What is the pathophysiology of macular hole?
Best insight from top research papers
The pathophysiology of macular hole involves vitreous traction and dynamic forces on the macula. Vitreous anteroposterior traction and tangential traction play important roles in the formation and expansion of macular holes . In idiopathic macular holes, abnormal vitreous traction from incomplete vitreous detachment and dynamic forces caused by mobile posterior cortical vitreous with fluid currents contribute to hole development . Muller cells have also been implicated in the pathogenesis of macular holes . Traumatic macular holes result from sudden compression and expansion of the globe, leading to vitreous traction . The severity of disruption to the photoreceptors and retinal pigment epithelial cells determines the final visual acuity in traumatic macular holes . In the pediatric population, macular holes are often the result of direct ocular trauma, and surgical management poses unique challenges . Persistent symptomatic vitreomacular adhesions and epiretinal membrane formation can also contribute to macular hole development .
Answers from top 4 papers
More filters
| Papers (4) | Insight |
|---|---|
| The pathophysiology of macular hole involves vitreous traction on the retina, posterior vitreous detachment, and continuous adhesion. | |
| The pathophysiology of macular hole involves vitreous traction on the foveal center, leading to the development of a hole in the macula. | |
3 Citations | The pathomechanism of traumatic macular hole involves vitreous traction caused by sudden compression and expansion of the globe. |
| The pathophysiology of macular hole is a slow, degenerative process of progressive vitreoretinal traction, except in pediatric cases where it is caused by direct ocular trauma. |
Related Questions
What is the pathophysiology of diabetes?4 answersThe pathophysiology of diabetes involves complex mechanisms related to insulin levels and utilization in the body. In type 1 diabetes, there is a total lack of insulin due to autoimmune destruction of insulin-producing β cells. On the other hand, type 2 diabetes is characterized by peripheral tissue resistance to insulin effects, impaired regulation of hepatic glucose production, and declining β-cell function leading to β-cell death. Hyperglycemia, a key feature of diabetes, results from abnormalities in insulin secretion or action. Insulin is crucial for glucose homeostasis, as pancreatic beta cells release it in response to elevated blood glucose levels. Understanding the molecular processes involved in diabetes development, including the role of long-chain non-coding RNA, is essential for improving clinical care.
What is the current understanding of the pathophysiology of primary open angle glaucoma?5 answersPrimary open-angle glaucoma (POAG) is a progressive optic neuropathy characterized by the loss of retinal ganglion cells and narrowing of visual fields. The pathophysiology of POAG involves multiple mechanisms, including increased intraocular pressure (IOP), circulatory disorders, trabecular meshwork (TM) dysfunction, chronic inflammation, and genetic predisposition. Chronic inflammation and immune damage play a significant role in POAG, leading to hypersecretion of inflammatory mediators and infiltration of inflammatory cells into ischemic tissue, exacerbating the effects of increased IOP and ischemia. Mutations in the Toll-like receptor 4 (TLR4) gene have been associated with both infectious and non-infectious diseases, including POAG. TLR4 activation initiates TM fibrosis, increases IOP, and activates retinal ganglion cell apoptosis. Cerebral hemodynamic dysfunction is also implicated in POAG, affecting brain regions involved in visual processing, somatosensory processing, motor control, emotional regulation, and cognitive functions. Additionally, oxidative stress, excitotoxicity, and compromised neuroprotective mechanisms contribute to cell death in glaucoma. Further research is needed to understand the genetic and molecular mechanisms underlying POAG and develop innovative treatment strategies.
What is the pathophysiology of ADHD?5 answersThe pathophysiology of ADHD involves structural and functional changes in the brain, alterations in neurotransmitter transporters and genes, and abnormalities in neuronal networks and resting-state activity. These changes primarily affect the prefrontal cortex, corpus striatum, and cerebellum, which are involved in attention, impulse control, and motor coordination. Dopamine and norepinephrine, key neurotransmitters, play a role in the pathophysiology of ADHD. Inflammation may also be involved, as ADHD is associated with inflammatory and autoimmune disorders. The cortico-basal ganglia-thalamocortical circuitry, including the frontal cortex and basal ganglia, shows dysfunction in ADHD. Neurofeedback, a treatment approach that allows participants to gain control over specific brain activity, may be helpful in addressing the cognitive and motivational problems associated with ADHD. Further research is needed to fully understand the pathophysiology of ADHD.
What is a macular hole?4 answersA macular hole is a full-thickness defect in the neurosensory layers of the retina at the center of the macula. It is a retinal disease that can lead to reduced vision, especially in individuals over 60 years old. Macular holes can be classified into different subtypes, including full-thickness macular holes, lamellar macular holes, myopic macular holes, and traumatic macular holes. The pathogenesis of macular holes involves complex tractional forces exerted by the vitreomacular interface, epiretinal tissue, and progressive scleral ectasia of the posterior ocular globe wall. Surgical intervention, such as vitrectomy, is the standard treatment for macular holes, but closure of the hole is not always successful. Various surgical techniques and technological advancements have been developed to improve the outcomes of macular hole repair.
What is the pathophysiology of blurred vision?4 answersBlurred vision can have various pathophysiologies. In cases of dural ectasia, it is caused by cerebrospinal fluid accumulation within the expanded nerve sheath around the optic nerve. In uncontrolled diabetes mellitus, blurred vision can be a presenting symptom, resulting from increased glycosylated hemoglobin. In Parkinson's disease, blurry vision can have different underlying causes, such as strabismus, convergence insufficiency, or higher order visual processing deficits. In exophthalmic goiter (Graves' disease), blurred vision can be due to changes in refraction, corneal exposure, glaucoma, or optic nerve disorders. The visual system involves neuronal stations, non-neuronal structures, and specific pathways from the retina to the visual cortex. Overall, the pathophysiology of blurred vision can vary depending on the underlying condition or disease.
What's Pathophysiology of herpes?3 answersThe pathophysiology of herpes involves the infection and replication of the herpes simplex virus (HSV) in various tissues and cells of the body. HSV-1 primarily causes orofacial and genital infections, while HSV-2 primarily causes genital infections. In ocular herpes, HSV-1 enters corneal epithelial cells through interactions with cell surface receptors, leading to corneal lesions and potential blindness. The specific patterns of accumulation of porphyrins and their toxic precursors in porphyrias result in a variety of clinical manifestations, including acute neurovisceral attacks, skin lesions, and liver disease. Postherpetic neuralgia (PHN), a complication of herpes, is believed to involve multiple mechanisms operating simultaneously, leading to a constellation of painful sensations and sensory loss. Genital herpes is considered a chronic rather than an intermittent disease, with recurrent shedding of the virus even in the absence of clinical signs.