Acute dystonic reactions are involuntary movements (muscle spasms, protruding tongue, torticollis, etc.), usually appear within a few days of starting neuroleptic treatment and can appear as oculogyric crisis (dystonic posturing of neck, face, and eyes) or combination of focal dystonias. They are frightening but also very responsive to injected anticholinergic or antihistamine drugs. They do not tend to recur during neuroleptic treatment.

These tree reactions occur commonly in the first few weeks, often declining with time, and they are reversible on stopping drug treatment. The occurrence of acute dystonias is consistent with block of DA-nergic nigrostriatal pathway.

Tardive dyskinesia develops after months or years in 20-40% of patients treated with classical antipsychotic drugs, and is one of the main problems of antipsychotic therapy. It characterized by involuntary and excessive oral-facial movements. Sever tardive dyskinesia can cause feeding and breathing to be impaired as well as be disfiguring. There are several theories about the mechanism of tardive dyskinesia. One is that it is associated with a gradual increase in the number or hypersensitivity of D2 receptor sites in striatum (up-regulation), which is less marked with the atypical antipsychotic drugs. Another possibility is that chronic block of inhibitory D2-receptors enchances catecholamones and/or glutamate release in the striatum, leading to excitotoxic neurodegeneration.