PT  - JOURNAL ARTICLE
AU  - Diana E van Rooijen
AU  - Erica J Geraedts
AU  - Johan Marinus
AU  - Joseph Jankovic
AU  - Jacobus J van Hilten
TI  - Peripheral trauma and movement disorders: a systematic review of reported cases
AID  - 10.1136/jnnp.2010.232504
DP  - 2011 Aug 01
TA  - Journal of Neurology, Neurosurgery & Psychiatry
PG  - 892--898
VI  - 82
IP  - 8
4099  - http://jnnp.bmj.com/content/82/8/892.short
4100  - http://jnnp.bmj.com/content/82/8/892.full
SO  - J Neurol Neurosurg Psychiatry2011 Aug 01; 82
AB  - Objective To perform a systematic review of cases reported in the literature in which a peripheral trauma preceded the onset of a movement disorder (MD).Methods Two reviewers independently searched Medline and EMBASE. Data regarding patient characteristics, type of MD and type of injury were collected, as well as information on the spread of MD, predisposing factors, psychological characteristics, presence of nerve lesions and treatment.Results 133 publications presenting findings on 713 patients with peripherally induced movement disorders (PIMDs) were included. MDs were more frequent in women. The most commonly reported PIMD was fixed dystonia, which was often associated with pain and sensory abnormalities of the affected body part. In 26% of patients, a nerve injury was identified. More than one-third of patients had complex regional pain syndrome; these patients were younger, had a shorter interval before developing MDs and more often showed spread of MD to other body parts. Nearly 15% were diagnosed with a psychogenic movement disorder (PMD). PMD was associated with higher frequencies of fixed dystonia and tremor. In general, response to various treatments, including botulinum toxin administrations, was disappointing.Conclusions While there is overlap in clinical characteristics between PIMDs and PMDs, the current review indicates that there are many well documented organic cases of PIMDs. This suggests that MDs, such as dystonia, tremor, myoclonus and tics, may under certain circumstances (eg, nerve lesions or genetic predisposition) be triggered by peripheral trauma. Potential mechanisms that may explain the underlying pathophysiology are addressed.