What are the neurologic effects of caffeine?

Updated: Jun 14, 2018
  • Author: Jasvinder Chawla, MD, MBA; Chief Editor: Nicholas Lorenzo, MD, CPE, MHCM, FAAPL  more...
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Caffeine is the most widely used psychoactive substance and has sometimes been considered a drug of abuse. This article summarizes the available data on its neurologic effects.

Classic drugs of abuse lead to specific increases in cerebral functional activity and dopamine release in the shell of the nucleus accumbens (the key neural structure for reward, motivation, and addiction). In contrast, caffeine at doses reflecting daily human consumption does not induce a release of dopamine in the shell of the nucleus accumbens but leads to a release of dopamine in the prefrontal cortex, which is consistent with its reinforcing properties.

Furthermore, caffeine increases glucose utilization in the shell of the nucleus accumbens only at high concentrations; this, in turn, nonspecifically stimulates most brain structures and thus likely reflects the side effects linked to high caffeine ingestion alone. Moreover, this dose is 5-10 times higher than the dose necessary to stimulate the caudate nucleus (extrapyramidal motor system) and the neural structures regulating the sleep-wake cycle, the 2 functions that are most sensitive to caffeine.

Thus, although caffeine fulfills some of the criteria for drug dependence and shares with amphetamine and cocaine a certain specificity of action on the cerebral dopaminergic system, it does not act on the dopaminergic structures related to reward, motivation, and addiction.

Tolerance to caffeine-induced stimulation of locomotor activity has been shown in animals. In humans, tolerance to some subjective effects of caffeine may occur, but most of the time, complete tolerance to many effects of caffeine on the central nervous system (CNS) does not occur. In animals, caffeine can act as a reinforcer, but only in a more limited range of conditions than classic drugs of dependence do. In humans, the reinforcing stimulus functions of caffeine are limited to low or moderate doses, while high doses usually are avoided.

Dietary sources include coffee, tea, cola drinks, and chocolate, as well as energy drinks. [1] The most notable behavioral effects of caffeine occur after consumption of low-to-moderate doses (50-300 mg) and include increased alertness, energy, and ability to concentrate. Whereas moderate consumption rarely leads to health risks, higher doses induce negative effects such as anxiety, restlessness, insomnia, and tachycardia. After sudden caffeine cessation, withdrawal symptoms develop in a modest number of cases but are typically moderate and transient.

The negative effects of high-dose caffeine consumption are seen primarily in a small group of individuals who are caffeine-sensitive. [2] However, caffeine was considered in one study as a potential drug of abuse and has even been described as a model drug of abuse. On the basis of a review of science and clinical data, the possibility of adding caffeine withdrawal, but not abuse and dependence, to diagnostic manuals is being considered in the United States.

For patient education resources, see the Substance Abuse Center, as well as Drug Dependence and Abuse and Substance Abuse.

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