Biomedical subjects
Publications and source records attributed to R L Ruff.
Thirty-five cases of benign acute childhood myositis followed infections with influenza A or B. Two children had recurrent myositis associated with infections of different influenza types. None of the children had acute-phase antibody titers to the infecting type of influenza. These results are consistent with the proposal that benign acute childhood myositis can occur only with the initial infection of a viral type.
We explored the possibility that glucocorticoid-induced muscle weakness and atrophy resulted from impaired muscle membrane excitability. Male Sprague-Dawley rats received intramuscular injections of dexamethasone, cortisone acetate (equivalent anti-inflammatory doses), or saline for up to 28 days. Temporal patterns of change in muscle mass, twitch and tetanic tension, and membrane potential, cable parameters, and excitability were studied in vitro in the extensor digitorum longus (EDL), soleus (SOL), omohyoid (OMO), caudofemoralis (CF), and the sternomastoid muscles (membrane potential only). the membrane properties of EDL fibers were also studied in vivo (pentobarbital anesthesia). The relative severity of atrophy was OMO greater than CF greater than EDL greater than SOL. Reduction in twitch or tetanic tension never preceded atrophy. The twitch and tetanic tension (per g muscle) increased with glucocorticoid treatment. There were no significant changes in the time course of the twitch or tetanus. Dexamethasone produced more severe atrophy and force reduction than did cortisone acetate. Glucocorticoid treatment produced a depolarization of EDL muscle fibers measured in vitro at 23 degrees C, but this did not appear to be physiologically significant because EDL fibers studied in vivo were not depolarized and had normal action potential amplitudes and thresholds. Glucocorticoid treatment did not change the membrane resistance or capacitance. We conclude that glucocorticoid treatment did not produce muscle weakness by impairing sarcolemmal excitability or excitation-contraction coupling, but that the weakness resulted from muscle atrophy.
The effect of the local anesthetic QX222 on the kinetics of miniature end-plate currents (MEPC)and acetylcholine-induced end-plate current fluctuations was studied in voltage-clamped frog cutaneous pectoris neuromuscular junctions. The rate constants for a kinetic scheme of local anesthetic blockage of end-plate channels were calculated from the MEPC decay parameters. At 18 degrees C the blocking rate constant was 1.1 +/- 0.3 x 10(7) exp (-0.009 +/- 0.003 x V)s -1M-1, and the unblocking rate constant was 5.7 +/- 0.6 exp (0.011 +/- 0.002 x V)s -1. The dissociation constant was close to 10 microM at -80 mV. End-plate fluctuations indicated that the local anesthetic QX222 lowered the effective single-channel conductance, suggesting a finite blocked state conductance that was calculated to be 1.6 pS. The apparent differences between QX222 interaction with end-plate and extrajunctional channels are discussed.
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Four patients with environmental reduplication, a specific form of spatial disorientation and confabulation are described. The patients maintained that their hospital rooms were located in their homes. Each patients had evidence of right frontal or right parietal injury based upon computed tomography, neurosurgery, and neuropsychological testing. The factors associated with environmental reduplication were: impaired spatial perception and visual memory, inability of the patients to recognise the inconsistency between their believed location and their actual location, confusion soon after admission to hospital, and a strong desire to be at home.
A 15-year-old right-handed woman had selective impairment of speech--aphemia--after drainage of a left frontal hematoma caused by an arteriovenous malformation. There was no buccofacial or pharyngeal muscle dysfunction. Computerized tomography demonstrated residual injury extending from the Broca area to the inferior left precentral gyrus. Aphemia may have resulted from disruption of the connection between Broca's area and the portion of the motor cortex that controls oral and pharyngeal muscles.
Of 217 patients with clinical diagnosis of acute stroke 23% had nonischemic lesions diagnosed by computed tomography (CT) or lumbar puncture (LP). CT demonstrated all 37 cases of intracerebral hemorrhagic lesions; 9 were detected by LP. CT failed to demonstrate 8 of 17 cases of subarachnoid hemorrhage, but only 1 of these lacked headache or stiff neck. In 7 of 342 patients who were treated with anticoagulants after LP, spinal hematoma followed LP ( 5 with paraparesis). CT evaluation reduced the incidence of fatal cerebral hemorrhage during anticoagulant therapy of acute stroke. However, even if patients were evaluated with both CT and LP, the incidence of fatal cerebral hemorrhage resulting from intravenous anticoagulant therapy was 2.4%.
Concentrations of n-hexane greater than the threshold limit value (TLV) of 500 ppm are known to produce peripheral neuropathy. This report describes the case of a worker who developed peripheral neuropathy, with a histologic pattern characteristic of n-hexane toxicity, after chronic on-the-job exposure to n-hexane at concentrations less than 450 ppm. We suggest that the current TLV for n-hexane be reevaluated.
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A middleaged woman with a four year history of behavioural change including episodes of catatonia is described. Despite a persistently abnormal electroencephalogram, the patient was diagnosed repeatedly as suffering from a primary psychiatric disorder. Neurological examination and psychological testing suggested frontal lobe dysfunction, which was confirmed by the finding of isolated frontal lobe atrophy on computed axial tomography.
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