Prevalence of hyperactive digastric muscles during swallowing as measured by electromyography in patients with myofascial pain dysfunction syndrome.

One purpose of this clinical study is to establish a relationship between the hyper activity of the digastric muscles and predisposition of an individual to MPDS (myofacial pain dysfunction syndrome). If a population predisposed to MPD could be identified by an early diagnosis, intervention and treatment could eliminate potential pain in adulthood. Secondly, can the employment of electromyography to aid in the diagnosis of patients with MPD be helpful in establishing a program of prevention and treatment? Thirty-one patients, male and female, were randomly selected from among those routinely diagnosed as having myofascial pain dysfunction syndrome by the dental staff at the Long Island Center for Craniofacial Pain. Eighteen patients who did not experience any symptoms of facial pain comprised the control group in the study. This study demonstrated that the average trace readings which indicate the activity of the digastric muscles, as measured by the electromyogram from patients experiencing facial pain were significantly higher than those from patients without pain symptoms. In every instance, the correlation between facial pain and abnormal swallow patterns which are a cause of hyperactivity of the digastrics was confirmed.

Activation of factor XI in plasma is dependent on factor XII.

The activation of factor XI initiates the intrinsic coagulation pathway. Until recently it was believed that the main activator of factor XI is factor XIIa in conjunction with the cofactor high molecular weight kininogen on a negatively charged surface. Two recent reports have presented evidence that in a purified system factor XI is activatable by thrombin together with the soluble polyanion dextran sulfate. To assess the physiological relevance of these findings we studied the activation of factor XI in normal and factor XII-deficient plasma. We used either kaolin/cephalin or dextran sulfate as a surface for the intrinsic coagulation pathway, tissue factor to generate thrombin via the extrinsic pathway, or the addition of alpha-thrombin directly. 125I-factor XI, added to factor XI-deficient plasma at physiologic concentrations (35 nmol/L), is rapidly cleaved on incubation with kaolin. The kinetics appear to be exponential with half the maximum cleavage at 5 minutes. Similar kinetics of factor XI cleavage are seen when 40 nmol/L factor XIIa (equal to 10% of factor XII activation) is added to factor XII-deficient plasma if an activating surface is provided. Tissue factor (1:500) added to plasma did not induce cleavage of factor XI during a 90-minute incubation, although fibrin formation within 30 seconds indicated that thrombin was generated via the extrinsic pathway. Adding 1 mumol/L alpha-thrombin (equivalent to 50% prothrombin activation) directly to factor XII deficient or normal plasma (with or without kaolin/cephalin/Ca2+ or dextran sulfate) led to instantaneous fibrinogen cleavage, but again no cleavage of factor XI was observable. We conclude that in plasma surroundings factor XI is not activated by thrombin, and that proposals of thrombin initiation of the intrinsic coagulation cascade are not supportable.