Delayed segmental motor paralysis following laminoplasty: two case reports.

STUDY DESIGN: Two patients who experienced the onset of segmental motor paralysis several years after laminoplasty are presented. OBJECTIVES: To discuss the mechanism of development of delayed segmental motor paralysis following laminoplasty. SETTING: A department of orthopaedic surgery in Japan. METHODS: One patient experienced motor weakness in his deltoid and biceps muscles on the left side 5 years after laminoplasty. The other patient noticed motor weakness in his deltoid and biceps on the right side 7 years after laminoplasty. CT myelography revealed posterior spur formation and hypertrophic facet joints on the hinged side at the C4-C5 level in both patients. RESULTS: Posterior foraminotomy was performed at the C4-C5 level on the hinged side in both patients. Postoperatively, motor weakness in the deltoid and biceps muscles was improved in both patients. CONCLUSIONS: Although spondylotic changes, including spur formation and disc herniation, have occasionally developed in operated segments after laminoplasty, few patients have required additional surgery for treatment of relapse of neurological deficits. It has been believed that spinal cord is rarely compressed by the spondylotic changes since it shifts posteriorly in the enlarged spinal canal. However, laminoplasty disturbs the facet joints since the medial portion of dorsal cortex and cancellous bone in facet joints is drilled out to make a trough. Facet joints disturbed in this fashion undergo degeneration over time after surgery. Nerve roots may occasionally be compressed by degenerated facet joints and spurs that have developed at the entrance of root canal, resulting in segmental motor paralysis several years after laminoplasty. Careful long-term observation is necessary after this procedure.

Complications associated with intraarterial administration of papaverine for vasospasm following subarachnoid hemorrhage--two case reports.

Complications associated with intraarterial papaverine infusion occurred in two patients treated for vasospasm due to subarachnoid hemorrhage (SAH). A 42-year-old male with an anterior communicating artery aneurysm underwent craniotomy and aneurysm clipping. Five days after the SAH occurred, angiography demonstrated moderate vasospasm in spite of hypervolemic-hypertensive therapy. During papaverine infusion into the carotid artery, he suffered loss of consciousness due to a seizure for a few minutes. A 61-year-old female with a right internal carotid-posterior communicating artery aneurysm underwent clipping. Six days after the SAH occurred, angiography demonstrated severe vasospasm in spite of hypervolemic-hypertensive therapy. Angiography performed immediately after papaverine infusion into the carotid artery revealed exacerbation of the vasospasm. Finally she suffered cerebral infarction and died. Complications of intraarterial papaverine infusion are potentially dangerous. We recommend trial administration of papaverine with angiography and neurological examination before full dose infusion to avoid complications.

Differential effects of pressure or volume overload on myocardial MMP levels and inhibitory control.

Left ventricular (LV) pressure (PO) or volume (VO) overload is accompanied by myocardial remodeling, but mechanisms that contribute to this progressive remodeling process remain unclear. The matrix metalloproteinases (MMPs) contribute to tissue remodeling in a number of disease states. This study tested the hypothesis that increased MMP expression and activity occur after the induction of an LV overload, which is accompanied by a loss of endogenous MMP inhibitory control. LV MMP zymographic activity and species abundance were measured in dogs under the following conditions: acute PO induced by ascending aortic balloon inflation (6 h, n = 9), prolonged PO by aortic banding (10 days, n = 5), acute VO through mitral regurgitation secondary to chordal rupture (6 h, n = 6), prolonged VO due to mitral regurgitation (14 days, n = 7), and sham controls (n = 11). MMP zymographic activity in the 92-kDa region, indicative of MMP-9 activity, increased over threefold in acute PO and VO and fell to control levels in prolonged PO and VO. The MMP-9 activity-to-abundance ratio increased by over fourfold with acute VO and twofold in acute PO, suggesting a loss of inhibitory control. Endogenous MMP inhibitor content was unchanged with either PO or VO. Interstitial collagenase (MMP-1) content decreased by 50% with acute VO but not with acute PO. Stromelysin (MMP-3) levels increased by 40% with acute VO and increased by 80% with prolonged PO. Although changes in LV myocardial MMP activity and inhibitory control occurred in both acute and prolonged PO and VO states, these changes were not identical. These results suggest that the type of overload stimulus may selectively influence myocardial MMP activity and expression, which in turn would affect the overall LV myocardial remodeling process in LV overload.

Successful treatment using high-dose intravenous immunoglobulin in a patient with rapidly progressive interstitial pneumonia associated with dermatomyositis.

Abstract A 36-year-old male patient with dermatomyo-sitis (DM) associated with rapidly progressive interstitial pneumonia (IP) was successfully treated by high-dose intravenous immunoglobulin (IVIG). He suffered from myopathy, skin lesions, and IP. In spite of the treatment with a high-dose corticosteroid, IP progressed rapidly. Then high-dose intravenous immunoglobulin (20 g/day, 4 days) was administered. The skin lesions, myopathy, and pulmonary lesions improved. High-dose IVIG was considered to be a relatively safe and effective treatment for progressive IP associated with DM.

Translational mechanisms accelerate the rate of protein synthesis during canine pressure-overload hypertrophy.

This study examined how translational mechanisms regulate the rate of cardiac protein synthesis during canine pressure overload in vivo. Acute aortic stenosis (AS) was produced by inflating a balloon catheter in the ascending aorta for 6 h; sustained AS was created by controlled banding of the ascending aorta. AS caused significant hypertrophy as reflected by increased left ventricular (LV) mass after 5 and 10 days. To monitor LV protein synthesis in vivo, myosin heavy chain (MHC) synthesis was measured by continuous infusion of radiolabeled leucine. Acute AS accelerated the rate of myosin synthesis without a corresponding increase in ribosomal RNA, indicating an increase in translational efficiency. Total MHC synthesis (mg MHC/LV per day) was significantly increased at 5 and 10 days of sustained AS. Total MHC degradation was not significantly altered at 5 days of AS but increased at 10 days of AS in concordance with a new steady state with respect to growth. Translational capacity (mg total RNA/LV) was significantly increased after 5 and 10 days of AS and was preceded by an increase in the rate of ribosome formation. MHC mRNA levels remained unchanged during AS. These findings demonstrate that cardiac protein synthesis is accelerated in response to pressure overload by an initial increase in translational efficiency, followed by an adaptive increase in translational capacity during sustained hypertrophic growth.

Mechanisms of cardiac hypertrophy in canine volume overload.

This study tested whether the modest hypertrophy that develops in dogs in response to mitral regurgitation is due to a relatively small change in the rate of protein synthesis or, alternatively, is due to a decreased rate of protein degradation. After 3 mo of severe experimental mitral regurgitation, the left ventricular (LV) mass-to-body weight ratio increased by 23% compared with baseline values. This increase in LV mass occurred with a small, but not statistically significant, increase in the fractional rate of myosin heavy chain (MHC) synthesis (Ks), as measured using continuous infusion with [3H]leucine in dogs at 2 wk, 4 wk, and 3 mo after creation of severe mitral regurgitation. Translational efficiency was unaffected by mitral regurgitation as measured by the distribution of MHC mRNA in polysome gradients. Furthermore, there was no detectable increase in translational capacity as measured by either total RNA content or the rate of ribosome formation. These data indicate that translational mechanisms that accelerate the rate of cardiac protein synthesis are not responsive to the stimulus of mitral regurgitation. Most of the growth after mitral regurgitation was accounted for by a decrease in the fractional rate of protein degradation, calculated by subtracting fractional rates of protein accumulation at each time point from the corresponding Ks values. We conclude that 1) volume overload produced by severe mitral regurgitation does not trigger substantial increases in the rate of protein synthesis and 2) the modest increase in LV mass results primarily from a decrease in the rate of protein degradation.

Increased expression of interleukin-2 receptor alpha on peripheral blood mononuclear cells in HTLV-I tax/rex mRNA-positive asymptomatic carriers.

Using the double-nested reverse transcription-polymerase chain reaction, we assayed human T-cell leukemia virus type I (HTLV-I) tax/rex-encoded mRNA in the peripheral blood mononuclear cells (PBMCs) of asymptomatic carriers as an index of the expression of HTLV-I in vivo in relation to the proviral DNA level. HTLV-I tax/rex mRNA was detected in only 1 (3.3%) of 30 samples with medium or lower proviral DNA levels, but it was detected in 11 (39.3%) of 28 samples with high HTLV-I proviral DNA levels, estimated as equal to or more than the proviral DNA of 10 ng of HUT102 (i.e., HUT102 cells were used as positive controls). The mean number of interleukin-2 receptor alpha (IL-2R alpha)-positive cells as a percentage of the total number of PBMCs was higher (13.2%) in the tax/rex mRNA-positive carriers with high proviral DNA levels than in the carriers who were mRNA negative (8.4%) (p = 0.004, Wilcoxon test). These results suggest that virus activation as indicated by the presence of tax/rex mRNA in asymptomatic carriers with high proviral DNA levels is associated with an elevation of the IL-2R alpha-positive cells in vivo.

Prevalence of genotypes of Orientia tsutsugamushi in patients with scrub typhus in Miyazaki Prefecture.

The genotypes of Orientia tsutsugamushi in patients with scrub typhus in Miyazaki Prefecture were examined by polymerase chain reaction (PCR) and the restriction fragment length polymorphism method. Specific patterns for genotypes Irie, Hirano, Tazume and Yoshimura were detected in 26, 6, 5 and 2 of 39 DNA samples obtained from peripheral blood mononuclear cells, respectively. DNA sequences of the PCR products from the Tazume strain were genetically very close to the Hirano strain and the Yoshimura strain was also very close to the Karp strain. Furthermore, the DNA sequences from the Irie and Tazume strains were completely homologous to the reported sequences of the Kawasaki and Kuroki strains, respectively.

[FLAIR images of cerebral and brain stem infarction].

FLAIR (fluid-attenuated inversion recovery) images are MR images obtained with an inversion recovery sequence having a long inversion time (TI) and a long echo time (TE). We examined 47 cases (56 graphics) of lacunar infarction (LI), 28 cases (32 graphics) of cortical infarction (CI) and 16 cases (23 graphics) of stem infarction (SI) with a FLAIR sequence having a repetitive time (TR) of 6500 msec, a TI of 1700 msec and a TE of 110 msec, and compared these graphics with T2-weighted images by spin-echo sequence (TR 2500 msec, TE 90 msec). LI and CI were better demonstrated with FLAIR images than with conventional T2-weighted images. FLAIR images were very useful in detecting lesions adjacent to the lateral ventricles and the cerebral sulci in particular, because the cerebrospinal fluid signals in the lateral ventricles and the cerebral sulci were low-intensity, with brain tissue appearing as high-intensity areas. In a number of old infarctions, FLAIR images revealed cystic structures, constructed out of internal low-intensity areas and peripheral high-intensity areas. These structural changes suggested that FLAIR images can provide information on pathological changes.

Proadrenomedullin N-terminal 20 peptide is rapidly cleaved by neutral endopeptidase.

Proadrenomedullin N-terminal 20 peptide (PAMP) is a novel hypotensive peptide which is processed from an adrenomedullin precursor. PAMP is rapidly cleaved by human neutral endopeptidase (NEP), a protease which plays a key role in the degradation of human atrial natriuretic peptide (ANP). A double reciprocal plot indicated that Km of NEP as a substrate of PAMP was 6.1 microM and V(max) was 3.1 mmol/min/mg of NEP. EDTA, phosphoramidon and thiorphan inhibit the proteolysis of PAMP by NEP. NEP cleaves at least 6 peptide bonds in human PAMP; Arg2-Leu3, Glu8-Phe9, Lys12-Trp13, Lys15-Trp16, Trp16-Ala17 and Ala17-Leu18. The present data suggest that NEP may be involved in the circulation control by degrading PAMP as well as ANP.

Genotypic identification of Rickettsia tsutsugamushi by restriction fragment length polymorphism analysis of DNA amplified by the polymerase chain reaction.

We combined the nested polymerase chain reaction and restriction fragment length polymorphism (PCR-RFLP) for genotypic identification of Rickettsia tsutsugamushi. Four primers were selected from the DNA sequence of the gene encoding a 56-kD serotype-specific antigen of the Karp strain. Nested PCR produced rickettsia-specific products of approximately 0.6 kb in the amplification of DNA prepared from three reference strains (Gilliam, Karp, and Kato) and two prototype strains (Irie and Hirano) prevalent in the Miyazaki Prefecture of Japan. When the nested PCR products obtained from these five strains were digested with Hha I, profiles specific to each strain were generated. Fourteen of 17 DNA samples of peripheral blood mononuclear cells from patients with scrub typhus tested positive in the nested-PCR, providing a rickettsia-specific band. The serotype of infected rickettsia of 10 patients were diagnosed as Irie and those of four patients were diagnosed as Hirano by indirect immunofluorescence methods. The fragment profiles of the PCR products of these 14 patients after digestion with Hha I corresponded closely with those serotypes. However, the PCR products from two of four samples, which were similar to Hirano strain by a serologic method and by the pattern of digestion with Hha I, produced different RFLP profiles upon further digestion with Hinf I and Alu I. These results may suggest that genetic variation exists within serotypes. Genotypic identification of R. tsutsugamushi by means of PCR-RFLP using three restriction enzymes is apparently useful.

Increased plasma adrenomedullin levels in chronic congestive heart failure.

Adrenomedullin is a potent vasodilator peptide and occurs in circulating blood of human beings and experimental animals. Because it is produced in intact aorta of rats and in cultured vascular endothelial cells, adrenomedullin seems to participate in regulation of local vascular tone. To determine the pathophysiological roles of adrenomedullin, we investigated its plasma concentrations in 49 patients with heart failure. Plasma adrenomedullin levels increased significantly with advancing severity of the disease (New York Heart Association functional class I, 4.1 +/- 1.0; II, 5.6 +/- 1.6; III, 6.4 +/- 0.8; IV, 13.2 +/- 6.8 (fmol/l). Plasma adrenomedullin was correlated with pulmonary artery pressure (r = 0.44, p = 0.0114) and pulmonary capillary wedge pressure (r = 0.53, p = 0.0002). These findings indicate that adrenomedullin may play some important role in the pathophysiologic makeup of heart failure by its vasodilating effects against the concomitant exaggeration of humor pressor agents such as catecholamine and the renin-angiotensin system. Hemodynamic changes in pulmonary circulation may have some influence on the increased synthesis and secretion of plasma adrenomedullin in chronic congestive heart failure.

Extramedullary plasmacytoma of the jejunum.

A case of extramedullary plasmacytoma (EMP) of the jejunum, an uncommon neoplasia, is reported. A 56-year-old Japanese woman who experienced intermittent upper abdominal pain and weight loss had a large movable mass in the upper abdomen. The mass was hypervascular in an angiographic study and positive for gallium-67 citrate scintigraphy. Immunoelectrophoresis showed the presence of an M-component of immunoglobulin (Ig) A-lambda in the serum. It was identified as an EMP immunohistochemically positive for IgA-lambda. This M-component disappeared after resection and chemotherapy. The clinical features of this rare neoplastic disorder are discussed.

Increased plasma adrenomedullin in acute myocardial infarction.

Adrenomedullin has a potent vasodilating effect comparable to that of calcitonin gene-related peptide. To investigate the pathophysiologic role of endogenous adrenomedullin, we determined sequentially the plasma adrenomedullin level in 15 consecutive patients with acute myocardial infarction (AMI). Plasma adrenomedullin was higher immediately after the onset of AMI and decreased gradually; plasma levels during the 3-week period after the AMI were higher than plasma levels in 15 healthy control subjects (p < 0.001), with higher levels in patients with congestive heart failure than in patients without congestive heart failure throughout the period of the study (p < 0.05). Plasma adrenomedullin was positively correlated with pulmonary capillary wedge pressure, pulmonary arterial pressure, right atrial pressure, and heart rate in the early stage of AMI. These findings suggest that the elevation of plasma adrenomedullin is related to the retention of body fluid volume, the enhancement of sympathetic activity, and/or the elevation of pressure in pulmonary vascular beds. Adrenomedullin may act against excessive vasoconstrictors increased in AMI.

Enhanced engraftment of HTLV-I-infected human T cells in severe combined immunodeficiency mice by anti-asialo GM-1 antibody treatment.

The effects of anti-asialo GM-1 antibody (AAGM) treatment on the engraftment of human T-cell leukemia virus type I (HTLV-I)-infected human T cells in severe combined immunodeficiency (SCID) mice were studied. The frequency of tumor formation in an HTLV-I-transformed human T-cell line, MT-2 cells, at the site of inoculation was significantly higher in AAGM-treated than untreated mice (P<0.05): 16/18 (89%) and 16/26 (62%), respectively. The promotive effect of AAGM treatment on tumor development was marked in the early stage (less than 3 weeks), suggesting that the immediate reaction of natural killers to the inoculated cells may be important for the prevention of tumor development. The surface phenotypes and clonality of the tumor cells were the same as the MT-2 cells inoculated. Inoculation of peripheral blood mononuclear cells (PBMC) from one of the 4 adult T-cell leukemia/lymphoma (ATL) patients resulted in the development of tumors in AAGM-treated SCID mice. However, the surface phenotypes of the cells from these tumors were a mixture of B cells and T cells, suggesting that these tumors consisted of Epstein-Barr virus-transformed B cells and HTLV-I-transformed T cells. In addition, HTLV-I was detected by polymerase chain reaction in various organs of the mice inoculated with PBMC from the ATL patient and the asymptomatic carrier examined. These results suggest that elimination of natural killer function by AAGM treatment is important, although such treatment is not always necessary for the engraftment of HTLV-I-infected cells in SCID mice.

Recovery from primary deep cerebral venous sinus thrombosis with recanalisation.

A 50-year-old woman with idiopathic deep cerebral sinus and vein thrombosis (DCVT) had cerebellar disturbance prior to impaired consciousness. CT and MRI revealed haemorrhagic infarction in the cerebellum and signal changes suggesting infarction in the thalamus and basal ganglia bilaterally. The straight sinus and internal cerebral vein (ICV) were dense on CT. On angiography, the vein of Galen (VG) and straight sinus were not seen. Following clinical recovery, CT and MRI became normal, and angiography showed recanalization of the VG and ICV. The relationship between cerebellar infarction and DCVT, and signal changes on CT and MRI are discussed.

Alteration of intracellular metabolite diffusion in rat brain in vivo during ischemia and reperfusion.

BACKGROUND AND PURPOSE: Diffusion-weighted MRI can demonstrate decreases of the apparent diffusion coefficient (ADC) of brain tissue water shortly after the onset of ischemia. To further elucidate underlying mechanisms, this study extended diffusion assessment to intracellular metabolites in rat brain in vivo before, during, and after ischemia. METHODS: Changes in molecular mobility were studied in a rat model of global forebrain ischemia (n = 8, 20-minute occlusion, 120-minute reperfusion) with the use of diffusion-weighted localized proton MR spectroscopy. During ischemia and early reperfusion the time course of ADC changes was monitored by strongly diffusion-weighted spectra. ADC values of N-acetylaspartate, creatines, cholines, and myo-inositol were evaluated from series of differently diffusion-weighted spectra before ischemia, 90 minutes after reperfusion, and 60 minutes postmortem. RESULTS: Parallel to a rise in diffusion-weighted water signal (133 +/- 20%), pertinent intensities of all brain metabolites increased during ischemia. Changes were most pronounced for myo-inositol (46 +/- 9%) and smallest for N-acetylaspartate (12 +/- 4%). During reperfusion water ADC values returned to basal values, whereas metabolite ADC values were decreased by 22% (after 40 minutes). Postmortem ADC values (after 60 minutes) were reduced by 46% for water and 38% for metabolites. CONCLUSIONS: The present findings indicate that water ADC changes during ischemic stroke are accompanied by significant alterations in intracellular mobility in both neuronal and glial cell populations as reflected by N-acetylaspartate and myo-inositol, respectively. Altered metabolite ADC values during reperfusion are consistent with irreversible tissue damage in this model and offer new means to assess circulatory and metabolic compromise.

Dynamic monitoring of cerebral metabolites during and after transient global ischemia in rats by quantitative proton NMR spectroscopy in vivo.

Localized proton NMR spectroscopy was used to dynamically monitor alterations of cerebral metabolites before, during, and after a 10 min period of global forebrain ischemia in anesthetized rats. Metabolic assessment was based on user-independent determination of absolute brain concentrations at a nominal temporal resolution of 1.6 min. While the concentrations of N-acetyl aspartate (neuronal marker), creatines, cholines, and myo-inositol (glial marker) remained constant, ischemia induced a rapid decline of brain glucose. One hour after reperfusion, glucose recovered to 4.1 +/- 2.2 mmol/kg wet weight significantly above the basal value of 2.3 +/- 1.3 mmol/kg wet weight. Mirroring glucose depletion, lactate increased from 1.0 +/- 0.6 to 13.5 +/- 1.5 mmol/kg wet weight 10-15 min after the onset of ischemia. During reperfusion lactate clearance was characterized by a first-order rate constant of 0.03/min. The time courses of glucose and lactate reflect the rapid onset of anaerobic glycolysis during states of critically diminished blood flow. Assuming complete ischemia the production of lactate from glucose and cerebral glycogen stores yields a brain glycogen concentration of 4.7 +/- 0.9 mmol glycosyl unit/kg wet weight. Elevation of brain glucose during early reperfusion suggests a transient mismatch of glucose uptake and consumption during the first 1-2 hours post ischemia.

[A case of Plasmodium ovale malaria with thrombocytopenia and an abnormality grade in FDP concentration despite the use of chloroquine as a malaria prophylaxis].

A 45-year-old Japanese male, who had been to the Central African Republic, was admitted to our hospital because of high fever with chills on July 29, 1994. He used chloroquine as a malaria prophylaxis during his stay and for 6 weeks after his return to Japan. On admission, Plasmodium ovale was detected in his blood smears and in the DNA analysis. He was treated successfully with chloroquine (1500 mg over 3 day period) and primaquine (15 mg/day for 14 days beginning day 4). Disappearance of malarial parasites in the peripheral blood smear occurred on the third day and his temperature returned to normal on the 4th day. Interestingly, he had thrombocytopenia and an abnormal grade in fibrin degradation products (FDP) concentration. This led to the suspicion of disseminated intravascular coagulation (DIC). This report indicates the importance of thrombocytopenia which may develop into DIC even though P. ovale malaria infection rarely becomes severe. This is the second report of a P. ovale malaria case in the Central African Republic.