Purpose. To examine the most prevalent risk factors found in patients with permanent obstetric brachial plexus injury (OBPI) to identify better predictors of injury. Methods. A population-based study was performed on 241 OBPI patients who underwent surgical treatment at the Texas Nerve and Paralysis Institute. Results. Shoulder dystocia (97%) was the most prevalent risk factor. We found that 80% of the patients in this study were not macrosomic, and 43% weighed less than 4000 g at birth. The rate of instrument use was 41% , which is 4-fold higher than the 10% predicted for all vaginal deliveries in the United States. Posterior subluxation and glenoid version measurements in children with no finger movement at birth indicated a less severe shoulder deformity in comparison with those with finger movement. Conclusions. The average birth weight in this study was indistinguishable from the average birth weight reported for all brachial plexus injuries. Higher birth weight does not, therefore, affect the prognosis of brachial plexus injury. We found forceps/vacuum delivery to be an independent risk factor for OBPI, regardless of birth weight. Permanently injured patients with finger movement at birth develop more severe bony deformities of the shoulder than patients without finger movement.
nous acyclovir and levofloxacin treatments were initiated. MRI of the brain was normal. Later, her level of consciousness improved, but there were still considerable memory impairment and slowing of the cognitive functions. The patient had a generalized seizure. EEG showed slow wave activity and irritative changes in the lateral left hemisphere. Intravenous phenytoin treatment was initiated. CSF examination showed 3 ϫ 10 6 /L leukocytes with negative bacterial and viral cultures and normal protein level (384 mg/L). On MRI, an increased signal intensity (edema) could be seen in the left hippocampal area (figure, A). There was no enhancement of the lesion after gadolinium infusion. On control MRI 6 weeks later, the edema had diminished (see figure, B).Serologic testing of serum and CSF samples was performed. C pneumoniae antibodies were detected using an enzyme immunoassay (EIA; Labsystems, Helsinki, Finland). On 27 August, a high concentration of 317 U/L was measured for C pneumoniae IgG in the serum and also IgA, but no IgM-type antibodies were detected. There were no antibodies against C pneumoniae in the CSF. On 8 September, there were 241 U/L anti-C pneumoniae IgG with positive IgA and negative IgM antibodies in the serum and 16 U/L IgG-type antibodies against C pneumoniae in the CSF but no anti-chlamydial IgM or IgA. Serologic tests (IgG and IgM, serum and CSF) were also performed for Borrelia burgdorferi, Mycoplasma pneumoniae, HIV, herpes simplex, varicella zoster, and cytomegalo-, adeno-, parainfluenza-, entero-, Sindbis-and parvoviruses, with negative diagnostic findings. CSF samples were tested by PCR for the presence of C pneumoniae, B burgdorferi, herpes simplex, and enteroviruses with negative findings.The patient was dismissed from the hospital on 10 September, and she continued taking azithromycin for a further 3-week period because of the suspected C pneumoniae infection. In January 2000, the CSF antibody titer for C pneumoniae was negative. The concentration of anti-chlamydial IgG in serum was 218 U/L, but no IgA or IgM-type antibodies were detected. The temporal lesions in the MRI had disappeared. In neuropsychological testing, the patient's memory was moderately impaired. She is still treated for symptomatic epilepsy.Discussion. The appearance of C pneumoniae antibodies in the CSF during the course of encephalitis suggests that C pneumoniae was responsible for the CNS involvement. The serum/CSF C pneumoniae IgG ratio was 15:1, which suggests that anti-C pneumoniae antibodies were intrathecally produced (normal ratio 200 to 300:1). There were no signs of blood-brain barrier leakage; the CSF protein concentration was not elevated, the CSF albumin index (CSF IgG concentration/CSF albumin concentration) was 0.12 (within the normal range), and the CSF sample was free of red blood cells. There was also no enhancement with contrast medium in the MRI. Importantly, there were no detectable antibodies against any other microbes in the CSF, despite considerable antibody concentrations in the serum of anti-...
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