Process S represents the drive for sleep, increasing during wakefulness and decreasing during sleep, until a defined threshold level, while Process C is the oscillator responsible for these levels. When being sleep deprived, homeostatic pressure accumulates to the point that waking functions will be degraded even at the highest circadian drive for wakefulness. Microsleeps
Microsleeps are periods of brief sleep that most frequently occur when a person has a significant level of sleep deprivation. Microsleeps usually last for a few seconds, usually no longer than 15 seconds, and happen most frequently when a person is trying to stay awake when they are feeling sleepy. The person usually falls into microsleep while doing a monotonous task like driving, reading a book, or staring at a computer. Microsleeps are similar to blackouts and a person experiencing them is not consciously aware that they are occurring. An even lighter type of sleep has been seen in rats that have been kept awake for long periods of time. In a process known as local sleep, specific localized brain regions went into periods of short (~80 ms) but frequent (~40/min) NREM-like states. Despite the on and off periods where neurons shut off, the rats appeared to be awake, although they performed poorly at tests. Cardiovascular morbidity
Decreased sleep duration is associated with many adverse cardiovascular consequences. The American Heart Association has stated that sleep restriction is a risk factor for adverse cardiometabolic profiles and outcomes.
Types
Based on the presence of extraocular findings, such as neurological, auditory, and integumentary manifestations, the "revised diagnostic criteria" of 2001 classify the disease as complete (eyes along with both neurological and skin), incomplete (eyes along with either neurological or skin), or probable (eyes without either neurological or skin) . By definition, for research homogeneity purposes, the two exclusion criteria are previous ocular penetrating trauma or surgery, and other concomitant ocular disease similar to VKH disease. Management
The acute uveitis]phase of VKH is usually responsive to high-dose oral corticosteroids; parenteral administration is usually not required. However, ocular complications may require a subtenon or intravitreous injection of corticosteroids or bevacizumab. In refractory situations, other immunosuppressives such as cyclosporine, or tacrolimus, antimetabolites (azathioprine, mycophenolate mofetil or methotrexate), or biological agents such as intravenous immunoglobulins (IVIG) or infliximab may be needed. Outcomes
Visual prognosis is generally good with prompt diagnosis and aggressive immunomodulatory treatment. Inner ear symptoms usually respond to corticosteroid therapy within weeks to months; hearing usually recovers completely. Chronic eye effects such as cataracts, glaucoma, and optic atrophy can occur. Skin changes usually persist despite therapy. Eponym
VKH syndrome is named for ophthalmologists Alfred Vogt from Switzerland and Yoshizo Koyanagi and Einosuke Harada from Japan. Several authors, including Arabic doctor Mohammad-al-Ghâfiqî in the 12th century ,as well as Jacobi, Nettelship, and Tay in the 19th century, had described poliosis, neuralgias, and hearing disorders. This constellation was probably often due to sympathetic ophthalmia, but likely included examples of VKH.