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Dystonia

Dystonia may occur in association with untreated PD, such as action-induced bending (flexion) of the foot that worsens with walking. More specifically, there may be inward turning of the heel and upward bending (flexion) of the sole of the foot (equinovarus deformity), with flexion of the second to fifth toes and backward flexion (i.e., upward bending or dorsiflexion) of the great toes. As mentioned earlier, adult-onset lower limb dystonia suggests the possibility of PD or other parkinsonism syndromes.

Many PD patients also may develop dystonic flexion of the trunk during the disease course. Less commonly, untreated PD patients may be affected by dystonia of the upper limbs. In addition, there have been a few reports in which untreated individuals developed hemidystonia or focal dystonia of muscles of the eyelids (blepharospasm); jaw, mouth, and lower face (oromandibular dystonia); or neck (cervical dystonia). However, some researchers have questioned the significance of such findings, indicating that the frequency of focal dystonia in PD is similar to its expected frequency in the same age group. As mentioned earlier, dystonia may also develop as a complication of therapy for PD, occurring secondary to the administration of L-dopa.

The specific cause of PD remains unknown. Ongoing research has focused on the role that various genes, exposure to certain chemicals, and other mechanisms may play in potentially causing the disorder. The symptoms and findings associated with PD are thought to primarily result from progressive loss of nerve cells within a certain region of the substantia nigra and the striatum (nigrostriatal system) of the brain and associated deficient production of the neurotransmitter dopamine.

Source:  Dystonia


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