Lattice corneal dystrophy type II is characterized by an accumulation of protein globs called amyloid deposits in cells throughout the body. It is made up of numerous layers of tissue, and in lattice corneal dystrophy type II, the amyloid deposits develop in the stromal layer. They commonly lead to vision impairment because these protein deposits cloud the cornea. On top of that, affected people can have recurrent corneal disintegrations, which are triggered by splitting up of specific layers of the cornea from one another. Corneal disintegrations are very unpleasant and can cause level of sensitivity to brilliant light. As lattice corneal dystrophy type II progresses, the nerves come to be included, usually starting in an individual's forties. It is thought that the amyloid deposits interrupt nerve function. Dysfunction of the nerves in the head and face can cause paralysis of facial muscular tissues; decreased feelings in the face; and trouble talking, chewing, and swallowing. Dysfunction of the nerves that attach the brain and spinal cord to muscles and to sensory cells that identify sensations such as pain, touch, and heat can cause loss of experience and weak point in the limbs. The skin is also generally affected in people with lattice corneal dystrophy type II, commonly beginning in a person's forties. People with this problem might have enlarged, sagging skin, specifically on the scalp and forehead, and a condition called cutis laxa, which is characterized by loosened skin that does not have elasticity. The skin can be dry and itchy. People with lattice corneal dystrophy type II can have a face expression that appears unfortunate due to the fact that of loose skin and muscle mass paralysis in the face.
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