Movement disorders and psychosis, a complex marriage

[anon79999497]

The relationship between psychosis and movement disorders has been described for more than a century often referring to stereotypies (purposeless, meaningless actions), and mannerisms (peculiar ways of carrying out normal actions), but also to non-drug induced dyskinesia or parkinsonism and catatonia. However, nowadays most clinicians relate parkinsonism and dyskinesia directly to acute and tardive drug induced movement disorders. Acute drug induced movement disorders Acute drug induced movement disorders such as acute dystonia, parkinsonism, and akathisia, are very common side effects of dopamine blocking agents. If antipsychotic naïve psychotic patients without clinical signs of movement disorders receive antipsychotics and develop these side effects, which disappear after dose reduction or cessation of the antipsychotics and this on-off mechanism can be repeated, the causal relationship between these movement disorders and antipsychotics is beyond any doubt. Tardive syndromes The relationship between tardive syndromes and antipsychotics is far more complex because they start after months to years of treatment with antipsychotics and can also be suppressed by antipsychotics. Tardive suggest drug induced, but also spontaneous hyperkinetic dyskinesia’s, such as “grimacing” and “irregular movements of tongue and lips” (and also parkinsonism), are prevalent in antipsychotic naïve psychotic patients and have been described by Kraepelin and Bleuler more than 100 years ago. Also, recent studies show that the numbers of spontaneous movement disorders such as dyskinesia, bradykinesia and soft neurological signs related to schizophrenia are substantial and increasing with age [1; 2; 3; 4; 5; 6; 7]. There is no test to differentiate in psychotic patients with long-term use of antipsychotics, between tardive drug induced movement disorders and spontaneous movement disorders. A metanalysis showed that in antipsychotic naïve patients with schizophrenia the risk of dyskinesia and parkinsonism are respectively, three and five times higher than in healthy controls [8]. Another study in antipsychotic naïve patients showed a prevalence of clinical signs of dyskinesia and parkinsonism of respectively, 13 and 18% which increased to 20% and 28% respectively, with the use of instrumental assessment [9]. On the other hand several findings suggest a direct relationship between antipsychotics and tardive dyskinesia. First, non-psychiatric patients may also develop tardive dyskinesia after long term use of dopamine blocking agents e.g. long term use of metoclopramide in nausea, or long term use of antipsychotics for insomnia [10; 11].

http://journal.frontiersin.org/Journal/122284/full