ObjectiveTo ascertain the etiology of non-traumatic plexopathy and clarify the clinical, electrophysiological characteristics according to its etiology.MethodWe performed a retrospective analysis of 63 non-traumatic plexopathy patients that had been diagnosed by nerve conduction studies (NCS) and needle electromyography (EMG). Clinical, electrophysiological, imaging findings were obtained from medical records.ResultsWe identified 36 cases with brachial plexopathy (BP) and 27 cases with lumbosacral plexopathy (LSP). The causes of plexopathy were neoplastic (36.1%), thoracic outlet syndrome (TOS) (25.0%), radiation induced (16.7%), neuralgic amyotrophy (8.3%), perioperative (5.6%), unknown (8.3%) in BP, while neoplastic (59.3%), radiation induced (22.2%), neuralgic amyotrophy (7.4%), psoas muscle abscess (3.7%), and unknown (7.4%) in LSP. In neoplastic plexopathy, pain presented as the first symptom in most patients (82.8%), with the lower trunk of the brachial plexus predominantly involved. In radiation induced plexopathy (RIP), pain was a common initial symptom, but the proportion was smaller (50%), and predominant involvements of bilateral lumbosacral plexus and whole trunk of brachial or lumbosacral plexus were characteristic. Myokymic discharges were noted in 41.7% patients with RIP. Abnormal NCS finding in the medial antebrachial cutaneous nerve was the most sensitive to diagnose TOS. Neuralgic amyotrophy of the brachial plexus showed upper trunk involvement in all cases.ConclusionBy integrating anatomic, pathophysiologic knowledge with detailed clinical assessment and the results of ancillary studies, physicians can make an accurate diagnosis and prognosis.
ObjectiveTo investigate the clinical usefulness of the Schedule for Oral-Motor Assessment (SOMA) in children with dysphagia by comparing findings of SOMA with those of the videofluoroscopic swallowing study (VFSS).MethodBoth SOMA and VFSS were performed in 33 children with dysphagia (21 boys and 12 girls; mean age 17.3±12.1 months) who were referred for oropharyngeal evaluation. Ratings of oral-motor functions indicated by SOMA were based upon the cutting score of each specific texture of food (puree, semi-solids, solids, cracker, liquid-bottle, and liquid-cup). Abnormalities of either the oral phase, or the pharyngeal phase as indicated by VFSS were assessed by a physician and a speech-language pathologist.ResultsThere was significant consistency between the findings of SOMA and the oral phase evaluation by VFSS (Kappa=0.419, p=0.023). SOMA reached 87.5% sensitivity, 66.6% specificity, and 95.4% positive predictive value when compared with the oral phase of the VFSS. We were able to evaluate oral-motor function by using SOMA in 6 children who were unable to complete the oral phase evaluation by VFSS, due to fear and crying during the study. The findings of SOMA failed to show any consistency with the pharyngeal phase evaluation by VFSS (Kappa=-0.105, p=0.509).ConclusionThese results suggest that SOMA is a reliable method for evaluation of oral-motor function in children with dysphagia. In particular, SOMA is recommended for children that were unable to complete the oral phase evaluation by VFSS due to poor cooperation.
Warfarin is a frequently prescribed anticoagulant in rehabilitation patients. Adverse drug reactions of warfarin were reported as bleeding and cutaneous microvascular thrombosis. Major bleeding, such as intracranial hemorrhage and psoas hematoma, in patients receiving anticoagulation therapy is a rare condition, but sometimes very serious complication that can even be fatal. Patient-specific factors (eg, age, body size, race, concurrent diseases, and medications) explain some of the individual variability in warfarin dose, but genetic factors, which influence warfarin response, explain a significantly higher proportion of the variability in the dose. There are two identified genes that are responsible for the main proportion of the genetic effect: CYP2C9, which codes for the enzyme cytochrome P450 2C9 that metabolizes S-warfarin, and VKORC1, which codes for warfarin's target, vitamin K epoxide reductase. We report a case of intolerance to warfarin dosing, due to impaired drug metabolism in a patient with CYP2C9*1/*3 and VKORC 1173TT. Fortunately, there are no severe complications.
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