Cerebral Polyopia
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Polyopia, or the perception of multiple images, can be caused by occipital lobe disease from trauma, ischemia, epilepsy, or migraines. The proposed mechanisms include cortical spreading depression, abnormal visual synthesis in the brain, and disruption of signal transmission from the posterior parietal cortex to the frontal eye field to midbrain structures via the holonomic brain theory, leading to convergence insufficiency and horizontal diplopia.
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Visual pathway ppt
1. The visual pathway begins in the retina and passes through the optic nerve, optic chiasm, optic tracts, lateral geniculate bodies, optic radiations, and terminates in the visual cortex.
2. The optic nerve has four parts - intraocular, intraorbital, intracanalicular, and intracranial parts. It carries nerve fibers from the retina and is surrounded by meninges and receives its blood supply from branches of the internal carotid artery.
3. The lateral geniculate bodies contain six layers of neurons that receive input from the retina via the optic tracts and relay this information to the visual cortex via the optic radiations.
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Neural tube defects a case series - copy
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Balint syndrome: an unusual triad, Balint syndrome: an unusual triad
The paper investigates a case of sudden loss of vision in a patient with recent history of blurred vision of right eye
diagnosed with Central retinal artery occlusion (CRAO). The point of interest of this case report is that the clinical
features are something different from those of a CRAO and revealed cardinal triad of simultanagnosia, optic ataxia,
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Presentation1.pptx, congenital malformation of the brain.
More than 2000 congenital brain malformations have been described. Magnetic resonance imaging is useful for studying these conditions. The document provides an overview of important congenital brain malformations, including disorders of organogenesis like Chiari malformations, holoprosencephaly, and cephaloceles. Disorders of histogenesis and cytogenesis such as neurocutaneous syndromes, vascular malformations, and tumors are also discussed. The imaging features of various malformations are presented to aid diagnosis.
Multiple sclerosis
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Ophthalmology 5th year, 7th lecture (Dr. Bakhtyar)
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Visual Impairment in Cerebral Venous Thrombosis.pptx
Visual Impairment in Cerebral Venous Thrombosis.pptx
Balint syndrome: an unusual triad, Balint syndrome: an unusual triad
Balint syndrome: an unusual triad, Balint syndrome: an unusual triad
Presentation1.pptx, congenital malformation of the brain.
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Management of Motor Fluctuations in Parkinson Disease.pptx
- Motor fluctuations are a common complication of Parkinson's disease that occur in approximately one-third of patients after 2 years of levodopa therapy. They involve unpredictable switching between "on" periods where symptoms are relieved and "off" periods where symptoms return.
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Transient Epileptic Amnesia.pptx
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Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
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Cerebral Polyopia
- 1. Ade Wijaya, MD – February 2021
- 2. Definition “Duplication of images (doublets, triplets, and more) in the absence of a refractive error, fascicular cranial nerve disease, orbital pathology, or brainstem disease” Kesserwani H. A Novel Case of Cerebral Diplopia Secondary to a Posterior Parietal Cortex Ischemic Infarct: Proposal of a Mechanism of Generation of Polyopia Due to Convergence Insufficiency.
- 3. Etiology Occipital lobe disease due to: - Trauma - Ischemia - Epilepsy - Migraine Kesserwani H. A Novel Case of Cerebral Diplopia Secondary to a Posterior Parietal Cortex Ischemic Infarct: Proposal of a Mechanism of Generation of Polyopia Due to Convergence Insufficiency.
- 4. Mechanism Cortical spreading depression Abnormal visual synthesis Holonomic brain theory: - Posterior parietal cortex frontal eye field midbrain and paramedian pontine reticular formation. leading to convergence insufficiency and subsequent horizontal diplopia. Kesserwani H (September 07, 2020) An Analytic Dissection of a Case of Cerebral Diplopia: Is the Human Brain a Holographic Device?. Cureus 12(9): e10292. doi:10.7759/cureus.10292 Kesserwani H: The Zeitraffer phenomenon: a strategic ischemic infarct of the banks of the parieto-occipitalsulcus - a unique case report and a side note on the neuroanatomy of visual perception. Cureus. 2020,12:e9443.
- 5. Kesserwani H. A Novel Case of Cerebral Diplopia Secondary to a Posterior Parietal Cortex Ischemic Infarct: Proposal of a Mechanism of Generation of Polyopia Due to Convergence Insufficiency.
- 6. Kesserwani H. A Novel Case of Cerebral Diplopia Secondary to a Posterior Parietal Cortex Ischemic Infarct: Proposal of a Mechanism of Generation of Polyopia Due to Convergence Insufficiency.
- 7. Kesserwani H. A Novel Case of Cerebral Diplopia Secondary to a Posterior Parietal Cortex Ischemic Infarct: Proposal of a Mechanism of Generation of Polyopia Due to Convergence Insufficiency.
- 8. Summary Polyopia Diplopia of cerebral origin Etiology: occipital lobe disease Mechanism: Cortical spreading depression Abnormal visual synthesis Holonomic brain theory: - Posterior parietal cortex frontal eye field midbrain and paramedian pontine reticular formation