and visual evoked potentials, and disturbance of complex visual functions such as in reading ability, visuospatial function, and the naming and identification of objects. Pathological changes have also been reported affecting the crystalline lens, retina, optic nerve, and visual cortex. Clinically, issues such as cataract surgery, correcting the refractive error, quality of life, falls, visual impairment and eye care for dementia have been addressed. Summary Many visual changes occur across dementias, are controversial, often based on limited patient numbers, and no single feature can be regarded as diagnostic of any specific dementia. Nevertheless, visual hallucinations may be more characteristic of dementia with Lewy bodies and Parkinson's disease dementia than Alzheimer's disease or frontotemporal dementia. Differences in saccadic eye movement dysfunction may also help to distinguish Alzheimer's disease from frontotemporal dementia and Parkinson's disease dementia from dementia with Lewy bodies. Eye care professionals need to keep informed of the growing literature in vision/dementia, be attentive to signs and symptoms suggestive of cognitive impairment, and be able to adapt their practice and clinical interventions to best serve patients with dementia.

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Why patients with Alzheimer’s disease may show increased sensitivity to tropicamide eye drops: role of locus coeruleus

Abstract: The potentiation of tropicamide-evoked pupil dilatation by clonidine may be due to the abolition of the increase in parasympathetically mediated pupil constriction due to reduced LC activity.

Cited by 16 publications

References 63 publications

Arousal and the pupil: why diazepam-induced sedation is not accompanied by miosis

Arousal and the pupil: why diazepam-induced sedation is not accompanied by miosis

Ocular Biomarkers for Early Detection of Alzheimer's Disease

Oculo‐visual changes and clinical considerations affecting older patients with dementia

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