Severe progression of glaucomatous optic neuropathy in patients with Alzheimer’s disease

Abstract

209stimulating hormone level of 21.7 mu/l (normal 0.5-5.0), but serum thyroxine was normal. Other routine bloods including full blood count, urea and electrolytes, serum glucose and liver function tests were also normal. Thyroid autoantibodies and TSH receptor assays were not performed. This subclinical hypothyroidism 1 supported our diagnosis of dysthyroid ocular myopathy. Treatment with oral thyroxine was commenced with a subsequent reduction in this patient's serum cholesterol. He remains visually asymptomatic with normal visual fields, unchanged disc appearances, and normal intraocular pressures in the primary gaze position. CommentThe English, medieval, Franciscan, philosopher William of Occam, proposed the principle of Pluralitas non est ponenda sine necessitate meaning that plurality should not be posited without necessity. Physicians understand this to mean that a patient's diverse symptoms and signs be explained by a single pathophysiology.Our asymptomatic patient's abnormal lipids and IOP were discovered by separate, ad hoc 'screening' procedures. Initially they were considered separate matters; ultimately a common causation became clearillustrating Occam's razor.Both elevated lipids 1 and intra-ocular pressure 2 are recognised features of hypothyroidism in Graves disease. Elevated intra-ocular pressure is due to the inelastic inferior rectus muscle compressing the globe as it fails to relax against the upward pull of its antagonist. 3 Failure to recognise underlying hypothyroidism was of practical importance for this patient, who suffered the adverse effects from oral lipid lowering agents, lipid levels only becoming controlled on treatment with Thyroxine. In addition topical Timolol treatment was been shown to cause lipid derangement in healthy volunteers. 4 We feel that hypothyroidism should be considered in patients who present with elevated lipids 1 and elevated IOP-especially when optic discs or visual fields are normal.Subclinical hypothyroidism may present with a spectrum of clinical ophthalmic signs, but the presence of raised IOP particularly on up gaze, lid lag on down gaze, and the presence of deranged thyroid profiles are sufficient evidence of dysthyroid ocular myopathy in our case. In our opinion the presence of raised intraocular pressure in these patients contraindicates the use of ocular hypotensives in the presence of normal disc appearances and visual fields.

Ocular Biomarkers for Early Detection of Alzheimer's Disease

“…A greater than 10%/year decay in visual field and optic disc cupping were demonstrated in glaucoma patients who were later diagnosed with AD, whereas an average 3%/year decay in visual field was observed in glaucoma patients who did not develop AD, indicating that AD accelerates the progression of glaucoma symptoms [126]. However, increased rates of visual field defects and/or optic disc cupping have also been reported in Parkinson's disease [125] and since these changes are observed in the common eye disease glaucoma, they are unlikely to provide a test that has specificity for AD.…”

“…This change in protein levels is similar to that observed in the CSF in AD. Given the retinal degeneration observed in AD [119][120][121][122][123] and the recently reported common features between AD and glaucoma [61,107,[121][122][123][124][125][126][127][128][129][130], the vitreous humor is an interesting focus for future research into ocular protein changes in AD.…”

How strong is the relationship between glaucoma, the retinal nerve fibre layer, and neurodegenerative diseases such as Alzheimer’s disease and multiple sclerosis?

“…However, given no AD patients had ocular hypertension (in comparison with 7.5% of controls) and had no family history of glaucoma, it may be visual field abnormalities were not due to glaucoma and reflect difficulties in performing psychophysical visual field tests in AD patients. A subsequent study by the same authors 54 showed an accelerated progression of visual field defects in patients with open-angle glaucoma and AD when compared with patients with open-angle glaucoma but without AD. However, given possible selection bias, a small sample size, non-blinded observers, and use of fundus photographs rather than more objective RNFL measures, these results need to be considered with caution.…”

Critical Review on the Relationship between Glaucoma and Alzheimer's Disease

“…In favor of this hypothesis, some studies have reported that amyloid-beta, a substance found in cerebral tissues of AD patients, is also implicated in RGC death [10]. Conversely, other studies have shown a relatively higher occurrence of POAG in AD patients [11][12][13][14][15][16][17][18]. …”