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22.06.2014
AbstractVitiligo reflects a systemic process that has important implications beyond the skin. Melanocytes are present not only within the skin and hair follicles, but also in the eyes and other parts of the central nervous system. In addition to ocular pathologies, other neurological abnormalities are associated with vitiligo in Alezzandrini and VKH syndromes. Vitiligo is one of a number of skin disorders characterized by displaying a tendency to expand into traumatized or otherwise altered skin, an occurrence known as the Koebner phenomenon. In the absence of pre-existent vitiligo, induction may occur secondary to a reaction to a variety of compounds. Waardenburg syndrome is a rare autosomal-dominant disorder associated with piebaldism.[14] Affected individuals often have hypomelanotic macules. Tuberous sclerosis (TS) may be first evident through the appearance of characteristic depigmented spots.[15] TS macules are usually hypomelanotic, as opposed to chalk-white, have an ash-leaf shape, and may have a segmental distribution.
Enhancement Of The Eighth Cranial Nerve And Labyrinth On MR …Panied by pressure in the ears, tinnitus, vertigo, and disequilibrium. SYMPTOMS FROM MINERAL DEFICIENCES Some Symptoms Of Boron …In ears (Tinnitus) Lack of concentration . Case ReportsEpstein–Barr virus (EBV) appears to be the strongest predisposing factor. High Incidence Of Nasopharyngeal Carcinoma In AsiaTion, tinnitus, pain, and cranial nerve pal sy.
A dysfunction of the vestibular system that causes sudden and severe VERTIGO (sensation of spinning) with accompanying NAUSEA, VOMITING, and balance disturbances. The distinguishing symptoms of vestibular neuronitis are severe vertigo and one-sided balance disturbances without TINNITUS or HEARING LOSS. The diagnostic path is fairly straightforward; any pattern of vestibular disturbance that includes additional symptoms is likely to have a different cause. Imaging procedures are not likely to offer diagnostic information unless the doctor is uncertain of the diagnosis, in which case MAGNETIC RESONANCE IMAGING (MRI) or COMPUTED TOMOGRAPHY (CT) SCAN can rule out other conditions such as ACOUSTIC NEUROMA.
The VIRUS causing the vestibular neuronitis must run its course, which typically takes 10 to 14 days. Because doctors do not know for certain what causes vestibular neuronitis, they cannot identify risk factors or preventive measures. High intensity interval training (HIIT) has been growing in popularity in the past few years. It may be linked with Hashimoto's thyroiditis, diabetes mellitus, Addison's disease, and other autoimmune processes.
Vitiligo may be induced by chemicals typically from an occupational exposure to phenolic germicides.[2] It is unclear whether use of certain oral medications may also be associated with vitiligo.
To diagnose vitiligo, one should be able to differentiate among a complete absence of pigment, hypopigmentation, and normal skin.
These may be differentiated from vitiliginous macules by the variability of the pigmentation of the lesions (ranging from amelanotic to hyperpigmented), their distribution (typically sparing the hands, feet, and periorificial areas), stability, and tendency to be congenital.


They may be seen in a confetti-like pattern that is difficult to differentiate from vitiligo. Diffuse scleroderma may result in areas of skin hyper- or hypopigmentation.[17] The presence of macules with any degree of pigmentation or macules with varied pigmentation would favor this diagnosis over vitiligo.
The same process, autoimmune destruction of melanocytes, is thought to be responsible for both melanoma-associated vitiliginous depigmentation and common vitiligo.[18] They appear identical histologically. Epidemiology of vitiligo and associated autoimmune diseases in Caucasian probands and their families.
The transcription factors SOX9 and SOX10 are vitiligo autoantigens in autoimmune polyendocrine syndrome type I. Melanocyte destruction after antigen-specific immunotherapy of melanoma: direct evidence of t cell-mediated vitiligo. During this time, certain ANTIHISTAMINE MEDICATIONS used to treat motion sickness can provide relief from the vertigo and associated nausea. Prompt diagnosis and treatment help relieve symptoms more quickly but do not appear to alter the course of the inflammation or affect the likelihood of RECURRENCE. Alezzandrini syndrome and Vogt-Koyanagi-Harada syndrome particularly exemplify this relationship.
It may be associated with ocular abnormalities, exclusively, or as part of a constellation of symptoms, as it is in Alezzandrini syndrome or Vogt-Koyanagi-Harada (VKH) syndrome.
Vitiligo and poliosis, as well as alopecia areata, are all possible cutaneous disturbances.
Systemic components of Waardenburg syndrome include bilateral congenital deafness, heterochromic irides, a broadened nasal root, and a white forelock.
The course of these ash-leaf lesions differs from that of vitiliginous ones in that these TS stigmata are congenital or develop within the few years of life, and remain stable. A confetti-like pattern of depigmentation may also be seen with this disease, necessitating differentiation from confetti vitiligo.
As immune system effectors circulate freely in the plasma, the sites of depigmentation do not necessarily have to be near the actual melanoma and, in fact, can be quite distant from it. Because hearing remains unaffected, doctors believe the INFECTION inflames the vestibular NERVE, the branch of the eighth cranial nerve (vestibulocochlear nerve) leading from the vestibular structures to the BRAIN.
These antihistamines include the prescription medications hydroxyzine (Atarax, Vistaril) and promethazine (Phenergan) and the over-the-counter products dimenhydrinate (Dramamine), meclizine (Antivert, Bonine) and diphenhydramine (Benadryl).
In addition, vitiligo may be confused with other systemic disorders, including tuberous sclerosis, progressive systemic sclerosis (scleroderma), melanoma, and, in endemic regions, leprosy. There is usually no loss of visual acuity, so clinicians managing patients with vitiligo need to have a high index of suspicion. The initiating event may be a cutaneous insult, such as generalized erythema or a physical trauma to the skin. Characteristic systemic signs and symptoms as well as histological examination may be helpful in making the proper diagnosis. In TS, there is hamartoma formation in many organs, resulting in numerous systemic abnormalities, including low intelligence, epilepsy, and pituitary adrenal dysfunction.[16] A child with seizures may need to be examined in Wood's light to detect any ash-leaf spots.


Systemic signs of the disease include essential vasomotor disturbances, such as Raynaud's phenomenon, fibrosis, and abnormalities of the lungs, kidneys, digestive system, and heart.
The major difference between vitiligo resulting from melanoma and common vitiligo is the distribution.
INFLAMMATION causes the vestibular nerve to transmit confused and erroneous signals to the brain.
The two prescription medications diazepam (Valium) and clonazepam (Klonopin) appear to act on the vestibular system directly to subdue the vertigo, though cause more sedation than antihistamines and can be addictive when used for an extended period of time. Chorioretinitis can often be diagnosed by detection of choroid or retinal pigmented epithelial lesions typical of this pathology.[2] The most specific sign of chorioretinitis, however, is the finding of a characteristic focal scar.
The disease process usually begins in the meningoencephalic phase, which has primarily neurologic symptoms, advances to the ophthalmic phase, in which retinal detachment may occur, and ends in the convalescent phase, where the cutaneous pathologies develop. Discoid plaques of lupus erythematous may also appear, markedly devoid of pigmentation, but atrophy is usually evident. The former is said to usually begin centrally, on the chin, neck, and trunk, for example, and spread to the periphery. The brain responds to the incoming signals as though they were legitimate, instructing the body to react to movement that is not occurring or failing to direct reaction when there is movement. The symptoms often are debilitating, with the person falling toward the affected side when attempting to walk and sometimes when attempting to sit upright.
The cutaneous loss of melanocytes is often accompanied by a similar depigmentation of the two pigment layers of the retina. Generalized vitiliginous lesions usually begin distally, on the hands and feet, and then advance to involve the trunk.[19] Systemic signs and symptoms are not usually useful in differentiating them.
Symptoms appear abruptly though often follow a cold or occur among groups of people who are in close contact. Most people recover completely and are free from residual consequences in three to four weeks. This causes the retina to have alternating whitish streaks, coming from capillaries being visualized through the depigmented patches, and darkened areas of normal choroid pigment.
Both common vitiligo vulgaris and melanoma-associated vitiligo may have uveitis and poliosis. A small percentage experiences recurrent episodes over the following months to years, though the severity of symptoms diminishes with each episode. Alternatively, if a reactive proliferation of glial cells is triggered by choroid destruction, a homogeneous, yellowish discoloration of the retina may result.



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