ABSTRACT
An 81-year-old woman presented with blurred vision in the left eye. Best corrected visual acuity was 20/100. Ophthalmologic examination in the left eye revealed tilted disc syndrome with exudative change at the margin of inferior staphyloma. The exudative change persisted despite monthly intravitreal ranibizumab injections for 5 months. Subsequently, two intravitreal aflibercept injections 1 month apart were substituted for the ranibizumab injections, resulting in successful resolution of the exudative change.
Subject(s)
Angiogenesis Inhibitors/therapeutic use , Antibodies, Monoclonal, Humanized/therapeutic use , Eye Abnormalities/drug therapy , Optic Disk/abnormalities , Receptors, Vascular Endothelial Growth Factor/therapeutic use , Recombinant Fusion Proteins/therapeutic use , Retinal Diseases/drug therapy , Subretinal Fluid/drug effects , Aged, 80 and over , Coloring Agents , Drug Substitution , Epiretinal Membrane/diagnosis , Epiretinal Membrane/drug therapy , Eye Abnormalities/diagnosis , Female , Fluorescein Angiography , Humans , Indocyanine Green , Intravitreal Injections , Macular Edema/diagnosis , Macular Edema/drug therapy , Ranibizumab , Retinal Detachment/diagnosis , Retinal Detachment/drug therapy , Retinal Diseases/diagnosis , Retinal Pigment Epithelium/drug effects , Retinal Pigment Epithelium/pathology , Tomography, Optical Coherence , Vascular Endothelial Growth Factor A/antagonists & inhibitorsABSTRACT
We review the utility of serum anticholinergic activity (SAA) as a peripheral marker of anticholinergic activity (AA) in the central nervous system (CAA). We hypothesize that the compensatory mechanisms of the cholinergic system do not contribute to SAA if their system is intact and that if central cholinergic system deteriorates alone in conditions such as Alzheimer's disease or Lewy body dementia, CAA and SAA are caused by way of hyperactivity of inflammatory system and SAA is a marker of the anticholinergic burden in CNS. Taking into account the diurnal variations in the plasma levels of corticosteroids, which are thought to affect SAA, it should be measured at noon or just afterward.
Subject(s)
Acetylcholine/blood , Alzheimer Disease/blood , Central Nervous System/metabolism , Biomarkers/blood , HumansABSTRACT
We report the case of a 74-year-old woman who presented with amnesia and positive serum anticholinergic activity (SAA), which disappeared after treatment with the cholinesterase inhibitor donepezil for 1 year. Her only other regular medications were topical glaucoma preparations. We suggest that mental stress, mild cognitive impairment and Alzheimer's disease pathology combined to generate SAA in this patient. We also consider that SAA may have subsequently become negative because of upregulation of acetylcholine production by donepezil, and because the patient's other medications and physical condition (including glaucoma) remained unchanged during the 1-year period.
Subject(s)
Amnesia/drug therapy , Cholinesterase Inhibitors/therapeutic use , Cognitive Dysfunction/drug therapy , Indans/therapeutic use , Nootropic Agents/therapeutic use , Piperidines/therapeutic use , Aged , Amnesia/diagnosis , Cognitive Dysfunction/diagnosis , Donepezil , Female , HumansABSTRACT
We previously speculated that anticholinergic activity (AA) endogenously appeared in Alzheimer's disease (AD) and accelerated AD pathology. In this article we introduce manuscripts supporting the endogenous appearance of AA in AD and the acceleration of AD pathology. We speculate that acethylcholine (ACh) not only is related to cognitive functions but also regulates the inflammatory system. Therefore in AD, in which the ACh system is down-regulated, the hyperactivity of the inflammatory system may be caused and among cyctokines, substances having anticholinergic properties may appear. We also refer to a case in which serum anticholinergic activity (SAA) disappeared with the prescription of memantine (an antidementia agent that has the property of the N-methyl-D-aspartate (NMDA) receptor blocker) and speculate that because the hyperactivity of the inflammatory system occurs by way of the hyperactivity of NMDA receptor, memantine could abolish the AA.