NSAIDs, including acetylsalicylic acid, are frequently classified as peripherally-acting analgesics. This is based on the fact that these substances, among other effects, inhibit the biosynthesis of prostaglandines. A few solid arguments, however, stand against an exclusively peripheral mode of the analgesic action of NSAIDs in the sense of an inhibition of prostaglandin synthesis. It should be noted here that the analgesically-effective doses do not suffice to block prostaglandin synthesis. Furthermore, the inhibiting effects of paracetamol and metamizol are far weaker or are not at all present, although both substances are reliably-effective analgesics. The NSAIDs indometacin, ibuprofen, and diclofenac are capable of suppressing the sensory response of the nociceptive system via a central effect. In experimental studies with rats under urethane anesthesia, the nociceptive activity of individual neurons of the thalamus (the dorsomedial part of the ventral nucleus) was measured. The activity was triggered via an electric stimulation of afferent C-fibres in the ipsilateral or contralateral sural nerve. The NSAIDs named suppressed the evoked nociceptive activity in a dose-dependent manner. At the highest doses, the suppression resulted in a difference of approx. 60% of the control activity. The ED50 values were 5 mg/kg for indometacin, 10.9 mg/kg for diclofenac, and 15.6 mg/kg for ibuprofen. These results support the theory that the central effects of NSAIDs contribute to their analgesic efficacy. The possible mechanisms of these effects will be discussed. A practical significance of the central analgesic effects of NSAIDs could be that their therapeutic applicability is not limited only to the treatment of pain, which results from an activation of nociceptors.