The various forms of dystonia can be classified into two broad groups: primary dystonias and secondary dystonias. Primary dystonias are largely genetic in origin whereas secondary dystonias result from apparent outside factors and are usually attributed to a specific cause, such as exposure to certain medications, trauma, toxins, infections, or stroke.
Secondary dystonia is defined as a dystonic disorder that develops mainly as the result of environmental factors that provide insult to the brain. Spinal cord injury, head, and peripheral injury are also recognised contributors to dystonia. Other examples of secondary dystonias include levodopa-induced dystonia in the treatment of parkinsonism; acute and tardive dystonia due to dopamine receptor blocking agents; and dystonias associated with cerebral palsy, cerebral hypoxia, cerebrovascular disease, cerebral infections and post infectious states, stroke, encephalitis, brain tumor, and toxicants such as manganese, cyanide, and 3-nitroproprionic acid.
A number of disorders in this group, such as infectious and toxicant-induced neurodegenerations, do not present as pure dystonia, but, with a mixture of other neurologic features, often present parkinsonian features of bradykinesia and rigidity.
Many of the ascribed causes of secondary dystonias are based on historical information or subtle clinical findings and have no diagnostic, radiologic, serologic, or other pathologic marker. One issue debated regarding secondary dystonias is the causal relationship with environmental factors, specifically neuroleptic exposure, perinatal asphyxia, and head and peripheral trauma. It is unclear whether these common insults alone are sufficient to cause dystonia or, as proposed in several studies, if they precipitate or exacerbate symptoms in genetically predisposed individuals. Research continues to better understand these various manifestations of dystonia.