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Biomedical subjects

K L Kaye

Publications and source records attributed to K L Kaye.

4 recordsLinked to original sources

Cervical flexion myelopathy after valproic acid overdose.

STUDY DESIGN: Case report and literature review of cervical flexion myelopathies. OBJECTIVE: To increase awareness that prolonged extreme neck flexion, in association with profound muscular relaxation, can produce a severe cervical myelopathy. SUMMARY OF BACKGROUND DATA: Similar case reports of cervical myelopathies have been documented in the neurosurgical literature after intraoperative prolonged neck flexion, and after forcible prolonged neck flexion during a robbery. To the authors' best knowledge, this is the first report of a cervical flexion myelopathy after a medication overdose, and the only clinical-pathologic correlation. METHODS: Retrospective case report with clinical, radiographic, and postmortem data available for analysis. RESULTS: A transverse myelopathy at the sixth cervical level developed in a 25-year-old woman after an overdose of valproic acid in a suicide attempt. She was found in the sitting position, with her neck in extreme flexion, where she had been for an estimated 18 hours. Magnetic resonance imaging showed that her cervical cord was enlarged, maximally at C6, with prominent paraspinal soft tissue swelling. The patient died of pulmonary embolism and pneumonia. Pathologic findings included transverse spinal cord necrosis at C6; central gray matter necrosis extended to several segments below this. CONCLUSION: Prolonged extreme neck flexion, in association with profound muscular relaxation, can produce a severe myelopathy that is at least partly related to compromise of the spinal cord's microcirculation.

Adult↗

Human cerebrovascular nerve fibers immunoreactive for synaptophysin, chromogranin A and tyrosine hydroxylase.

The innervation of human cerebral blood vessels has been examined using synaptophysin, a marker of synaptic vesicles, and chromogranin A, a marker of large dense-core vesicles. The catecholaminergic marker tyrosine hydroxylase was used for comparison. Synaptophysin and tyrosine hydroxylase demonstrated a similar distribution of nerve fibers whereas chromogranin A terminals were only sparsely evident. Our results suggest that there is not a subset of nerve fibers in existence which has a distribution different than that of catecholaminergic fibers. Furthermore, in view of its unexpected sparse distribution, chromogranin A in the nervi vasorum is not likely to be a significant contributor to cerebral blood flow regulation.

Adult↗

Cerebritis due to group B streptococcus.

A premature infant who died of early-onset group B streptococcal meningitis was found to have cerebritis with direct bacterial infection of the basal ganglia. Although the organism was sensitive to penicillin by in vitro testing, it was not eradicated from the cerebrospinal fluid after 48 h of antibiotic treatment. These findings illustrate that suppurative extension with cerebritis of the basal ganglia as a complication of group B streptococcal meningitis may be one of the factors responsible for treatment failure.

Basal Ganglia Diseases↗

Therapy for experimental endocarditis due to Staphylococcus epidermidis.

Vancomycin was evaluated with and without gentamicin and/or rifampin in therapy for endocarditis due to methicillin-resistant Staphylococcus epidermidis in rabbits. Vancomycin (30 mg/kg iv every 12 hr), gentamicin (3.5 mg/kg im every 8 hr), rifampin (20 mg/kg im every 12 hr), combinations of vancomycin plus gentamicin, vancomycin plus rifampin, and vancomycin plus gentamicin plus rifampin were injected for two days, and the number of bacteria in vegetations was determined. Ratios of minimal inhibitory concentrations to minimal bactericidal concentrations (microgram/ml) for S. epidermidis were 3.1:25 for vancomycin, 0.2:0.8 for gentamicin, and 0.4:0.4 for rifampin. After two days of therapy, mean log colony-forming units +/- SD in vegetations were 7.1 +/- 1.5 (none of eight animals were sterile) for vancomycin; 4.6 +/- 2.2 (two of nine) for gentamicin; 4.5 +/- 2.2 (two of eight) for rifampin; 3.3 +/- 1.3 (three of 10) for vancomycin plus gentamicin; 2.7 +/- 1.2 (three of nine) for vancomycin plus rifampin; 2.1 +/- 0.2 (eight of nine) for vancomycin plus gentamicin plus rifampin; and 8.1 +/- 1.3 (none of 12) for the control group. Gentamicin, rifampin, vancomycin plus gentamicin, and vancomycin plus rifampin were significantly more effective than was vancomycin; vancomycin plus rifampin was more effective than was gentamicin alone; and the combination of vancomycin plus gentamicin plus rifampin was more effective than were the drugs administered alone or in the combinations vancomycin plus gentamicin and vancomycin plus rifampin. Two days of treatment followed by seven days of no treatment resulted in 71%, 29%, and 14% sterile vegetations in rabbits receiving the combination therapy vancomycin plus gentamicin plus rifampin, vancomycin plus rifampin, and vancomycin plus gentamicin, respectively.

Animals↗