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Movement Disorders Clinic, Department of Neurology,
Baylor College of Medicine, Houston, Texas, USA
Correspondence to: Professor J Jankovic, Movement Disorders Clinic, Department of Neurology, Baylor College of Medicine, 6550 Fannin, Suite 1801, Houston, Texas 77030-3498, USA. Telephone 001 713 798 5998; fax 001 713 798 6808.
Received 19 December 1997 and in revised form 29 April 1998;
Accepted 2 May 1998
OBJECTIVES
Oromandibular dystonia (OMD) is a
focal dystonia manifested by involuntary muscle contractions producing
repetitive, patterned mouth, jaw, and tongue movements. Dystonia is
usually idiopathic (primary), but in some cases it follows peripheral
injury. Peripherally induced cervical and limb dystonia is well
recognised, and the aim of this study was to characterise peripherally
induced OMD.
METHODSThe following inclusion criteria were used
for peripherally induced OMD: (1) the onset of the dystonia was within
a few days or months (up to 1 year) after the injury; (2) the trauma
was well documented by the patient's history or a review of their medical and dental records; and (3) the onset of dystonia was anatomically related to the site of injury (facial and oral).
RESULTSTwenty seven patients were
identified in the database with OMD, temporally and anatomically
related to prior injury or surgery. No additional precipitant other
than trauma could be detected. None of the patients had any litigation
pending. The mean age at onset was 50.11 (SD 14.15) (range 23-74)
years and there was a 2:1 female preponderance. Mean latency between
the initial trauma and the onset of OMD was 65 days (range 1 day-1
year). Ten (37%) patients had some evidence of predisposing factors
such as family history of movement disorders, prior exposure to
neuroleptic drugs, and associated dystonia affecting other regions or
essential tremor. When compared with 21 patients with primary OMD,
there was no difference for age at onset, female preponderance, and
phenomenology. The frequency of dystonic writer's cramp, spasmodic
dysphonia, bruxism, essential tremor, and family history of movement
disorder, however, was lower in the post-traumatic group (p<0.05). In
both groups the response to botulinum toxin treatment was superior to
medical therapy (p<0.005). Surgical intervention for
temporomandibular disorders was more frequent in the post-traumatic
group and was associated with worsening of dystonia.
CONCLUSIONThe study indicates that
oromandibular-facial trauma, including dental procedures, may
precipitate the onset of OMD, especially in predisposed people. Prompt
recognition and treatment may prevent further complications.
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  G Abbruzzese, A Berardelli, P Girlanda, R Marchese, D Martino, F Morgante, L Avanzino, C Colosimo, and G Defazio Long-term assessment of the risk of spread in primary late-onset focal dystonia J. Neurol. Neurosurg. Psychiatry, April 1, 2008; 79(4): 392 - 396. [Abstract] [Full Text] [PDF]
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 G. Defazio, A. Berardelli, and M. Hallett Do primary adult-onset focal dystonias share aetiological factors? Brain, May 1, 2007; 130(5): 1183 - 1193. [Abstract] [Full Text] [PDF]
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D. Martino, G. Defazio, G. Abbruzzese, P. Girlanda, M. Tinazzi, G. Fabbrini, M. S. Aniello, L. Avanzino, C. Colosimo, G. Majorana, et al. Head trauma in primary cranial dystonias: a multicentre case-control study J. Neurol. Neurosurg. Psychiatry, March 1, 2007; 78(3): 260 - 263. [Abstract] [Full Text] [PDF]
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E.-K. Tan and J. Jankovic Tardive and idiopathic oromandibular dystonia: a clinical comparison J. Neurol. Neurosurg. Psychiatry, February 1, 2000; 68(2): 186 - 190. [Abstract] [Full Text] [PDF]
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 E.-K. TAN and J. JANKOVIC TREATING SEVERE BRUXISM WITH BOTULINUM TOXIN J Am Dent Assoc, February 1, 2000; 131(2): 211 - 216. [Abstract] [Full Text] [PDF]
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 E.-K. Tan and J. Jankovic Botulinum toxin A in patients with oromandibular dystonia: Long-term follow-up Neurology, December 1, 1999; 53(9): 2102 - 2102. [Abstract] [Full Text]
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