Extrapyramidal tracts are chiefly found in the reticular formation of the pons and medulla, and target neurons in the spinal cord involved in reflexes, locomotion, complex movements, and postural control. These tracts are in turn modulated by various parts of the central nervous system, including the nigrostriatal pathway, the basal ganglia, the cerebellum, the vestibular nuclei, and different sensory areas of the cerebral cortex. All of these regulatory components can be considered part of the extrapyramidal system, in that they modulate motor activity without directly innervating motor neurons.
The extrapyramidal system can be affected in a number of ways, which are revealed in a range of extrapyramidal symptoms such as akinesia (inability to initiate movement) and akathisia (inability to remain motionless).
Extrapyramidal symptoms (EPS) are the various movement disorders such as tardive dyskinesia suffered as a result of taking dopamine antagonists, usually antipsychotic (neuroleptic) drugs, which are often used to control psychosis, especially schizophrenia. Other antidopaminergic drugs like the antiemetic metoclopramide or the tricyclic antidepressant amoxapine can also cause extrapyramidal side effects.
The best known EPS is tardive dyskinesia (involuntary, irregular muscle movements, usually in the face). Other common EPS include akathisia (restlessness), dystonia (muscular spasms of neck - torticollis, eyes - oculogyric crisis, tongue, or jaw; more frequent in children), drug-induced parkinsonism (muscular lead-pipe rigidity, bradykinesia/akinesia, resting tremor, postural instability; more frequent in adults and the elderly),
Although Parkinson's Disease is primarily a disease of the nigrostriatal pathway and not the extrapyramidal system, loss of dopaminergic neurons in the substantia nigra leads to dysregulation of the extrapyramidal system. Since this system regulates posture and skeletal muscle tone, a result is the characteristic bradykinesia of Parkinson's.
Extrapyramidal symptoms can also be caused by brain damage, as in athetotic cerebral palsy, which is involuntary writhing movements caused by prenatal or perinatal brain damage.
Anticholinergic drugs are used to control neuroleptic-induced EPS, although akathisia may require beta blockers or even benzodiazepines. If the EPS are induced by a typical antipsychotic, EPS may be reduced by dose titration or by switching to an atypical antipsychotic, such as aripiprazole, ziprasidone, quetiapine, olanzapine, risperidone or clozapine. These medications possess an additional mode of action that is believed to negate their effect on the nigrostriatal pathway, which means they are associated with fewer extrapyramidal side effects than "conventional" antipsychotics (chlorpromazine, haloperidol, etc.).