Sleep deprivation increases this propensity, which can be measured by polysomnography (PSG), as a reduction in sleep latency (the time needed to fall asleep). An indicator of sleep propensity can also be seen in the shortening of transition from light stages of non-REM sleep to deeper slow-waves oscillations can also be measured as indicator of sleep propensity.On average, the latency in healthy adults decreases by a few minutes after a night without sleep, and the latency from sleep onset to slow-wave sleep is halved. Sleep latency is generally measured with the multiple sleep latency test (MSLT). In contrast, the maintenance of wakefulness test (MWT) also uses sleep latency, but this time as a measure of the capacity of the participants to stay awake (when asked to) instead of falling asleep. Sleep-wake cycle
People aged 18 to 64 need seven to nine hours of sleep per night. Research studying sleep deprivation shows its impact on mood, cognitive and motor functioning, due to dysregulation of the sleep-wake cycle and augmented sleep propensity. Multiple studies that identified the role of the hypothalamus and multiple neural systems controlling circadian rhythms and homeostasis have been helpful in understanding sleep deprivation better. To describe the temporal course of the sleep-wake cycle, the two-process model of sleep regulation can be mentioned.This model proposes a homeostatic process (Process S) and a circadian process (Process C) that interact to define the time and intensity of sleep.
Causes
The cause of Todds paresis has been attributed to the affected cortex being ‘exhausted’ or silenced due to increased inhibition, but these conjectures are not supported. It has been observed that the impairments that follow seizures are similar to those that follow strokes, where for a period of time blood flow to certain areas of the brain is restricted and these areas are starved of oxygen. Diagnosis
The most significant issue regarding the Todds paresis is its differentiation from a stroke. The issue is further complicated by the fact that some strokes trigger a focal seizure during the acute phase. A Todds paresis in this context may overestimate the extent of neurological deficit due to the vascular process itself resulting in erroneous decisions with regards to acute stroke therapy  such as thrombolysis. For this reason a seizure during an acute stroke is generally accepted to be a relative contraindication to thrombolytic therapy, especially in the absence of documented cerebrovascular occlusion using vascular imaging techniques.An infant with Todds paresis does not necessarily preclude the diagnosis of a febrile convulsion. This view is as a result of a recent study that showed the incidence of Todds paresis to be in 0.4% of infants that have been diagnosed with a febrile convulsion. Treatment
There is no treatment for Todds paralysis. Individuals must rest as comfortably as possible until the paralysis disappears. Prognosis
An occurrence of Todds paralysis indicates that a seizure has occurred. The prognosis for the patient depends upon the effects of the seizure, not the occurrence of the paralysis.