Caffeine and other xanthine derivatives, including aminophylline, are CNS stimulants that excite all levels of the CNS, with the cortex being the most sensitive. Caffeine increases energy metabolism throughout the brain but decreases cerebral blood flow, inducing a relative brain hypoperfusion. The drug activates noradrenaline neurons and may act as a second messenger at dopamine receptors to affect the local release of dopamine. U Mobilization of intracellular calcium and inhibition of specific phosphodiesterases occurs at high, nonphysiological concentrations of caffeine. The most likely mechanism of action of methylxanthine is the antagonism at the level of adenosine receptors.

Caffeine's psychostimulant action on humans is often subtle and difficult to detect. Its effects on learning, memory, performance, and coordination are related to methylxanthine-induced arousal, vigilance, and fatigue. An increased awareness of the environment or hyperesthesia may be an unpleasant experience to some patients. The patient becomes loquacious and restless, and often complains of ringing in the ears and giddiness. In high doses, xanthines affect the spinal cord, resulting in increased reflex excitability, tremulous extremities, and tense muscles. [i] Caffeine clearly alters sleep patterns, and if taken within 1 hour of attempted sleep, it increases sleep latency, decreases total sleep time, and worsens the subject's estimate of sleep quality. Less time is spent in stage 3 and 4 sleep and more in stage 2 sleep. Xanthine-associated seizures are seen as a complication of aminophylline therapy, especially when the drug is administered intravenously. They are usually generalized but can be focal. Cessation of the use of products containing caffeine can cause a withdrawal syndrome that includes headaches, drowsiness, fatigue, decreased performance, and in some instances, nausea and vomiting. These symptoms begin within 12 to 24 hours after the last use of caffeine, peak at 20 to 48 hours, and last approximately 1 week.y

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