This form of neuropathic pain can be any combination of itching, tingling, burning, or searing experienced spontaneously or from stimuli.Allodynia and dysaesthesia replace numbness between one week and a few months after a thalamic stroke. In general, once the development of pain has stopped, the type and severity of pain will be unchanging and if untreated, persist throughout life. Consequentially, many will undergo some form of pain treatment and adjust to their new lives as best they can.Pain associated with Dejerine–Roussy syndrome is sometimes coupled with anosognosia or somatoparaphrenia which causes a patient having undergone a right-parietal, or right-sided stroke to deny any paralysis of the left side when indeed there is, or deny the paralyzed limb(s) belong to them. Although debatable, these symptoms are rare and considered part of a "thalamic phenomenon", and are not normally considered a characteristic of Dejerine–Roussy syndrome. Mechanism
Although there are many contributing factors and risks associated with strokes, there are very few associated with Dejerine–Roussy syndrome and thalamic lesions specifically. In general, strokes damage one hemisphere of the brain, which can include the thalamus. The thalamus is generally believed to relay sensory information between a variety of subcortical areas and the cerebral cortex. It is known that sensory information from environmental stimuli travels to the thalamus for processing and then to the somatosensory cortex for interpretation. The final product of this communication is the ability to see, hear or feel something as interpreted by the brain. Dejerine–Roussy syndrome most often compromises tactile sensation.
Granular corneal dystrophy  is a slowly progressive corneal dystrophy that most often begins in early childhood. Granular corneal dystrophy has two types:

Granular corneal dystrophy type I, also corneal dystrophy Groenouw type I, is a rare form of human corneal dystrophy. It was first described by German ophthalmologist Arthur Groenouw in 1890. Granular corneal dystrophy type II, also called Avellino corneal dystrophy or combined granular-lattice corneal dystrophy is also a rare form of corneal dystrophy. The disorder was first described by Folberg et al. in 1988. The name Avellino corneal dystrophy comes from the first four patients in the original study each tracing their family origin to the Italian province of Avellino. Presentation
Granular corneal dystrophy is diagnosed during an eye examination by an ophthalmologist or optometrist. The lesions consist of central, fine, whitish granular lesions in the cornea. Visual acuity is slightly reduced. Genetics
Granular corneal dystrophy is caused by a mutation in the TGFBI gene, located on chromosome 5q31. The disorder is inherited in an autosomal dominant manner. This indicates that the defective gene responsible for the disorder is located on an autosome (chromosome 5 is an autosome), and only one copy of the gene is sufficient to cause the disorder, when inherited from a parent who has the disorder. The gene TGFBI encodes the protein keratoepithelin. Diagnosis
Treatment
Corneal transplant is not needed except in very severe and late cases. Light sensitivity may be overcome by wearing tinted glasses. See also
Corneal dystrophy


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