Vogt–Koyanagi–Harada disease at the University of Tokyo, in 1911. It was the much later article, published in 1929, that definitively associated Koyanagi with the disease. Harada's 1926 paper is recognized for its comprehensive description of what is now known as Vogt–Koyanagi–Harada disease. Vogt–Koyanagi–Harada disease Vogt–Koyanagi–Harada disease (VKH), also known as Vogt–Koyanagi–Harada syndrome, uveomeningitis syndrome and uveomeningoencephalitic syndrome, is a multisystem disease of presumed autoimmune cause, that affects pigmented tissues, which have melanin. The most significant manifestation is bilateral, diffuse uveitis, which affects the eye. VKH may variably also involve the inner ear with effects on hearing, the skin, and the meninges of
Hypothalamic disease act on the pituitary gland. Hypothalamic disease therefore affects the functioning of the pituitary and the target organs controlled by the pituitary, including the adrenal glands, ovaries and testes, and the thyroid gland. Numerous dysfunctions manifest as a result of hypothalamic disease. Damage to the hypothalamus may cause disruptions in body temperature regulation, growth, weight, sodium and water balance, milk production, emotions, and sleep cycles. Hypopituitarism, neurogenic diabetes insipidus, tertiary hypothyroidism, and developmental disorders are examples of precipitating conditions caused by hypothalamic disease. The hypothalamus and pituitary gland are tightly integrated. Damage to the hypothalamus will impact the responsiveness and