Proglottids leave the body through the anus and fall to the ground, where they may be eaten with grass by a grazing animal such as a cow. This animal then becomes an intermediate host, the oncosphere boring through the gut wall and migrating to another part of the body such as the muscle. Here it encysts, forming a cysticercus. The parasite completes its lifecycle when the intermediate host passes on the parasite to the definitive host, usually when the definitive host eats contaminated parts of the intermediate host, for example a human eating raw or undercooked meat. Another two-phase lifecycle is exhibited by Anoplocephala perfoliata, the definitive host being an equine and the intermediate host an oribatid mite.Diphyllobothrium exhibits a more complex, three-phase lifecycle. If the eggs are laid in water, they develop into free-swimming oncosphere larvae. After ingestion by a suitable freshwater crustacean such as a copepod, the first intermediate host, they develop into procercoid larvae. When the copepod is eaten by a suitable second intermediate host, typically a minnow or other small freshwater fish, the procercoid larvae migrate into the fishs flesh where they develop into plerocercoid larvae. These are the infective stages for the mammalian definitive host. If the small fish is eaten by a predatory fish, its muscles too can become infected.Schistocephalus solidus is another three-phase example. The intermediate hosts are copepods and small fish, and the definitive hosts are waterbirds. This species has been used to demonstrate that cross-fertilisation produces a higher infective success rate than self-fertilisation.
The most common treatment is dopamine replacement therapy, which consists in the administration of levodopa (L-Dopa) or dopamine agonists (such as pramipexole or ropinirole) to patients. Dopamine replacement therapy is well known to improve motor symptoms but its effects in cognitive and behavioral symptoms are more complex. Dopamine has been related to the normal learning of stimuli with behavioral and motivational significance, attention, and most importantly the reward system. In accordance with the role of dopamine in reward processing, addictive drugs stimulate dopamine release. Although the exact mechanism has yet to be elucidated, the role of dopamine in the reward system and addiction has been proposed as the origin of DDS. Models of addiction have been used to explain how dopamine replacement therapy produces DDS. One of these models of addiction proposes that over the usage course of a drug there is a habituation to the rewarding effects that it produces at the initial stages. This habituation is thought to be dopamine mediated. With long-term administration of L-dopa the reward system gets used to it and needs higher quantities. As the user increases drug intake there is a loss of dopaminergic receptors in the striatum which acts in addition to an impairment in goal-direction mental functions to produce an enhancement of sensitization to dopamine therapy. The behavioral and mood symptoms of the syndrome are produced by the dopamine overdose. Diagnosis
Diagnosis of the syndrome is clinical since there are no laboratory tests to confirm it.