Tinnitus is a debilitating condition from which some 0.5-1% of the population of the Western world suffer sufficiently badly as to interfere with their normal working and leisure life. There is no satisfactory treatment at the present time and the uncertainty surrounding the mechanism of its generation makes it difficult to devise an effective cure. After much debate, the consensus of opinion amongst researchers regarding its site of origin is that it is primarily a central nervous system pathology although there certainly exists a class of patients whose tinnitus is peripherally based. In this paper, we provide some speculative ideas on how an initial auditory insult can be translated into central neurological substrates that represent tinnitus. Plastic changes arising from sensory deprivation trigger a change in synaptology and neurotransmission with a consequent change in receptor configuration. From neuroanatomical considerations and analogies with other clinical conditions, we postulate the involvement of serotonin (5-HT) in these plastic changes and consider the evidence available from the use of serotonergic drugs in different conditions. A possible relationship between 5-HT and lidocaine is also discussed.