Search results
Results from the WOW.Com Content Network
Chronic solvent-induced encephalopathy (CSE) is a condition induced by long-term exposure to organic solvents, often—but not always—in the workplace, that lead to a wide variety of persisting sensorimotor polyneuropathies and neurobehavioral deficits even after solvent exposure has been removed.
Toxic encephalopathy is a neurologic disorder caused by exposure to neurotoxic organic solvents such as toluene, following exposure to heavy metals such as manganese, as a side effect of melarsoprol treatment for African trypanosomiasis, adverse effects to prescription drugs, or exposure to extreme concentrations of any natural toxin such as cyanotoxins found in shellfish or freshwater ...
They may include limb weakness or numbness, loss of memory, vision, and/or intellect, uncontrollable obsessive and/or compulsive behaviors, delusions, headache, cognitive and behavioral problems and sexual dysfunction. Chronic mold exposure in homes can lead to neurotoxicity which may not appear for months to years of exposure. [6]
Most causes of vision loss can cause varying degrees of damage, from total blindness to a negligible effect. Media opacity occurs in the presence of opacities in the eye tissues or fluid, distorting and/or blocking the image prior to contact with the photoreceptor cells. Vision loss often results despite correctly functioning retinal receptors.
For premium support please call: 800-290-4726 more ways to reach us
The internal wall of the canal is very delicate and allows the fluid to filter due to the high pressure of the fluid within the eye. [7] The secondary route is the uveoscleral drainage , and is independent of the intraocular pressure, the aqueous flows through here, but to a lesser extent than through the trabecular meshwork (approx. 10% of the ...
Long-term contact lens use can lead to alterations in corneal thickness, stromal thickness, curvature, corneal sensitivity, cell density, and epithelial oxygen uptake. . Other structural changes may include the formation of epithelial vacuoles and microcysts (containing cellular debris), corneal neovascularization, as well as the emergence of polymegethism in the corneal endoth
The breakdown of the tight endothelial junctions that make up the blood–brain barrier causes extravasation of fluid, ions, and plasma proteins, such as albumin, into the brain parenchyma. [18] Accumulation of extracellular fluid increases brain volume and then intracranial pressure causing the symptoms of cerebral edema. [1]