Sankhla C, Lai E C, Jankovic J
Movement Disorders Clinic, Department of Neurology, Baylor College of Medicine, Houston, Texas 77030-3498, USA.
J Neurol Neurosurg Psychiatry. 1998 Nov;65(5):722-8. doi: 10.1136/jnnp.65.5.722.
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.
The 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).
Twenty 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.
The 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.
口下颌肌张力障碍（OMD）是一种局灶性肌张力障碍，表现为非自主性肌肉收缩，产生重复性、有规律的口部、下颌和舌部运动。肌张力障碍通常为特发性（原发性），但在某些情况下继发于周围神经损伤。周围神经损伤诱发的颈部和肢体肌张力障碍已得到充分认识，本研究的目的是明确周围神经损伤诱发的OMD的特征。
周围神经损伤诱发的OMD采用以下纳入标准：（1）肌张力障碍在损伤后数天或数月（最长1年）内起病；（2）患者病史或其医疗及牙科记录能充分证明有外伤史；（3）肌张力障碍的起病在解剖学上与损伤部位（面部和口腔）相关。
数据库中识别出27例OMD患者，其发病时间和解剖部位与既往损伤或手术相关。除外伤外未发现其他诱发因素。所有患者均无未决诉讼。发病时的平均年龄为50.11（标准差14.15）（范围23 - 74）岁，女性占比为2:1。初次外伤至OMD起病的平均潜伏期为65天（范围1天至1年）。10例（37%）患者有一些易感因素的证据，如运动障碍家族史、既往接触过抗精神病药物、伴有影响其他部位的肌张力障碍或特发性震颤。与21例原发性OMD患者相比，发病年龄、女性占比和临床表现无差异。然而，创伤后组肌张力障碍性书写痉挛、痉挛性发音障碍、磨牙症、特发性震颤和运动障碍家族史的发生率较低（p<0.05）。两组中肉毒毒素治疗的反应均优于药物治疗（p<0.005）。创伤后组颞下颌关节紊乱的手术干预更为频繁，且与肌张力障碍加重有关。
该研究表明，包括牙科手术在内的口下颌面部创伤可能促使OMD起病，尤其是在易感人群中。及时识别和治疗可预防进一步的并发症。
