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PURPOSE: In this study, we describe common demographic and clinical characteristics of the glaucoma patient population attending vision rehabilitation. DESIGN: Cross-sectional study. PARTICIPANTS: Patients attending a hospital-based vision rehabilitation center with a primary ocular diagnosis of glaucoma. METHODS: Participants' charts were retrospectively reviewed. Data extracted from medical records included demographics, referring physician, ocular history, glaucoma diagnosis, past ocular surgery, intraocular pressure, optic nerve findings, results of a functional intake assessing activities of daily living, depression, visual hallucinations, best-corrected visual acuity (BCVA), mean deviation (MD) scores on visual field testing, and log contrast sensitivity (CS). MAIN OUTCOME MEASURES: Participant demographic information, ocular history, self-reported difficulty with activities of daily living, depression, visual hallucinations, BCVA, visual field, and CS. RESULTS: The mean age of patients in this study was 77 years and ranged from 8 to 103 years. Ninety percent of patients were referred to vision rehabilitation by an ophthalmologist. Median BCVA was 20/50. Fifty-five percent of patients were functionally monocular, and for all patients, there was a median 9-line difference in BCVA between eyes. Median MD score was -13.95 decibels (dB). Median CS was 1.05. Patients reported having the greatest difficulty with reading (88%), writing (72%), and mobility (67%). Seventy-eight percent of patients stopped driving, and 12% reported difficulty driving. Among those experiencing depression, there was a 4:1 ratio of depressed patients having difficulty with mobility. One-third of patients experienced visual hallucinations. CONCLUSIONS: Most glaucoma patients attending vision rehabilitation are not legally blind, but many are functionally monocular. This may cause greater difficulty performing functions that require the use of binocularity. Increasing the referral of younger glaucoma patients to vision rehabilitation may help patients learn to cope with the loss of visual function that occurs over time.
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Actividades Cotidianas , Glaucoma , Adolescente , Adulto , Anciano , Anciano de 80 o más Años , Niño , Estudios Transversales , Glaucoma/diagnóstico , Glaucoma/epidemiología , Humanos , Persona de Mediana Edad , Estudios Retrospectivos , Adulto JovenRESUMEN
Endotheliitis is the inflammation of the corneal endothelium resulting in edema and subsequent loss of vision. Bacterial causes of corneal inflammation primarily of the epithelium with subsequent, secondary involvement of the endothelium have previously been described. Notably, however, there are no reports of isolated endotheliitis related to a bacterial pathogen. We report, for the first time, a case of corneal endotheliitis associated with a pyogenic liver abscess caused by methicillin resistant Staphylococcus aureus (MRSA). Treatment targeting the underlying source of infection led to visual recovery in our patient.
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Altered brain energy homeostasis is a key adaptation occurring in the cocaine-addicted brain, but the effect of cocaine on the fundamental source of energy, mitochondria, is unknown. We demonstrate an increase of dynamin-related protein-1 (Drp1), the mitochondrial fission mediator, in nucleus accumbens (NAc) after repeated cocaine exposure and in cocaine-dependent individuals. Mdivi-1, a demonstrated fission inhibitor, blunts cocaine seeking and locomotor sensitization, while blocking c-Fos induction and excitatory input onto dopamine receptor-1 (D1) containing NAc medium spiny neurons (MSNs). Drp1 and fission promoting Drp1 are increased in D1-MSNs, consistent with increased smaller mitochondria in D1-MSN dendrites after repeated cocaine. Knockdown of Drp1 in D1-MSNs blocks drug seeking after cocaine self-administration, while enhancing the fission promoting Drp1 enhances seeking after long-term abstinence from cocaine. We demonstrate a role for altered mitochondrial fission in the NAc, during early cocaine abstinence, suggesting potential therapeutic treatment of disrupting mitochondrial fission in cocaine addiction.
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Cocaína/farmacología , Neuronas Dopaminérgicas/efectos de los fármacos , Dinaminas/metabolismo , Locomoción/efectos de los fármacos , Mitocondrias/metabolismo , Receptores de Dopamina D1/metabolismo , Animales , Cocaína/administración & dosificación , Condicionamiento Operante/efectos de los fármacos , Condicionamiento Operante/fisiología , Inhibidores de Captación de Dopamina/administración & dosificación , Inhibidores de Captación de Dopamina/farmacología , Neuronas Dopaminérgicas/ultraestructura , Dinaminas/genética , Inhibidores Enzimáticos/farmacología , Regulación de la Expresión Génica/efectos de los fármacos , Regulación de la Expresión Génica/genética , Locomoción/genética , Ratones , Ratones Endogámicos C57BL , Ratones Transgénicos , Mitocondrias/efectos de los fármacos , Plasticidad Neuronal/efectos de los fármacos , Plasticidad Neuronal/genética , Núcleo Accumbens/citología , Quinazolinonas/farmacología , Receptores de Dopamina D1/genética , Receptores de Dopamina D2/genética , Receptores de Dopamina D2/metabolismo , AutoadministraciónRESUMEN
Among children with the most severe presentation of Marfan syndrome (MFS), an inherited disorder of connective tissue caused by a deficiency of extracellular fibrillin-1, heart failure is the leading cause of death. Here, we show that, while MFS mice (Fbn1C1039G/+ mice) typically have normal cardiac function, pressure overload (PO) induces an acute and severe dilated cardiomyopathy in association with fibrosis and myocyte enlargement. Failing MFS hearts show high expression of TGF-ß ligands, with increased TGF-ß signaling in both nonmyocytes and myocytes; pathologic ERK activation is restricted to the nonmyocyte compartment. Informatively, TGF-ß, angiotensin II type 1 receptor (AT1R), or ERK antagonism (with neutralizing antibody, losartan, or MEK inhibitor, respectively) prevents load-induced cardiac decompensation in MFS mice, despite persistent PO. In situ analyses revealed an unanticipated axis of activation in nonmyocytes, with AT1R-dependent ERK activation driving TGF-ß ligand expression that culminates in both autocrine and paracrine overdrive of TGF-ß signaling. The full compensation seen in wild-type mice exposed to mild PO correlates with enhanced deposition of extracellular fibrillin-1. Taken together, these data suggest that fibrillin-1 contributes to cardiac reserve in the face of hemodynamic stress, critically implicate nonmyocytes in disease pathogenesis, and validate ERK as a therapeutic target in MFS-related cardiac decompensation.
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RATIONALE AND OBJECTIVE: There is evidence that cue-induced sucrose seeking progressively increases after cessation of oral sucrose self-administration (incubation of sucrose craving) in both adolescent and adult rats. The synaptic plasticity changes associated with this incubation at different age groups are unknown. We assessed whether incubation of sucrose craving in rats trained to self-administer sucrose as young adolescents, adolescents, or adults is associated with changes in 2-amino-3-(3-hydroxy-5-methyl-isoxazol-4-yl)propanoic acid (AMPA)/N-methyl-D-aspartate (NMDA) ratio (a measure of postsynaptic changes in synaptic strength) in nucleus accumbens. METHODS: Three age groups initiated oral sucrose self-administration training (10 days) on postnatal day (P) 35 (young adolescents), P42 (adolescents), or P70 (adults). They were then tested for cue-induced sucrose seeking (assessed in an extinction test) on abstinence days 1 and 21. Separate groups of rats were trained to self-administer sucrose or water (a control condition), and assessed for AMPA/NMDA ratio in nucleus accumbens on abstinence days 1-3 and 21. RESULTS: Adult rats earned more sucrose rewards, but sucrose intake per body weight was higher in young adolescent rats. Time-dependent increases in cue-induced sucrose seeking (incubation of sucrose craving) were more pronounced in adult rats, less pronounced in adolescents, and not detected in young adolescents. On abstinence day 21, but not days 1-3, AMPA/NMDA ratio in nucleus accumbens were decreased in rats that self-administered sucrose as adults and adolescents, but not young adolescents. CONCLUSIONS: Our data demonstrate age-dependent changes in magnitude of incubation of sucrose craving and nucleus accumbens synaptic plasticity after cessation of sucrose self-administration.